Theodore A. Stern, MD

From SIG: E CAPS to CAGE and WWHHHHIMPS, mnemonics help practitioners and trainees recall important lists (such as criteria for depression, screening questions for alcoholism, or life-threatening causes of delirium, respectively). Mnemonics’ efficacy rests on the principle that grouped information is easier to remember than individual points of data.

Not everyone loves mnemonics, but recollecting diagnostic criteria is useful in clinical practice and research, on board examinations, and for insurance reimbursement. Thus, tools that assist in recalling diagnostic criteria have a role in psychiatric practice and teaching.

In this article, we present 32 mnemonics to help clinicians diagnose:

• affective disorders (Box 1)^1,2
• anxiety disorders (Box 2)^3-6
• medication adverse effects (Box 3)^7,8
• personality disorders (Box 4)^9-11
• addiction disorders (Box 5)^12,13
• causes of delirium (Box 6).¹⁴

We also discuss how mnemonics improve one’s memory, based on the principles of learning theory.

How mnemonics work

A mnemonic—from the Greek word “mnemonikos” (“of memory”)—links new data with previously learned information. Mnemonics assist in learning by reducing the amount of information (“cognitive load”) that needs to be stored for long-term processing and retrieval.¹⁵

Memory, defined as the “persistence of learning in a state that can be revealed at a later time,”¹⁶ can be divided into 2 types:

• declarative (a conscious recollection of facts, such as remembering a relative’s birthday)
• procedural (skills-based learning, such as riding a bicycle).

Declarative memory has a conscious component and may be mediated by the medial temporal lobe and cortical association structures. Procedural memory has less of a conscious component; it may involve the basal ganglia, cerebellum, and a variety of cortical sensory-perceptive regions.¹⁷

BOX 1.

Declarative memory can be subdivided into working memory and long-term memory.

With working memory, new items of information are held briefly so that encoding and eventual storage can take place.

Working memory guides decision-making and future planning and is intricately related to attention.^18-21 Functional MRI and positron emission tomography as well as neurocognitive testing have shown that working memory tasks activate the prefrontal cortex and brain regions specific to language and visuospatial memory.

The hippocampus is thought to rapidly absorb new information, and this data is consolidated and permanently stored via the prefrontal cortex.^22-26 Given the hippocampus’ limited storage capacity, new information (such as what you ate for breakfast 3 weeks ago) will disappear if it is not repeated regularly.¹⁷

Long-term memory, on the other hand, is encoded knowledge that is linked to facts learned in the past; it is consolidated in the brain and can be readily retrieved. Neuroimaging studies have demonstrated opposing patterns of activation in the hippocampus and prefrontal cortex, depending on whether the memory being recalled is:

• new (high hippocampal activity, low prefrontal cortex activity)
• old (low hippocampal activity, high prefrontal cortex activity).²⁷

Mnemonics are thought to affect working memory by reducing the introduced cognitive load and increasing the efficiency of memory acquisition and encoding. They reduce cognitive load by grouping objects into a single verbal or visual cue that can be introduced into working memory. Learning is optimized when the load on working memory is minimized, enabling long-term memory to be facilitated.²⁸

BOX 2.

BOX 3.

Mnemonics may use rhyme, music, or visual cues to enhance memory. Most mnemonics used in medical practice and education are word-based, including:

• Acronyms—words, each letter of which stands for a particular piece of information to be recalled (such as RICE for treatment of a sprained joint: rest, ice, compression, elevation).
• Acrostics—sentences with the first letter of each word prompting the desired recollection (such as “To Zanzibar by motor car” for the branches of the facial nerve: temporal, zygomatic, buccal, mandibular, cervical).
• Alphabetical sequences (such as ABCDE of trauma assessment: airway, breathing, circulation, disability, exposure).²⁹

An appropriate teaching tool?

Dozens of mnemonics addressing psychiatric diagnosis and treatment have been published, but relatively few are widely used. Psychiatric educators may resist teaching with mnemonics, believing they might erode a humanistic approach to patients by reducing psychopathology to “a laundry list” of symptoms and the art of psychiatric diagnosis to a “check-box” endeavor. Mnemonics that use humor may be rejected as irreverent or unprofessional.³⁰ Publishing a novel mnemonic may be viewed with disdain by some as an “easy” way of padding a curriculum vitae.

BOX 4.

Entire Web sites exist to share mnemonics for medical education (see Related Resources). Thus it is likely that trainees are using them with or without their teachers’ supervision. Psychiatric educators need to be aware of the mnemonics their trainees are using and to:

• screen these tools for factual errors (such as incomplete diagnostic criteria)
• remind trainees that although mnemonics are useful, psychiatrists should approach patients as individuals without the prejudice of a potentially pejorative label.

Our methodology

In preparing this article, we gathered numerous mnemonics (some published and some novel) designed to capture the learner’s attention and impart information pertinent to psychiatric diagnosis and treatment. Whenever possible, we credited each mnemonic to its creator, but—given the difficulty in confirming authorship of (what in many cases has become) oral history—we’ve listed some mnemonics without citation.

Our list is far from complete because we likely are unaware of many mnemonics, and we have excluded some that seemed obscure, unwieldy, or redundant. We have not excluded mnemonics that some may view as pejorative but merely report their existence. Including them does not mean that we endorse them.

This article lists 32 mnemonics related to psychiatric diagnosis. Thus, it seems odd that an informal survey of >60 residents at the Massachusetts General Hospital (MGH)/McLean Residency Training Program in Psychiatry revealed that most were aware of only 2 or 3 psychiatric mnemonics, typically:

• SIG: E CAPS (a tool to recall the criteria for depression)
• DIG FAST (a list of criteria for diagnosing mania)
• WWHHHHIMPS (a tool for recalling life-threatening causes of delirium).

Although this unscientific survey may be biased because faculty or trainees at MGH created the above 3 mnemonics, it nonetheless begs the question of what qualities make a mnemonic memorable.

Learning theory provides several clues. George Miller’s classic 1956 paper, “The magical number seven, plus or minus two: some limits on our capacity for processing information,” discussed the finding that 7 seems to be the upper limit of individual pieces of data that can be easily remembered.³¹ Research also has shown that recruiting the limbic system (potentially through the use of humor) aids in the recall of otherwise dry, cortical information.^32,33

Intuitively, it would seem that nonrepeating letters would facilitate the recall of the linked data, allowing each letter to provide a distinct cue, without any clouding by redundancy. Of the 3 most popular psychiatric mnemonics, however, only DIG FAST fits the learning theory. It contains 7 letters, repeats no letters, and has the limbic cue of allowing the learner to imagine a person with mania digging furiously.

BOX 5.

SIG: E CAPS falls within the range of 7 plus or minus 2, includes a limbic cue (although often forgotten, it refers to the prescription of energy capsules for depression), but repeats the letter S.

WWHHHHIMPS, with 10 letters, exceeds the recommended range, repeats the W (appearing twice) and the H (appearing 4 times), and provides no clear limbic cue.

BOX 6.

It may be that recruiting the limbic system provides the greatest likelihood of recall. Recruiting this system may add increased valence to a particular mnemonic for a specific individual, but this same limbic valence may limit its usefulness in a professional context.

Related resources

• Free searchable database of medical mnemonics. www.medicalmnemonics.com.
• Robinson DJ. Mnemonics and more for psychiatry. Port Huron, MI: Rapid Psychler Press, 2001.

From SIG: E CAPS to CAGE and WWHHHHIMPS, mnemonics help practitioners and trainees recall important lists (such as criteria for depression, screening questions for alcoholism, or life-threatening causes of delirium, respectively). Mnemonics’ efficacy rests on the principle that grouped information is easier to remember than individual points of data.

Not everyone loves mnemonics, but recollecting diagnostic criteria is useful in clinical practice and research, on board examinations, and for insurance reimbursement. Thus, tools that assist in recalling diagnostic criteria have a role in psychiatric practice and teaching.

In this article, we present 32 mnemonics to help clinicians diagnose:

• affective disorders (Box 1)^1,2
• anxiety disorders (Box 2)^3-6
• medication adverse effects (Box 3)^7,8
• personality disorders (Box 4)^9-11
• addiction disorders (Box 5)^12,13
• causes of delirium (Box 6).¹⁴

We also discuss how mnemonics improve one’s memory, based on the principles of learning theory.

How mnemonics work

A mnemonic—from the Greek word “mnemonikos” (“of memory”)—links new data with previously learned information. Mnemonics assist in learning by reducing the amount of information (“cognitive load”) that needs to be stored for long-term processing and retrieval.¹⁵

Memory, defined as the “persistence of learning in a state that can be revealed at a later time,”¹⁶ can be divided into 2 types:

• declarative (a conscious recollection of facts, such as remembering a relative’s birthday)
• procedural (skills-based learning, such as riding a bicycle).

Declarative memory has a conscious component and may be mediated by the medial temporal lobe and cortical association structures. Procedural memory has less of a conscious component; it may involve the basal ganglia, cerebellum, and a variety of cortical sensory-perceptive regions.¹⁷

BOX 1.

Declarative memory can be subdivided into working memory and long-term memory.

With working memory, new items of information are held briefly so that encoding and eventual storage can take place.

Working memory guides decision-making and future planning and is intricately related to attention.^18-21 Functional MRI and positron emission tomography as well as neurocognitive testing have shown that working memory tasks activate the prefrontal cortex and brain regions specific to language and visuospatial memory.

The hippocampus is thought to rapidly absorb new information, and this data is consolidated and permanently stored via the prefrontal cortex.^22-26 Given the hippocampus’ limited storage capacity, new information (such as what you ate for breakfast 3 weeks ago) will disappear if it is not repeated regularly.¹⁷

Long-term memory, on the other hand, is encoded knowledge that is linked to facts learned in the past; it is consolidated in the brain and can be readily retrieved. Neuroimaging studies have demonstrated opposing patterns of activation in the hippocampus and prefrontal cortex, depending on whether the memory being recalled is:

• new (high hippocampal activity, low prefrontal cortex activity)
• old (low hippocampal activity, high prefrontal cortex activity).²⁷

Mnemonics are thought to affect working memory by reducing the introduced cognitive load and increasing the efficiency of memory acquisition and encoding. They reduce cognitive load by grouping objects into a single verbal or visual cue that can be introduced into working memory. Learning is optimized when the load on working memory is minimized, enabling long-term memory to be facilitated.²⁸

BOX 2.

BOX 3.

Mnemonics may use rhyme, music, or visual cues to enhance memory. Most mnemonics used in medical practice and education are word-based, including:

• Acronyms—words, each letter of which stands for a particular piece of information to be recalled (such as RICE for treatment of a sprained joint: rest, ice, compression, elevation).
• Acrostics—sentences with the first letter of each word prompting the desired recollection (such as “To Zanzibar by motor car” for the branches of the facial nerve: temporal, zygomatic, buccal, mandibular, cervical).
• Alphabetical sequences (such as ABCDE of trauma assessment: airway, breathing, circulation, disability, exposure).²⁹

An appropriate teaching tool?

Dozens of mnemonics addressing psychiatric diagnosis and treatment have been published, but relatively few are widely used. Psychiatric educators may resist teaching with mnemonics, believing they might erode a humanistic approach to patients by reducing psychopathology to “a laundry list” of symptoms and the art of psychiatric diagnosis to a “check-box” endeavor. Mnemonics that use humor may be rejected as irreverent or unprofessional.³⁰ Publishing a novel mnemonic may be viewed with disdain by some as an “easy” way of padding a curriculum vitae.

BOX 4.

Entire Web sites exist to share mnemonics for medical education (see Related Resources). Thus it is likely that trainees are using them with or without their teachers’ supervision. Psychiatric educators need to be aware of the mnemonics their trainees are using and to:

• screen these tools for factual errors (such as incomplete diagnostic criteria)
• remind trainees that although mnemonics are useful, psychiatrists should approach patients as individuals without the prejudice of a potentially pejorative label.

Our methodology

In preparing this article, we gathered numerous mnemonics (some published and some novel) designed to capture the learner’s attention and impart information pertinent to psychiatric diagnosis and treatment. Whenever possible, we credited each mnemonic to its creator, but—given the difficulty in confirming authorship of (what in many cases has become) oral history—we’ve listed some mnemonics without citation.

Our list is far from complete because we likely are unaware of many mnemonics, and we have excluded some that seemed obscure, unwieldy, or redundant. We have not excluded mnemonics that some may view as pejorative but merely report their existence. Including them does not mean that we endorse them.

This article lists 32 mnemonics related to psychiatric diagnosis. Thus, it seems odd that an informal survey of >60 residents at the Massachusetts General Hospital (MGH)/McLean Residency Training Program in Psychiatry revealed that most were aware of only 2 or 3 psychiatric mnemonics, typically:

• SIG: E CAPS (a tool to recall the criteria for depression)
• DIG FAST (a list of criteria for diagnosing mania)
• WWHHHHIMPS (a tool for recalling life-threatening causes of delirium).

Although this unscientific survey may be biased because faculty or trainees at MGH created the above 3 mnemonics, it nonetheless begs the question of what qualities make a mnemonic memorable.

Learning theory provides several clues. George Miller’s classic 1956 paper, “The magical number seven, plus or minus two: some limits on our capacity for processing information,” discussed the finding that 7 seems to be the upper limit of individual pieces of data that can be easily remembered.³¹ Research also has shown that recruiting the limbic system (potentially through the use of humor) aids in the recall of otherwise dry, cortical information.^32,33

Intuitively, it would seem that nonrepeating letters would facilitate the recall of the linked data, allowing each letter to provide a distinct cue, without any clouding by redundancy. Of the 3 most popular psychiatric mnemonics, however, only DIG FAST fits the learning theory. It contains 7 letters, repeats no letters, and has the limbic cue of allowing the learner to imagine a person with mania digging furiously.

BOX 5.

SIG: E CAPS falls within the range of 7 plus or minus 2, includes a limbic cue (although often forgotten, it refers to the prescription of energy capsules for depression), but repeats the letter S.

WWHHHHIMPS, with 10 letters, exceeds the recommended range, repeats the W (appearing twice) and the H (appearing 4 times), and provides no clear limbic cue.

BOX 6.

It may be that recruiting the limbic system provides the greatest likelihood of recall. Recruiting this system may add increased valence to a particular mnemonic for a specific individual, but this same limbic valence may limit its usefulness in a professional context.

Related resources

• Free searchable database of medical mnemonics. www.medicalmnemonics.com.
• Robinson DJ. Mnemonics and more for psychiatry. Port Huron, MI: Rapid Psychler Press, 2001.

From SIG: E CAPS to CAGE and WWHHHHIMPS, mnemonics help practitioners and trainees recall important lists (such as criteria for depression, screening questions for alcoholism, or life-threatening causes of delirium, respectively). Mnemonics’ efficacy rests on the principle that grouped information is easier to remember than individual points of data.

Not everyone loves mnemonics, but recollecting diagnostic criteria is useful in clinical practice and research, on board examinations, and for insurance reimbursement. Thus, tools that assist in recalling diagnostic criteria have a role in psychiatric practice and teaching.

In this article, we present 32 mnemonics to help clinicians diagnose:

• affective disorders (Box 1)^1,2
• anxiety disorders (Box 2)^3-6
• medication adverse effects (Box 3)^7,8
• personality disorders (Box 4)^9-11
• addiction disorders (Box 5)^12,13
• causes of delirium (Box 6).¹⁴

We also discuss how mnemonics improve one’s memory, based on the principles of learning theory.

How mnemonics work

A mnemonic—from the Greek word “mnemonikos” (“of memory”)—links new data with previously learned information. Mnemonics assist in learning by reducing the amount of information (“cognitive load”) that needs to be stored for long-term processing and retrieval.¹⁵

Memory, defined as the “persistence of learning in a state that can be revealed at a later time,”¹⁶ can be divided into 2 types:

• declarative (a conscious recollection of facts, such as remembering a relative’s birthday)
• procedural (skills-based learning, such as riding a bicycle).

Declarative memory has a conscious component and may be mediated by the medial temporal lobe and cortical association structures. Procedural memory has less of a conscious component; it may involve the basal ganglia, cerebellum, and a variety of cortical sensory-perceptive regions.¹⁷

BOX 1.

Declarative memory can be subdivided into working memory and long-term memory.

With working memory, new items of information are held briefly so that encoding and eventual storage can take place.

Working memory guides decision-making and future planning and is intricately related to attention.^18-21 Functional MRI and positron emission tomography as well as neurocognitive testing have shown that working memory tasks activate the prefrontal cortex and brain regions specific to language and visuospatial memory.

The hippocampus is thought to rapidly absorb new information, and this data is consolidated and permanently stored via the prefrontal cortex.^22-26 Given the hippocampus’ limited storage capacity, new information (such as what you ate for breakfast 3 weeks ago) will disappear if it is not repeated regularly.¹⁷

Long-term memory, on the other hand, is encoded knowledge that is linked to facts learned in the past; it is consolidated in the brain and can be readily retrieved. Neuroimaging studies have demonstrated opposing patterns of activation in the hippocampus and prefrontal cortex, depending on whether the memory being recalled is:

• new (high hippocampal activity, low prefrontal cortex activity)
• old (low hippocampal activity, high prefrontal cortex activity).²⁷

Mnemonics are thought to affect working memory by reducing the introduced cognitive load and increasing the efficiency of memory acquisition and encoding. They reduce cognitive load by grouping objects into a single verbal or visual cue that can be introduced into working memory. Learning is optimized when the load on working memory is minimized, enabling long-term memory to be facilitated.²⁸

BOX 2.

BOX 3.

Mnemonics may use rhyme, music, or visual cues to enhance memory. Most mnemonics used in medical practice and education are word-based, including:

• Acronyms—words, each letter of which stands for a particular piece of information to be recalled (such as RICE for treatment of a sprained joint: rest, ice, compression, elevation).
• Acrostics—sentences with the first letter of each word prompting the desired recollection (such as “To Zanzibar by motor car” for the branches of the facial nerve: temporal, zygomatic, buccal, mandibular, cervical).
• Alphabetical sequences (such as ABCDE of trauma assessment: airway, breathing, circulation, disability, exposure).²⁹

An appropriate teaching tool?

Dozens of mnemonics addressing psychiatric diagnosis and treatment have been published, but relatively few are widely used. Psychiatric educators may resist teaching with mnemonics, believing they might erode a humanistic approach to patients by reducing psychopathology to “a laundry list” of symptoms and the art of psychiatric diagnosis to a “check-box” endeavor. Mnemonics that use humor may be rejected as irreverent or unprofessional.³⁰ Publishing a novel mnemonic may be viewed with disdain by some as an “easy” way of padding a curriculum vitae.

BOX 4.

Entire Web sites exist to share mnemonics for medical education (see Related Resources). Thus it is likely that trainees are using them with or without their teachers’ supervision. Psychiatric educators need to be aware of the mnemonics their trainees are using and to:

• screen these tools for factual errors (such as incomplete diagnostic criteria)
• remind trainees that although mnemonics are useful, psychiatrists should approach patients as individuals without the prejudice of a potentially pejorative label.

Our methodology

In preparing this article, we gathered numerous mnemonics (some published and some novel) designed to capture the learner’s attention and impart information pertinent to psychiatric diagnosis and treatment. Whenever possible, we credited each mnemonic to its creator, but—given the difficulty in confirming authorship of (what in many cases has become) oral history—we’ve listed some mnemonics without citation.

Our list is far from complete because we likely are unaware of many mnemonics, and we have excluded some that seemed obscure, unwieldy, or redundant. We have not excluded mnemonics that some may view as pejorative but merely report their existence. Including them does not mean that we endorse them.

This article lists 32 mnemonics related to psychiatric diagnosis. Thus, it seems odd that an informal survey of >60 residents at the Massachusetts General Hospital (MGH)/McLean Residency Training Program in Psychiatry revealed that most were aware of only 2 or 3 psychiatric mnemonics, typically:

• SIG: E CAPS (a tool to recall the criteria for depression)
• DIG FAST (a list of criteria for diagnosing mania)
• WWHHHHIMPS (a tool for recalling life-threatening causes of delirium).

Although this unscientific survey may be biased because faculty or trainees at MGH created the above 3 mnemonics, it nonetheless begs the question of what qualities make a mnemonic memorable.

Learning theory provides several clues. George Miller’s classic 1956 paper, “The magical number seven, plus or minus two: some limits on our capacity for processing information,” discussed the finding that 7 seems to be the upper limit of individual pieces of data that can be easily remembered.³¹ Research also has shown that recruiting the limbic system (potentially through the use of humor) aids in the recall of otherwise dry, cortical information.^32,33

Intuitively, it would seem that nonrepeating letters would facilitate the recall of the linked data, allowing each letter to provide a distinct cue, without any clouding by redundancy. Of the 3 most popular psychiatric mnemonics, however, only DIG FAST fits the learning theory. It contains 7 letters, repeats no letters, and has the limbic cue of allowing the learner to imagine a person with mania digging furiously.

BOX 5.

SIG: E CAPS falls within the range of 7 plus or minus 2, includes a limbic cue (although often forgotten, it refers to the prescription of energy capsules for depression), but repeats the letter S.

WWHHHHIMPS, with 10 letters, exceeds the recommended range, repeats the W (appearing twice) and the H (appearing 4 times), and provides no clear limbic cue.

BOX 6.

It may be that recruiting the limbic system provides the greatest likelihood of recall. Recruiting this system may add increased valence to a particular mnemonic for a specific individual, but this same limbic valence may limit its usefulness in a professional context.

Related resources

• Free searchable database of medical mnemonics. www.medicalmnemonics.com.
• Robinson DJ. Mnemonics and more for psychiatry. Port Huron, MI: Rapid Psychler Press, 2001.

Ms. J, age 33, arrives at the emergency department (ED) complaining of chest pain and shortness of breath—symptoms she says are similar to those she had during episodes of pulmonary embolism. Routine laboratory workup, including chest CT and ultrasound of the lower extremities, indicate a very low likelihood of PE, but she insists that she be admitted.

On the medical floor, nursing staff note that Ms. J appears short of breath only when directly observed. Medical records reveal multiple visits to other hospitals with repeated requests for admission. When gently confronted, she maintains she will die
if she is not treated.

Has your hospital’s medical staff ever been puzzled by a patient’s inconsistent presentation or unsettled by a concern that he or she was not being straightforward with them? Have they suspected that a patient such as Ms. J may be voluntarily producing his or her symptoms?

This article suggests a 3-step approach by which the consultation-liaison psychiatrist can help medical staff identify and manage patients with factitious illness.

Cardinal features

In factitious illness, the patient’s symptoms are:

• under voluntary control and consciously produced
  
• not a direct result of a medical or psychiatric condition
  
• produced to assume the sick role (not to accrue secondary gain—a core feature of malingering).
  

CASE: Self-inflicted injury

Ms. H, age 50, surprises even the most seasoned clinicians when she presents to the ED with brain parenchyma herniating from an open wound in her skull. She denies having picked at her scalp and does not endorse a history of obsessive-compulsive disorder or trichotillomania.

On the medical floor, however, she is seen picking at the wound, which leaves blood on her protective mittens. Surgical repair is repeatedly attempted, and her case is complicated by chronic infections and a nonhealing wound.

Clinical presentation

Factitious disorder presents 3 diagnostic and treatment challenges for a hospital’s medical staff:

• To recognize and treat (even self-inflicted) serious medical conditions that can be life-threatening.
  
• To orchestrate appropriate diagnostic evaluation. (Remember that factitious illness is a diagnosis of exclusion.)
  
• To handle countertransference reactions to patients that can be intense; physicians may experience anger, frustration, resignation, and hatred.
  

CASE: ‘Suicidal’ but not depressed

Mr. B, age 48, presents to the ED with thoughts of suicide and profoundly depressed mood. On examination, however, he does not appear depressed. He repeatedly requests food, cigarettes, and assistance in finding shelter, which lead to concern that his main goal is secondary gain. However, because Mr. B has a history of serious suicide attempts—including some while an inpatient—the ED physician is reluctant to dismiss his complaints and unsure about how to proceed.

3-step diagnostic approach

Treating factitious illness is predicated upon making the correct diagnosis, which requires the medical team to investigate and gather data from collateral sources, such as outside hospital medical records and other providers. The diagnostic process can be summarized in 3 steps:

Step 1. Determine whether the patient has an identifiable medical or psychiatric problem that could explain the symptoms.

Step 2. Determine whether the symptoms are consciously or unconsciously produced. Somatoform disorders—such as conversion disorder and somatization disorder, for example—are thought to result from processes outside the patient’s control.

Step 3. Distinguish if the motivation is to obtain the sick role (consider factitious illness) or if material benefits are the goal (consider malingering). Both motivations may be operative in a given patient.

Table 1

Medical clues to a patient with factitious illness

• a patient’s behavior is notably different when he believes he is being directly observed and when he believes he is alone³
  
• psychiatric symptoms do not readily fit into diagnostic categories (such as a vague mix of memory loss, suicidal thoughts, and psychosis)
  
• the patient is suggestible or provides a diffusely positive review of systems (for example, he may report additional symptoms after having observed other patients).
  

The psychiatric presentations of Munchausen syndrome can be especially complicated, as they are usually associated with less objective evidence than are medical presentations (Box).^4-10 Clarity of the history and diagnosis may be in the eye of the beholder.

Admission characteristics

Somatic complaints. Chaos often surrounds the hospitalized patient with factitious illness. The ED commonly is their gateway, and they tend to arrive in the evening or on weekends when less experienced staff are on call.¹¹

Box

Escalating demands. During the hospital stay, patients with factitious illness may make repeated requests for care, which may escalate into demands if their needs are not met.¹³ At this point, staff often start to experience negative countertransference reactions. As medical tests reveal little to no evidence of an organic basis for their symptoms and no cohesive psychiatric diagnosis is reached, patients may complain of misdiagnosis and mistreatment.¹³

Patients usually leave before psychiatric consultation can be obtained, and the underlying suffering that led to their factitious complaints remains unaddressed. Typically, patients are lost to follow-up until the next presentation at another hospital, where the process begins again.

What motivates patients?

The motivation behind factitious presentations can be bewildering. Asher’s paper on Munchausen syndrome described several possible reasons for patients’ behavior, such as desire to be the center of attention, holding a grudge against the medical profession, drug seeking, looking for shelter, and running from police.⁵ This list, however, includes correlates of secondary gain, which with today’s psychiatric nomenclature would lead to a diagnosis of malingering.

Psychological factors. Some clinicians have tried to address underlying psychiatric factors, but data on evaluation and management are limited because these patients usually eschew psychiatric examination. Although the patient is voluntarily producing the symptoms, unconscious psychological factors are at play and are an essential part of the picture.¹⁴

When assessed, patients appear to have lived rootless lives with few attachments, which may have been the result of sadistic and unsatisfying relationships with authority figures of their youth.^15,16 Their grandiosity and distortion of the truth suggest a narcissistic need to overcome feelings of incompetence or impotence.¹⁷ Their ambivalent relationship to hospitals and physicians may reflect a need for caretaking, arising from early relationships and past caretakers.

Lastly, there is a component of masochism; this makes some individuals (erroneously) believe that if you don’t inflict pain you don’t care about them.¹³

Treatment challenges

Because patients with factitious disorder are not easily studied, no particular treatment is well-supported in the literature. Approaches that have been reported include preventing patients from being re-admitted to medical facilities, admitting patients for psychiatric treatment, and providing outpatient therapies such as individual psychodynamic psychotherapy, behavioral modification, and group psychotherapy.¹⁸

Other management strategies suggested in the literature include:

• reframing cognitive distortions
  
• drawing up a set of realistic hospitalization goals (with a written contract)
  
• maximizing the therapeutic alliance
  
• avoiding team splitting
  
• minimizing iatrogenic harm.¹⁹
  

Table 2

Recommended care for a patient with factitious illness

Nevertheless, prepare the physician for the patient to respond to confrontation with denial and resistance because he or she feels exposed and humiliated. If the physician makes it clear that ongoing medical care will still be available—even if the symptoms are fabricated—the patient may be more willing to accept psychiatric treatment.¹³

Related resources

• Barsky AJ, Stern TA, Greenberg DB, Cassem NH. Functional somatic symptoms and somatoform disorders. In: Stern TA, Fricchione GL, Cassem NH, et al, eds. The Massachusetts General Hospital handbook of general hospital psychiatry 5th ed. Philadelphia: Mosby/Elsevier; 2004:269-91.
  
• Elwyn TS, Ahmed I. Factitious disorder. EMedicine from WebMD. Last updated April 13, 2006. www.emedicine.com/med/topic3125.htm.
  

Ms. J, age 33, arrives at the emergency department (ED) complaining of chest pain and shortness of breath—symptoms she says are similar to those she had during episodes of pulmonary embolism. Routine laboratory workup, including chest CT and ultrasound of the lower extremities, indicate a very low likelihood of PE, but she insists that she be admitted.

On the medical floor, nursing staff note that Ms. J appears short of breath only when directly observed. Medical records reveal multiple visits to other hospitals with repeated requests for admission. When gently confronted, she maintains she will die
if she is not treated.

Has your hospital’s medical staff ever been puzzled by a patient’s inconsistent presentation or unsettled by a concern that he or she was not being straightforward with them? Have they suspected that a patient such as Ms. J may be voluntarily producing his or her symptoms?

This article suggests a 3-step approach by which the consultation-liaison psychiatrist can help medical staff identify and manage patients with factitious illness.

Cardinal features

In factitious illness, the patient’s symptoms are:

• under voluntary control and consciously produced
  
• not a direct result of a medical or psychiatric condition
  
• produced to assume the sick role (not to accrue secondary gain—a core feature of malingering).
  

CASE: Self-inflicted injury

Ms. H, age 50, surprises even the most seasoned clinicians when she presents to the ED with brain parenchyma herniating from an open wound in her skull. She denies having picked at her scalp and does not endorse a history of obsessive-compulsive disorder or trichotillomania.

On the medical floor, however, she is seen picking at the wound, which leaves blood on her protective mittens. Surgical repair is repeatedly attempted, and her case is complicated by chronic infections and a nonhealing wound.

Clinical presentation

Factitious disorder presents 3 diagnostic and treatment challenges for a hospital’s medical staff:

• To recognize and treat (even self-inflicted) serious medical conditions that can be life-threatening.
  
• To orchestrate appropriate diagnostic evaluation. (Remember that factitious illness is a diagnosis of exclusion.)
  
• To handle countertransference reactions to patients that can be intense; physicians may experience anger, frustration, resignation, and hatred.
  

CASE: ‘Suicidal’ but not depressed

Mr. B, age 48, presents to the ED with thoughts of suicide and profoundly depressed mood. On examination, however, he does not appear depressed. He repeatedly requests food, cigarettes, and assistance in finding shelter, which lead to concern that his main goal is secondary gain. However, because Mr. B has a history of serious suicide attempts—including some while an inpatient—the ED physician is reluctant to dismiss his complaints and unsure about how to proceed.

3-step diagnostic approach

Treating factitious illness is predicated upon making the correct diagnosis, which requires the medical team to investigate and gather data from collateral sources, such as outside hospital medical records and other providers. The diagnostic process can be summarized in 3 steps:

Step 1. Determine whether the patient has an identifiable medical or psychiatric problem that could explain the symptoms.

Step 2. Determine whether the symptoms are consciously or unconsciously produced. Somatoform disorders—such as conversion disorder and somatization disorder, for example—are thought to result from processes outside the patient’s control.

Step 3. Distinguish if the motivation is to obtain the sick role (consider factitious illness) or if material benefits are the goal (consider malingering). Both motivations may be operative in a given patient.

Table 1

Medical clues to a patient with factitious illness

• a patient’s behavior is notably different when he believes he is being directly observed and when he believes he is alone³
  
• psychiatric symptoms do not readily fit into diagnostic categories (such as a vague mix of memory loss, suicidal thoughts, and psychosis)
  
• the patient is suggestible or provides a diffusely positive review of systems (for example, he may report additional symptoms after having observed other patients).
  

The psychiatric presentations of Munchausen syndrome can be especially complicated, as they are usually associated with less objective evidence than are medical presentations (Box).^4-10 Clarity of the history and diagnosis may be in the eye of the beholder.

Admission characteristics

Somatic complaints. Chaos often surrounds the hospitalized patient with factitious illness. The ED commonly is their gateway, and they tend to arrive in the evening or on weekends when less experienced staff are on call.¹¹

Box

Escalating demands. During the hospital stay, patients with factitious illness may make repeated requests for care, which may escalate into demands if their needs are not met.¹³ At this point, staff often start to experience negative countertransference reactions. As medical tests reveal little to no evidence of an organic basis for their symptoms and no cohesive psychiatric diagnosis is reached, patients may complain of misdiagnosis and mistreatment.¹³

Patients usually leave before psychiatric consultation can be obtained, and the underlying suffering that led to their factitious complaints remains unaddressed. Typically, patients are lost to follow-up until the next presentation at another hospital, where the process begins again.

What motivates patients?

The motivation behind factitious presentations can be bewildering. Asher’s paper on Munchausen syndrome described several possible reasons for patients’ behavior, such as desire to be the center of attention, holding a grudge against the medical profession, drug seeking, looking for shelter, and running from police.⁵ This list, however, includes correlates of secondary gain, which with today’s psychiatric nomenclature would lead to a diagnosis of malingering.

Psychological factors. Some clinicians have tried to address underlying psychiatric factors, but data on evaluation and management are limited because these patients usually eschew psychiatric examination. Although the patient is voluntarily producing the symptoms, unconscious psychological factors are at play and are an essential part of the picture.¹⁴

When assessed, patients appear to have lived rootless lives with few attachments, which may have been the result of sadistic and unsatisfying relationships with authority figures of their youth.^15,16 Their grandiosity and distortion of the truth suggest a narcissistic need to overcome feelings of incompetence or impotence.¹⁷ Their ambivalent relationship to hospitals and physicians may reflect a need for caretaking, arising from early relationships and past caretakers.

Lastly, there is a component of masochism; this makes some individuals (erroneously) believe that if you don’t inflict pain you don’t care about them.¹³

Treatment challenges

Because patients with factitious disorder are not easily studied, no particular treatment is well-supported in the literature. Approaches that have been reported include preventing patients from being re-admitted to medical facilities, admitting patients for psychiatric treatment, and providing outpatient therapies such as individual psychodynamic psychotherapy, behavioral modification, and group psychotherapy.¹⁸

Other management strategies suggested in the literature include:

• reframing cognitive distortions
  
• drawing up a set of realistic hospitalization goals (with a written contract)
  
• maximizing the therapeutic alliance
  
• avoiding team splitting
  
• minimizing iatrogenic harm.¹⁹
  

Table 2

Recommended care for a patient with factitious illness

Nevertheless, prepare the physician for the patient to respond to confrontation with denial and resistance because he or she feels exposed and humiliated. If the physician makes it clear that ongoing medical care will still be available—even if the symptoms are fabricated—the patient may be more willing to accept psychiatric treatment.¹³

Related resources

• Barsky AJ, Stern TA, Greenberg DB, Cassem NH. Functional somatic symptoms and somatoform disorders. In: Stern TA, Fricchione GL, Cassem NH, et al, eds. The Massachusetts General Hospital handbook of general hospital psychiatry 5th ed. Philadelphia: Mosby/Elsevier; 2004:269-91.
  
• Elwyn TS, Ahmed I. Factitious disorder. EMedicine from WebMD. Last updated April 13, 2006. www.emedicine.com/med/topic3125.htm.
  

Ms. J, age 33, arrives at the emergency department (ED) complaining of chest pain and shortness of breath—symptoms she says are similar to those she had during episodes of pulmonary embolism. Routine laboratory workup, including chest CT and ultrasound of the lower extremities, indicate a very low likelihood of PE, but she insists that she be admitted.

On the medical floor, nursing staff note that Ms. J appears short of breath only when directly observed. Medical records reveal multiple visits to other hospitals with repeated requests for admission. When gently confronted, she maintains she will die
if she is not treated.

Has your hospital’s medical staff ever been puzzled by a patient’s inconsistent presentation or unsettled by a concern that he or she was not being straightforward with them? Have they suspected that a patient such as Ms. J may be voluntarily producing his or her symptoms?

This article suggests a 3-step approach by which the consultation-liaison psychiatrist can help medical staff identify and manage patients with factitious illness.

Cardinal features

In factitious illness, the patient’s symptoms are:

• under voluntary control and consciously produced
  
• not a direct result of a medical or psychiatric condition
  
• produced to assume the sick role (not to accrue secondary gain—a core feature of malingering).
  

CASE: Self-inflicted injury

Ms. H, age 50, surprises even the most seasoned clinicians when she presents to the ED with brain parenchyma herniating from an open wound in her skull. She denies having picked at her scalp and does not endorse a history of obsessive-compulsive disorder or trichotillomania.

On the medical floor, however, she is seen picking at the wound, which leaves blood on her protective mittens. Surgical repair is repeatedly attempted, and her case is complicated by chronic infections and a nonhealing wound.

Clinical presentation

Factitious disorder presents 3 diagnostic and treatment challenges for a hospital’s medical staff:

• To recognize and treat (even self-inflicted) serious medical conditions that can be life-threatening.
  
• To orchestrate appropriate diagnostic evaluation. (Remember that factitious illness is a diagnosis of exclusion.)
  
• To handle countertransference reactions to patients that can be intense; physicians may experience anger, frustration, resignation, and hatred.
  

CASE: ‘Suicidal’ but not depressed

Mr. B, age 48, presents to the ED with thoughts of suicide and profoundly depressed mood. On examination, however, he does not appear depressed. He repeatedly requests food, cigarettes, and assistance in finding shelter, which lead to concern that his main goal is secondary gain. However, because Mr. B has a history of serious suicide attempts—including some while an inpatient—the ED physician is reluctant to dismiss his complaints and unsure about how to proceed.

3-step diagnostic approach

Treating factitious illness is predicated upon making the correct diagnosis, which requires the medical team to investigate and gather data from collateral sources, such as outside hospital medical records and other providers. The diagnostic process can be summarized in 3 steps:

Step 1. Determine whether the patient has an identifiable medical or psychiatric problem that could explain the symptoms.

Step 2. Determine whether the symptoms are consciously or unconsciously produced. Somatoform disorders—such as conversion disorder and somatization disorder, for example—are thought to result from processes outside the patient’s control.

Step 3. Distinguish if the motivation is to obtain the sick role (consider factitious illness) or if material benefits are the goal (consider malingering). Both motivations may be operative in a given patient.

Table 1

Medical clues to a patient with factitious illness

• a patient’s behavior is notably different when he believes he is being directly observed and when he believes he is alone³
  
• psychiatric symptoms do not readily fit into diagnostic categories (such as a vague mix of memory loss, suicidal thoughts, and psychosis)
  
• the patient is suggestible or provides a diffusely positive review of systems (for example, he may report additional symptoms after having observed other patients).
  

The psychiatric presentations of Munchausen syndrome can be especially complicated, as they are usually associated with less objective evidence than are medical presentations (Box).^4-10 Clarity of the history and diagnosis may be in the eye of the beholder.

Admission characteristics

Somatic complaints. Chaos often surrounds the hospitalized patient with factitious illness. The ED commonly is their gateway, and they tend to arrive in the evening or on weekends when less experienced staff are on call.¹¹

Box

Escalating demands. During the hospital stay, patients with factitious illness may make repeated requests for care, which may escalate into demands if their needs are not met.¹³ At this point, staff often start to experience negative countertransference reactions. As medical tests reveal little to no evidence of an organic basis for their symptoms and no cohesive psychiatric diagnosis is reached, patients may complain of misdiagnosis and mistreatment.¹³

Patients usually leave before psychiatric consultation can be obtained, and the underlying suffering that led to their factitious complaints remains unaddressed. Typically, patients are lost to follow-up until the next presentation at another hospital, where the process begins again.

What motivates patients?

The motivation behind factitious presentations can be bewildering. Asher’s paper on Munchausen syndrome described several possible reasons for patients’ behavior, such as desire to be the center of attention, holding a grudge against the medical profession, drug seeking, looking for shelter, and running from police.⁵ This list, however, includes correlates of secondary gain, which with today’s psychiatric nomenclature would lead to a diagnosis of malingering.

Psychological factors. Some clinicians have tried to address underlying psychiatric factors, but data on evaluation and management are limited because these patients usually eschew psychiatric examination. Although the patient is voluntarily producing the symptoms, unconscious psychological factors are at play and are an essential part of the picture.¹⁴

When assessed, patients appear to have lived rootless lives with few attachments, which may have been the result of sadistic and unsatisfying relationships with authority figures of their youth.^15,16 Their grandiosity and distortion of the truth suggest a narcissistic need to overcome feelings of incompetence or impotence.¹⁷ Their ambivalent relationship to hospitals and physicians may reflect a need for caretaking, arising from early relationships and past caretakers.

Lastly, there is a component of masochism; this makes some individuals (erroneously) believe that if you don’t inflict pain you don’t care about them.¹³

Treatment challenges

Because patients with factitious disorder are not easily studied, no particular treatment is well-supported in the literature. Approaches that have been reported include preventing patients from being re-admitted to medical facilities, admitting patients for psychiatric treatment, and providing outpatient therapies such as individual psychodynamic psychotherapy, behavioral modification, and group psychotherapy.¹⁸

Other management strategies suggested in the literature include:

• reframing cognitive distortions
  
• drawing up a set of realistic hospitalization goals (with a written contract)
  
• maximizing the therapeutic alliance
  
• avoiding team splitting
  
• minimizing iatrogenic harm.¹⁹
  

Table 2

Recommended care for a patient with factitious illness

Nevertheless, prepare the physician for the patient to respond to confrontation with denial and resistance because he or she feels exposed and humiliated. If the physician makes it clear that ongoing medical care will still be available—even if the symptoms are fabricated—the patient may be more willing to accept psychiatric treatment.¹³

Related resources

• Barsky AJ, Stern TA, Greenberg DB, Cassem NH. Functional somatic symptoms and somatoform disorders. In: Stern TA, Fricchione GL, Cassem NH, et al, eds. The Massachusetts General Hospital handbook of general hospital psychiatry 5th ed. Philadelphia: Mosby/Elsevier; 2004:269-91.
  
• Elwyn TS, Ahmed I. Factitious disorder. EMedicine from WebMD. Last updated April 13, 2006. www.emedicine.com/med/topic3125.htm.
  

Medical history

• No other significant medical or psychiatric problems
• Married, with 2 teenaged children
• Employed as an administrator for an insurance company (>50 hrs/wk)
• Drinks 3 to 4 alcoholic beverages/wk
• Does not smoke
• Enjoys fishing and other outdoor activities
• Both parents had hypertension; father also had peripheral vascular disease

Examination

• Patient is in no acute distress
• Approximately 30 pounds over ideal body weight
• Other vital signs are normal
• Normal retinal examination, no carotid bruits, and clear lungs. Cardiac rate and rhythm are regular; no abdominal bruits
• Laboratory studies reveal normal renal function; cholesterol, 184 mg/dL; low-density lipoprotein (LDL) cholesterol, 129 mg/dL; high-density lipoprotein (HDL) cholesterol, 55 mg/dL; triglycerides, 163 mg/dL. Electrocardiogram shows no current or prior evidence of ischemia or left-ventricular strain.

Additional information is required in a number of domains. Blood pressure readings should be repeated to make an accurate diagnosis of hypertension. While the patient may have hypertension, only a single blood pressure reading is elevated. The Joint National Committee on Blood Pressure (JNC 7) specifications¹ state that 2 such readings on different days are needed to confirm a diagnosis of hypertension. The symptoms of claudication should be investigated. Physical examination should focus on auscultation for bruits and on the examination of eye grounds to further investigate the possibility of peripheral vascular disease (PVD). In addition, a lipid profile should be drawn. While guidelines are conflicting, consideration should be given to assessing a fasting glucose, potassium, and renal function. Other tests, such as a C-reactive protein, are more controversial.²

The patient opts for drug treatment of his hypertension, and begins taking atenolol 50 mg/d (in addition to aspirin 81 mg/d). He is scheduled to follow-up by phone in 1 week to assure compliance and in 3 months in the office.

On further questioning he reports that he initially tolerated the beta-blocker without problem, but more recently has experienced low energy and poor sleep (with early morning awakening); he acknowledges decreases in libido, interest in pleasurable activities (eg, hunting, fishing), and his ability to concentrate. He has gained 5 to 10 pounds in the last month.

Although he denies feeling “sad,” he says his emotions seem “flat.” He denies having thoughts of suicide, increased anxiety, symptoms of hypomania, or psychotic symptoms. He describes a mild increase in stress at work, and he feels that the process of preparing for his son to go to college had been “a big burden.” He says there are no other stressors.

The patient’s alcohol use has not changed significantly, and he reports being compliant with his new medication regimen.

When his father died 6 years earlier, he experienced similar symptoms; at no other time have such symptoms occurred. The patient reports no other new physical symptoms, and his physical examination is essentially unchanged from the exam conducted 3 months earlier. His vital signs are normal, including a blood pressure of 128/84 mm Hg.

Consider the differential diagnosis of the patient’s abnormal mood and neurovegetative symptoms. In the primary care setting, the differential diagnosis of depressed mood is broad (Table 1 ), including medical disorders and a variety of psychiatric syndromes.

Medical conditions to consider include a medication induced side effect, hypothyroidism (a metabolic masquerader of depression), anemia, sleep disorder (eg, sleep apnea), and alcohol abuse. PVD should also be considered—his symptoms may be secondary to poor perfusion of the cerebral cortex.

TABLE 1

Partial differential diagnosis of depressed mood and neurovegetative symptoms

Psychiatrist’s comments

It is important to distinguish major depression from other, less severe depressive syndromes. In major depression, 5 out of 9 symptoms (including depressed mood or anhedonia) are present most of the day nearly every day for 2 weeks.

With adjustment disorder and so-called minor depression, symptoms are fewer or less persistent (Table 2).

This distinction is important, as antidepressants are effective for major depression, but they have not yet been shown effective for adjustment disorders or minor depression. Major depression is the “hypertension of mental illness in primary care”—common, often undiagnosed, and associated with poor outcomes. Therefore, accurate diagnosis and appropriate treatment for major depression are essential.

Given the possibility of a depressive syndrome, gather further information to determine the duration of ongoing symptoms, and obtain answers to a short questionnaire (eg, the Beck Depression Inventory [BDI]³ or the PHQ-9⁴). Elicit a family history of mood disorder, or personal history suggestive of thyroid dysfunction, a sleep disorder, or alcohol or drug abuse. Order a complete blood count (CBC) to evaluate for anemia, a thyroid-stimulating hormone (TSH) to evaluate for hypothyroidism, and, if indicated by history, a sleep study.

Beta-blockers and depression. The patient’s symptoms developed in the context of beta-blocker therapy. From the 1970s through the 1990s, the lore was that beta-blockers caused depression and should be avoided in patients with a history of depression. Because of this, many patients with myocardial infarction (MI) and congestive heart failure (CHF) have been denied treatment with beta-blockers when otherwise indicated.

Fortunately, a recent rigorous academic study of this issue was conducted by Ko and colleagues⁵ to rationally guide treatment. This study involved a meta-analysis of 15 randomized controlled trials of beta-blocker therapy in patients with MI, CHF, or hypertension; the authors found that beta-blockers were associated with a slight (though statistically significant) increase in fatigue and sexual dysfunction, and that their use was not associated with depressive symptoms. This is the best review to date of beta-blockers and depression, and it debunks the myth that beta-blockers cause depression—a myth that has prevented many post-MI patients from receiving much-needed beta-blocker therapy. In short, although idiosyncratic reactions are possible, it is unlikely the patient’s use of atenolol caused his apparent depressive symptoms.

TABLE 2

Major depression, minor depression, and adjustment disorder

Further primary care evaluation

The patient has no cold intolerance or other symptoms of thyroid dysfunction. He does report a long history of snoring, confirmed by his wife. However, he did not notice feeling more fatigued after starting atenolol.Nonetheless, you switch his antihypertensive medication from atenolol to hydrochlorothiazide. In addition, you order a CBC, serum chemistries, a thyroid panel, and a sleep study. The patient is told to return for a follow-up appointment in 2 weeks and to call before that if symptoms worsen.

In this situation, the evidence (depressive symptoms in the context of good blood-pressure control) was insufficient to justify a switch from a beta-blocker to hydrochlorothiazide. One could argue that the switch was reasonable regardless of his depressive symptoms; the most recent guidelines from JNC 7¹ indicate that thiazide diuretics are first-line therapy for hypertension in patients without CAD, and that beta-blockers are not the first-line agent in the patient’s clinical situation.

But discontinuing atenolol because of ongoing depressive symptoms is not supported. The patient may well need a beta-blocker in the future (eg, if he were to develop CAD). By prematurely concluding that the beta-blocker caused adverse effects, we may be denying him an important treatment down the road.

Option 1: 2-week drug holiday

If there was concern that the patient was having an idiosyncratic reaction to atenolol, or if he developed substantial fatigue or sexual dysfunction, a 2-week drug holiday could be conducted while carefully monitoring blood pressure and depressive symptoms. Atenolol could then be restarted to identify a temporal relationship between the symptoms and the medication.

Option 2: Treat for depression

Another option would be to treat the patient as if his symptoms represented depression. Exhibiting 4 of the necessary diagnostic criteria, the patient nearly qualifies for a diagnosis of current major depression. An antidepressant could be started, exercise could be prescribed, or a referral could be made for psychotherapy. However, again there is insufficient evidence that his subsyndromal depression will respond to standard treatments designed for major depressive disorder.

The patient returns as scheduled 2 weeks later. He has tolerated the change in blood pressure medications without difficulty, but he is experiencing persistent anhedonia, terminal insomnia, and low levels of concentration, energy, and libido. He has felt increasingly hopeless and worthless over the past 2 weeks, though he denies having thoughts of suicide. Results on CBC, serum chemistries, thyroid panel, and sleep study are all unremarkable.

The patient now clearly meets criteria for a major depressive episode. As a first step, he should be educated about depression. An excellent self-help book is Getting Your Life Back by Wright and Basco.⁶ The patient should be taught to monitor his symptoms with the BDI³ or the PHQ-9⁴ to better assess the severity of the current episode, to monitor changes in his symptoms, and to rapidly identify relapses.

Most physicians would start an antidepressant, unless the patient had significant objections. Other treatment options, alone or in concert with antidepressant treatment, include exercise or psychotherapy. The patient is an excellent candidate for exercise, given that he has 3 risk factors for CAD: hypertension, a sedentary lifestyle, and obesity (4, if you include depression). Exercising for at least 30 minutes, 2 to 3 times per week, would likely benefit his physical and mental health. In addition to its cardiac benefits, exercise 3 times weekly was found in at least one trial to be as effective as sertraline in treating major depression in outpatients.⁷

Choosing an antidepressant. A number of factors should be considered in choosing antidepressants, including efficacy, side effect profile, and cost. Table 3 outlines some of the main considerations in the choice of antidepressants for this patient. Note that tricyclic antidepressants are not listed, being contraindicated in CAD because of their tendency to contribute to arrhythmias in the post-MI period. In this patient’s case, mirtazapine should be avoided because of the possibility of weight gain; venlafaxine should be avoided because of hypertension. Sertraline would be an appropriate choice, given that it has been relatively well-studied in persons with CAD.

The patient begins treatment with fluoxetine (10 mg/d, which is then increased to 20 mg/d after several days). His depressive symptoms gradually diminish; he achieves a “50%” reduction of symptoms at follow-up visit 3 weeks later. Two months after fluoxetine was initiated, the patient is nearly euthymic, reporting only 2 depressive symptoms, and is again engaging in usual recreational activities.

TABLE 3

A comparison of antidepressants in the treatment of depressed patients in cardiac populations

Whether depression is a risk factor for CAD depends on how one defines a risk factor and whether one is discussing “major” or “minor” risk factors. At least 15 narrative reviews have been written on the relationship between depression and heart disease, but none has examined the epidemiologic evidence for depression as a major risk factor for CAD (Table 4).⁸

In looking at the 7 main epidemiologic criteria for a risk factor, depression does very well on 4: strength of association, consistency, dose-response effect, and predictability. Numerous studies have shown that depression is clearly and consistently associated with the development of CAD, and that clinical depression appears to predict CAD more robustly than does depressed mood alone.^9-12

On 2 of the criteria, specificity and biological plausibility, there is fair evidence for depression as a CAD risk factor. We do not yet know the relative importance of recurrent major depression, dysthymia, BDI scores of 10 or greater, or some other marker of depression as predictors of CAD.

Because mild depressive symptoms may predict CAD, it is unclear what levels of depression increase the risk of CAD and require intervention. Excellent work exists regarding the development of plausible mechanisms by which depression may lead to CAD; however, these mechanisms have yet to be proven. Therefore, the evidence in this domain can only be rated as fair.

Finally, the evidence is incomplete for one important criterion: response to treatment. Only one study has been designed to examine the effect of depression treatments on cardiac risk reduction. This study (the ENRICHD trial¹³) was a treatment study of post-MI depression that found that cognitive-behavioral therapy did not have a significant impact on reducing recurrent cardiac events.

Based on the most stringent epidemiologic criteria, depression is almost, but not quite, a risk factor for CAD. However, depression is a minor risk factor for CAD, and may someday be considered a major risk factor. While the mechanisms by which depression may lead to CAD have not yet been established, the association between depression and subsequent CAD likely occurs via 2 pathways.

The first pathway is behavioral. Patients with depression have diminished self-care, possibly increasing other CAD risk factors such as smoking, poor diet/hyperlipidemia, diabetes, physical inactivity, and obesity.

The second pathway by which depression may lead to CAD is neuroendocrine. Hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis and hyperactive sympathomedullary activity may result in elevated cytokine levels, platelet activation, and vascular damage, thereby contributing to CAD.⁸

TABLE 4

Depression as a risk factor for CAD: a “report card”⁸

· Acknowledgments ·

Portions of this article were presented at the Association of Medicine and Psychiatry Annual Meeting, San Diego, California, November 19, 2003.

Medical history

• No other significant medical or psychiatric problems
• Married, with 2 teenaged children
• Employed as an administrator for an insurance company (>50 hrs/wk)
• Drinks 3 to 4 alcoholic beverages/wk
• Does not smoke
• Enjoys fishing and other outdoor activities
• Both parents had hypertension; father also had peripheral vascular disease

Examination

• Patient is in no acute distress
• Approximately 30 pounds over ideal body weight
• Other vital signs are normal
• Normal retinal examination, no carotid bruits, and clear lungs. Cardiac rate and rhythm are regular; no abdominal bruits
• Laboratory studies reveal normal renal function; cholesterol, 184 mg/dL; low-density lipoprotein (LDL) cholesterol, 129 mg/dL; high-density lipoprotein (HDL) cholesterol, 55 mg/dL; triglycerides, 163 mg/dL. Electrocardiogram shows no current or prior evidence of ischemia or left-ventricular strain.

Additional information is required in a number of domains. Blood pressure readings should be repeated to make an accurate diagnosis of hypertension. While the patient may have hypertension, only a single blood pressure reading is elevated. The Joint National Committee on Blood Pressure (JNC 7) specifications¹ state that 2 such readings on different days are needed to confirm a diagnosis of hypertension. The symptoms of claudication should be investigated. Physical examination should focus on auscultation for bruits and on the examination of eye grounds to further investigate the possibility of peripheral vascular disease (PVD). In addition, a lipid profile should be drawn. While guidelines are conflicting, consideration should be given to assessing a fasting glucose, potassium, and renal function. Other tests, such as a C-reactive protein, are more controversial.²

The patient opts for drug treatment of his hypertension, and begins taking atenolol 50 mg/d (in addition to aspirin 81 mg/d). He is scheduled to follow-up by phone in 1 week to assure compliance and in 3 months in the office.

On further questioning he reports that he initially tolerated the beta-blocker without problem, but more recently has experienced low energy and poor sleep (with early morning awakening); he acknowledges decreases in libido, interest in pleasurable activities (eg, hunting, fishing), and his ability to concentrate. He has gained 5 to 10 pounds in the last month.

Although he denies feeling “sad,” he says his emotions seem “flat.” He denies having thoughts of suicide, increased anxiety, symptoms of hypomania, or psychotic symptoms. He describes a mild increase in stress at work, and he feels that the process of preparing for his son to go to college had been “a big burden.” He says there are no other stressors.

The patient’s alcohol use has not changed significantly, and he reports being compliant with his new medication regimen.

When his father died 6 years earlier, he experienced similar symptoms; at no other time have such symptoms occurred. The patient reports no other new physical symptoms, and his physical examination is essentially unchanged from the exam conducted 3 months earlier. His vital signs are normal, including a blood pressure of 128/84 mm Hg.

Consider the differential diagnosis of the patient’s abnormal mood and neurovegetative symptoms. In the primary care setting, the differential diagnosis of depressed mood is broad (Table 1 ), including medical disorders and a variety of psychiatric syndromes.

Medical conditions to consider include a medication induced side effect, hypothyroidism (a metabolic masquerader of depression), anemia, sleep disorder (eg, sleep apnea), and alcohol abuse. PVD should also be considered—his symptoms may be secondary to poor perfusion of the cerebral cortex.

TABLE 1

Partial differential diagnosis of depressed mood and neurovegetative symptoms

Psychiatrist’s comments

It is important to distinguish major depression from other, less severe depressive syndromes. In major depression, 5 out of 9 symptoms (including depressed mood or anhedonia) are present most of the day nearly every day for 2 weeks.

With adjustment disorder and so-called minor depression, symptoms are fewer or less persistent (Table 2).

This distinction is important, as antidepressants are effective for major depression, but they have not yet been shown effective for adjustment disorders or minor depression. Major depression is the “hypertension of mental illness in primary care”—common, often undiagnosed, and associated with poor outcomes. Therefore, accurate diagnosis and appropriate treatment for major depression are essential.

Given the possibility of a depressive syndrome, gather further information to determine the duration of ongoing symptoms, and obtain answers to a short questionnaire (eg, the Beck Depression Inventory [BDI]³ or the PHQ-9⁴). Elicit a family history of mood disorder, or personal history suggestive of thyroid dysfunction, a sleep disorder, or alcohol or drug abuse. Order a complete blood count (CBC) to evaluate for anemia, a thyroid-stimulating hormone (TSH) to evaluate for hypothyroidism, and, if indicated by history, a sleep study.

Beta-blockers and depression. The patient’s symptoms developed in the context of beta-blocker therapy. From the 1970s through the 1990s, the lore was that beta-blockers caused depression and should be avoided in patients with a history of depression. Because of this, many patients with myocardial infarction (MI) and congestive heart failure (CHF) have been denied treatment with beta-blockers when otherwise indicated.

Fortunately, a recent rigorous academic study of this issue was conducted by Ko and colleagues⁵ to rationally guide treatment. This study involved a meta-analysis of 15 randomized controlled trials of beta-blocker therapy in patients with MI, CHF, or hypertension; the authors found that beta-blockers were associated with a slight (though statistically significant) increase in fatigue and sexual dysfunction, and that their use was not associated with depressive symptoms. This is the best review to date of beta-blockers and depression, and it debunks the myth that beta-blockers cause depression—a myth that has prevented many post-MI patients from receiving much-needed beta-blocker therapy. In short, although idiosyncratic reactions are possible, it is unlikely the patient’s use of atenolol caused his apparent depressive symptoms.

TABLE 2

Major depression, minor depression, and adjustment disorder

Further primary care evaluation

The patient has no cold intolerance or other symptoms of thyroid dysfunction. He does report a long history of snoring, confirmed by his wife. However, he did not notice feeling more fatigued after starting atenolol.Nonetheless, you switch his antihypertensive medication from atenolol to hydrochlorothiazide. In addition, you order a CBC, serum chemistries, a thyroid panel, and a sleep study. The patient is told to return for a follow-up appointment in 2 weeks and to call before that if symptoms worsen.

In this situation, the evidence (depressive symptoms in the context of good blood-pressure control) was insufficient to justify a switch from a beta-blocker to hydrochlorothiazide. One could argue that the switch was reasonable regardless of his depressive symptoms; the most recent guidelines from JNC 7¹ indicate that thiazide diuretics are first-line therapy for hypertension in patients without CAD, and that beta-blockers are not the first-line agent in the patient’s clinical situation.

But discontinuing atenolol because of ongoing depressive symptoms is not supported. The patient may well need a beta-blocker in the future (eg, if he were to develop CAD). By prematurely concluding that the beta-blocker caused adverse effects, we may be denying him an important treatment down the road.

Option 1: 2-week drug holiday

If there was concern that the patient was having an idiosyncratic reaction to atenolol, or if he developed substantial fatigue or sexual dysfunction, a 2-week drug holiday could be conducted while carefully monitoring blood pressure and depressive symptoms. Atenolol could then be restarted to identify a temporal relationship between the symptoms and the medication.

Option 2: Treat for depression

Another option would be to treat the patient as if his symptoms represented depression. Exhibiting 4 of the necessary diagnostic criteria, the patient nearly qualifies for a diagnosis of current major depression. An antidepressant could be started, exercise could be prescribed, or a referral could be made for psychotherapy. However, again there is insufficient evidence that his subsyndromal depression will respond to standard treatments designed for major depressive disorder.

The patient returns as scheduled 2 weeks later. He has tolerated the change in blood pressure medications without difficulty, but he is experiencing persistent anhedonia, terminal insomnia, and low levels of concentration, energy, and libido. He has felt increasingly hopeless and worthless over the past 2 weeks, though he denies having thoughts of suicide. Results on CBC, serum chemistries, thyroid panel, and sleep study are all unremarkable.

The patient now clearly meets criteria for a major depressive episode. As a first step, he should be educated about depression. An excellent self-help book is Getting Your Life Back by Wright and Basco.⁶ The patient should be taught to monitor his symptoms with the BDI³ or the PHQ-9⁴ to better assess the severity of the current episode, to monitor changes in his symptoms, and to rapidly identify relapses.

Most physicians would start an antidepressant, unless the patient had significant objections. Other treatment options, alone or in concert with antidepressant treatment, include exercise or psychotherapy. The patient is an excellent candidate for exercise, given that he has 3 risk factors for CAD: hypertension, a sedentary lifestyle, and obesity (4, if you include depression). Exercising for at least 30 minutes, 2 to 3 times per week, would likely benefit his physical and mental health. In addition to its cardiac benefits, exercise 3 times weekly was found in at least one trial to be as effective as sertraline in treating major depression in outpatients.⁷

Choosing an antidepressant. A number of factors should be considered in choosing antidepressants, including efficacy, side effect profile, and cost. Table 3 outlines some of the main considerations in the choice of antidepressants for this patient. Note that tricyclic antidepressants are not listed, being contraindicated in CAD because of their tendency to contribute to arrhythmias in the post-MI period. In this patient’s case, mirtazapine should be avoided because of the possibility of weight gain; venlafaxine should be avoided because of hypertension. Sertraline would be an appropriate choice, given that it has been relatively well-studied in persons with CAD.

The patient begins treatment with fluoxetine (10 mg/d, which is then increased to 20 mg/d after several days). His depressive symptoms gradually diminish; he achieves a “50%” reduction of symptoms at follow-up visit 3 weeks later. Two months after fluoxetine was initiated, the patient is nearly euthymic, reporting only 2 depressive symptoms, and is again engaging in usual recreational activities.

TABLE 3

A comparison of antidepressants in the treatment of depressed patients in cardiac populations

Whether depression is a risk factor for CAD depends on how one defines a risk factor and whether one is discussing “major” or “minor” risk factors. At least 15 narrative reviews have been written on the relationship between depression and heart disease, but none has examined the epidemiologic evidence for depression as a major risk factor for CAD (Table 4).⁸

In looking at the 7 main epidemiologic criteria for a risk factor, depression does very well on 4: strength of association, consistency, dose-response effect, and predictability. Numerous studies have shown that depression is clearly and consistently associated with the development of CAD, and that clinical depression appears to predict CAD more robustly than does depressed mood alone.^9-12

On 2 of the criteria, specificity and biological plausibility, there is fair evidence for depression as a CAD risk factor. We do not yet know the relative importance of recurrent major depression, dysthymia, BDI scores of 10 or greater, or some other marker of depression as predictors of CAD.

Because mild depressive symptoms may predict CAD, it is unclear what levels of depression increase the risk of CAD and require intervention. Excellent work exists regarding the development of plausible mechanisms by which depression may lead to CAD; however, these mechanisms have yet to be proven. Therefore, the evidence in this domain can only be rated as fair.

Finally, the evidence is incomplete for one important criterion: response to treatment. Only one study has been designed to examine the effect of depression treatments on cardiac risk reduction. This study (the ENRICHD trial¹³) was a treatment study of post-MI depression that found that cognitive-behavioral therapy did not have a significant impact on reducing recurrent cardiac events.

Based on the most stringent epidemiologic criteria, depression is almost, but not quite, a risk factor for CAD. However, depression is a minor risk factor for CAD, and may someday be considered a major risk factor. While the mechanisms by which depression may lead to CAD have not yet been established, the association between depression and subsequent CAD likely occurs via 2 pathways.

The first pathway is behavioral. Patients with depression have diminished self-care, possibly increasing other CAD risk factors such as smoking, poor diet/hyperlipidemia, diabetes, physical inactivity, and obesity.

The second pathway by which depression may lead to CAD is neuroendocrine. Hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis and hyperactive sympathomedullary activity may result in elevated cytokine levels, platelet activation, and vascular damage, thereby contributing to CAD.⁸

TABLE 4

Depression as a risk factor for CAD: a “report card”⁸

· Acknowledgments ·

Portions of this article were presented at the Association of Medicine and Psychiatry Annual Meeting, San Diego, California, November 19, 2003.

Medical history

• No other significant medical or psychiatric problems
• Married, with 2 teenaged children
• Employed as an administrator for an insurance company (>50 hrs/wk)
• Drinks 3 to 4 alcoholic beverages/wk
• Does not smoke
• Enjoys fishing and other outdoor activities
• Both parents had hypertension; father also had peripheral vascular disease

Examination

• Patient is in no acute distress
• Approximately 30 pounds over ideal body weight
• Other vital signs are normal
• Normal retinal examination, no carotid bruits, and clear lungs. Cardiac rate and rhythm are regular; no abdominal bruits
• Laboratory studies reveal normal renal function; cholesterol, 184 mg/dL; low-density lipoprotein (LDL) cholesterol, 129 mg/dL; high-density lipoprotein (HDL) cholesterol, 55 mg/dL; triglycerides, 163 mg/dL. Electrocardiogram shows no current or prior evidence of ischemia or left-ventricular strain.

Additional information is required in a number of domains. Blood pressure readings should be repeated to make an accurate diagnosis of hypertension. While the patient may have hypertension, only a single blood pressure reading is elevated. The Joint National Committee on Blood Pressure (JNC 7) specifications¹ state that 2 such readings on different days are needed to confirm a diagnosis of hypertension. The symptoms of claudication should be investigated. Physical examination should focus on auscultation for bruits and on the examination of eye grounds to further investigate the possibility of peripheral vascular disease (PVD). In addition, a lipid profile should be drawn. While guidelines are conflicting, consideration should be given to assessing a fasting glucose, potassium, and renal function. Other tests, such as a C-reactive protein, are more controversial.²

The patient opts for drug treatment of his hypertension, and begins taking atenolol 50 mg/d (in addition to aspirin 81 mg/d). He is scheduled to follow-up by phone in 1 week to assure compliance and in 3 months in the office.

On further questioning he reports that he initially tolerated the beta-blocker without problem, but more recently has experienced low energy and poor sleep (with early morning awakening); he acknowledges decreases in libido, interest in pleasurable activities (eg, hunting, fishing), and his ability to concentrate. He has gained 5 to 10 pounds in the last month.

Although he denies feeling “sad,” he says his emotions seem “flat.” He denies having thoughts of suicide, increased anxiety, symptoms of hypomania, or psychotic symptoms. He describes a mild increase in stress at work, and he feels that the process of preparing for his son to go to college had been “a big burden.” He says there are no other stressors.

The patient’s alcohol use has not changed significantly, and he reports being compliant with his new medication regimen.

When his father died 6 years earlier, he experienced similar symptoms; at no other time have such symptoms occurred. The patient reports no other new physical symptoms, and his physical examination is essentially unchanged from the exam conducted 3 months earlier. His vital signs are normal, including a blood pressure of 128/84 mm Hg.

Consider the differential diagnosis of the patient’s abnormal mood and neurovegetative symptoms. In the primary care setting, the differential diagnosis of depressed mood is broad (Table 1 ), including medical disorders and a variety of psychiatric syndromes.

Medical conditions to consider include a medication induced side effect, hypothyroidism (a metabolic masquerader of depression), anemia, sleep disorder (eg, sleep apnea), and alcohol abuse. PVD should also be considered—his symptoms may be secondary to poor perfusion of the cerebral cortex.

TABLE 1

Partial differential diagnosis of depressed mood and neurovegetative symptoms

Psychiatrist’s comments

It is important to distinguish major depression from other, less severe depressive syndromes. In major depression, 5 out of 9 symptoms (including depressed mood or anhedonia) are present most of the day nearly every day for 2 weeks.

With adjustment disorder and so-called minor depression, symptoms are fewer or less persistent (Table 2).

This distinction is important, as antidepressants are effective for major depression, but they have not yet been shown effective for adjustment disorders or minor depression. Major depression is the “hypertension of mental illness in primary care”—common, often undiagnosed, and associated with poor outcomes. Therefore, accurate diagnosis and appropriate treatment for major depression are essential.

Given the possibility of a depressive syndrome, gather further information to determine the duration of ongoing symptoms, and obtain answers to a short questionnaire (eg, the Beck Depression Inventory [BDI]³ or the PHQ-9⁴). Elicit a family history of mood disorder, or personal history suggestive of thyroid dysfunction, a sleep disorder, or alcohol or drug abuse. Order a complete blood count (CBC) to evaluate for anemia, a thyroid-stimulating hormone (TSH) to evaluate for hypothyroidism, and, if indicated by history, a sleep study.

Beta-blockers and depression. The patient’s symptoms developed in the context of beta-blocker therapy. From the 1970s through the 1990s, the lore was that beta-blockers caused depression and should be avoided in patients with a history of depression. Because of this, many patients with myocardial infarction (MI) and congestive heart failure (CHF) have been denied treatment with beta-blockers when otherwise indicated.

Fortunately, a recent rigorous academic study of this issue was conducted by Ko and colleagues⁵ to rationally guide treatment. This study involved a meta-analysis of 15 randomized controlled trials of beta-blocker therapy in patients with MI, CHF, or hypertension; the authors found that beta-blockers were associated with a slight (though statistically significant) increase in fatigue and sexual dysfunction, and that their use was not associated with depressive symptoms. This is the best review to date of beta-blockers and depression, and it debunks the myth that beta-blockers cause depression—a myth that has prevented many post-MI patients from receiving much-needed beta-blocker therapy. In short, although idiosyncratic reactions are possible, it is unlikely the patient’s use of atenolol caused his apparent depressive symptoms.

TABLE 2

Major depression, minor depression, and adjustment disorder

Further primary care evaluation

The patient has no cold intolerance or other symptoms of thyroid dysfunction. He does report a long history of snoring, confirmed by his wife. However, he did not notice feeling more fatigued after starting atenolol.Nonetheless, you switch his antihypertensive medication from atenolol to hydrochlorothiazide. In addition, you order a CBC, serum chemistries, a thyroid panel, and a sleep study. The patient is told to return for a follow-up appointment in 2 weeks and to call before that if symptoms worsen.

In this situation, the evidence (depressive symptoms in the context of good blood-pressure control) was insufficient to justify a switch from a beta-blocker to hydrochlorothiazide. One could argue that the switch was reasonable regardless of his depressive symptoms; the most recent guidelines from JNC 7¹ indicate that thiazide diuretics are first-line therapy for hypertension in patients without CAD, and that beta-blockers are not the first-line agent in the patient’s clinical situation.

But discontinuing atenolol because of ongoing depressive symptoms is not supported. The patient may well need a beta-blocker in the future (eg, if he were to develop CAD). By prematurely concluding that the beta-blocker caused adverse effects, we may be denying him an important treatment down the road.

Option 1: 2-week drug holiday

If there was concern that the patient was having an idiosyncratic reaction to atenolol, or if he developed substantial fatigue or sexual dysfunction, a 2-week drug holiday could be conducted while carefully monitoring blood pressure and depressive symptoms. Atenolol could then be restarted to identify a temporal relationship between the symptoms and the medication.

Option 2: Treat for depression

Another option would be to treat the patient as if his symptoms represented depression. Exhibiting 4 of the necessary diagnostic criteria, the patient nearly qualifies for a diagnosis of current major depression. An antidepressant could be started, exercise could be prescribed, or a referral could be made for psychotherapy. However, again there is insufficient evidence that his subsyndromal depression will respond to standard treatments designed for major depressive disorder.

The patient returns as scheduled 2 weeks later. He has tolerated the change in blood pressure medications without difficulty, but he is experiencing persistent anhedonia, terminal insomnia, and low levels of concentration, energy, and libido. He has felt increasingly hopeless and worthless over the past 2 weeks, though he denies having thoughts of suicide. Results on CBC, serum chemistries, thyroid panel, and sleep study are all unremarkable.

The patient now clearly meets criteria for a major depressive episode. As a first step, he should be educated about depression. An excellent self-help book is Getting Your Life Back by Wright and Basco.⁶ The patient should be taught to monitor his symptoms with the BDI³ or the PHQ-9⁴ to better assess the severity of the current episode, to monitor changes in his symptoms, and to rapidly identify relapses.

Most physicians would start an antidepressant, unless the patient had significant objections. Other treatment options, alone or in concert with antidepressant treatment, include exercise or psychotherapy. The patient is an excellent candidate for exercise, given that he has 3 risk factors for CAD: hypertension, a sedentary lifestyle, and obesity (4, if you include depression). Exercising for at least 30 minutes, 2 to 3 times per week, would likely benefit his physical and mental health. In addition to its cardiac benefits, exercise 3 times weekly was found in at least one trial to be as effective as sertraline in treating major depression in outpatients.⁷

Choosing an antidepressant. A number of factors should be considered in choosing antidepressants, including efficacy, side effect profile, and cost. Table 3 outlines some of the main considerations in the choice of antidepressants for this patient. Note that tricyclic antidepressants are not listed, being contraindicated in CAD because of their tendency to contribute to arrhythmias in the post-MI period. In this patient’s case, mirtazapine should be avoided because of the possibility of weight gain; venlafaxine should be avoided because of hypertension. Sertraline would be an appropriate choice, given that it has been relatively well-studied in persons with CAD.

The patient begins treatment with fluoxetine (10 mg/d, which is then increased to 20 mg/d after several days). His depressive symptoms gradually diminish; he achieves a “50%” reduction of symptoms at follow-up visit 3 weeks later. Two months after fluoxetine was initiated, the patient is nearly euthymic, reporting only 2 depressive symptoms, and is again engaging in usual recreational activities.

TABLE 3

A comparison of antidepressants in the treatment of depressed patients in cardiac populations

Whether depression is a risk factor for CAD depends on how one defines a risk factor and whether one is discussing “major” or “minor” risk factors. At least 15 narrative reviews have been written on the relationship between depression and heart disease, but none has examined the epidemiologic evidence for depression as a major risk factor for CAD (Table 4).⁸

In looking at the 7 main epidemiologic criteria for a risk factor, depression does very well on 4: strength of association, consistency, dose-response effect, and predictability. Numerous studies have shown that depression is clearly and consistently associated with the development of CAD, and that clinical depression appears to predict CAD more robustly than does depressed mood alone.^9-12

On 2 of the criteria, specificity and biological plausibility, there is fair evidence for depression as a CAD risk factor. We do not yet know the relative importance of recurrent major depression, dysthymia, BDI scores of 10 or greater, or some other marker of depression as predictors of CAD.

Because mild depressive symptoms may predict CAD, it is unclear what levels of depression increase the risk of CAD and require intervention. Excellent work exists regarding the development of plausible mechanisms by which depression may lead to CAD; however, these mechanisms have yet to be proven. Therefore, the evidence in this domain can only be rated as fair.

Finally, the evidence is incomplete for one important criterion: response to treatment. Only one study has been designed to examine the effect of depression treatments on cardiac risk reduction. This study (the ENRICHD trial¹³) was a treatment study of post-MI depression that found that cognitive-behavioral therapy did not have a significant impact on reducing recurrent cardiac events.

Based on the most stringent epidemiologic criteria, depression is almost, but not quite, a risk factor for CAD. However, depression is a minor risk factor for CAD, and may someday be considered a major risk factor. While the mechanisms by which depression may lead to CAD have not yet been established, the association between depression and subsequent CAD likely occurs via 2 pathways.

The first pathway is behavioral. Patients with depression have diminished self-care, possibly increasing other CAD risk factors such as smoking, poor diet/hyperlipidemia, diabetes, physical inactivity, and obesity.

The second pathway by which depression may lead to CAD is neuroendocrine. Hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis and hyperactive sympathomedullary activity may result in elevated cytokine levels, platelet activation, and vascular damage, thereby contributing to CAD.⁸

TABLE 4

Depression as a risk factor for CAD: a “report card”⁸

· Acknowledgments ·

Portions of this article were presented at the Association of Medicine and Psychiatry Annual Meeting, San Diego, California, November 19, 2003.