When a psychiatrist is sued for negligence, the legal system asks, “Did the doctor depart from the standard of care, and—if so—did that departure proximately cause the harm?” To determine proximate cause, the legal system then asks whether the harm was a “reasonably foreseeable” result of the negligent act.

Inadequate evaluation leads to patient’s suicide, plaintiff alleges

Dallas County (TX) District Court

In 1997, 1 year after suffering a stroke, a 56-year-old man was admitted to a rehabilitation center and seen by a psychiatrist for depression. In February 2000, the patient died after jumping from the center’s fifth-floor window.

The patient’s estate charged that the psychiatrist was negligent and did not adequately evaluate or treat the patient. The defense disputed the charge.

• The jury found for the defense.
  

Dr. Grant’s observations

In this case, the psychiatrist presumably assessed the patient, determined whether he was depressed, and made appropriate treatment interventions. Three years later, the patient killed himself.

Although 3 years passed between the consultation and the suicide, under the law an intervening act that is the reasonably foreseeable result of negligence does not break the causal chain. For example, if the psychiatrist told the patient he needed no treatment and did not need to follow-up with another clinician, the causal chain arguably would still exist. Thus, proper care, not time, will prevent such a suit.

To win a negligence case, the plaintiff must show that the psychiatrist’s actions proximately caused the harm. In order to defend your treatment decisions, document and discuss with the patient:

• the diagnosis and illness severity
  
• possible illness course based on patient history and the illness in question
  
• the need to monitor mood symptoms
  
• basis for treatment recommendations
  
• the possible need for continued treatment and to arrange follow-up care.
  

Plaintiff: Improper treatment caused fatal altercation

Cuyahoga County (OH) Court of Common Pleas

A man in his early 30s was admitted to the hospital’s psychiatric unit for depression, mood disorder, and adjustment disorder secondary to myasthenia gravis. He was estranged from his wife, who was dating another man. The treating psychiatrist discharged the patient after 5 days.

Approximately 40 hours after discharge, the patient went to the other man’s home and confronted him about his relationship with the patient’s wife. The two men then fought, and the other man fatally shot the patient. During the fight, the patient stabbed the other man in the neck with a knife; this man required care and subsequently developed a scar.

The other man and the patient’s estate charged that the psychiatrist did not appropriately evaluate and treat the patient. They claimed that a more thorough evaluation would have resulted in continued hospitalization and prevented the fight.

The defendant argued that the evaluation was thorough, that the discharge met the guidelines of appropriate care, and that the patient posed no risk to himself or others when he was discharged.

• The jury decided for the defense.
  

Dr. Grant’s observations

This case raises the clinically difficult issue of assessing a patient’s danger to self or others and whether this danger is reasonably foreseeable. Although Hughes reports that 17% of psychiatric emergency room patients are homicidal,¹ the American Psychiatric Association notes that 2 of 3 predictions of patient violence are wrong.²

In Tarasoff v Regents of the University of California, the California Supreme Court ruled that clinicians must warn potential victims of, and protect them from, a patient’s intent to harm.³ You should become familiar with the Tarasoff-type legislations in your state. But even if the patient shows no violent intent, the possibility of future violence cannot be ruled out.

During admission, assess and document an inpatient’s risk of violence.⁴ Factors that may increase a depressed patient’s risk of becoming homicidal include:

• past violence
  
• current substance abuse
  
• psychopathy
  
• having suffered physical abuse as a child
  
• violent thoughts.^4-6
  

If sexual infidelity, real or fantasized, precipitated the depression—as it might have in this case—a depressed patient may be at increased risk for homicide.

Check the patient’s records for a history of recurrent violence. Culling this information from the chart is necessary because:

• past violent behavior may predict future violence
  
• patients rarely reveal homicidal thoughts or behavior spontaneously.⁶
  

Knowing a patient’s violent past may aid in treatment. For example, you might order a longer hospitalization or establish more-intensive outpatient services focusing on avoiding aggression and violence. Make sure that follow-up care meets the patient’s needs after discharge.⁷

A psychiatrist may be found negligent after a patient’s violent act if the violence was foreseeable. However, after having seen the patient for 5 days in an inpatient setting, the psychiatrist in this case apparently could clearly document that the patient was not dangerous to himself or others before discharge.

When a psychiatrist is sued for negligence, the legal system asks, “Did the doctor depart from the standard of care, and—if so—did that departure proximately cause the harm?” To determine proximate cause, the legal system then asks whether the harm was a “reasonably foreseeable” result of the negligent act.

Inadequate evaluation leads to patient’s suicide, plaintiff alleges

Dallas County (TX) District Court

In 1997, 1 year after suffering a stroke, a 56-year-old man was admitted to a rehabilitation center and seen by a psychiatrist for depression. In February 2000, the patient died after jumping from the center’s fifth-floor window.

The patient’s estate charged that the psychiatrist was negligent and did not adequately evaluate or treat the patient. The defense disputed the charge.

• The jury found for the defense.
  

Dr. Grant’s observations

In this case, the psychiatrist presumably assessed the patient, determined whether he was depressed, and made appropriate treatment interventions. Three years later, the patient killed himself.

Although 3 years passed between the consultation and the suicide, under the law an intervening act that is the reasonably foreseeable result of negligence does not break the causal chain. For example, if the psychiatrist told the patient he needed no treatment and did not need to follow-up with another clinician, the causal chain arguably would still exist. Thus, proper care, not time, will prevent such a suit.

To win a negligence case, the plaintiff must show that the psychiatrist’s actions proximately caused the harm. In order to defend your treatment decisions, document and discuss with the patient:

• the diagnosis and illness severity
  
• possible illness course based on patient history and the illness in question
  
• the need to monitor mood symptoms
  
• basis for treatment recommendations
  
• the possible need for continued treatment and to arrange follow-up care.
  

Plaintiff: Improper treatment caused fatal altercation

Cuyahoga County (OH) Court of Common Pleas

A man in his early 30s was admitted to the hospital’s psychiatric unit for depression, mood disorder, and adjustment disorder secondary to myasthenia gravis. He was estranged from his wife, who was dating another man. The treating psychiatrist discharged the patient after 5 days.

Approximately 40 hours after discharge, the patient went to the other man’s home and confronted him about his relationship with the patient’s wife. The two men then fought, and the other man fatally shot the patient. During the fight, the patient stabbed the other man in the neck with a knife; this man required care and subsequently developed a scar.

The other man and the patient’s estate charged that the psychiatrist did not appropriately evaluate and treat the patient. They claimed that a more thorough evaluation would have resulted in continued hospitalization and prevented the fight.

The defendant argued that the evaluation was thorough, that the discharge met the guidelines of appropriate care, and that the patient posed no risk to himself or others when he was discharged.

• The jury decided for the defense.
  

Dr. Grant’s observations

This case raises the clinically difficult issue of assessing a patient’s danger to self or others and whether this danger is reasonably foreseeable. Although Hughes reports that 17% of psychiatric emergency room patients are homicidal,¹ the American Psychiatric Association notes that 2 of 3 predictions of patient violence are wrong.²

In Tarasoff v Regents of the University of California, the California Supreme Court ruled that clinicians must warn potential victims of, and protect them from, a patient’s intent to harm.³ You should become familiar with the Tarasoff-type legislations in your state. But even if the patient shows no violent intent, the possibility of future violence cannot be ruled out.

During admission, assess and document an inpatient’s risk of violence.⁴ Factors that may increase a depressed patient’s risk of becoming homicidal include:

• past violence
  
• current substance abuse
  
• psychopathy
  
• having suffered physical abuse as a child
  
• violent thoughts.^4-6
  

If sexual infidelity, real or fantasized, precipitated the depression—as it might have in this case—a depressed patient may be at increased risk for homicide.

Check the patient’s records for a history of recurrent violence. Culling this information from the chart is necessary because:

• past violent behavior may predict future violence
  
• patients rarely reveal homicidal thoughts or behavior spontaneously.⁶
  

Knowing a patient’s violent past may aid in treatment. For example, you might order a longer hospitalization or establish more-intensive outpatient services focusing on avoiding aggression and violence. Make sure that follow-up care meets the patient’s needs after discharge.⁷

A psychiatrist may be found negligent after a patient’s violent act if the violence was foreseeable. However, after having seen the patient for 5 days in an inpatient setting, the psychiatrist in this case apparently could clearly document that the patient was not dangerous to himself or others before discharge.

When a psychiatrist is sued for negligence, the legal system asks, “Did the doctor depart from the standard of care, and—if so—did that departure proximately cause the harm?” To determine proximate cause, the legal system then asks whether the harm was a “reasonably foreseeable” result of the negligent act.

Inadequate evaluation leads to patient’s suicide, plaintiff alleges

Dallas County (TX) District Court

In 1997, 1 year after suffering a stroke, a 56-year-old man was admitted to a rehabilitation center and seen by a psychiatrist for depression. In February 2000, the patient died after jumping from the center’s fifth-floor window.

The patient’s estate charged that the psychiatrist was negligent and did not adequately evaluate or treat the patient. The defense disputed the charge.

• The jury found for the defense.
  

Dr. Grant’s observations

In this case, the psychiatrist presumably assessed the patient, determined whether he was depressed, and made appropriate treatment interventions. Three years later, the patient killed himself.

Although 3 years passed between the consultation and the suicide, under the law an intervening act that is the reasonably foreseeable result of negligence does not break the causal chain. For example, if the psychiatrist told the patient he needed no treatment and did not need to follow-up with another clinician, the causal chain arguably would still exist. Thus, proper care, not time, will prevent such a suit.

To win a negligence case, the plaintiff must show that the psychiatrist’s actions proximately caused the harm. In order to defend your treatment decisions, document and discuss with the patient:

• the diagnosis and illness severity
  
• possible illness course based on patient history and the illness in question
  
• the need to monitor mood symptoms
  
• basis for treatment recommendations
  
• the possible need for continued treatment and to arrange follow-up care.
  

Plaintiff: Improper treatment caused fatal altercation

Cuyahoga County (OH) Court of Common Pleas

A man in his early 30s was admitted to the hospital’s psychiatric unit for depression, mood disorder, and adjustment disorder secondary to myasthenia gravis. He was estranged from his wife, who was dating another man. The treating psychiatrist discharged the patient after 5 days.

Approximately 40 hours after discharge, the patient went to the other man’s home and confronted him about his relationship with the patient’s wife. The two men then fought, and the other man fatally shot the patient. During the fight, the patient stabbed the other man in the neck with a knife; this man required care and subsequently developed a scar.

The other man and the patient’s estate charged that the psychiatrist did not appropriately evaluate and treat the patient. They claimed that a more thorough evaluation would have resulted in continued hospitalization and prevented the fight.

The defendant argued that the evaluation was thorough, that the discharge met the guidelines of appropriate care, and that the patient posed no risk to himself or others when he was discharged.

• The jury decided for the defense.
  

Dr. Grant’s observations

This case raises the clinically difficult issue of assessing a patient’s danger to self or others and whether this danger is reasonably foreseeable. Although Hughes reports that 17% of psychiatric emergency room patients are homicidal,¹ the American Psychiatric Association notes that 2 of 3 predictions of patient violence are wrong.²

In Tarasoff v Regents of the University of California, the California Supreme Court ruled that clinicians must warn potential victims of, and protect them from, a patient’s intent to harm.³ You should become familiar with the Tarasoff-type legislations in your state. But even if the patient shows no violent intent, the possibility of future violence cannot be ruled out.

During admission, assess and document an inpatient’s risk of violence.⁴ Factors that may increase a depressed patient’s risk of becoming homicidal include:

• past violence
  
• current substance abuse
  
• psychopathy
  
• having suffered physical abuse as a child
  
• violent thoughts.^4-6
  

If sexual infidelity, real or fantasized, precipitated the depression—as it might have in this case—a depressed patient may be at increased risk for homicide.

Check the patient’s records for a history of recurrent violence. Culling this information from the chart is necessary because:

• past violent behavior may predict future violence
  
• patients rarely reveal homicidal thoughts or behavior spontaneously.⁶
  

Knowing a patient’s violent past may aid in treatment. For example, you might order a longer hospitalization or establish more-intensive outpatient services focusing on avoiding aggression and violence. Make sure that follow-up care meets the patient’s needs after discharge.⁷

A psychiatrist may be found negligent after a patient’s violent act if the violence was foreseeable. However, after having seen the patient for 5 days in an inpatient setting, the psychiatrist in this case apparently could clearly document that the patient was not dangerous to himself or others before discharge.

A recently described cutaneous fibrosing disorder could be mistaken for scleroderma, but there are some key differences, said Dr. Collier.

Worldwide, there have been only 170 cases of nephrogenic fibrosing dermopathy (NFD) reported since it was first described in 1997, he said. Yet “I think it's far more common than we're led to believe,” he added.

The typical presentation of NFD consists of acute, lumpy, plaquelike indurations involving the lower limbs and occasionally the upper limbs and torso, he said.

Usually, scleroderma starts on the hands and face. But in NFD, these are almost always spared, he said.

The most common distribution of NFD skin presentation is between the ankles and the mid-thighs and between the wrists and mid-upper arms bilaterally, he said. Skin-colored to erythematous papules coalesce into brawny plaques with a peau d'orange appearance. There is a distinctive, irregular edge with amoeboid projections and islands of sparing within the indurated plaque. Eventually, the skin becomes markedly thickened and woody. Pruritis and causalgia are prominent features.

Unlike scleroderma, NFD often causes severe sharp pains in the affected areas, and renal insufficiency is necessary for the diagnosis.

The biopsy will show deposits of collagen and elastin—spindle cells, dendritic cells, and mucin deposits—“which is different from what we see in scleroderma.”

Although NFD was initially thought to be only a cutaneous disease, there now appears to be a severe myopathic component. Joint contractures may develop within days or weeks of onset, likely resulting from facial and muscle fibrosis, Dr. Collier noted.

The abrupt emergence of this disease suggests that toxic exposures, infectious agents, or medical techniques may be involved.

Document

70303_fx1.sml

NFD plaques typically take on a peau d'orange appearence. Courtesy Dr. David H. Collier

A recently described cutaneous fibrosing disorder could be mistaken for scleroderma, but there are some key differences, said Dr. Collier.

Worldwide, there have been only 170 cases of nephrogenic fibrosing dermopathy (NFD) reported since it was first described in 1997, he said. Yet “I think it's far more common than we're led to believe,” he added.

The typical presentation of NFD consists of acute, lumpy, plaquelike indurations involving the lower limbs and occasionally the upper limbs and torso, he said.

Usually, scleroderma starts on the hands and face. But in NFD, these are almost always spared, he said.

The most common distribution of NFD skin presentation is between the ankles and the mid-thighs and between the wrists and mid-upper arms bilaterally, he said. Skin-colored to erythematous papules coalesce into brawny plaques with a peau d'orange appearance. There is a distinctive, irregular edge with amoeboid projections and islands of sparing within the indurated plaque. Eventually, the skin becomes markedly thickened and woody. Pruritis and causalgia are prominent features.

Unlike scleroderma, NFD often causes severe sharp pains in the affected areas, and renal insufficiency is necessary for the diagnosis.

The biopsy will show deposits of collagen and elastin—spindle cells, dendritic cells, and mucin deposits—“which is different from what we see in scleroderma.”

Although NFD was initially thought to be only a cutaneous disease, there now appears to be a severe myopathic component. Joint contractures may develop within days or weeks of onset, likely resulting from facial and muscle fibrosis, Dr. Collier noted.

The abrupt emergence of this disease suggests that toxic exposures, infectious agents, or medical techniques may be involved.

Document

70303_fx1.sml

NFD plaques typically take on a peau d'orange appearence. Courtesy Dr. David H. Collier

A recently described cutaneous fibrosing disorder could be mistaken for scleroderma, but there are some key differences, said Dr. Collier.

Worldwide, there have been only 170 cases of nephrogenic fibrosing dermopathy (NFD) reported since it was first described in 1997, he said. Yet “I think it's far more common than we're led to believe,” he added.

The typical presentation of NFD consists of acute, lumpy, plaquelike indurations involving the lower limbs and occasionally the upper limbs and torso, he said.

Usually, scleroderma starts on the hands and face. But in NFD, these are almost always spared, he said.

The most common distribution of NFD skin presentation is between the ankles and the mid-thighs and between the wrists and mid-upper arms bilaterally, he said. Skin-colored to erythematous papules coalesce into brawny plaques with a peau d'orange appearance. There is a distinctive, irregular edge with amoeboid projections and islands of sparing within the indurated plaque. Eventually, the skin becomes markedly thickened and woody. Pruritis and causalgia are prominent features.

Unlike scleroderma, NFD often causes severe sharp pains in the affected areas, and renal insufficiency is necessary for the diagnosis.

The biopsy will show deposits of collagen and elastin—spindle cells, dendritic cells, and mucin deposits—“which is different from what we see in scleroderma.”

Although NFD was initially thought to be only a cutaneous disease, there now appears to be a severe myopathic component. Joint contractures may develop within days or weeks of onset, likely resulting from facial and muscle fibrosis, Dr. Collier noted.

The abrupt emergence of this disease suggests that toxic exposures, infectious agents, or medical techniques may be involved.

Document

70303_fx1.sml

NFD plaques typically take on a peau d'orange appearence. Courtesy Dr. David H. Collier

SNOWMASS, COLO — The most significant predictor of progression to scleroderma in a patient with new onset Raynaud's phenomenon is the presence of capillary abnormalities at the proximal nail fold, according to David H. Collier, M.D.

Although scleroderma is primarily managed by rheumatologists, it is dermatologists who most commonly identify the early skin manifestations of the disorder, said Dr. Collier of the University of Colorado, Denver, and chief of rheumatology at Denver Health Medical Center.

In addition to Raynaud's, these manifestations include skin thickening, ulceration, telangiectases, calcinosis, and pigmentation changes.

Speaking at a clinical dermatology seminar sponsored by Medicis, Dr. Collier explained that Raynaud's phenomenon is an almost universal component of systemic sclerosis, and yet the vast majority of patients with Raynaud's never progress to scleroderma.

“Up to 10% of adult women can have Raynaud's, and less then 0.1% can go on to develop scleroderma,” he said in an interview, adding that about 77% of Raynaud's patients are female.

By examining the periungual area of the finger, under gel with an opthalmoscope, the physician can easily assess capillary abnormalities at the proximal nail fold, he said.

“Instead of thin little loops of capillaries that you would see in a normal patient, you see capillary dilation and areas that are denuded or dropped out altogether,” he said, explaining that capillary dilation occurs early in the disease, and after about 10 years, only denudation is typically visible.

“A patient with abnormal capilloscopy should be followed every 3-6 months for signs of progression to systemic sclerosis,” he advised, adding that early identification of scleroderma and referral can allow for a prompt pulmonary evaluation and establishment of gastroesophageal reflux prevention/management.

Pitting or ulceration of the fingertips is another indication that a Raynaud's patient has scleroderma, said Dr. Collier.

“Primary Raynaud's disease does not give you pitting. So if you see pits—especially fingertip pits and ulceration—that's a red light [indicating] that you're dealing with an autoimmune disease. It's almost always Raynaud's secondary to scleroderma or mixed connective tissue disease, or occasionally lupus,” he said.

In addition to the evaluation for capillary abnormalities, the scleroderma work-up for patients presenting with Raynaud's should also include autoantibody testing, he said.

“If they also have the antibodies, that's the subgroup that I worry about the most for progressing to scleroderma, but it's not universal. I've certainly followed people with autoantibodies, and they didn't progress.”

Anticentromere antibodies are seen in 20%-30% of scleroderma patients and are the most predictive of risk to progression to limited systemic sclerosis, although they are also commonly seen in primary biliary cirrhosis and, rarely, in other connective tissue diseases, such as rheumatoid arthritis, systemic lupus erythematosus, mixed connective tissue disease, and polymyositis, he said.

Anti-topoisomerase-1 antibodies (e.g., anti-scleroderma [Scl]-70) are present in 9%-20% of scleroderma patients. Anti-RNA polymerase 1-3 antibodies are seen in 20%. Antifibrillarin/anti-U3 ribonucleoprotein (anti-U3 RNP) antibodies are seen in 10%, and anti-neutrophilic cytoplasmic antibodies (ANCA) are seen in about 4%, though mostly in patients with diffuse systemic sclerosis. Finally, antipolymyositis /Scl (anti-PM Scl) and anti-Th/To (which recognizes certain RNA processing enzymes) antibodies are seen in about 2% of scleroderma patients.

SNOWMASS, COLO — The most significant predictor of progression to scleroderma in a patient with new onset Raynaud's phenomenon is the presence of capillary abnormalities at the proximal nail fold, according to David H. Collier, M.D.

Although scleroderma is primarily managed by rheumatologists, it is dermatologists who most commonly identify the early skin manifestations of the disorder, said Dr. Collier of the University of Colorado, Denver, and chief of rheumatology at Denver Health Medical Center.

In addition to Raynaud's, these manifestations include skin thickening, ulceration, telangiectases, calcinosis, and pigmentation changes.

Speaking at a clinical dermatology seminar sponsored by Medicis, Dr. Collier explained that Raynaud's phenomenon is an almost universal component of systemic sclerosis, and yet the vast majority of patients with Raynaud's never progress to scleroderma.

“Up to 10% of adult women can have Raynaud's, and less then 0.1% can go on to develop scleroderma,” he said in an interview, adding that about 77% of Raynaud's patients are female.

By examining the periungual area of the finger, under gel with an opthalmoscope, the physician can easily assess capillary abnormalities at the proximal nail fold, he said.

“Instead of thin little loops of capillaries that you would see in a normal patient, you see capillary dilation and areas that are denuded or dropped out altogether,” he said, explaining that capillary dilation occurs early in the disease, and after about 10 years, only denudation is typically visible.

“A patient with abnormal capilloscopy should be followed every 3-6 months for signs of progression to systemic sclerosis,” he advised, adding that early identification of scleroderma and referral can allow for a prompt pulmonary evaluation and establishment of gastroesophageal reflux prevention/management.

Pitting or ulceration of the fingertips is another indication that a Raynaud's patient has scleroderma, said Dr. Collier.

“Primary Raynaud's disease does not give you pitting. So if you see pits—especially fingertip pits and ulceration—that's a red light [indicating] that you're dealing with an autoimmune disease. It's almost always Raynaud's secondary to scleroderma or mixed connective tissue disease, or occasionally lupus,” he said.

In addition to the evaluation for capillary abnormalities, the scleroderma work-up for patients presenting with Raynaud's should also include autoantibody testing, he said.

“If they also have the antibodies, that's the subgroup that I worry about the most for progressing to scleroderma, but it's not universal. I've certainly followed people with autoantibodies, and they didn't progress.”

Anticentromere antibodies are seen in 20%-30% of scleroderma patients and are the most predictive of risk to progression to limited systemic sclerosis, although they are also commonly seen in primary biliary cirrhosis and, rarely, in other connective tissue diseases, such as rheumatoid arthritis, systemic lupus erythematosus, mixed connective tissue disease, and polymyositis, he said.

Anti-topoisomerase-1 antibodies (e.g., anti-scleroderma [Scl]-70) are present in 9%-20% of scleroderma patients. Anti-RNA polymerase 1-3 antibodies are seen in 20%. Antifibrillarin/anti-U3 ribonucleoprotein (anti-U3 RNP) antibodies are seen in 10%, and anti-neutrophilic cytoplasmic antibodies (ANCA) are seen in about 4%, though mostly in patients with diffuse systemic sclerosis. Finally, antipolymyositis /Scl (anti-PM Scl) and anti-Th/To (which recognizes certain RNA processing enzymes) antibodies are seen in about 2% of scleroderma patients.

SNOWMASS, COLO — The most significant predictor of progression to scleroderma in a patient with new onset Raynaud's phenomenon is the presence of capillary abnormalities at the proximal nail fold, according to David H. Collier, M.D.

Although scleroderma is primarily managed by rheumatologists, it is dermatologists who most commonly identify the early skin manifestations of the disorder, said Dr. Collier of the University of Colorado, Denver, and chief of rheumatology at Denver Health Medical Center.

In addition to Raynaud's, these manifestations include skin thickening, ulceration, telangiectases, calcinosis, and pigmentation changes.

Speaking at a clinical dermatology seminar sponsored by Medicis, Dr. Collier explained that Raynaud's phenomenon is an almost universal component of systemic sclerosis, and yet the vast majority of patients with Raynaud's never progress to scleroderma.

“Up to 10% of adult women can have Raynaud's, and less then 0.1% can go on to develop scleroderma,” he said in an interview, adding that about 77% of Raynaud's patients are female.

By examining the periungual area of the finger, under gel with an opthalmoscope, the physician can easily assess capillary abnormalities at the proximal nail fold, he said.

“Instead of thin little loops of capillaries that you would see in a normal patient, you see capillary dilation and areas that are denuded or dropped out altogether,” he said, explaining that capillary dilation occurs early in the disease, and after about 10 years, only denudation is typically visible.

“A patient with abnormal capilloscopy should be followed every 3-6 months for signs of progression to systemic sclerosis,” he advised, adding that early identification of scleroderma and referral can allow for a prompt pulmonary evaluation and establishment of gastroesophageal reflux prevention/management.

Pitting or ulceration of the fingertips is another indication that a Raynaud's patient has scleroderma, said Dr. Collier.

“Primary Raynaud's disease does not give you pitting. So if you see pits—especially fingertip pits and ulceration—that's a red light [indicating] that you're dealing with an autoimmune disease. It's almost always Raynaud's secondary to scleroderma or mixed connective tissue disease, or occasionally lupus,” he said.

In addition to the evaluation for capillary abnormalities, the scleroderma work-up for patients presenting with Raynaud's should also include autoantibody testing, he said.

“If they also have the antibodies, that's the subgroup that I worry about the most for progressing to scleroderma, but it's not universal. I've certainly followed people with autoantibodies, and they didn't progress.”

Anticentromere antibodies are seen in 20%-30% of scleroderma patients and are the most predictive of risk to progression to limited systemic sclerosis, although they are also commonly seen in primary biliary cirrhosis and, rarely, in other connective tissue diseases, such as rheumatoid arthritis, systemic lupus erythematosus, mixed connective tissue disease, and polymyositis, he said.

Anti-topoisomerase-1 antibodies (e.g., anti-scleroderma [Scl]-70) are present in 9%-20% of scleroderma patients. Anti-RNA polymerase 1-3 antibodies are seen in 20%. Antifibrillarin/anti-U3 ribonucleoprotein (anti-U3 RNP) antibodies are seen in 10%, and anti-neutrophilic cytoplasmic antibodies (ANCA) are seen in about 4%, though mostly in patients with diffuse systemic sclerosis. Finally, antipolymyositis /Scl (anti-PM Scl) and anti-Th/To (which recognizes certain RNA processing enzymes) antibodies are seen in about 2% of scleroderma patients.

Etanercept does not impact maintenance of remission in patients with Wegener's granulomatosis, according to results from a multicenter, randomized, placebo-controlled trial.

“Our results underscore three points,” according to John H. Stone, M.D., of the Johns Hopkins Vasculitis Center, Baltimore. “Standard therapy fails to induce durable remissions in the majority of patients, etanercept does not enhance the effects of standard therapy, and even with the shorter courses of cyclophosphamide, now regarded as the standard of care, adverse events are common and frequently severe, with or without the addition of a specific tumor necrosis factor-? blockade.”

Dr. Stone and other members of the Wegener's Granulomatosis Etanercept Trial Research Group evaluated etanercept for maintenance of remission in 180 patients with Wegener's granulomatosis (N. Engl. J. Med. 2005;352:351-61). Of the total, 89 received 25 mg etanercept twice a week via subcutaneous injection, and 91 received placebo. Each patient received standard therapy that consisted of glucocorticoids plus cyclophosphamide or methotrexate.

During the mean 27-month follow-up period, there were no differences between the etanercept group and the controls in terms of sustained remission (70% vs. 75%, respectively), sustained periods of low-level disease activity (87% vs. 91%, respectively), or the time required to achieve those measures.

In addition, 118 flares occurred in the etanercept group, compared with 134 in the control group, a difference that was not statistically significant.

Etanercept does not impact maintenance of remission in patients with Wegener's granulomatosis, according to results from a multicenter, randomized, placebo-controlled trial.

“Our results underscore three points,” according to John H. Stone, M.D., of the Johns Hopkins Vasculitis Center, Baltimore. “Standard therapy fails to induce durable remissions in the majority of patients, etanercept does not enhance the effects of standard therapy, and even with the shorter courses of cyclophosphamide, now regarded as the standard of care, adverse events are common and frequently severe, with or without the addition of a specific tumor necrosis factor-? blockade.”

Dr. Stone and other members of the Wegener's Granulomatosis Etanercept Trial Research Group evaluated etanercept for maintenance of remission in 180 patients with Wegener's granulomatosis (N. Engl. J. Med. 2005;352:351-61). Of the total, 89 received 25 mg etanercept twice a week via subcutaneous injection, and 91 received placebo. Each patient received standard therapy that consisted of glucocorticoids plus cyclophosphamide or methotrexate.

During the mean 27-month follow-up period, there were no differences between the etanercept group and the controls in terms of sustained remission (70% vs. 75%, respectively), sustained periods of low-level disease activity (87% vs. 91%, respectively), or the time required to achieve those measures.

In addition, 118 flares occurred in the etanercept group, compared with 134 in the control group, a difference that was not statistically significant.

Etanercept does not impact maintenance of remission in patients with Wegener's granulomatosis, according to results from a multicenter, randomized, placebo-controlled trial.

“Our results underscore three points,” according to John H. Stone, M.D., of the Johns Hopkins Vasculitis Center, Baltimore. “Standard therapy fails to induce durable remissions in the majority of patients, etanercept does not enhance the effects of standard therapy, and even with the shorter courses of cyclophosphamide, now regarded as the standard of care, adverse events are common and frequently severe, with or without the addition of a specific tumor necrosis factor-? blockade.”

Dr. Stone and other members of the Wegener's Granulomatosis Etanercept Trial Research Group evaluated etanercept for maintenance of remission in 180 patients with Wegener's granulomatosis (N. Engl. J. Med. 2005;352:351-61). Of the total, 89 received 25 mg etanercept twice a week via subcutaneous injection, and 91 received placebo. Each patient received standard therapy that consisted of glucocorticoids plus cyclophosphamide or methotrexate.

During the mean 27-month follow-up period, there were no differences between the etanercept group and the controls in terms of sustained remission (70% vs. 75%, respectively), sustained periods of low-level disease activity (87% vs. 91%, respectively), or the time required to achieve those measures.

In addition, 118 flares occurred in the etanercept group, compared with 134 in the control group, a difference that was not statistically significant.

SNOWMASS, COLO. — Antimalarials may not only treat active lupus, but also benefit the heart, W. Joseph McCune, M.D., said at a symposium sponsored by the American College of Rheumatology.

Lupus patients have an elevated risk of heart disease, and antimalarials have been shown to have a number of cardioprotective properties, said Dr. McCune, professor of internal medicine at the University of Michigan, Ann Arbor.

Such benefits may help offset the deleterious effects of prednisone, which has been shown to increase cholesterol levels. Each 10-mg titration in prednisone dosage is estimated to increase serum cholesterol by 7.5 mg/dL.

Several studies have shown that antimalarials are associated with lipid profile improvements in lupus patients. Each of those studies has treated patients somewhat differently and has shown slightly different results. “But the body of the studies clearly show that when a benefit is looked for, it is found mostly in lowering LDL cholesterol,” Dr. McCune said.

In one study involving lupus patients not on corticosteroids, antimalarial therapy was associated with a 4% drop in total cholesterol at 3 months and a 1% drop at 6 months, compared with baseline levels. In patients on a corticosteroid, antimalarial therapy was associated with an 11% drop in total cholesterol at 3 months and a 9% drop at 6 months (J. Rheumatol. 1999;26:325-30).

Among diabetes patients, antimalarials have been shown to lower glucose levels in non-insulin-dependent patients. They also reduce insulin requirements in insulin-dependent patients. The dosages used have tended to be much higher than those typically used in rheumatology. However, even at the lower dosages used for treating lupus, it's believed that there is some positive effect on glucose tolerance, Dr. McCune said.

Dehydroepiandrosterone, which can be steroid sparing when it is added to lupus treatment, may produce increases in bone density that could offset steroid-induced osteopenia. But this has not been shown in patients with lupus, and the evidence is not definitive.

Statins clearly have immunomodulatory effects and have been shown to help prevent transplant rejection and to improve rheumatoid arthritis symptoms. However, at present there are no trials of statins used in patients with lupus, Dr. McCune said.

SNOWMASS, COLO. — Antimalarials may not only treat active lupus, but also benefit the heart, W. Joseph McCune, M.D., said at a symposium sponsored by the American College of Rheumatology.

Lupus patients have an elevated risk of heart disease, and antimalarials have been shown to have a number of cardioprotective properties, said Dr. McCune, professor of internal medicine at the University of Michigan, Ann Arbor.

Such benefits may help offset the deleterious effects of prednisone, which has been shown to increase cholesterol levels. Each 10-mg titration in prednisone dosage is estimated to increase serum cholesterol by 7.5 mg/dL.

Several studies have shown that antimalarials are associated with lipid profile improvements in lupus patients. Each of those studies has treated patients somewhat differently and has shown slightly different results. “But the body of the studies clearly show that when a benefit is looked for, it is found mostly in lowering LDL cholesterol,” Dr. McCune said.

In one study involving lupus patients not on corticosteroids, antimalarial therapy was associated with a 4% drop in total cholesterol at 3 months and a 1% drop at 6 months, compared with baseline levels. In patients on a corticosteroid, antimalarial therapy was associated with an 11% drop in total cholesterol at 3 months and a 9% drop at 6 months (J. Rheumatol. 1999;26:325-30).

Among diabetes patients, antimalarials have been shown to lower glucose levels in non-insulin-dependent patients. They also reduce insulin requirements in insulin-dependent patients. The dosages used have tended to be much higher than those typically used in rheumatology. However, even at the lower dosages used for treating lupus, it's believed that there is some positive effect on glucose tolerance, Dr. McCune said.

Dehydroepiandrosterone, which can be steroid sparing when it is added to lupus treatment, may produce increases in bone density that could offset steroid-induced osteopenia. But this has not been shown in patients with lupus, and the evidence is not definitive.

Statins clearly have immunomodulatory effects and have been shown to help prevent transplant rejection and to improve rheumatoid arthritis symptoms. However, at present there are no trials of statins used in patients with lupus, Dr. McCune said.

SNOWMASS, COLO. — Antimalarials may not only treat active lupus, but also benefit the heart, W. Joseph McCune, M.D., said at a symposium sponsored by the American College of Rheumatology.

Lupus patients have an elevated risk of heart disease, and antimalarials have been shown to have a number of cardioprotective properties, said Dr. McCune, professor of internal medicine at the University of Michigan, Ann Arbor.

Such benefits may help offset the deleterious effects of prednisone, which has been shown to increase cholesterol levels. Each 10-mg titration in prednisone dosage is estimated to increase serum cholesterol by 7.5 mg/dL.

Several studies have shown that antimalarials are associated with lipid profile improvements in lupus patients. Each of those studies has treated patients somewhat differently and has shown slightly different results. “But the body of the studies clearly show that when a benefit is looked for, it is found mostly in lowering LDL cholesterol,” Dr. McCune said.

In one study involving lupus patients not on corticosteroids, antimalarial therapy was associated with a 4% drop in total cholesterol at 3 months and a 1% drop at 6 months, compared with baseline levels. In patients on a corticosteroid, antimalarial therapy was associated with an 11% drop in total cholesterol at 3 months and a 9% drop at 6 months (J. Rheumatol. 1999;26:325-30).

Among diabetes patients, antimalarials have been shown to lower glucose levels in non-insulin-dependent patients. They also reduce insulin requirements in insulin-dependent patients. The dosages used have tended to be much higher than those typically used in rheumatology. However, even at the lower dosages used for treating lupus, it's believed that there is some positive effect on glucose tolerance, Dr. McCune said.

Dehydroepiandrosterone, which can be steroid sparing when it is added to lupus treatment, may produce increases in bone density that could offset steroid-induced osteopenia. But this has not been shown in patients with lupus, and the evidence is not definitive.

Statins clearly have immunomodulatory effects and have been shown to help prevent transplant rejection and to improve rheumatoid arthritis symptoms. However, at present there are no trials of statins used in patients with lupus, Dr. McCune said.

BOSTON — High-dose intravenous chemotherapy and autologous stem cell transplantation significantly improve the survival and organ response of some patients with primary amyloidosis, a longitudinal analysis has shown.

Until recently, the prognosis for patients with primary amyloidosis has been poor, with median survival rates of just 1-2 years, said Martha Skinner, M.D., at a meeting on advances in rheumatology sponsored by Harvard Medical School.

Primary amyloidosis, also called AL amyloidosis, involves an overproduction of amyloid light (AL) chain proteins caused by an underlying plasma cell abnormality. The excess proteins build up in tissues and organs, disrupting the structure and function of the heart, liver, kidneys, spleen, intestines, skin, and nervous system. Amyloid cardiomyopathy is a particularly fatal complication of the disease.

Conventional treatment with low-dose oral melphalan has been associated with a very low response rate, said Dr. Skinner, director of the amyloid program at Boston University Medical Center. Recently, however, aggressive treatment with high-dose intravenous melphalan followed by stem cell replacement or rescue has proven to be a more effective therapy, she said. In selected patients, this regimen has resulted in hematologic remission, improved survival rates, and reversal of amyloid-related disease, according to a review of outcome data.

Dr. Skinner and her colleagues analyzed data for 701 consecutive patients with AL amyloidosis who participated in six separate trials over a period of 8 years. They looked for evidence of persistent disease after treatment, and they assessed duration of survival and organ function.

Of the combined study populations, 394 patients were eligible for high-dose melphalan (100-200 mg/m2) and stem cell transplantation based on organ involvement and clinical status. Of these, 312 patients initiated treatment. The remaining 82 eligible patients did not proceed with treatment by choice or because of disease progression.

Among the treated patients, 40% had a complete hematologic response, defined as no evidence of an underlying plasma cell dyscrasia 1 year after treatment. Of those who remained in complete remission 1 year after treatment, 8% had relapses within 2 years, but none had relapses after 2 years, said Dr. Skinner.

Patients with a complete hematologic response had greater statistically significant improvements in end-organ disease, compared with treated patients who had evidence of persistent plasma cell dyscrasia, she said.

The hematologic and end-organ responses to treatment were accompanied by measurable and sustained quality of life improvements based on Short-Form Health Survey (SF-36) scores, said Dr. Skinner. At baseline, the scores were significantly lower on all eight SF-36 scales, compared with age-matched population norms. At 1 year, all of the scores had improved, with the mental component summary scores reaching the population norm. The physical component summary scores, which were lower than the population norm but still improved, were higher in the subgroup of patients who achieved a complete hematologic response, she said.

Mortality within 100 days of treatment was 13%, said Dr. Skinner, noting that patients in the treatment group who had cardiomyopathy had the highest mortality, compared with the other patients in the treatment group. The median survival of the treatment group was 4.6 years, Dr. Skinner said. Of 137 treated patients with heart involvement, approximately half were alive after 1.5 years, compared with 6.5 years for those treated patients without heart involvement. Half of the patients who were not eligible for the aggressive treatment died within 4 months.

The results should be taken in context, Dr. Skinner advised. “Patients were collected from multiple studies.”

BOSTON — High-dose intravenous chemotherapy and autologous stem cell transplantation significantly improve the survival and organ response of some patients with primary amyloidosis, a longitudinal analysis has shown.

Until recently, the prognosis for patients with primary amyloidosis has been poor, with median survival rates of just 1-2 years, said Martha Skinner, M.D., at a meeting on advances in rheumatology sponsored by Harvard Medical School.

Primary amyloidosis, also called AL amyloidosis, involves an overproduction of amyloid light (AL) chain proteins caused by an underlying plasma cell abnormality. The excess proteins build up in tissues and organs, disrupting the structure and function of the heart, liver, kidneys, spleen, intestines, skin, and nervous system. Amyloid cardiomyopathy is a particularly fatal complication of the disease.

Conventional treatment with low-dose oral melphalan has been associated with a very low response rate, said Dr. Skinner, director of the amyloid program at Boston University Medical Center. Recently, however, aggressive treatment with high-dose intravenous melphalan followed by stem cell replacement or rescue has proven to be a more effective therapy, she said. In selected patients, this regimen has resulted in hematologic remission, improved survival rates, and reversal of amyloid-related disease, according to a review of outcome data.

Dr. Skinner and her colleagues analyzed data for 701 consecutive patients with AL amyloidosis who participated in six separate trials over a period of 8 years. They looked for evidence of persistent disease after treatment, and they assessed duration of survival and organ function.

Of the combined study populations, 394 patients were eligible for high-dose melphalan (100-200 mg/m2) and stem cell transplantation based on organ involvement and clinical status. Of these, 312 patients initiated treatment. The remaining 82 eligible patients did not proceed with treatment by choice or because of disease progression.

Among the treated patients, 40% had a complete hematologic response, defined as no evidence of an underlying plasma cell dyscrasia 1 year after treatment. Of those who remained in complete remission 1 year after treatment, 8% had relapses within 2 years, but none had relapses after 2 years, said Dr. Skinner.

Patients with a complete hematologic response had greater statistically significant improvements in end-organ disease, compared with treated patients who had evidence of persistent plasma cell dyscrasia, she said.

The hematologic and end-organ responses to treatment were accompanied by measurable and sustained quality of life improvements based on Short-Form Health Survey (SF-36) scores, said Dr. Skinner. At baseline, the scores were significantly lower on all eight SF-36 scales, compared with age-matched population norms. At 1 year, all of the scores had improved, with the mental component summary scores reaching the population norm. The physical component summary scores, which were lower than the population norm but still improved, were higher in the subgroup of patients who achieved a complete hematologic response, she said.

Mortality within 100 days of treatment was 13%, said Dr. Skinner, noting that patients in the treatment group who had cardiomyopathy had the highest mortality, compared with the other patients in the treatment group. The median survival of the treatment group was 4.6 years, Dr. Skinner said. Of 137 treated patients with heart involvement, approximately half were alive after 1.5 years, compared with 6.5 years for those treated patients without heart involvement. Half of the patients who were not eligible for the aggressive treatment died within 4 months.

The results should be taken in context, Dr. Skinner advised. “Patients were collected from multiple studies.”

BOSTON — High-dose intravenous chemotherapy and autologous stem cell transplantation significantly improve the survival and organ response of some patients with primary amyloidosis, a longitudinal analysis has shown.

Until recently, the prognosis for patients with primary amyloidosis has been poor, with median survival rates of just 1-2 years, said Martha Skinner, M.D., at a meeting on advances in rheumatology sponsored by Harvard Medical School.

Primary amyloidosis, also called AL amyloidosis, involves an overproduction of amyloid light (AL) chain proteins caused by an underlying plasma cell abnormality. The excess proteins build up in tissues and organs, disrupting the structure and function of the heart, liver, kidneys, spleen, intestines, skin, and nervous system. Amyloid cardiomyopathy is a particularly fatal complication of the disease.

Conventional treatment with low-dose oral melphalan has been associated with a very low response rate, said Dr. Skinner, director of the amyloid program at Boston University Medical Center. Recently, however, aggressive treatment with high-dose intravenous melphalan followed by stem cell replacement or rescue has proven to be a more effective therapy, she said. In selected patients, this regimen has resulted in hematologic remission, improved survival rates, and reversal of amyloid-related disease, according to a review of outcome data.

Dr. Skinner and her colleagues analyzed data for 701 consecutive patients with AL amyloidosis who participated in six separate trials over a period of 8 years. They looked for evidence of persistent disease after treatment, and they assessed duration of survival and organ function.

Of the combined study populations, 394 patients were eligible for high-dose melphalan (100-200 mg/m2) and stem cell transplantation based on organ involvement and clinical status. Of these, 312 patients initiated treatment. The remaining 82 eligible patients did not proceed with treatment by choice or because of disease progression.

Among the treated patients, 40% had a complete hematologic response, defined as no evidence of an underlying plasma cell dyscrasia 1 year after treatment. Of those who remained in complete remission 1 year after treatment, 8% had relapses within 2 years, but none had relapses after 2 years, said Dr. Skinner.

Patients with a complete hematologic response had greater statistically significant improvements in end-organ disease, compared with treated patients who had evidence of persistent plasma cell dyscrasia, she said.

The hematologic and end-organ responses to treatment were accompanied by measurable and sustained quality of life improvements based on Short-Form Health Survey (SF-36) scores, said Dr. Skinner. At baseline, the scores were significantly lower on all eight SF-36 scales, compared with age-matched population norms. At 1 year, all of the scores had improved, with the mental component summary scores reaching the population norm. The physical component summary scores, which were lower than the population norm but still improved, were higher in the subgroup of patients who achieved a complete hematologic response, she said.

Mortality within 100 days of treatment was 13%, said Dr. Skinner, noting that patients in the treatment group who had cardiomyopathy had the highest mortality, compared with the other patients in the treatment group. The median survival of the treatment group was 4.6 years, Dr. Skinner said. Of 137 treated patients with heart involvement, approximately half were alive after 1.5 years, compared with 6.5 years for those treated patients without heart involvement. Half of the patients who were not eligible for the aggressive treatment died within 4 months.

The results should be taken in context, Dr. Skinner advised. “Patients were collected from multiple studies.”

NEW ORLEANS — Younger women with acute MI are a particularly high-priority target population in terms of screening for and treatment of postinfarct depression, Susmita Mallik, M.D., said at the annual scientific sessions of the American Heart Association.

She reported on 2,501 patients admitted with acute MI to 19 U.S. medical centers participating in the Prospective Registry Evaluating Outcomes After Myocardial Infarction: Events and Recovery (PREMIER) study. Roughly half the patients were age 60 or younger, and 815 participants were women.

The prevalence of in-hospital depression—defined by a score of at least 10 on the Primary Care Evaluation of Mental Disorders Brief Patient Health Questionnaire—was 40% in women and 22% in men age 60 or younger, and 21% among women and 16% in men over age 60, said Dr. Mallik of Emory University, Atlanta.

After adjusting for race, comorbid conditions, smoking status, and other potential confounders, the odds of experiencing in-hospital depression following an acute MI were nearly fourfold greater in women under age 60 than in men over age 60.

This observation supports community-based studies showing that the prevalence of depression is higher in young women than in the general population, she added.

NEW ORLEANS — Younger women with acute MI are a particularly high-priority target population in terms of screening for and treatment of postinfarct depression, Susmita Mallik, M.D., said at the annual scientific sessions of the American Heart Association.

She reported on 2,501 patients admitted with acute MI to 19 U.S. medical centers participating in the Prospective Registry Evaluating Outcomes After Myocardial Infarction: Events and Recovery (PREMIER) study. Roughly half the patients were age 60 or younger, and 815 participants were women.

The prevalence of in-hospital depression—defined by a score of at least 10 on the Primary Care Evaluation of Mental Disorders Brief Patient Health Questionnaire—was 40% in women and 22% in men age 60 or younger, and 21% among women and 16% in men over age 60, said Dr. Mallik of Emory University, Atlanta.

After adjusting for race, comorbid conditions, smoking status, and other potential confounders, the odds of experiencing in-hospital depression following an acute MI were nearly fourfold greater in women under age 60 than in men over age 60.

This observation supports community-based studies showing that the prevalence of depression is higher in young women than in the general population, she added.

NEW ORLEANS — Younger women with acute MI are a particularly high-priority target population in terms of screening for and treatment of postinfarct depression, Susmita Mallik, M.D., said at the annual scientific sessions of the American Heart Association.

She reported on 2,501 patients admitted with acute MI to 19 U.S. medical centers participating in the Prospective Registry Evaluating Outcomes After Myocardial Infarction: Events and Recovery (PREMIER) study. Roughly half the patients were age 60 or younger, and 815 participants were women.

The prevalence of in-hospital depression—defined by a score of at least 10 on the Primary Care Evaluation of Mental Disorders Brief Patient Health Questionnaire—was 40% in women and 22% in men age 60 or younger, and 21% among women and 16% in men over age 60, said Dr. Mallik of Emory University, Atlanta.

After adjusting for race, comorbid conditions, smoking status, and other potential confounders, the odds of experiencing in-hospital depression following an acute MI were nearly fourfold greater in women under age 60 than in men over age 60.

This observation supports community-based studies showing that the prevalence of depression is higher in young women than in the general population, she added.

NEW ORLEANS — Mortality is extraordinarily high in the year after acute MI in patients with renal failure—and the explanation may lie largely in their strikingly different clinical characteristics as compared with the general MI population.

In this regard, dialysis patients and those with non-dialysis-dependent chronic renal insufficiency look much more alike as a group, and distinctly different from acute MI patients without a history of renal impairment, Charles A. Herzog, M.D., said at the annual scientific sessions of the American Heart Association.

Dialysis patients have a “dismal” 60% 1-year mortality following acute MI, noted Dr. Herzog, a cardiologist with the U.S. Renal Data System and Minneapolis Medical Foundation.

In an effort to understand why patients with renal failure fare so poorly after an MI, he and his coinvestigators constructed a unique database by cross matching the records of the U.S. Renal Data System and the National Registry of Myocardial Infarction-3, a large Genentech-sponsored registry of MI patients. This yielded a study population consisting of 2,720 renal dialysis patients with MI; 35,950 MI patients with non-dialysis-dependent renal insufficiency; and 384,415 MI patients with no history of chronic renal disease. None of the study participants was transferred for MI care.

Many statistically and clinically significant differences were apparent between the renal patients and those in the general population. (See box.)

Among the differences that may have had the greatest bearing on the poor long-term prognosis of patients with renal disease were their lesser likelihood of presenting with chest pain, in Killip class I, or with ST-elevation MI, as well as the lower diagnostic suspicion of MI upon presentation. By ECG criteria, a much lower percentage of renal failure patients were eligible for any sort of reperfusion therapy, Dr. Herzog said.

There was no major difference between the groups in terms of prehospital delay, which averaged about 5.5 hours from symptom onset to hospital presentation, so an educational campaign aimed at increasing renal patients' awareness of MI signs and symptoms isn't likely to yield major improvements in long-term outcome, Dr. Herzog said.

In response to audience expressions of surprise that the patients with non-dialysis-dependent renal insufficiency fared as poorly post MI as patients requiring dialysis, Dr. Herzog replied that this appeared to be largely an age-driven phenomenon.

Advanced age has long been recognized as an important predictor of worse outcome after an MI, he noted, and in this study the non-dialysis-dependent renal patients were significantly older than the other two groups, with a mean age of 75 years, compared with 68 years in the dialysis patients and 69 years in MI patients without renal disease.

NEW ORLEANS — Mortality is extraordinarily high in the year after acute MI in patients with renal failure—and the explanation may lie largely in their strikingly different clinical characteristics as compared with the general MI population.

In this regard, dialysis patients and those with non-dialysis-dependent chronic renal insufficiency look much more alike as a group, and distinctly different from acute MI patients without a history of renal impairment, Charles A. Herzog, M.D., said at the annual scientific sessions of the American Heart Association.

Dialysis patients have a “dismal” 60% 1-year mortality following acute MI, noted Dr. Herzog, a cardiologist with the U.S. Renal Data System and Minneapolis Medical Foundation.

In an effort to understand why patients with renal failure fare so poorly after an MI, he and his coinvestigators constructed a unique database by cross matching the records of the U.S. Renal Data System and the National Registry of Myocardial Infarction-3, a large Genentech-sponsored registry of MI patients. This yielded a study population consisting of 2,720 renal dialysis patients with MI; 35,950 MI patients with non-dialysis-dependent renal insufficiency; and 384,415 MI patients with no history of chronic renal disease. None of the study participants was transferred for MI care.

Many statistically and clinically significant differences were apparent between the renal patients and those in the general population. (See box.)

Among the differences that may have had the greatest bearing on the poor long-term prognosis of patients with renal disease were their lesser likelihood of presenting with chest pain, in Killip class I, or with ST-elevation MI, as well as the lower diagnostic suspicion of MI upon presentation. By ECG criteria, a much lower percentage of renal failure patients were eligible for any sort of reperfusion therapy, Dr. Herzog said.

There was no major difference between the groups in terms of prehospital delay, which averaged about 5.5 hours from symptom onset to hospital presentation, so an educational campaign aimed at increasing renal patients' awareness of MI signs and symptoms isn't likely to yield major improvements in long-term outcome, Dr. Herzog said.

In response to audience expressions of surprise that the patients with non-dialysis-dependent renal insufficiency fared as poorly post MI as patients requiring dialysis, Dr. Herzog replied that this appeared to be largely an age-driven phenomenon.

Advanced age has long been recognized as an important predictor of worse outcome after an MI, he noted, and in this study the non-dialysis-dependent renal patients were significantly older than the other two groups, with a mean age of 75 years, compared with 68 years in the dialysis patients and 69 years in MI patients without renal disease.

NEW ORLEANS — Mortality is extraordinarily high in the year after acute MI in patients with renal failure—and the explanation may lie largely in their strikingly different clinical characteristics as compared with the general MI population.

In this regard, dialysis patients and those with non-dialysis-dependent chronic renal insufficiency look much more alike as a group, and distinctly different from acute MI patients without a history of renal impairment, Charles A. Herzog, M.D., said at the annual scientific sessions of the American Heart Association.

Dialysis patients have a “dismal” 60% 1-year mortality following acute MI, noted Dr. Herzog, a cardiologist with the U.S. Renal Data System and Minneapolis Medical Foundation.

In an effort to understand why patients with renal failure fare so poorly after an MI, he and his coinvestigators constructed a unique database by cross matching the records of the U.S. Renal Data System and the National Registry of Myocardial Infarction-3, a large Genentech-sponsored registry of MI patients. This yielded a study population consisting of 2,720 renal dialysis patients with MI; 35,950 MI patients with non-dialysis-dependent renal insufficiency; and 384,415 MI patients with no history of chronic renal disease. None of the study participants was transferred for MI care.

Many statistically and clinically significant differences were apparent between the renal patients and those in the general population. (See box.)

Among the differences that may have had the greatest bearing on the poor long-term prognosis of patients with renal disease were their lesser likelihood of presenting with chest pain, in Killip class I, or with ST-elevation MI, as well as the lower diagnostic suspicion of MI upon presentation. By ECG criteria, a much lower percentage of renal failure patients were eligible for any sort of reperfusion therapy, Dr. Herzog said.

There was no major difference between the groups in terms of prehospital delay, which averaged about 5.5 hours from symptom onset to hospital presentation, so an educational campaign aimed at increasing renal patients' awareness of MI signs and symptoms isn't likely to yield major improvements in long-term outcome, Dr. Herzog said.

In response to audience expressions of surprise that the patients with non-dialysis-dependent renal insufficiency fared as poorly post MI as patients requiring dialysis, Dr. Herzog replied that this appeared to be largely an age-driven phenomenon.

Advanced age has long been recognized as an important predictor of worse outcome after an MI, he noted, and in this study the non-dialysis-dependent renal patients were significantly older than the other two groups, with a mean age of 75 years, compared with 68 years in the dialysis patients and 69 years in MI patients without renal disease.

NEW ORLEANS — Use of intravenous morphine in patients with acute coronary syndromes is a long-standing common practice—and the focus of new safety questions.

Data from the CRUSADE national quality-improvement registry indicate nearly 30% of patients hospitalized with non-ST segment elevation acute coronary syndrome (NSTE ACS) receive intravenous morphine within the first 24 hours of presentation.

Patients who received morphine had increased rates of mortality and other in-hospital adverse outcomes than did those who did not, even after controlling for differences in patient, hospital, and physician characteristics, Trip J. Meine, M.D., reported at the annual scientific sessions of the American Heart Association.

Morphine has been used for management of refractory chest pain in patients with MI since at least 1912. The practice has never been the subject of a randomized trial, nor even—until CRUSADE—a large observational study. Yet it enjoys a class I-C recommendation in the AHA/American College of Cardiology guidelines, noted Dr. Meine of the Duke Clinical Research Institute, Durham, N.C.

He reported that of 57,039 patients who presented with NSTE ACS in 2001-2003 to more than 400 U.S. hospitals participating in CRUSADE (Can Rapid Risk Stratification of Unstable Angina Patients Suppress Adverse Outcomes With Early Implementation of the ACC/AHA Guidelines), 30% received intravenous morphine within the first 24 hours.

“That was the first surprise. It's a really common practice,” he observed.

Morphine-treated patients presented with more high-risk features, such as ST-segment depression and positive biomarkers, than patients who didn't get morphine.

Perhaps for this reason, morphine recipients also were more likely to get evidence-based medications in accord with ACC/AHA guidelines, including ?-blockers, aspirin, and glycoprotein IIb/IIIa inhibitors. They also got speedier care and were more likely to undergo diagnostic cardiac catheterization and coronary revascularization, all of which indicates morphine use is not a marker for overall suboptimal care.

Morphine-treated patients had worse unadjusted in-hospital outcomes. Moreover, after extensive statistical adjustment for patient risk level, use of evidence-based therapies, and hospital and physician characteristics, they still had a 48% increased relative risk of death and a 34% increased risk of reinfarction, compared with patients who didn't get morphine.

Could morphine merely be a marker for more refractory ongoing chest pain and a particularly severe acute presentation? To examine this possibility, investigators looked at the more than 13,000 patients who got another agent widely prescribed for chest pain—intravenous nitroglycerin—but not morphine.

Like the morphine-treated patients, those on intravenous nitroglycerin presented with more high-risk characteristics and were more likely to receive evidence-based therapies than were patients on neither therapy. Yet their in-hospital combined death or reinfarction rate was only 6.5%, compared with 9.6% in the morphine group. After controlling for patient risk level and other relevant factors, morphine-treated patients still had a 40% greater risk of the combined end point than did those given intravenous nitroglycerin.

Clinical outcomes in the subset of CRUSADE participants who got both agents were worse than in those who received intravenous nitroglycerin alone.

It's worth noting, Dr. Meine continued, that nitroglycerin reduces ventricular wall tension and myocardial oxygen demand, both potentially beneficial effects on ischemic myocardium. In contrast, morphine has many side effects that reduce myocardial oxygen delivery and are thus potentially harmful to ischemic myocardium, including respiratory depression, bradycardia, and hypotension.

“I think it's important to bring up the question of whether morphine itself is a deleterious medication,” Dr. Meine said. “Clearly, a randomized controlled trial is warranted. … My gut feeling is morphine is probably often reached for much earlier than it needs to be, before trying maximum-dose IV nitroglycerin.”

NEW ORLEANS — Use of intravenous morphine in patients with acute coronary syndromes is a long-standing common practice—and the focus of new safety questions.

Data from the CRUSADE national quality-improvement registry indicate nearly 30% of patients hospitalized with non-ST segment elevation acute coronary syndrome (NSTE ACS) receive intravenous morphine within the first 24 hours of presentation.

Patients who received morphine had increased rates of mortality and other in-hospital adverse outcomes than did those who did not, even after controlling for differences in patient, hospital, and physician characteristics, Trip J. Meine, M.D., reported at the annual scientific sessions of the American Heart Association.

Morphine has been used for management of refractory chest pain in patients with MI since at least 1912. The practice has never been the subject of a randomized trial, nor even—until CRUSADE—a large observational study. Yet it enjoys a class I-C recommendation in the AHA/American College of Cardiology guidelines, noted Dr. Meine of the Duke Clinical Research Institute, Durham, N.C.

He reported that of 57,039 patients who presented with NSTE ACS in 2001-2003 to more than 400 U.S. hospitals participating in CRUSADE (Can Rapid Risk Stratification of Unstable Angina Patients Suppress Adverse Outcomes With Early Implementation of the ACC/AHA Guidelines), 30% received intravenous morphine within the first 24 hours.

“That was the first surprise. It's a really common practice,” he observed.

Morphine-treated patients presented with more high-risk features, such as ST-segment depression and positive biomarkers, than patients who didn't get morphine.

Perhaps for this reason, morphine recipients also were more likely to get evidence-based medications in accord with ACC/AHA guidelines, including ?-blockers, aspirin, and glycoprotein IIb/IIIa inhibitors. They also got speedier care and were more likely to undergo diagnostic cardiac catheterization and coronary revascularization, all of which indicates morphine use is not a marker for overall suboptimal care.

Morphine-treated patients had worse unadjusted in-hospital outcomes. Moreover, after extensive statistical adjustment for patient risk level, use of evidence-based therapies, and hospital and physician characteristics, they still had a 48% increased relative risk of death and a 34% increased risk of reinfarction, compared with patients who didn't get morphine.

Could morphine merely be a marker for more refractory ongoing chest pain and a particularly severe acute presentation? To examine this possibility, investigators looked at the more than 13,000 patients who got another agent widely prescribed for chest pain—intravenous nitroglycerin—but not morphine.

Like the morphine-treated patients, those on intravenous nitroglycerin presented with more high-risk characteristics and were more likely to receive evidence-based therapies than were patients on neither therapy. Yet their in-hospital combined death or reinfarction rate was only 6.5%, compared with 9.6% in the morphine group. After controlling for patient risk level and other relevant factors, morphine-treated patients still had a 40% greater risk of the combined end point than did those given intravenous nitroglycerin.

Clinical outcomes in the subset of CRUSADE participants who got both agents were worse than in those who received intravenous nitroglycerin alone.

It's worth noting, Dr. Meine continued, that nitroglycerin reduces ventricular wall tension and myocardial oxygen demand, both potentially beneficial effects on ischemic myocardium. In contrast, morphine has many side effects that reduce myocardial oxygen delivery and are thus potentially harmful to ischemic myocardium, including respiratory depression, bradycardia, and hypotension.

“I think it's important to bring up the question of whether morphine itself is a deleterious medication,” Dr. Meine said. “Clearly, a randomized controlled trial is warranted. … My gut feeling is morphine is probably often reached for much earlier than it needs to be, before trying maximum-dose IV nitroglycerin.”

NEW ORLEANS — Use of intravenous morphine in patients with acute coronary syndromes is a long-standing common practice—and the focus of new safety questions.

Data from the CRUSADE national quality-improvement registry indicate nearly 30% of patients hospitalized with non-ST segment elevation acute coronary syndrome (NSTE ACS) receive intravenous morphine within the first 24 hours of presentation.

Patients who received morphine had increased rates of mortality and other in-hospital adverse outcomes than did those who did not, even after controlling for differences in patient, hospital, and physician characteristics, Trip J. Meine, M.D., reported at the annual scientific sessions of the American Heart Association.

Morphine has been used for management of refractory chest pain in patients with MI since at least 1912. The practice has never been the subject of a randomized trial, nor even—until CRUSADE—a large observational study. Yet it enjoys a class I-C recommendation in the AHA/American College of Cardiology guidelines, noted Dr. Meine of the Duke Clinical Research Institute, Durham, N.C.

He reported that of 57,039 patients who presented with NSTE ACS in 2001-2003 to more than 400 U.S. hospitals participating in CRUSADE (Can Rapid Risk Stratification of Unstable Angina Patients Suppress Adverse Outcomes With Early Implementation of the ACC/AHA Guidelines), 30% received intravenous morphine within the first 24 hours.

“That was the first surprise. It's a really common practice,” he observed.

Morphine-treated patients presented with more high-risk features, such as ST-segment depression and positive biomarkers, than patients who didn't get morphine.

Perhaps for this reason, morphine recipients also were more likely to get evidence-based medications in accord with ACC/AHA guidelines, including ?-blockers, aspirin, and glycoprotein IIb/IIIa inhibitors. They also got speedier care and were more likely to undergo diagnostic cardiac catheterization and coronary revascularization, all of which indicates morphine use is not a marker for overall suboptimal care.

Morphine-treated patients had worse unadjusted in-hospital outcomes. Moreover, after extensive statistical adjustment for patient risk level, use of evidence-based therapies, and hospital and physician characteristics, they still had a 48% increased relative risk of death and a 34% increased risk of reinfarction, compared with patients who didn't get morphine.

Could morphine merely be a marker for more refractory ongoing chest pain and a particularly severe acute presentation? To examine this possibility, investigators looked at the more than 13,000 patients who got another agent widely prescribed for chest pain—intravenous nitroglycerin—but not morphine.

Like the morphine-treated patients, those on intravenous nitroglycerin presented with more high-risk characteristics and were more likely to receive evidence-based therapies than were patients on neither therapy. Yet their in-hospital combined death or reinfarction rate was only 6.5%, compared with 9.6% in the morphine group. After controlling for patient risk level and other relevant factors, morphine-treated patients still had a 40% greater risk of the combined end point than did those given intravenous nitroglycerin.

Clinical outcomes in the subset of CRUSADE participants who got both agents were worse than in those who received intravenous nitroglycerin alone.

It's worth noting, Dr. Meine continued, that nitroglycerin reduces ventricular wall tension and myocardial oxygen demand, both potentially beneficial effects on ischemic myocardium. In contrast, morphine has many side effects that reduce myocardial oxygen delivery and are thus potentially harmful to ischemic myocardium, including respiratory depression, bradycardia, and hypotension.

“I think it's important to bring up the question of whether morphine itself is a deleterious medication,” Dr. Meine said. “Clearly, a randomized controlled trial is warranted. … My gut feeling is morphine is probably often reached for much earlier than it needs to be, before trying maximum-dose IV nitroglycerin.”

NEW ORLEANS — Treatment with abciximab failed to improve the outcomes of patients with diabetes who underwent elective percutaneous coronary interventions in a randomized study with 701 patients.

All patients in the study received a loading dose of 600 mg of the antiplatelet drug clopidogrel at least 2 hours before their percutaneous coronary intervention (PCI), which suggested that clopidogrel treatment “may obviate the need for abciximab during elective PCI in patients at low to intermediate risk,” Julinda Mehilli, M.D., reported at the annual scientific sessions of the American Heart Association.

But the results from this German study, which was not sponsored by a pharmaceutical company, cannot be considered the last word on using a glycoprotein IIb/IIIa platelet inhibitor in patients with diabetes undergoing PCI, said some experts at the meeting.

One limitation is that the current study excluded patients with acute coronary syndrome, an acute myocardial infarction, or visible thrombus. “These patients have been the sweet spot for abciximab and other IIb/IIIa inhibitors,” commented Gregg W. Stone, M.D., director of cardiovascular research and education at the Cardiovascular Research Foundation of Lenox Hill Hospital in New York.

Other shortcomings of the study included its enrollment of a relatively small number of insulin-dependent diabetics, and the fact that it was underpowered to prove that patients did just as well without abciximab as they did with the drug, commented Eric R. Bates, M.D., a professor of medicine at the University of Michigan, Ann Arbor.

The study was designed as a superiority trial, to prove that abciximab-treated patients fared better than those who didn't get the drug. Dr. Bates was also skeptical that physicians who now use abciximab to treat diabetic patients undergoing elective PCI would be persuaded to change their practice based on the results of a single study.

The study was done at three German hospitals from January 2001 to October 2003. Patients were enrolled if they were on active treatment with either insulin or an oral hypoglycemic agent and were scheduled to undergo an elective PCI in a native coronary vessel. The study's primary end point was the incidence of death or MI during the first 12 months following the procedure.

All patients received a loading dose of clopidogrel plus 500 mg aspirin. Following randomization, patients in the abciximab group received a 0.25-mg/kg bolus followed by a 0.125-mcg/kg per minute infusion for 12 hours, along with 70 U/kg of unfractionated heparin.

Patients in the placebo group received a placebo bolus and infusion, along with a 140-U/kg bolus of heparin. Following their procedure, all patients received a 200-mg daily aspirin dosage that was continued indefinitely. Patients also received 75 mg clopidogrel b.i.d. until discharge or for a maximum of 3 days, and then continued on 75 mg clopidogrel daily for at least 6 months. Patients received other medications as indicated.

After 1 year of follow-up, the incidence of death or MI was essentially identical in the two groups: 8.3% among the 351 patients treated with abciximab, and 8.6% among those treated with placebo, reported Dr. Mehilli of the German Heart Center in Munich.

The secondary end point of the study was the incidence of angiographic restenosis at follow-up. By this criterion, the abciximab group did better: Angiographic restenosis occurred in 28.9% of the patients in the abciximab group, compared with 37.8% of placebo patients, a statistically significant difference.

But this result is already outdated because the study was done largely before the advent of drug-eluting stents. Only 10% of the patients received drug-eluting stents; in this small subgroup, treatment with abciximab conferred no significant advantage over placebo.

The edge in restenosis conferred by abciximab “would have been a very important finding 2 years ago, but now it's too little too late,” said Dr. Stone. “Drug-eluting stents are clearly the treatment of choice to reduce restenosis in patients with diabetes, and no drug has been shown to reduce restenosis when used on top of drug-eluting stents,” he said.

NEW ORLEANS — Treatment with abciximab failed to improve the outcomes of patients with diabetes who underwent elective percutaneous coronary interventions in a randomized study with 701 patients.

All patients in the study received a loading dose of 600 mg of the antiplatelet drug clopidogrel at least 2 hours before their percutaneous coronary intervention (PCI), which suggested that clopidogrel treatment “may obviate the need for abciximab during elective PCI in patients at low to intermediate risk,” Julinda Mehilli, M.D., reported at the annual scientific sessions of the American Heart Association.

But the results from this German study, which was not sponsored by a pharmaceutical company, cannot be considered the last word on using a glycoprotein IIb/IIIa platelet inhibitor in patients with diabetes undergoing PCI, said some experts at the meeting.

One limitation is that the current study excluded patients with acute coronary syndrome, an acute myocardial infarction, or visible thrombus. “These patients have been the sweet spot for abciximab and other IIb/IIIa inhibitors,” commented Gregg W. Stone, M.D., director of cardiovascular research and education at the Cardiovascular Research Foundation of Lenox Hill Hospital in New York.

Other shortcomings of the study included its enrollment of a relatively small number of insulin-dependent diabetics, and the fact that it was underpowered to prove that patients did just as well without abciximab as they did with the drug, commented Eric R. Bates, M.D., a professor of medicine at the University of Michigan, Ann Arbor.

The study was designed as a superiority trial, to prove that abciximab-treated patients fared better than those who didn't get the drug. Dr. Bates was also skeptical that physicians who now use abciximab to treat diabetic patients undergoing elective PCI would be persuaded to change their practice based on the results of a single study.

The study was done at three German hospitals from January 2001 to October 2003. Patients were enrolled if they were on active treatment with either insulin or an oral hypoglycemic agent and were scheduled to undergo an elective PCI in a native coronary vessel. The study's primary end point was the incidence of death or MI during the first 12 months following the procedure.

All patients received a loading dose of clopidogrel plus 500 mg aspirin. Following randomization, patients in the abciximab group received a 0.25-mg/kg bolus followed by a 0.125-mcg/kg per minute infusion for 12 hours, along with 70 U/kg of unfractionated heparin.

Patients in the placebo group received a placebo bolus and infusion, along with a 140-U/kg bolus of heparin. Following their procedure, all patients received a 200-mg daily aspirin dosage that was continued indefinitely. Patients also received 75 mg clopidogrel b.i.d. until discharge or for a maximum of 3 days, and then continued on 75 mg clopidogrel daily for at least 6 months. Patients received other medications as indicated.

After 1 year of follow-up, the incidence of death or MI was essentially identical in the two groups: 8.3% among the 351 patients treated with abciximab, and 8.6% among those treated with placebo, reported Dr. Mehilli of the German Heart Center in Munich.

The secondary end point of the study was the incidence of angiographic restenosis at follow-up. By this criterion, the abciximab group did better: Angiographic restenosis occurred in 28.9% of the patients in the abciximab group, compared with 37.8% of placebo patients, a statistically significant difference.

But this result is already outdated because the study was done largely before the advent of drug-eluting stents. Only 10% of the patients received drug-eluting stents; in this small subgroup, treatment with abciximab conferred no significant advantage over placebo.

The edge in restenosis conferred by abciximab “would have been a very important finding 2 years ago, but now it's too little too late,” said Dr. Stone. “Drug-eluting stents are clearly the treatment of choice to reduce restenosis in patients with diabetes, and no drug has been shown to reduce restenosis when used on top of drug-eluting stents,” he said.

NEW ORLEANS — Treatment with abciximab failed to improve the outcomes of patients with diabetes who underwent elective percutaneous coronary interventions in a randomized study with 701 patients.

All patients in the study received a loading dose of 600 mg of the antiplatelet drug clopidogrel at least 2 hours before their percutaneous coronary intervention (PCI), which suggested that clopidogrel treatment “may obviate the need for abciximab during elective PCI in patients at low to intermediate risk,” Julinda Mehilli, M.D., reported at the annual scientific sessions of the American Heart Association.

But the results from this German study, which was not sponsored by a pharmaceutical company, cannot be considered the last word on using a glycoprotein IIb/IIIa platelet inhibitor in patients with diabetes undergoing PCI, said some experts at the meeting.

One limitation is that the current study excluded patients with acute coronary syndrome, an acute myocardial infarction, or visible thrombus. “These patients have been the sweet spot for abciximab and other IIb/IIIa inhibitors,” commented Gregg W. Stone, M.D., director of cardiovascular research and education at the Cardiovascular Research Foundation of Lenox Hill Hospital in New York.

Other shortcomings of the study included its enrollment of a relatively small number of insulin-dependent diabetics, and the fact that it was underpowered to prove that patients did just as well without abciximab as they did with the drug, commented Eric R. Bates, M.D., a professor of medicine at the University of Michigan, Ann Arbor.

The study was designed as a superiority trial, to prove that abciximab-treated patients fared better than those who didn't get the drug. Dr. Bates was also skeptical that physicians who now use abciximab to treat diabetic patients undergoing elective PCI would be persuaded to change their practice based on the results of a single study.

The study was done at three German hospitals from January 2001 to October 2003. Patients were enrolled if they were on active treatment with either insulin or an oral hypoglycemic agent and were scheduled to undergo an elective PCI in a native coronary vessel. The study's primary end point was the incidence of death or MI during the first 12 months following the procedure.

All patients received a loading dose of clopidogrel plus 500 mg aspirin. Following randomization, patients in the abciximab group received a 0.25-mg/kg bolus followed by a 0.125-mcg/kg per minute infusion for 12 hours, along with 70 U/kg of unfractionated heparin.

Patients in the placebo group received a placebo bolus and infusion, along with a 140-U/kg bolus of heparin. Following their procedure, all patients received a 200-mg daily aspirin dosage that was continued indefinitely. Patients also received 75 mg clopidogrel b.i.d. until discharge or for a maximum of 3 days, and then continued on 75 mg clopidogrel daily for at least 6 months. Patients received other medications as indicated.

After 1 year of follow-up, the incidence of death or MI was essentially identical in the two groups: 8.3% among the 351 patients treated with abciximab, and 8.6% among those treated with placebo, reported Dr. Mehilli of the German Heart Center in Munich.

The secondary end point of the study was the incidence of angiographic restenosis at follow-up. By this criterion, the abciximab group did better: Angiographic restenosis occurred in 28.9% of the patients in the abciximab group, compared with 37.8% of placebo patients, a statistically significant difference.

But this result is already outdated because the study was done largely before the advent of drug-eluting stents. Only 10% of the patients received drug-eluting stents; in this small subgroup, treatment with abciximab conferred no significant advantage over placebo.

The edge in restenosis conferred by abciximab “would have been a very important finding 2 years ago, but now it's too little too late,” said Dr. Stone. “Drug-eluting stents are clearly the treatment of choice to reduce restenosis in patients with diabetes, and no drug has been shown to reduce restenosis when used on top of drug-eluting stents,” he said.