Does early repolarization on ECG increase the risk of cardiac death in healthy people?

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Does early repolarization on ECG increase the risk of cardiac death in healthy people?
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Ziad SayedAhmad, MD
Fahed Darmoch, MD
Yasser Al-Khadra, MD
Amjad Kabach, MD
M. Chadi Alraies, MD, FACP

No. The early repolarization pattern on electrocardiography (ECG) in asymp­tomatic patients is nearly always a benign incidental finding. However, in a patient with a history of idiopathic ventricular fibrillation or a family history of sudden cardiac death, the finding warrants further evaluation.

DEFINING EARLY REPOLARIZATION

Figure 1. Early repolarization with and without QRS notch or slur.
Figure 1. Early repolarization with and without QRS notch or slur.
Published studies differ in their definitions of the early repolarization pattern. In 2016, Patton et al described it as ST-segment elevation in the absence of chest pain, with terminal QRS slur or terminal QRS notch.1 However, Mcfarlane et al2 described it as a J-point elevation of at least 0.1 mV in 2 or more contiguous leads on 12-lead ECG, excluding leads V1 to V3, with the presence of terminal QRS notch or slur and QRS duration less than 120 msec. They defined the J point as either the peak of QRS notch or the beginning of QRS slur (Figure 1).2 J-point elevation and QRS notch or slur are most commonly seen in left lateral leads and less often in inferior leads.

The early repolarization pattern may mimic patterns seen in myocardial infarction, pericarditis, ventricular aneurysm, hyperkalemia, and hypothermia,1,3 and misinterpreting the pattern can lead to unnecessary laboratory testing, imaging, medication use, and hospital admissions. On the other hand, misinterpreting it as benign in the presence of certain features of the history or clinical presentation can delay the diagnosis and treatment of a potentially critical condition.

PREVALENCE AND MECHANISMS

The prevalence of the early repolarization pattern in the general population ranges from 5% to 15%; the wide range reflects differences in the definition, as well as variability in the pattern of early repolarization over time.4

The early repolarization pattern is more commonly seen in African American men and in young, physically active individuals.3 In one study, it was observed in 15% of cases of idiopathic ventricular fibrillation and sudden cardiac death, especially in people ages 35 to 45.4 While there is evidence of a heritable basis in the general population, a family history of early repolarization is not known to increase the risk of sudden cardiac death.

A proposed mechanism for the early repolarization pattern is an imbalance in the ion channel system, resulting in variable refractoriness of multiple myocardial regions and varying excitability in the myocardium. This can produce a voltage gradient between myocardial regions, which is believed to cause the major hallmarks of the early repolarization pattern, ie, ST-segment elevation and QRS notching or slurring.3

Table 1. Early repolarization: High-risk features
Although the mechanistic basis of ventricular arrhythmia in patients with early repolarization is still incompletely understood, certain associations may help define the ECG phenotype that suggests increased risk of sudden cardiac death (Table 1).

MANAGEMENT

The early repolarization pattern is nearly always a benign incidental finding on ECG, with no specific signs or symptoms attributed to it. High-risk features on ECG are associated with a modest increase in absolute risk of sudden cardiac death and warrant clinical correlation.

In the absence of syncope or family history of sudden cardiac death, early repolarization does not merit further workup.2

In patients with a history of unexplained syncope and a family history of sudden cardiac death, early repolarization should be considered in overall risk stratification.1 Early repolarization in a patient with previous idiopathic ventricular fibrillation warrants referral for electrophysiologic study and, if indicated, insertion of an implantable cardiac defibrillator for secondary prevention.5

References
  1. Patton KK, Ellinor PT, Ezekowitz M, et al; American Heart Association Electrocardiography and Arrhythmias Committee of the Council on Clinical Cardiology and Council on Functional Genomics and Translational Biology. Electrocardiographic early repolarization: a scientific statement from the American Heart Association. Circulation 2016; 133(15):1520–1529. doi:10.1161/CIR.0000000000000388
  2. Macfarlane PW, Antzelevitch C, Haissaguerre M, et al. The early repolarization pattern: a consensus paper. J Am Coll Cardiol 2015; 66(4):470–477. doi:10.1016/j.jacc.2015.05.033
  3. Benito B, Guasch E, Rivard L, Nattel S. Clinical and mechanistic issues in early repolarization of normal variants and lethal arrhythmia syndromes. J Am Coll Cardiol 2010; 56(15):1177–1186. doi:10.1016/j.jacc.2010.05.037
  4. Maury P, Rollin A. Prevalence of early repolarisation/J wave patterns in the normal population. J Electrocardiol 2013; 46(5):411–416. doi:10.1016/j.jelectrocard.2013.06.014
  5. Mahida S, Sacher F, Berte B, et al. Evaluation of patients with early repolarization syndrome. J Atr Fibrillation 2014; 7(3):1083. doi:10.4022/jafib.1083
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Ziad SayedAhmad, MD
Beaumont Hospital, Department of Internal Medicine, Royal Oak, MI

Fahed Darmoch, MD
Department of Internal Medicine, Cleveland Clinic

Yasser Al-Khadra, MD
Department of Internal Medicine, Cleveland Clinic

Amjad Kabach, MD
Department of Cardiovascular Medicine, Creighton University, School of Medicine, Omaha, NE

M. Chadi Alraies, MD
Department of Cardiovascular Medicine, Wayne State University/Detroit Medical Center, Detroit, MI

Address: M. Chadi Alraies, MD, Wayne State University, Detroit Medical Center, 311 Mack Avenue, Detroit, MI 48201; alraies@hotmail.com

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Fahed Darmoch, MD
Yasser Al-Khadra, MD
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M. Chadi Alraies, MD, FACP
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Ziad SayedAhmad, MD
Fahed Darmoch, MD
Yasser Al-Khadra, MD
Amjad Kabach, MD
M. Chadi Alraies, MD, FACP
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Ziad SayedAhmad, MD
Beaumont Hospital, Department of Internal Medicine, Royal Oak, MI

Fahed Darmoch, MD
Department of Internal Medicine, Cleveland Clinic

Yasser Al-Khadra, MD
Department of Internal Medicine, Cleveland Clinic

Amjad Kabach, MD
Department of Cardiovascular Medicine, Creighton University, School of Medicine, Omaha, NE

M. Chadi Alraies, MD
Department of Cardiovascular Medicine, Wayne State University/Detroit Medical Center, Detroit, MI

Address: M. Chadi Alraies, MD, Wayne State University, Detroit Medical Center, 311 Mack Avenue, Detroit, MI 48201; alraies@hotmail.com

Author and Disclosure Information

Ziad SayedAhmad, MD
Beaumont Hospital, Department of Internal Medicine, Royal Oak, MI

Fahed Darmoch, MD
Department of Internal Medicine, Cleveland Clinic

Yasser Al-Khadra, MD
Department of Internal Medicine, Cleveland Clinic

Amjad Kabach, MD
Department of Cardiovascular Medicine, Creighton University, School of Medicine, Omaha, NE

M. Chadi Alraies, MD
Department of Cardiovascular Medicine, Wayne State University/Detroit Medical Center, Detroit, MI

Address: M. Chadi Alraies, MD, Wayne State University, Detroit Medical Center, 311 Mack Avenue, Detroit, MI 48201; alraies@hotmail.com

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Related Articles
ST-segment elevation: Differential diagnosis, caveats

No. The early repolarization pattern on electrocardiography (ECG) in asymp­tomatic patients is nearly always a benign incidental finding. However, in a patient with a history of idiopathic ventricular fibrillation or a family history of sudden cardiac death, the finding warrants further evaluation.

DEFINING EARLY REPOLARIZATION

Figure 1. Early repolarization with and without QRS notch or slur.
Figure 1. Early repolarization with and without QRS notch or slur.
Published studies differ in their definitions of the early repolarization pattern. In 2016, Patton et al described it as ST-segment elevation in the absence of chest pain, with terminal QRS slur or terminal QRS notch.1 However, Mcfarlane et al2 described it as a J-point elevation of at least 0.1 mV in 2 or more contiguous leads on 12-lead ECG, excluding leads V1 to V3, with the presence of terminal QRS notch or slur and QRS duration less than 120 msec. They defined the J point as either the peak of QRS notch or the beginning of QRS slur (Figure 1).2 J-point elevation and QRS notch or slur are most commonly seen in left lateral leads and less often in inferior leads.

The early repolarization pattern may mimic patterns seen in myocardial infarction, pericarditis, ventricular aneurysm, hyperkalemia, and hypothermia,1,3 and misinterpreting the pattern can lead to unnecessary laboratory testing, imaging, medication use, and hospital admissions. On the other hand, misinterpreting it as benign in the presence of certain features of the history or clinical presentation can delay the diagnosis and treatment of a potentially critical condition.

PREVALENCE AND MECHANISMS

The prevalence of the early repolarization pattern in the general population ranges from 5% to 15%; the wide range reflects differences in the definition, as well as variability in the pattern of early repolarization over time.4

The early repolarization pattern is more commonly seen in African American men and in young, physically active individuals.3 In one study, it was observed in 15% of cases of idiopathic ventricular fibrillation and sudden cardiac death, especially in people ages 35 to 45.4 While there is evidence of a heritable basis in the general population, a family history of early repolarization is not known to increase the risk of sudden cardiac death.

A proposed mechanism for the early repolarization pattern is an imbalance in the ion channel system, resulting in variable refractoriness of multiple myocardial regions and varying excitability in the myocardium. This can produce a voltage gradient between myocardial regions, which is believed to cause the major hallmarks of the early repolarization pattern, ie, ST-segment elevation and QRS notching or slurring.3

Table 1. Early repolarization: High-risk features
Although the mechanistic basis of ventricular arrhythmia in patients with early repolarization is still incompletely understood, certain associations may help define the ECG phenotype that suggests increased risk of sudden cardiac death (Table 1).

MANAGEMENT

The early repolarization pattern is nearly always a benign incidental finding on ECG, with no specific signs or symptoms attributed to it. High-risk features on ECG are associated with a modest increase in absolute risk of sudden cardiac death and warrant clinical correlation.

In the absence of syncope or family history of sudden cardiac death, early repolarization does not merit further workup.2

In patients with a history of unexplained syncope and a family history of sudden cardiac death, early repolarization should be considered in overall risk stratification.1 Early repolarization in a patient with previous idiopathic ventricular fibrillation warrants referral for electrophysiologic study and, if indicated, insertion of an implantable cardiac defibrillator for secondary prevention.5

No. The early repolarization pattern on electrocardiography (ECG) in asymp­tomatic patients is nearly always a benign incidental finding. However, in a patient with a history of idiopathic ventricular fibrillation or a family history of sudden cardiac death, the finding warrants further evaluation.

DEFINING EARLY REPOLARIZATION

Figure 1. Early repolarization with and without QRS notch or slur.
Figure 1. Early repolarization with and without QRS notch or slur.
Published studies differ in their definitions of the early repolarization pattern. In 2016, Patton et al described it as ST-segment elevation in the absence of chest pain, with terminal QRS slur or terminal QRS notch.1 However, Mcfarlane et al2 described it as a J-point elevation of at least 0.1 mV in 2 or more contiguous leads on 12-lead ECG, excluding leads V1 to V3, with the presence of terminal QRS notch or slur and QRS duration less than 120 msec. They defined the J point as either the peak of QRS notch or the beginning of QRS slur (Figure 1).2 J-point elevation and QRS notch or slur are most commonly seen in left lateral leads and less often in inferior leads.

The early repolarization pattern may mimic patterns seen in myocardial infarction, pericarditis, ventricular aneurysm, hyperkalemia, and hypothermia,1,3 and misinterpreting the pattern can lead to unnecessary laboratory testing, imaging, medication use, and hospital admissions. On the other hand, misinterpreting it as benign in the presence of certain features of the history or clinical presentation can delay the diagnosis and treatment of a potentially critical condition.

PREVALENCE AND MECHANISMS

The prevalence of the early repolarization pattern in the general population ranges from 5% to 15%; the wide range reflects differences in the definition, as well as variability in the pattern of early repolarization over time.4

The early repolarization pattern is more commonly seen in African American men and in young, physically active individuals.3 In one study, it was observed in 15% of cases of idiopathic ventricular fibrillation and sudden cardiac death, especially in people ages 35 to 45.4 While there is evidence of a heritable basis in the general population, a family history of early repolarization is not known to increase the risk of sudden cardiac death.

A proposed mechanism for the early repolarization pattern is an imbalance in the ion channel system, resulting in variable refractoriness of multiple myocardial regions and varying excitability in the myocardium. This can produce a voltage gradient between myocardial regions, which is believed to cause the major hallmarks of the early repolarization pattern, ie, ST-segment elevation and QRS notching or slurring.3

Table 1. Early repolarization: High-risk features
Although the mechanistic basis of ventricular arrhythmia in patients with early repolarization is still incompletely understood, certain associations may help define the ECG phenotype that suggests increased risk of sudden cardiac death (Table 1).

MANAGEMENT

The early repolarization pattern is nearly always a benign incidental finding on ECG, with no specific signs or symptoms attributed to it. High-risk features on ECG are associated with a modest increase in absolute risk of sudden cardiac death and warrant clinical correlation.

In the absence of syncope or family history of sudden cardiac death, early repolarization does not merit further workup.2

In patients with a history of unexplained syncope and a family history of sudden cardiac death, early repolarization should be considered in overall risk stratification.1 Early repolarization in a patient with previous idiopathic ventricular fibrillation warrants referral for electrophysiologic study and, if indicated, insertion of an implantable cardiac defibrillator for secondary prevention.5

References
  1. Patton KK, Ellinor PT, Ezekowitz M, et al; American Heart Association Electrocardiography and Arrhythmias Committee of the Council on Clinical Cardiology and Council on Functional Genomics and Translational Biology. Electrocardiographic early repolarization: a scientific statement from the American Heart Association. Circulation 2016; 133(15):1520–1529. doi:10.1161/CIR.0000000000000388
  2. Macfarlane PW, Antzelevitch C, Haissaguerre M, et al. The early repolarization pattern: a consensus paper. J Am Coll Cardiol 2015; 66(4):470–477. doi:10.1016/j.jacc.2015.05.033
  3. Benito B, Guasch E, Rivard L, Nattel S. Clinical and mechanistic issues in early repolarization of normal variants and lethal arrhythmia syndromes. J Am Coll Cardiol 2010; 56(15):1177–1186. doi:10.1016/j.jacc.2010.05.037
  4. Maury P, Rollin A. Prevalence of early repolarisation/J wave patterns in the normal population. J Electrocardiol 2013; 46(5):411–416. doi:10.1016/j.jelectrocard.2013.06.014
  5. Mahida S, Sacher F, Berte B, et al. Evaluation of patients with early repolarization syndrome. J Atr Fibrillation 2014; 7(3):1083. doi:10.4022/jafib.1083
References
  1. Patton KK, Ellinor PT, Ezekowitz M, et al; American Heart Association Electrocardiography and Arrhythmias Committee of the Council on Clinical Cardiology and Council on Functional Genomics and Translational Biology. Electrocardiographic early repolarization: a scientific statement from the American Heart Association. Circulation 2016; 133(15):1520–1529. doi:10.1161/CIR.0000000000000388
  2. Macfarlane PW, Antzelevitch C, Haissaguerre M, et al. The early repolarization pattern: a consensus paper. J Am Coll Cardiol 2015; 66(4):470–477. doi:10.1016/j.jacc.2015.05.033
  3. Benito B, Guasch E, Rivard L, Nattel S. Clinical and mechanistic issues in early repolarization of normal variants and lethal arrhythmia syndromes. J Am Coll Cardiol 2010; 56(15):1177–1186. doi:10.1016/j.jacc.2010.05.037
  4. Maury P, Rollin A. Prevalence of early repolarisation/J wave patterns in the normal population. J Electrocardiol 2013; 46(5):411–416. doi:10.1016/j.jelectrocard.2013.06.014
  5. Mahida S, Sacher F, Berte B, et al. Evaluation of patients with early repolarization syndrome. J Atr Fibrillation 2014; 7(3):1083. doi:10.4022/jafib.1083
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Does early repolarization on ECG increase the risk of cardiac death in healthy people?
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Can patients opt to turn off implantable cardioverter-defibrillators near the end of life?

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Can patients opt to turn off implantable cardioverter-defibrillators near the end of life?
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M. Motaz Baibars, MD, FACP
M. Chadi Alraies, MD, FACP
Amjad Kabach, MD
Marc Pritzker, MD, FACC

Yes. Although implantable cardioverter-defibrillators (ICDs) prevent sudden cardiac death in patients with advanced heart failure, their benefit in terminally ill patients is small.1 Furthermore, the shocks they deliver at the end of life can cause distress. Therefore, it is reasonable to consider ICD deactivation if the patient or family wishes.

See related commentary

A DIFFICULT DECISION

End-of-life decisions place significant emotional burdens on patients, their families, and their healthcare providers and can have social and legal consequences.

Turning off an ICD is an especially difficult decision, considering that these devices protect against sudden cardiac death and fatal arrhythmias. Also, patients and their representatives may find it more difficult to withdraw from active care than to forgo further interventions (more on this below), and they may misunderstand discussions about ICD deactivation, perceiving them as the beginning of abandonment.

ICD DEACTIVATION IS OFTEN DONE HAPHAZARDLY OR NOT AT ALL

Many healthcare providers are not trained in or comfortable with discussing end-of-life issues, and many hospitals and hospice programs lack policies and protocols for managing implanted devices at the end of life. Consequently, ICD management at the end of life varies among providers and tends to be suboptimal.2

In a report of a survey in 414 hospice facilities, 97% of facilities reported that they admitted patients with ICDs, but only 10% had a policy on device deactivation.3

In a survey of 47 European medical centers, only 4% said they addressed ICD deactivation with their patients.4

A study of 125 patients with ICDs who had died found that 52% had do-not-resuscitate orders. Nevertheless, in 100 patients the ICD had remained active in the last 24 hours of their life, and 31 of these patients had received shocks during their last 24 hours.5

In a survey of next of kin of patients with ICDs who had died of any cause,6 in only 27 of 100 cases had the clinician discussed ICD deactivation, and about three-fourths of these discussions had occurred during the last few days of life. Twenty-seven patients had received ICD discharges in the last month of life, and 8% had received a discharge during the final minutes.

TRAINING AND PROTOCOLS ARE NEEDED

Healthcare professionals need education about device deactivation at the end of life so that they are comfortable communicating with patients and families about this critical issue. To this end, several cardiac and palliative care societies have jointly released an expert statement on managing ICDs and other implantable devices in end-of-life situations.7

Many providers harbor a misunderstanding of the difference between withholding a device and withdrawing (or turning off) a device that is already implanted.2 Some mistakenly believe they would be committing a crime by deactivating an implanted life-sustaining device. Legally and ethically, there is no difference between withholding a device and withdrawing a device. Legally, carrying out a request to withdraw life-sustaining treatment is neither physician-assisted suicide nor euthanasia.

DISCUSSION SHOULD BEGIN EARLY AND SHOULD BE ONGOING

The discussion of ICD deactivation should begin before the device is implanted and should continue as the patient’s health status changes. In a survey, 40% of patients said they felt that ICD deactivation should be discussed before the device is implanted, and only 5% felt that this discussion should be undertaken in the last days of life.8

At the least, it is important to identify patients with ICDs on admission to hospice and to have policies in place that ensure adequate patient education to make an informed decision about ICD deactivation at the end of life.

The topic should be discussed when goals of care change and when do-not-resuscitate status is addressed, and also when advanced directives are being acknowledged. If the patient or his or her legal representative wishes to keep the ICD turned on, that wish should be respected. The essence of a discussion is not to impose the providers’ choice on the patient, but to help the patient make the right decision for himself or herself. Of note, patients entering hospice do not have to have do-not-resuscitate status.

We believe that device management in end-of-life circumstances should be part of the discussion of the goals of care. Accordingly, healthcare providers need to be familiar with device management and to have a higher comfort level in addressing such sensitive topics with patients facing the end of life, as well as with their families.

It is also advisable to apply protocols within hospice services to address ICD management options for the patient and the legal representative. An early decision regarding end-of-life deactivation will help patients avoid distressing ICD discharges and the related emotional distress in their last moments.

References
  1. Barsheshet A, Moss AJ, Huang DT, McNitt S, Zareba W, Goldenberg I. Applicability of a risk score for prediction of the long-term (8-year) benefit of the implantable cardioverter-defibrillator. J Am Coll Cardiol 2012; 59:2075–2079.
  2. Kapa S, Mueller PS, Hayes DL, Asirvatham SJ. Perspectives on withdrawing pacemaker and implantable cardioverter-defibrillator therapies at end of life: results of a survey of medical and legal professionals and patients. Mayo Clin Proc 2010; 85:981–990.
  3. Goldstein N, Carlson M, Livote E, Kutner JS. Brief communication: management of implantable cardioverter-defibrillators in hospice: a nationwide survey. Ann Intern Med 2010; 152:296–299.
  4. Marinskis G, van Erven L; EHRA Scientific Initiatives Committtee. Deactivation of implanted cardioverter-defibrillators at the end of life: results of the EHRA survey. Europace 2010; 12:1176–1177.
  5. Kinch Westerdahl A, Sjoblom J, Mattiasson AC, Rosenqvist M, Frykman V. Implantable cardioverter-defibrillator therapy before death: high risk for painful shocks at end of life. Circulation 2014; 129:422–429.
  6. Goldstein NE, Lampert R, Bradley E, Lynn J, Krumholz HM. Management of implantable cardioverter defibrillators in end-of-life care. Ann Intern Med 2004; 141:835–838.
  7. Lampert R, Hayes DL, Annas GJ, et al; American College of Cardiology; American Geriatrics Society; American Academy of Hospice and Palliative Medicine; American Heart Association; European Heart Rhythm Association; Hospice and Palliative Nurses Association. HRS expert consensus statement on the management of cardiovascular implantable electronic devices (CIEDs) in patients nearing end of life or requesting withdrawal of therapy. Heart Rhythm 2010; 7:1008–1026.
  8. Raphael CE, Koa-Wing M, Stain N, Wright I, Francis DP, Kanagaratnam P. Implantable cardioverter-defibrillator recipient attitudes towards device activation: how much do patients want to know? Pacing Clin Electrophysiol 2011; 34:1628–1633.
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M. Chadi Alraies, MD, FACP
Department of Medicine, Cardiovascular Division, University of Minnesota, Minneapolis

Amjad Kabach, MD
Department of Medicine, Creighton University, Omaha, NE

Marc Pritzker, MD, FACC
Professor of Medicine, Surgery and Biomedical Innovation; Director, Pulmonary Hypertension Service, University of Minnesota, Minneapolis

Address: M. Chadi Alraies, MD, FACP, Department of Medicine, Cardiovascular Division, University of Minnesota Medical Center, 420 Delaware Street SE, MMC 508, Minneapolis, MN 55455; e-mail: alrai005@umn.edu

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Department of Hospital Medicine, Peninsula Regional Medical Center, Salisbury, MD

M. Chadi Alraies, MD, FACP
Department of Medicine, Cardiovascular Division, University of Minnesota, Minneapolis

Amjad Kabach, MD
Department of Medicine, Creighton University, Omaha, NE

Marc Pritzker, MD, FACC
Professor of Medicine, Surgery and Biomedical Innovation; Director, Pulmonary Hypertension Service, University of Minnesota, Minneapolis

Address: M. Chadi Alraies, MD, FACP, Department of Medicine, Cardiovascular Division, University of Minnesota Medical Center, 420 Delaware Street SE, MMC 508, Minneapolis, MN 55455; e-mail: alrai005@umn.edu

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M. Motaz Baibars, MD, FACP
Department of Hospital Medicine, Peninsula Regional Medical Center, Salisbury, MD

M. Chadi Alraies, MD, FACP
Department of Medicine, Cardiovascular Division, University of Minnesota, Minneapolis

Amjad Kabach, MD
Department of Medicine, Creighton University, Omaha, NE

Marc Pritzker, MD, FACC
Professor of Medicine, Surgery and Biomedical Innovation; Director, Pulmonary Hypertension Service, University of Minnesota, Minneapolis

Address: M. Chadi Alraies, MD, FACP, Department of Medicine, Cardiovascular Division, University of Minnesota Medical Center, 420 Delaware Street SE, MMC 508, Minneapolis, MN 55455; e-mail: alrai005@umn.edu

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Related Articles
The ethics of ICDs: History and future directions

Yes. Although implantable cardioverter-defibrillators (ICDs) prevent sudden cardiac death in patients with advanced heart failure, their benefit in terminally ill patients is small.1 Furthermore, the shocks they deliver at the end of life can cause distress. Therefore, it is reasonable to consider ICD deactivation if the patient or family wishes.

See related commentary

A DIFFICULT DECISION

End-of-life decisions place significant emotional burdens on patients, their families, and their healthcare providers and can have social and legal consequences.

Turning off an ICD is an especially difficult decision, considering that these devices protect against sudden cardiac death and fatal arrhythmias. Also, patients and their representatives may find it more difficult to withdraw from active care than to forgo further interventions (more on this below), and they may misunderstand discussions about ICD deactivation, perceiving them as the beginning of abandonment.

ICD DEACTIVATION IS OFTEN DONE HAPHAZARDLY OR NOT AT ALL

Many healthcare providers are not trained in or comfortable with discussing end-of-life issues, and many hospitals and hospice programs lack policies and protocols for managing implanted devices at the end of life. Consequently, ICD management at the end of life varies among providers and tends to be suboptimal.2

In a report of a survey in 414 hospice facilities, 97% of facilities reported that they admitted patients with ICDs, but only 10% had a policy on device deactivation.3

In a survey of 47 European medical centers, only 4% said they addressed ICD deactivation with their patients.4

A study of 125 patients with ICDs who had died found that 52% had do-not-resuscitate orders. Nevertheless, in 100 patients the ICD had remained active in the last 24 hours of their life, and 31 of these patients had received shocks during their last 24 hours.5

In a survey of next of kin of patients with ICDs who had died of any cause,6 in only 27 of 100 cases had the clinician discussed ICD deactivation, and about three-fourths of these discussions had occurred during the last few days of life. Twenty-seven patients had received ICD discharges in the last month of life, and 8% had received a discharge during the final minutes.

TRAINING AND PROTOCOLS ARE NEEDED

Healthcare professionals need education about device deactivation at the end of life so that they are comfortable communicating with patients and families about this critical issue. To this end, several cardiac and palliative care societies have jointly released an expert statement on managing ICDs and other implantable devices in end-of-life situations.7

Many providers harbor a misunderstanding of the difference between withholding a device and withdrawing (or turning off) a device that is already implanted.2 Some mistakenly believe they would be committing a crime by deactivating an implanted life-sustaining device. Legally and ethically, there is no difference between withholding a device and withdrawing a device. Legally, carrying out a request to withdraw life-sustaining treatment is neither physician-assisted suicide nor euthanasia.

DISCUSSION SHOULD BEGIN EARLY AND SHOULD BE ONGOING

The discussion of ICD deactivation should begin before the device is implanted and should continue as the patient’s health status changes. In a survey, 40% of patients said they felt that ICD deactivation should be discussed before the device is implanted, and only 5% felt that this discussion should be undertaken in the last days of life.8

At the least, it is important to identify patients with ICDs on admission to hospice and to have policies in place that ensure adequate patient education to make an informed decision about ICD deactivation at the end of life.

The topic should be discussed when goals of care change and when do-not-resuscitate status is addressed, and also when advanced directives are being acknowledged. If the patient or his or her legal representative wishes to keep the ICD turned on, that wish should be respected. The essence of a discussion is not to impose the providers’ choice on the patient, but to help the patient make the right decision for himself or herself. Of note, patients entering hospice do not have to have do-not-resuscitate status.

We believe that device management in end-of-life circumstances should be part of the discussion of the goals of care. Accordingly, healthcare providers need to be familiar with device management and to have a higher comfort level in addressing such sensitive topics with patients facing the end of life, as well as with their families.

It is also advisable to apply protocols within hospice services to address ICD management options for the patient and the legal representative. An early decision regarding end-of-life deactivation will help patients avoid distressing ICD discharges and the related emotional distress in their last moments.

Yes. Although implantable cardioverter-defibrillators (ICDs) prevent sudden cardiac death in patients with advanced heart failure, their benefit in terminally ill patients is small.1 Furthermore, the shocks they deliver at the end of life can cause distress. Therefore, it is reasonable to consider ICD deactivation if the patient or family wishes.

See related commentary

A DIFFICULT DECISION

End-of-life decisions place significant emotional burdens on patients, their families, and their healthcare providers and can have social and legal consequences.

Turning off an ICD is an especially difficult decision, considering that these devices protect against sudden cardiac death and fatal arrhythmias. Also, patients and their representatives may find it more difficult to withdraw from active care than to forgo further interventions (more on this below), and they may misunderstand discussions about ICD deactivation, perceiving them as the beginning of abandonment.

ICD DEACTIVATION IS OFTEN DONE HAPHAZARDLY OR NOT AT ALL

Many healthcare providers are not trained in or comfortable with discussing end-of-life issues, and many hospitals and hospice programs lack policies and protocols for managing implanted devices at the end of life. Consequently, ICD management at the end of life varies among providers and tends to be suboptimal.2

In a report of a survey in 414 hospice facilities, 97% of facilities reported that they admitted patients with ICDs, but only 10% had a policy on device deactivation.3

In a survey of 47 European medical centers, only 4% said they addressed ICD deactivation with their patients.4

A study of 125 patients with ICDs who had died found that 52% had do-not-resuscitate orders. Nevertheless, in 100 patients the ICD had remained active in the last 24 hours of their life, and 31 of these patients had received shocks during their last 24 hours.5

In a survey of next of kin of patients with ICDs who had died of any cause,6 in only 27 of 100 cases had the clinician discussed ICD deactivation, and about three-fourths of these discussions had occurred during the last few days of life. Twenty-seven patients had received ICD discharges in the last month of life, and 8% had received a discharge during the final minutes.

TRAINING AND PROTOCOLS ARE NEEDED

Healthcare professionals need education about device deactivation at the end of life so that they are comfortable communicating with patients and families about this critical issue. To this end, several cardiac and palliative care societies have jointly released an expert statement on managing ICDs and other implantable devices in end-of-life situations.7

Many providers harbor a misunderstanding of the difference between withholding a device and withdrawing (or turning off) a device that is already implanted.2 Some mistakenly believe they would be committing a crime by deactivating an implanted life-sustaining device. Legally and ethically, there is no difference between withholding a device and withdrawing a device. Legally, carrying out a request to withdraw life-sustaining treatment is neither physician-assisted suicide nor euthanasia.

DISCUSSION SHOULD BEGIN EARLY AND SHOULD BE ONGOING

The discussion of ICD deactivation should begin before the device is implanted and should continue as the patient’s health status changes. In a survey, 40% of patients said they felt that ICD deactivation should be discussed before the device is implanted, and only 5% felt that this discussion should be undertaken in the last days of life.8

At the least, it is important to identify patients with ICDs on admission to hospice and to have policies in place that ensure adequate patient education to make an informed decision about ICD deactivation at the end of life.

The topic should be discussed when goals of care change and when do-not-resuscitate status is addressed, and also when advanced directives are being acknowledged. If the patient or his or her legal representative wishes to keep the ICD turned on, that wish should be respected. The essence of a discussion is not to impose the providers’ choice on the patient, but to help the patient make the right decision for himself or herself. Of note, patients entering hospice do not have to have do-not-resuscitate status.

We believe that device management in end-of-life circumstances should be part of the discussion of the goals of care. Accordingly, healthcare providers need to be familiar with device management and to have a higher comfort level in addressing such sensitive topics with patients facing the end of life, as well as with their families.

It is also advisable to apply protocols within hospice services to address ICD management options for the patient and the legal representative. An early decision regarding end-of-life deactivation will help patients avoid distressing ICD discharges and the related emotional distress in their last moments.

References
  1. Barsheshet A, Moss AJ, Huang DT, McNitt S, Zareba W, Goldenberg I. Applicability of a risk score for prediction of the long-term (8-year) benefit of the implantable cardioverter-defibrillator. J Am Coll Cardiol 2012; 59:2075–2079.
  2. Kapa S, Mueller PS, Hayes DL, Asirvatham SJ. Perspectives on withdrawing pacemaker and implantable cardioverter-defibrillator therapies at end of life: results of a survey of medical and legal professionals and patients. Mayo Clin Proc 2010; 85:981–990.
  3. Goldstein N, Carlson M, Livote E, Kutner JS. Brief communication: management of implantable cardioverter-defibrillators in hospice: a nationwide survey. Ann Intern Med 2010; 152:296–299.
  4. Marinskis G, van Erven L; EHRA Scientific Initiatives Committtee. Deactivation of implanted cardioverter-defibrillators at the end of life: results of the EHRA survey. Europace 2010; 12:1176–1177.
  5. Kinch Westerdahl A, Sjoblom J, Mattiasson AC, Rosenqvist M, Frykman V. Implantable cardioverter-defibrillator therapy before death: high risk for painful shocks at end of life. Circulation 2014; 129:422–429.
  6. Goldstein NE, Lampert R, Bradley E, Lynn J, Krumholz HM. Management of implantable cardioverter defibrillators in end-of-life care. Ann Intern Med 2004; 141:835–838.
  7. Lampert R, Hayes DL, Annas GJ, et al; American College of Cardiology; American Geriatrics Society; American Academy of Hospice and Palliative Medicine; American Heart Association; European Heart Rhythm Association; Hospice and Palliative Nurses Association. HRS expert consensus statement on the management of cardiovascular implantable electronic devices (CIEDs) in patients nearing end of life or requesting withdrawal of therapy. Heart Rhythm 2010; 7:1008–1026.
  8. Raphael CE, Koa-Wing M, Stain N, Wright I, Francis DP, Kanagaratnam P. Implantable cardioverter-defibrillator recipient attitudes towards device activation: how much do patients want to know? Pacing Clin Electrophysiol 2011; 34:1628–1633.
References
  1. Barsheshet A, Moss AJ, Huang DT, McNitt S, Zareba W, Goldenberg I. Applicability of a risk score for prediction of the long-term (8-year) benefit of the implantable cardioverter-defibrillator. J Am Coll Cardiol 2012; 59:2075–2079.
  2. Kapa S, Mueller PS, Hayes DL, Asirvatham SJ. Perspectives on withdrawing pacemaker and implantable cardioverter-defibrillator therapies at end of life: results of a survey of medical and legal professionals and patients. Mayo Clin Proc 2010; 85:981–990.
  3. Goldstein N, Carlson M, Livote E, Kutner JS. Brief communication: management of implantable cardioverter-defibrillators in hospice: a nationwide survey. Ann Intern Med 2010; 152:296–299.
  4. Marinskis G, van Erven L; EHRA Scientific Initiatives Committtee. Deactivation of implanted cardioverter-defibrillators at the end of life: results of the EHRA survey. Europace 2010; 12:1176–1177.
  5. Kinch Westerdahl A, Sjoblom J, Mattiasson AC, Rosenqvist M, Frykman V. Implantable cardioverter-defibrillator therapy before death: high risk for painful shocks at end of life. Circulation 2014; 129:422–429.
  6. Goldstein NE, Lampert R, Bradley E, Lynn J, Krumholz HM. Management of implantable cardioverter defibrillators in end-of-life care. Ann Intern Med 2004; 141:835–838.
  7. Lampert R, Hayes DL, Annas GJ, et al; American College of Cardiology; American Geriatrics Society; American Academy of Hospice and Palliative Medicine; American Heart Association; European Heart Rhythm Association; Hospice and Palliative Nurses Association. HRS expert consensus statement on the management of cardiovascular implantable electronic devices (CIEDs) in patients nearing end of life or requesting withdrawal of therapy. Heart Rhythm 2010; 7:1008–1026.
  8. Raphael CE, Koa-Wing M, Stain N, Wright I, Francis DP, Kanagaratnam P. Implantable cardioverter-defibrillator recipient attitudes towards device activation: how much do patients want to know? Pacing Clin Electrophysiol 2011; 34:1628–1633.
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Can patients opt to turn off implantable cardioverter-defibrillators near the end of life?
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Does stenting of severe renal artery stenosis improve outomes compared with medical therapy alone?

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Does stenting of severe renal artery stenosis improve outomes compared with medical therapy alone?
Author(s)
Amjad Kabach, MD
Osama Qasim Agha, MD
M. Motaz Baibars, MD, FACP
Abdul Hamid Alraiyes, MD, FCCP
M. Chadi Alraies, MD, FACP

No. In patients with severe atherosclerotic renal artery stenosis and hypertension or chronic kidney disease, renal artery stenting offers no additional benefit when added to comprehensive medical therapy.

See related editorial

In these patients, renal artery stenting in addition to antihypertensive drug therapy can improve blood pressure control modestly but has no significant effect on outcomes such as adverse cardiovascular events and death. And because renal artery stenting carries a risk of complications, medical management should continue to be the first-line therapy.

RENAL ARTERY STENOSIS

Renal artery stenosis is a common form of peripheral artery disease. Atherosclerosis is the most common cause, but it can also be caused by fibromuscular dysplasia or vasculitis (eg, Takayasu arteritis). It is most often unilateral, but bilateral disease has also been reported.

The prevalence of atherosclerotic renal vascular disease in the US Medicare population is 0.5%, and 5.5% in those with chronic kidney disease.1 Furthermore, renal artery stenosis is found in 6.8% of adults over age 65.2 The prevalence increases with age and is higher in patients with hyperlipidemia, peripheral arterial disease, and hypertension. The prevalence of renal artery stenosis in patients with atherosclerotic disease and renal dysfunction is as high as 50%.3

Patients with peripheral artery disease may be five times more likely to develop renal artery stenosis than people without peripheral artery disease.4 Significant stenosis can result in resistant arterial hypertension, renal insufficiency, left ventricular hypertrophy, and congestive heart failure.5

Renal artery stenting added to drug therapy can modestly improve blood pressure control, but has no significant effect on outcomes

Nephropathy due to renal artery stenosis is complex and is caused by hypoperfusion and chronic microatheroembolism. Renal artery stenosis leads to oxidative stress, inflammation, fibrosis in the stenotic kidney, and, over time, loss of kidney function. Hypoperfusion also leads to activation of the renin-angiotensin-aldosterone system, which plays a role in development of left ventricular hypertrophy.5,6

Adequate blood pressure control, goal-directed lipid-lowering therapy, smoking cessation, and other preventive measures are the foundation of management.

RENAL ARTERY STENOSIS AND HYPERTENSION

Figure 1. Pathophysiology of hypertension in renal artery stenosis.

Renal artery stenosis is a cause of secondary hypertension. The stenosis decreases renal perfusion pressure, activating the release of renin and the production of angiotensin II, which in turn raises the blood pressure by two mechanisms (Figure 1): directly, by causing generalized vasoconstriction, and indirectly, by stimulating the release of aldosterone, which in turn increases the reabsorption of sodium and causes hypervolemia. These two mechanisms play a major role in renal vascular hypertension when renal artery stenosis is bilateral. In unilateral renal artery stenosis, pressure diuresis in the unaffected kidney compensates for the reabsorption of sodium in the affected kidney, keeping the blood pressure down. However, with time, the unaffected kidney will develop hypertensive nephropathy, and pressure diuresis will be lost.7,8 In addition, the activation of the renin-angiotensin-aldosterone system results in structural heart disease, such as left ventricular hypertrophy,5 and may shorten survival.

STENTING PLUS ANTIHYPERTENSIVE DRUG THERAPY

Because observational studies showed improvement in blood pressure control after endovascular stenting of atherosclerotic renal artery stenosis,9,10 this approach became a treatment option for uncontrolled hypertension in these patients. The 2005 joint guidelines of the American College of Cardiology and the American Heart Association11 considered percutaneous revascularization a reasonable option (level of evidence B) for patients who meet one of the following criteria:

  • Hemodynamically significant stenosis and accelerated, resistant, or malignant hypertension, hypertension with an unexplained unilateral small kidney, or hypertension with intolerance to medication
  • Renal artery stenosis and progressive chronic kidney disease with bilateral stenosis or stenosis in a solitary functioning kidney
  • Hemodynamically significant stenosis and recurrent, unexplained congestive heart failure or sudden, unexplained pulmonary edema or unstable angina.11

However, no randomized study has shown a direct benefit of renal artery stenting on rates of cardiovascular events or renal function compared with drug therapy alone.

 

 

TRIALS OF STENTING VS MEDICAL THERAPY ALONE

Technical improvements have led to more widespread use of diagnostic and interventional endovascular tools for renal artery revascularization. Studies over the past 10 years examined the impact of stenting in patients with uncontrolled hypertension.

The STAR trial

In the Stent Placement and Blood Pressure and Lipid-lowering for the Prevention of Progression of Renal Dysfunction Caused by Atherosclerotic Ostial Stenosis of the Renal Artery (STAR) trial,9 patients with creatinine clearance less than 80 mL/min/1.73 m2, renal artery stenosis greater than 50%, and well-controlled blood pressure were randomized to either renal artery stenting plus medical therapy or medical therapy alone. The authors concluded that stenting had no effect on the progression of renal dysfunction but led to a small number of significant, procedure-related complications. The study was criticized for including patients with mild stenosis (< 50% stenosis) and for being underpowered for the primary end point.

The ASTRAL study

The Angioplasty and Stenting for Renal Artery Lesions (ASTRAL) study10 was a similar comparison with similar results, showing no benefit from stenting with respect to renal function, systolic blood pressure control, cardiovascular events, or death.

HERCULES

The Herculink Elite Cobalt Chromium Renal Stent Trial to Demonstrate Efficacy and Safety (HERCULES)12 was a prospective multicenter study of the effects of renal artery stenting in 202 patients with significant renal artery stenosis and uncontrolled hypertension. It showed a reduction in systolic blood pressure from baseline (P < .0001). However, follow-up was only 9 months, which was insufficient to show a significant effect on long-term cardiovascular and cerebrovascular outcomes.

The CORAL trial

The Cardiovascular Outcomes in Renal Atherosclerotic Lesions (CORAL) trial13 used more stringent definitions and longer follow-up. It randomized 947 patients to either stenting plus medical therapy or medical therapy alone. Patients had atherosclerotic renal artery stenosis, defined as stenosis of at least 80% or stenosis of 60% to 80% with a gradient of at least 20 mm Hg in the systolic pressure), and either systolic hypertension while taking two or more antihypertensive drugs or stage 3 or higher chronic kidney disease (glomerular filtration rate < 60 mL/min/1.73 m2 as calculated by the Modification of Diet in Renal Disease formula).

Complications of renal artery stenting are a limiting factor compared with drug therapy alone

Participants were followed for 43 months to detect the occurrence of adverse cardiovascular and renal events. There was no significant difference in primary outcome between stenting plus drug therapy and drug therapy alone (35.1% and 35.8%, respectively; P = .58). However, stenting plus drug therapy was associated with modestly lower systolic pressures compared with drug therapy alone (−2.3 mm Hg, 95% confidence interval −4.4 to −0.2 mm Hg, P = .03).13 This study provided strong evidence that renal artery stenting offers no significant benefit to patients with moderately severe atherosclerotic renal artery stenosis, and that stenting may actually pose an unnecessary risk.

COMPLICATIONS OF RENAL ARTERY STENTING

Complications of renal artery stenting are a limiting factor compared with drug therapy alone, especially since the procedure offers no significant benefit in outcome. Procedural complication rates of 10% to 15% have been reported.9,10,12 The CORAL trial reported arterial dissection in 2.2%, branch-vessel occlusion in 1.2%, and distal embolization in 1.2% of patients undergoing stenting.13 Other reported complications have included stent misplacement requiring an additional stent, access-vessel damage, stent embolization, renal artery thrombosis or occlusion, and death.10,12

References
  1. Kalra PA, Guo H, Kausz AT, et al. Atherosclerotic renovascular disease in United States patients aged 67 years or older: risk factors, revascularization, and prognosis. Kidney Int 2005; 68:293–301.
  2. Hansen KJ, Edwards MS, Craven TE, et al. Prevalence of renovascular disease in the elderly: a population-based study. J Vasc Surg 2002; 36:443–451.
  3. Uzu T, Takeji M, Yamada N, et al. Prevalence and outcome of renal artery stenosis in atherosclerotic patients with renal dysfunction. Hypertens Res 2002; 25:537–542.
  4. Benjamin MM, Fazel P, Filardo G, Choi JW, Stoler RC. Prevalence of and risk factors of renal artery stenosis in patients with resistant hypertension. Am J Cardiol 2014; 113:687–690.
  5. Wu S, Polavarapu N, Stouffer GA. Left ventricular hypertrophy in patients with renal artery stenosis. Am J Med Sci 2006; 332:334–338.
  6. Lerman LO, Textor SC, Grande JP. Mechanisms of tissue injury in renal artery stenosis: ischemia and beyond. Prog Cardiovasc Dis 2009; 52:196–203.
  7. Black HR, Glickman MG, Schiff M Jr, Pingoud EG. Renovascular hypertension: pathophysiology, diagnosis, and treatment. Yale J Biol Med 1978; 51:635–654.
  8. Tobe SW, Burgess E, Lebel M. Atherosclerotic renovascular disease. Can J Cardiol 2006; 22:623–628.
  9. Bax L, Mali WP, Buskens E, et al; STAR Study Group. The benefit of stent placement and blood pressure and lipid-lowering for the prevention of progression of renal dysfunction caused by atherosclerotic ostial stenosis of the renal artery. The STAR-study: rationale and study design. J Nephrol 2003; 16:807–812.
  10. ASTRAL Investigators; Wheatley K, Ives N, Gray R, et al. Revascularization versus medical therapy for renal-artery stenosis. N Engl J Med 2009; 361:1953–1962.
  11. Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): executive summary. J Am Coll Cardiol 2006; 47:1239–1312.
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Amjad Kabach, MD
Department of Medicine, Creighton University, Omaha, NE

Osama Qasim Agha, MD
Department of Internal Medicine, St. Joseph’s Hospital and Medical Center, Phoenix, AZ

M. Motaz Baibars, MD, FACP
Department of Hospital Medicine, Peninsula Regional Medical Center, Salisbury, MD

Abdul Hamid Alraiyes, MD, FCCP
Pulmonary, Allergy, and Critical Care Medicine, Respiratory Institute, Cleveland Clinic, Cleveland, OH

M. Chadi Alraies, MD, FACP
Department of Medicine, Cardiovascular Division, University of Minnesota, Minneapolis

Address: M. Chadi Alraies, MD, FACP, Department of Medicine, Cardiovascular Division, University of Minnesota Medical Center, 420 Delaware Street SE, MMC 508, Minneapolis, MN 55455; e-mail: alrai005@umn.edu

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Osama Qasim Agha, MD
M. Motaz Baibars, MD, FACP
Abdul Hamid Alraiyes, MD, FCCP
M. Chadi Alraies, MD, FACP
Author(s)
Amjad Kabach, MD
Osama Qasim Agha, MD
M. Motaz Baibars, MD, FACP
Abdul Hamid Alraiyes, MD, FCCP
M. Chadi Alraies, MD, FACP
Author and Disclosure Information

Amjad Kabach, MD
Department of Medicine, Creighton University, Omaha, NE

Osama Qasim Agha, MD
Department of Internal Medicine, St. Joseph’s Hospital and Medical Center, Phoenix, AZ

M. Motaz Baibars, MD, FACP
Department of Hospital Medicine, Peninsula Regional Medical Center, Salisbury, MD

Abdul Hamid Alraiyes, MD, FCCP
Pulmonary, Allergy, and Critical Care Medicine, Respiratory Institute, Cleveland Clinic, Cleveland, OH

M. Chadi Alraies, MD, FACP
Department of Medicine, Cardiovascular Division, University of Minnesota, Minneapolis

Address: M. Chadi Alraies, MD, FACP, Department of Medicine, Cardiovascular Division, University of Minnesota Medical Center, 420 Delaware Street SE, MMC 508, Minneapolis, MN 55455; e-mail: alrai005@umn.edu

Author and Disclosure Information

Amjad Kabach, MD
Department of Medicine, Creighton University, Omaha, NE

Osama Qasim Agha, MD
Department of Internal Medicine, St. Joseph’s Hospital and Medical Center, Phoenix, AZ

M. Motaz Baibars, MD, FACP
Department of Hospital Medicine, Peninsula Regional Medical Center, Salisbury, MD

Abdul Hamid Alraiyes, MD, FCCP
Pulmonary, Allergy, and Critical Care Medicine, Respiratory Institute, Cleveland Clinic, Cleveland, OH

M. Chadi Alraies, MD, FACP
Department of Medicine, Cardiovascular Division, University of Minnesota, Minneapolis

Address: M. Chadi Alraies, MD, FACP, Department of Medicine, Cardiovascular Division, University of Minnesota Medical Center, 420 Delaware Street SE, MMC 508, Minneapolis, MN 55455; e-mail: alrai005@umn.edu

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Related Articles
Stenting atherosclerotic renal arteries: Time to be less aggressive
Stenting for atherosclerotic renal artery stenosis: One poorly designed trial after another

No. In patients with severe atherosclerotic renal artery stenosis and hypertension or chronic kidney disease, renal artery stenting offers no additional benefit when added to comprehensive medical therapy.

See related editorial

In these patients, renal artery stenting in addition to antihypertensive drug therapy can improve blood pressure control modestly but has no significant effect on outcomes such as adverse cardiovascular events and death. And because renal artery stenting carries a risk of complications, medical management should continue to be the first-line therapy.

RENAL ARTERY STENOSIS

Renal artery stenosis is a common form of peripheral artery disease. Atherosclerosis is the most common cause, but it can also be caused by fibromuscular dysplasia or vasculitis (eg, Takayasu arteritis). It is most often unilateral, but bilateral disease has also been reported.

The prevalence of atherosclerotic renal vascular disease in the US Medicare population is 0.5%, and 5.5% in those with chronic kidney disease.1 Furthermore, renal artery stenosis is found in 6.8% of adults over age 65.2 The prevalence increases with age and is higher in patients with hyperlipidemia, peripheral arterial disease, and hypertension. The prevalence of renal artery stenosis in patients with atherosclerotic disease and renal dysfunction is as high as 50%.3

Patients with peripheral artery disease may be five times more likely to develop renal artery stenosis than people without peripheral artery disease.4 Significant stenosis can result in resistant arterial hypertension, renal insufficiency, left ventricular hypertrophy, and congestive heart failure.5

Renal artery stenting added to drug therapy can modestly improve blood pressure control, but has no significant effect on outcomes

Nephropathy due to renal artery stenosis is complex and is caused by hypoperfusion and chronic microatheroembolism. Renal artery stenosis leads to oxidative stress, inflammation, fibrosis in the stenotic kidney, and, over time, loss of kidney function. Hypoperfusion also leads to activation of the renin-angiotensin-aldosterone system, which plays a role in development of left ventricular hypertrophy.5,6

Adequate blood pressure control, goal-directed lipid-lowering therapy, smoking cessation, and other preventive measures are the foundation of management.

RENAL ARTERY STENOSIS AND HYPERTENSION

Figure 1. Pathophysiology of hypertension in renal artery stenosis.

Renal artery stenosis is a cause of secondary hypertension. The stenosis decreases renal perfusion pressure, activating the release of renin and the production of angiotensin II, which in turn raises the blood pressure by two mechanisms (Figure 1): directly, by causing generalized vasoconstriction, and indirectly, by stimulating the release of aldosterone, which in turn increases the reabsorption of sodium and causes hypervolemia. These two mechanisms play a major role in renal vascular hypertension when renal artery stenosis is bilateral. In unilateral renal artery stenosis, pressure diuresis in the unaffected kidney compensates for the reabsorption of sodium in the affected kidney, keeping the blood pressure down. However, with time, the unaffected kidney will develop hypertensive nephropathy, and pressure diuresis will be lost.7,8 In addition, the activation of the renin-angiotensin-aldosterone system results in structural heart disease, such as left ventricular hypertrophy,5 and may shorten survival.

STENTING PLUS ANTIHYPERTENSIVE DRUG THERAPY

Because observational studies showed improvement in blood pressure control after endovascular stenting of atherosclerotic renal artery stenosis,9,10 this approach became a treatment option for uncontrolled hypertension in these patients. The 2005 joint guidelines of the American College of Cardiology and the American Heart Association11 considered percutaneous revascularization a reasonable option (level of evidence B) for patients who meet one of the following criteria:

  • Hemodynamically significant stenosis and accelerated, resistant, or malignant hypertension, hypertension with an unexplained unilateral small kidney, or hypertension with intolerance to medication
  • Renal artery stenosis and progressive chronic kidney disease with bilateral stenosis or stenosis in a solitary functioning kidney
  • Hemodynamically significant stenosis and recurrent, unexplained congestive heart failure or sudden, unexplained pulmonary edema or unstable angina.11

However, no randomized study has shown a direct benefit of renal artery stenting on rates of cardiovascular events or renal function compared with drug therapy alone.

 

 

TRIALS OF STENTING VS MEDICAL THERAPY ALONE

Technical improvements have led to more widespread use of diagnostic and interventional endovascular tools for renal artery revascularization. Studies over the past 10 years examined the impact of stenting in patients with uncontrolled hypertension.

The STAR trial

In the Stent Placement and Blood Pressure and Lipid-lowering for the Prevention of Progression of Renal Dysfunction Caused by Atherosclerotic Ostial Stenosis of the Renal Artery (STAR) trial,9 patients with creatinine clearance less than 80 mL/min/1.73 m2, renal artery stenosis greater than 50%, and well-controlled blood pressure were randomized to either renal artery stenting plus medical therapy or medical therapy alone. The authors concluded that stenting had no effect on the progression of renal dysfunction but led to a small number of significant, procedure-related complications. The study was criticized for including patients with mild stenosis (< 50% stenosis) and for being underpowered for the primary end point.

The ASTRAL study

The Angioplasty and Stenting for Renal Artery Lesions (ASTRAL) study10 was a similar comparison with similar results, showing no benefit from stenting with respect to renal function, systolic blood pressure control, cardiovascular events, or death.

HERCULES

The Herculink Elite Cobalt Chromium Renal Stent Trial to Demonstrate Efficacy and Safety (HERCULES)12 was a prospective multicenter study of the effects of renal artery stenting in 202 patients with significant renal artery stenosis and uncontrolled hypertension. It showed a reduction in systolic blood pressure from baseline (P < .0001). However, follow-up was only 9 months, which was insufficient to show a significant effect on long-term cardiovascular and cerebrovascular outcomes.

The CORAL trial

The Cardiovascular Outcomes in Renal Atherosclerotic Lesions (CORAL) trial13 used more stringent definitions and longer follow-up. It randomized 947 patients to either stenting plus medical therapy or medical therapy alone. Patients had atherosclerotic renal artery stenosis, defined as stenosis of at least 80% or stenosis of 60% to 80% with a gradient of at least 20 mm Hg in the systolic pressure), and either systolic hypertension while taking two or more antihypertensive drugs or stage 3 or higher chronic kidney disease (glomerular filtration rate < 60 mL/min/1.73 m2 as calculated by the Modification of Diet in Renal Disease formula).

Complications of renal artery stenting are a limiting factor compared with drug therapy alone

Participants were followed for 43 months to detect the occurrence of adverse cardiovascular and renal events. There was no significant difference in primary outcome between stenting plus drug therapy and drug therapy alone (35.1% and 35.8%, respectively; P = .58). However, stenting plus drug therapy was associated with modestly lower systolic pressures compared with drug therapy alone (−2.3 mm Hg, 95% confidence interval −4.4 to −0.2 mm Hg, P = .03).13 This study provided strong evidence that renal artery stenting offers no significant benefit to patients with moderately severe atherosclerotic renal artery stenosis, and that stenting may actually pose an unnecessary risk.

COMPLICATIONS OF RENAL ARTERY STENTING

Complications of renal artery stenting are a limiting factor compared with drug therapy alone, especially since the procedure offers no significant benefit in outcome. Procedural complication rates of 10% to 15% have been reported.9,10,12 The CORAL trial reported arterial dissection in 2.2%, branch-vessel occlusion in 1.2%, and distal embolization in 1.2% of patients undergoing stenting.13 Other reported complications have included stent misplacement requiring an additional stent, access-vessel damage, stent embolization, renal artery thrombosis or occlusion, and death.10,12

No. In patients with severe atherosclerotic renal artery stenosis and hypertension or chronic kidney disease, renal artery stenting offers no additional benefit when added to comprehensive medical therapy.

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In these patients, renal artery stenting in addition to antihypertensive drug therapy can improve blood pressure control modestly but has no significant effect on outcomes such as adverse cardiovascular events and death. And because renal artery stenting carries a risk of complications, medical management should continue to be the first-line therapy.

RENAL ARTERY STENOSIS

Renal artery stenosis is a common form of peripheral artery disease. Atherosclerosis is the most common cause, but it can also be caused by fibromuscular dysplasia or vasculitis (eg, Takayasu arteritis). It is most often unilateral, but bilateral disease has also been reported.

The prevalence of atherosclerotic renal vascular disease in the US Medicare population is 0.5%, and 5.5% in those with chronic kidney disease.1 Furthermore, renal artery stenosis is found in 6.8% of adults over age 65.2 The prevalence increases with age and is higher in patients with hyperlipidemia, peripheral arterial disease, and hypertension. The prevalence of renal artery stenosis in patients with atherosclerotic disease and renal dysfunction is as high as 50%.3

Patients with peripheral artery disease may be five times more likely to develop renal artery stenosis than people without peripheral artery disease.4 Significant stenosis can result in resistant arterial hypertension, renal insufficiency, left ventricular hypertrophy, and congestive heart failure.5

Renal artery stenting added to drug therapy can modestly improve blood pressure control, but has no significant effect on outcomes

Nephropathy due to renal artery stenosis is complex and is caused by hypoperfusion and chronic microatheroembolism. Renal artery stenosis leads to oxidative stress, inflammation, fibrosis in the stenotic kidney, and, over time, loss of kidney function. Hypoperfusion also leads to activation of the renin-angiotensin-aldosterone system, which plays a role in development of left ventricular hypertrophy.5,6

Adequate blood pressure control, goal-directed lipid-lowering therapy, smoking cessation, and other preventive measures are the foundation of management.

RENAL ARTERY STENOSIS AND HYPERTENSION

Figure 1. Pathophysiology of hypertension in renal artery stenosis.

Renal artery stenosis is a cause of secondary hypertension. The stenosis decreases renal perfusion pressure, activating the release of renin and the production of angiotensin II, which in turn raises the blood pressure by two mechanisms (Figure 1): directly, by causing generalized vasoconstriction, and indirectly, by stimulating the release of aldosterone, which in turn increases the reabsorption of sodium and causes hypervolemia. These two mechanisms play a major role in renal vascular hypertension when renal artery stenosis is bilateral. In unilateral renal artery stenosis, pressure diuresis in the unaffected kidney compensates for the reabsorption of sodium in the affected kidney, keeping the blood pressure down. However, with time, the unaffected kidney will develop hypertensive nephropathy, and pressure diuresis will be lost.7,8 In addition, the activation of the renin-angiotensin-aldosterone system results in structural heart disease, such as left ventricular hypertrophy,5 and may shorten survival.

STENTING PLUS ANTIHYPERTENSIVE DRUG THERAPY

Because observational studies showed improvement in blood pressure control after endovascular stenting of atherosclerotic renal artery stenosis,9,10 this approach became a treatment option for uncontrolled hypertension in these patients. The 2005 joint guidelines of the American College of Cardiology and the American Heart Association11 considered percutaneous revascularization a reasonable option (level of evidence B) for patients who meet one of the following criteria:

  • Hemodynamically significant stenosis and accelerated, resistant, or malignant hypertension, hypertension with an unexplained unilateral small kidney, or hypertension with intolerance to medication
  • Renal artery stenosis and progressive chronic kidney disease with bilateral stenosis or stenosis in a solitary functioning kidney
  • Hemodynamically significant stenosis and recurrent, unexplained congestive heart failure or sudden, unexplained pulmonary edema or unstable angina.11

However, no randomized study has shown a direct benefit of renal artery stenting on rates of cardiovascular events or renal function compared with drug therapy alone.

 

 

TRIALS OF STENTING VS MEDICAL THERAPY ALONE

Technical improvements have led to more widespread use of diagnostic and interventional endovascular tools for renal artery revascularization. Studies over the past 10 years examined the impact of stenting in patients with uncontrolled hypertension.

The STAR trial

In the Stent Placement and Blood Pressure and Lipid-lowering for the Prevention of Progression of Renal Dysfunction Caused by Atherosclerotic Ostial Stenosis of the Renal Artery (STAR) trial,9 patients with creatinine clearance less than 80 mL/min/1.73 m2, renal artery stenosis greater than 50%, and well-controlled blood pressure were randomized to either renal artery stenting plus medical therapy or medical therapy alone. The authors concluded that stenting had no effect on the progression of renal dysfunction but led to a small number of significant, procedure-related complications. The study was criticized for including patients with mild stenosis (< 50% stenosis) and for being underpowered for the primary end point.

The ASTRAL study

The Angioplasty and Stenting for Renal Artery Lesions (ASTRAL) study10 was a similar comparison with similar results, showing no benefit from stenting with respect to renal function, systolic blood pressure control, cardiovascular events, or death.

HERCULES

The Herculink Elite Cobalt Chromium Renal Stent Trial to Demonstrate Efficacy and Safety (HERCULES)12 was a prospective multicenter study of the effects of renal artery stenting in 202 patients with significant renal artery stenosis and uncontrolled hypertension. It showed a reduction in systolic blood pressure from baseline (P < .0001). However, follow-up was only 9 months, which was insufficient to show a significant effect on long-term cardiovascular and cerebrovascular outcomes.

The CORAL trial

The Cardiovascular Outcomes in Renal Atherosclerotic Lesions (CORAL) trial13 used more stringent definitions and longer follow-up. It randomized 947 patients to either stenting plus medical therapy or medical therapy alone. Patients had atherosclerotic renal artery stenosis, defined as stenosis of at least 80% or stenosis of 60% to 80% with a gradient of at least 20 mm Hg in the systolic pressure), and either systolic hypertension while taking two or more antihypertensive drugs or stage 3 or higher chronic kidney disease (glomerular filtration rate < 60 mL/min/1.73 m2 as calculated by the Modification of Diet in Renal Disease formula).

Complications of renal artery stenting are a limiting factor compared with drug therapy alone

Participants were followed for 43 months to detect the occurrence of adverse cardiovascular and renal events. There was no significant difference in primary outcome between stenting plus drug therapy and drug therapy alone (35.1% and 35.8%, respectively; P = .58). However, stenting plus drug therapy was associated with modestly lower systolic pressures compared with drug therapy alone (−2.3 mm Hg, 95% confidence interval −4.4 to −0.2 mm Hg, P = .03).13 This study provided strong evidence that renal artery stenting offers no significant benefit to patients with moderately severe atherosclerotic renal artery stenosis, and that stenting may actually pose an unnecessary risk.

COMPLICATIONS OF RENAL ARTERY STENTING

Complications of renal artery stenting are a limiting factor compared with drug therapy alone, especially since the procedure offers no significant benefit in outcome. Procedural complication rates of 10% to 15% have been reported.9,10,12 The CORAL trial reported arterial dissection in 2.2%, branch-vessel occlusion in 1.2%, and distal embolization in 1.2% of patients undergoing stenting.13 Other reported complications have included stent misplacement requiring an additional stent, access-vessel damage, stent embolization, renal artery thrombosis or occlusion, and death.10,12

References
  1. Kalra PA, Guo H, Kausz AT, et al. Atherosclerotic renovascular disease in United States patients aged 67 years or older: risk factors, revascularization, and prognosis. Kidney Int 2005; 68:293–301.
  2. Hansen KJ, Edwards MS, Craven TE, et al. Prevalence of renovascular disease in the elderly: a population-based study. J Vasc Surg 2002; 36:443–451.
  3. Uzu T, Takeji M, Yamada N, et al. Prevalence and outcome of renal artery stenosis in atherosclerotic patients with renal dysfunction. Hypertens Res 2002; 25:537–542.
  4. Benjamin MM, Fazel P, Filardo G, Choi JW, Stoler RC. Prevalence of and risk factors of renal artery stenosis in patients with resistant hypertension. Am J Cardiol 2014; 113:687–690.
  5. Wu S, Polavarapu N, Stouffer GA. Left ventricular hypertrophy in patients with renal artery stenosis. Am J Med Sci 2006; 332:334–338.
  6. Lerman LO, Textor SC, Grande JP. Mechanisms of tissue injury in renal artery stenosis: ischemia and beyond. Prog Cardiovasc Dis 2009; 52:196–203.
  7. Black HR, Glickman MG, Schiff M Jr, Pingoud EG. Renovascular hypertension: pathophysiology, diagnosis, and treatment. Yale J Biol Med 1978; 51:635–654.
  8. Tobe SW, Burgess E, Lebel M. Atherosclerotic renovascular disease. Can J Cardiol 2006; 22:623–628.
  9. Bax L, Mali WP, Buskens E, et al; STAR Study Group. The benefit of stent placement and blood pressure and lipid-lowering for the prevention of progression of renal dysfunction caused by atherosclerotic ostial stenosis of the renal artery. The STAR-study: rationale and study design. J Nephrol 2003; 16:807–812.
  10. ASTRAL Investigators; Wheatley K, Ives N, Gray R, et al. Revascularization versus medical therapy for renal-artery stenosis. N Engl J Med 2009; 361:1953–1962.
  11. Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): executive summary. J Am Coll Cardiol 2006; 47:1239–1312.
References
  1. Kalra PA, Guo H, Kausz AT, et al. Atherosclerotic renovascular disease in United States patients aged 67 years or older: risk factors, revascularization, and prognosis. Kidney Int 2005; 68:293–301.
  2. Hansen KJ, Edwards MS, Craven TE, et al. Prevalence of renovascular disease in the elderly: a population-based study. J Vasc Surg 2002; 36:443–451.
  3. Uzu T, Takeji M, Yamada N, et al. Prevalence and outcome of renal artery stenosis in atherosclerotic patients with renal dysfunction. Hypertens Res 2002; 25:537–542.
  4. Benjamin MM, Fazel P, Filardo G, Choi JW, Stoler RC. Prevalence of and risk factors of renal artery stenosis in patients with resistant hypertension. Am J Cardiol 2014; 113:687–690.
  5. Wu S, Polavarapu N, Stouffer GA. Left ventricular hypertrophy in patients with renal artery stenosis. Am J Med Sci 2006; 332:334–338.
  6. Lerman LO, Textor SC, Grande JP. Mechanisms of tissue injury in renal artery stenosis: ischemia and beyond. Prog Cardiovasc Dis 2009; 52:196–203.
  7. Black HR, Glickman MG, Schiff M Jr, Pingoud EG. Renovascular hypertension: pathophysiology, diagnosis, and treatment. Yale J Biol Med 1978; 51:635–654.
  8. Tobe SW, Burgess E, Lebel M. Atherosclerotic renovascular disease. Can J Cardiol 2006; 22:623–628.
  9. Bax L, Mali WP, Buskens E, et al; STAR Study Group. The benefit of stent placement and blood pressure and lipid-lowering for the prevention of progression of renal dysfunction caused by atherosclerotic ostial stenosis of the renal artery. The STAR-study: rationale and study design. J Nephrol 2003; 16:807–812.
  10. ASTRAL Investigators; Wheatley K, Ives N, Gray R, et al. Revascularization versus medical therapy for renal-artery stenosis. N Engl J Med 2009; 361:1953–1962.
  11. Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): executive summary. J Am Coll Cardiol 2006; 47:1239–1312.
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Cleveland Clinic Journal of Medicine - 82(8)
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Cleveland Clinic Journal of Medicine - 82(8)
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491-494
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Does stenting of severe renal artery stenosis improve outomes compared with medical therapy alone?
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Does stenting of severe renal artery stenosis improve outomes compared with medical therapy alone?
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stenting, renal artery stenosis, renovascular hypertension, percutaneous transluminal renal angioplasty, Amjad Kabach, Osama Agha, Motaz Baibars, Abdul Hamid Alraiyes, M Chadi Alraies
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