Cocaine is among the most widely used recreational substances worldwide, with an estimated 18 million people using it globally. In the United States, cocaine consumption contributes significantly to morbidity and mortality, producing effects that range from long-term cognitive deficits to premature death. Cardiovascular complications are particularly important, accounting for over 64,000 emergency visits for chest pain annually and generating healthcare costs estimated between $155 million and $226 million each year. Cardiac events also rank among the leading causes of cocaine-related fatalities.
Although the association between cocaine and myocardial infarction has been extensively studied, the relationship between cocaine use and heart failure is less well characterized, even though it is widely recognized. The specific clinical, physiological, and structural features of cocaine-induced heart failure remain poorly defined. Despite numerous reviews examining cocaine’s role in acute coronary syndromes, there has been no comprehensive systematic review or meta-analysis to date that synthesizes the available evidence linking cocaine use to cardiomyopathy or heart failure.
Cocaine-related cardiomyopathy is a form of nonischemic cardiomyopathy that develops because of chronic or acute cocaine use. Cocaine is a powerful sympathomimetic agent that exerts toxic effects on the cardiovascular system through multiple mechanisms, including increased catecholamine release, coronary vasospasm, hypertension, arrhythmogenesis, and direct myocardial toxicity. These effects can result in structural and functional myocardial damage, ultimately leading to dilated cardiomyopathy and heart failure.
The condition is increasingly recognized due to the widespread use of cocaine worldwide and its association with significant morbidity and mortality among young and otherwise healthy individuals. Patients may present with chest pain, dyspnea, palpitations, or signs of acute decompensated heart failure. Importantly, the clinical course may vary, ranging from reversible myocardial dysfunction with abstinence to progressive, irreversible heart failure requiring advanced therapies such as implantable cardioverter-defibrillators or even cardiac transplantation.
Epidemiology
According to the 2018 National Survey on Drug Use and Health, an estimated 5.5 million individuals in the United States aged 12 years or older, representing about 2 percent of the population, reported having used cocaine at least once in their lifetime. This included approximately 757,000 people, or 0.3 percent of the population, who had used crack cocaine. The prevalence of past-year cocaine use in 2018 was comparable to the rates observed in 2016 and 2017, although it differed from most estimates between 2002 and 2015. In contrast, past-year crack cocaine use in 2018 was lower than the levels seen from 2002 to 2009 but remained like estimates between 2010 and 2017.
Most published data on cocaine-related cardiomyopathy are derived from case reports, suggesting that the condition may be relatively uncommon or potentially represent an idiosyncratic response. However, the actual incidence is likely underestimated. For example, Felker and colleagues documented 1,278 cases of dilated cardiomyopathy at Johns Hopkins, of which only 10 were attributed to cocaine exposure. Similarly, Bertolet and co-workers found that among chronic cocaine users without overt cardiac symptoms, 7 percent demonstrated left ventricular systolic dysfunction on radionuclide angiography. Importantly, no reports have linked cardiomyopathy to the therapeutic use of cocaine.
Anatomy
Pathophysiology
Etiology
Genetics
Prognostic Factors
Clinical History
Physical Examination
On physical examination, patients with cocaine-related cardiomyopathy often present with nonspecific findings that reflect heart failure rather than signs unique to cocaine use. They may appear dyspneic, anxious, or diaphoretic, particularly during acute intoxication or decompensation. Vital signs frequently reveal tachycardia and hypertension in acute use, whereas hypotension may occur in advanced cardiomyopathy. Cardiac examination may demonstrate a displaced, diffuse apical impulse suggestive of left ventricular enlargement, along with additional heart sounds such as an S3 gallop due to volume overload or an S4 indicating decreased ventricular compliance. Functional murmurs of mitral or tricuspid regurgitation may also be heard because of ventricular dilatation. Pulmonary auscultation often reveals bibasilar crackles consistent with pulmonary congestion or edema. Signs of right-sided heart failure, including jugular venous distension, hepatomegaly, ascites, and peripheral edema, may be evident. In severe cases, cool extremities and delayed capillary refill can indicate poor perfusion or cardiogenic shock. The clinical picture may also be influenced by complications of cocaine use, such as arrhythmias, myocardial ischemia, or hypertensive crisis, which should be carefully assessed during examination.
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Laboratory Studies
None
Imaging Studies
In patients with cardiomyopathy, chest radiographs often reveal cardiomegaly and features of congestive heart failure, although in many cases the radiograph may appear normal. If endocarditis is present, radiographic evidence of septic emboli can also be observed. Echocardiography typically demonstrates chamber enlargement with global ventricular dysfunction, while regional wall motion abnormalities may be noted in the setting of myocardial infarction. Studies have further shown that chronic cocaine users may have an increased left ventricular mass index and a tendency toward posterior wall thickening. A notable case involved a 58-year-old woman who developed Takotsubo cardiomyopathy two days after crack cocaine use, where bedside echocardiography in the emergency department suggested the diagnosis. Recognition of the characteristic echocardiographic finding of apical hypokinesis with left ventricular “ballooning” during systole can therefore be valuable for early identification. Cardiac catheterization in such patients generally reveals normal or minimally diseased coronary arteries, even when myocardial infarction is present, although coronary artery aneurysms have been documented in up to 30 percent of cocaine users. Electrocardiographic findings vary depending on the presentation: acute chest pain syndromes may show changes consistent with ischemia or infarction, while cardiomyopathy cases often display nonspecific features such as left ventricular hypertrophy, ST-T wave abnormalities, or arrhythmias, making continuous monitoring advisable.
Hypertension treatment
Patients who present with mild to moderate hypertension related to cocaine use often require no specific therapy beyond close observation and, when necessary, sedation with benzodiazepines. In situations where blood pressure elevation is more pronounced and consistent with a hypertensive crisis, intravenous vasodilators are typically indicated, with the addition of diuretics in select cases. Nitroglycerin is especially beneficial when there is evidence of myocardial ischemia. If sympathetic blockade is required to address arrhythmias or ischemic complications, beta blockers should not be administered as single agents, since this can result in unopposed alpha-adrenergic stimulation and worsening hypertension. Instead, beta blockers may be used in combination with alpha-adrenergic or ganglionic blockers to achieve safer hemodynamic control.
Myocardial Ischemia treatment
Chest pain is a frequent complaint among individuals who use cocaine and may result from myocardial ischemia or from musculoskeletal and other non-cardiac causes. An electrocardiogram is essential in all such cases to help distinguish between these possibilities. The use of beta blockers is contraindicated in patients with recent cocaine exposure who present with acute coronary syndrome, as this can increase the risk of coronary vasospasm. When myocardial ischemia is suspected without ST-segment elevation, intravenous nitroglycerin is the treatment of choice, with narcotic analgesics considered if pain persists despite nitrate therapy. In cases where ST-segment elevation is present, urgent cardiac catheterization should be pursued whenever possible. If catheterization is not immediately available, thrombolytic therapy may be considered, but clinicians must first rule out aortic dissection and intracranial hemorrhage, both of which have been associated with cocaine use.
Congestive heart failure treatment
A systematic review and meta-analysis published in 2020 highlighted that chronic cocaine use can induce structural and functional alterations in the myocardium, changes that are often more consistent with diastolic heart failure and may be reversible with beta-blocker therapy. Management of cocaine-related cardiomyopathy generally follows standard heart failure treatment protocols, including the use of diuretics and vasodilators when tolerated. In cases complicated by shock, inotropic support and vasopressors may be required. When ongoing myocardial ischemia is suspected, aggressive use of vasodilatory agents such as nitrates and calcium channel blockers is recommended to relieve coronary vasospasm. Advanced airway support, including endotracheal intubation, may be necessary in severe cases. Arrhythmias that compromise hemodynamic stability should be promptly addressed with appropriate therapy. Importantly, beta blockers should not be administered as sole agents, given the risk of unopposed alpha-adrenergic stimulation and worsening vasoconstriction.
Cocaine is among the most widely used recreational substances worldwide, with an estimated 18 million people using it globally. In the United States, cocaine consumption contributes significantly to morbidity and mortality, producing effects that range from long-term cognitive deficits to premature death. Cardiovascular complications are particularly important, accounting for over 64,000 emergency visits for chest pain annually and generating healthcare costs estimated between $155 million and $226 million each year. Cardiac events also rank among the leading causes of cocaine-related fatalities.
Although the association between cocaine and myocardial infarction has been extensively studied, the relationship between cocaine use and heart failure is less well characterized, even though it is widely recognized. The specific clinical, physiological, and structural features of cocaine-induced heart failure remain poorly defined. Despite numerous reviews examining cocaine’s role in acute coronary syndromes, there has been no comprehensive systematic review or meta-analysis to date that synthesizes the available evidence linking cocaine use to cardiomyopathy or heart failure.
Cocaine-related cardiomyopathy is a form of nonischemic cardiomyopathy that develops because of chronic or acute cocaine use. Cocaine is a powerful sympathomimetic agent that exerts toxic effects on the cardiovascular system through multiple mechanisms, including increased catecholamine release, coronary vasospasm, hypertension, arrhythmogenesis, and direct myocardial toxicity. These effects can result in structural and functional myocardial damage, ultimately leading to dilated cardiomyopathy and heart failure.
The condition is increasingly recognized due to the widespread use of cocaine worldwide and its association with significant morbidity and mortality among young and otherwise healthy individuals. Patients may present with chest pain, dyspnea, palpitations, or signs of acute decompensated heart failure. Importantly, the clinical course may vary, ranging from reversible myocardial dysfunction with abstinence to progressive, irreversible heart failure requiring advanced therapies such as implantable cardioverter-defibrillators or even cardiac transplantation.
According to the 2018 National Survey on Drug Use and Health, an estimated 5.5 million individuals in the United States aged 12 years or older, representing about 2 percent of the population, reported having used cocaine at least once in their lifetime. This included approximately 757,000 people, or 0.3 percent of the population, who had used crack cocaine. The prevalence of past-year cocaine use in 2018 was comparable to the rates observed in 2016 and 2017, although it differed from most estimates between 2002 and 2015. In contrast, past-year crack cocaine use in 2018 was lower than the levels seen from 2002 to 2009 but remained like estimates between 2010 and 2017.
Most published data on cocaine-related cardiomyopathy are derived from case reports, suggesting that the condition may be relatively uncommon or potentially represent an idiosyncratic response. However, the actual incidence is likely underestimated. For example, Felker and colleagues documented 1,278 cases of dilated cardiomyopathy at Johns Hopkins, of which only 10 were attributed to cocaine exposure. Similarly, Bertolet and co-workers found that among chronic cocaine users without overt cardiac symptoms, 7 percent demonstrated left ventricular systolic dysfunction on radionuclide angiography. Importantly, no reports have linked cardiomyopathy to the therapeutic use of cocaine.
On physical examination, patients with cocaine-related cardiomyopathy often present with nonspecific findings that reflect heart failure rather than signs unique to cocaine use. They may appear dyspneic, anxious, or diaphoretic, particularly during acute intoxication or decompensation. Vital signs frequently reveal tachycardia and hypertension in acute use, whereas hypotension may occur in advanced cardiomyopathy. Cardiac examination may demonstrate a displaced, diffuse apical impulse suggestive of left ventricular enlargement, along with additional heart sounds such as an S3 gallop due to volume overload or an S4 indicating decreased ventricular compliance. Functional murmurs of mitral or tricuspid regurgitation may also be heard because of ventricular dilatation. Pulmonary auscultation often reveals bibasilar crackles consistent with pulmonary congestion or edema. Signs of right-sided heart failure, including jugular venous distension, hepatomegaly, ascites, and peripheral edema, may be evident. In severe cases, cool extremities and delayed capillary refill can indicate poor perfusion or cardiogenic shock. The clinical picture may also be influenced by complications of cocaine use, such as arrhythmias, myocardial ischemia, or hypertensive crisis, which should be carefully assessed during examination.
None
In patients with cardiomyopathy, chest radiographs often reveal cardiomegaly and features of congestive heart failure, although in many cases the radiograph may appear normal. If endocarditis is present, radiographic evidence of septic emboli can also be observed. Echocardiography typically demonstrates chamber enlargement with global ventricular dysfunction, while regional wall motion abnormalities may be noted in the setting of myocardial infarction. Studies have further shown that chronic cocaine users may have an increased left ventricular mass index and a tendency toward posterior wall thickening. A notable case involved a 58-year-old woman who developed Takotsubo cardiomyopathy two days after crack cocaine use, where bedside echocardiography in the emergency department suggested the diagnosis. Recognition of the characteristic echocardiographic finding of apical hypokinesis with left ventricular “ballooning” during systole can therefore be valuable for early identification. Cardiac catheterization in such patients generally reveals normal or minimally diseased coronary arteries, even when myocardial infarction is present, although coronary artery aneurysms have been documented in up to 30 percent of cocaine users. Electrocardiographic findings vary depending on the presentation: acute chest pain syndromes may show changes consistent with ischemia or infarction, while cardiomyopathy cases often display nonspecific features such as left ventricular hypertrophy, ST-T wave abnormalities, or arrhythmias, making continuous monitoring advisable.
Hypertension treatment
Patients who present with mild to moderate hypertension related to cocaine use often require no specific therapy beyond close observation and, when necessary, sedation with benzodiazepines. In situations where blood pressure elevation is more pronounced and consistent with a hypertensive crisis, intravenous vasodilators are typically indicated, with the addition of diuretics in select cases. Nitroglycerin is especially beneficial when there is evidence of myocardial ischemia. If sympathetic blockade is required to address arrhythmias or ischemic complications, beta blockers should not be administered as single agents, since this can result in unopposed alpha-adrenergic stimulation and worsening hypertension. Instead, beta blockers may be used in combination with alpha-adrenergic or ganglionic blockers to achieve safer hemodynamic control.
Myocardial Ischemia treatment
Chest pain is a frequent complaint among individuals who use cocaine and may result from myocardial ischemia or from musculoskeletal and other non-cardiac causes. An electrocardiogram is essential in all such cases to help distinguish between these possibilities. The use of beta blockers is contraindicated in patients with recent cocaine exposure who present with acute coronary syndrome, as this can increase the risk of coronary vasospasm. When myocardial ischemia is suspected without ST-segment elevation, intravenous nitroglycerin is the treatment of choice, with narcotic analgesics considered if pain persists despite nitrate therapy. In cases where ST-segment elevation is present, urgent cardiac catheterization should be pursued whenever possible. If catheterization is not immediately available, thrombolytic therapy may be considered, but clinicians must first rule out aortic dissection and intracranial hemorrhage, both of which have been associated with cocaine use.
Congestive heart failure treatment
A systematic review and meta-analysis published in 2020 highlighted that chronic cocaine use can induce structural and functional alterations in the myocardium, changes that are often more consistent with diastolic heart failure and may be reversible with beta-blocker therapy. Management of cocaine-related cardiomyopathy generally follows standard heart failure treatment protocols, including the use of diuretics and vasodilators when tolerated. In cases complicated by shock, inotropic support and vasopressors may be required. When ongoing myocardial ischemia is suspected, aggressive use of vasodilatory agents such as nitrates and calcium channel blockers is recommended to relieve coronary vasospasm. Advanced airway support, including endotracheal intubation, may be necessary in severe cases. Arrhythmias that compromise hemodynamic stability should be promptly addressed with appropriate therapy. Importantly, beta blockers should not be administered as sole agents, given the risk of unopposed alpha-adrenergic stimulation and worsening vasoconstriction.
Cocaine is among the most widely used recreational substances worldwide, with an estimated 18 million people using it globally. In the United States, cocaine consumption contributes significantly to morbidity and mortality, producing effects that range from long-term cognitive deficits to premature death. Cardiovascular complications are particularly important, accounting for over 64,000 emergency visits for chest pain annually and generating healthcare costs estimated between $155 million and $226 million each year. Cardiac events also rank among the leading causes of cocaine-related fatalities.
Although the association between cocaine and myocardial infarction has been extensively studied, the relationship between cocaine use and heart failure is less well characterized, even though it is widely recognized. The specific clinical, physiological, and structural features of cocaine-induced heart failure remain poorly defined. Despite numerous reviews examining cocaine’s role in acute coronary syndromes, there has been no comprehensive systematic review or meta-analysis to date that synthesizes the available evidence linking cocaine use to cardiomyopathy or heart failure.
Cocaine-related cardiomyopathy is a form of nonischemic cardiomyopathy that develops because of chronic or acute cocaine use. Cocaine is a powerful sympathomimetic agent that exerts toxic effects on the cardiovascular system through multiple mechanisms, including increased catecholamine release, coronary vasospasm, hypertension, arrhythmogenesis, and direct myocardial toxicity. These effects can result in structural and functional myocardial damage, ultimately leading to dilated cardiomyopathy and heart failure.
The condition is increasingly recognized due to the widespread use of cocaine worldwide and its association with significant morbidity and mortality among young and otherwise healthy individuals. Patients may present with chest pain, dyspnea, palpitations, or signs of acute decompensated heart failure. Importantly, the clinical course may vary, ranging from reversible myocardial dysfunction with abstinence to progressive, irreversible heart failure requiring advanced therapies such as implantable cardioverter-defibrillators or even cardiac transplantation.
According to the 2018 National Survey on Drug Use and Health, an estimated 5.5 million individuals in the United States aged 12 years or older, representing about 2 percent of the population, reported having used cocaine at least once in their lifetime. This included approximately 757,000 people, or 0.3 percent of the population, who had used crack cocaine. The prevalence of past-year cocaine use in 2018 was comparable to the rates observed in 2016 and 2017, although it differed from most estimates between 2002 and 2015. In contrast, past-year crack cocaine use in 2018 was lower than the levels seen from 2002 to 2009 but remained like estimates between 2010 and 2017.
Most published data on cocaine-related cardiomyopathy are derived from case reports, suggesting that the condition may be relatively uncommon or potentially represent an idiosyncratic response. However, the actual incidence is likely underestimated. For example, Felker and colleagues documented 1,278 cases of dilated cardiomyopathy at Johns Hopkins, of which only 10 were attributed to cocaine exposure. Similarly, Bertolet and co-workers found that among chronic cocaine users without overt cardiac symptoms, 7 percent demonstrated left ventricular systolic dysfunction on radionuclide angiography. Importantly, no reports have linked cardiomyopathy to the therapeutic use of cocaine.
On physical examination, patients with cocaine-related cardiomyopathy often present with nonspecific findings that reflect heart failure rather than signs unique to cocaine use. They may appear dyspneic, anxious, or diaphoretic, particularly during acute intoxication or decompensation. Vital signs frequently reveal tachycardia and hypertension in acute use, whereas hypotension may occur in advanced cardiomyopathy. Cardiac examination may demonstrate a displaced, diffuse apical impulse suggestive of left ventricular enlargement, along with additional heart sounds such as an S3 gallop due to volume overload or an S4 indicating decreased ventricular compliance. Functional murmurs of mitral or tricuspid regurgitation may also be heard because of ventricular dilatation. Pulmonary auscultation often reveals bibasilar crackles consistent with pulmonary congestion or edema. Signs of right-sided heart failure, including jugular venous distension, hepatomegaly, ascites, and peripheral edema, may be evident. In severe cases, cool extremities and delayed capillary refill can indicate poor perfusion or cardiogenic shock. The clinical picture may also be influenced by complications of cocaine use, such as arrhythmias, myocardial ischemia, or hypertensive crisis, which should be carefully assessed during examination.
None
In patients with cardiomyopathy, chest radiographs often reveal cardiomegaly and features of congestive heart failure, although in many cases the radiograph may appear normal. If endocarditis is present, radiographic evidence of septic emboli can also be observed. Echocardiography typically demonstrates chamber enlargement with global ventricular dysfunction, while regional wall motion abnormalities may be noted in the setting of myocardial infarction. Studies have further shown that chronic cocaine users may have an increased left ventricular mass index and a tendency toward posterior wall thickening. A notable case involved a 58-year-old woman who developed Takotsubo cardiomyopathy two days after crack cocaine use, where bedside echocardiography in the emergency department suggested the diagnosis. Recognition of the characteristic echocardiographic finding of apical hypokinesis with left ventricular “ballooning” during systole can therefore be valuable for early identification. Cardiac catheterization in such patients generally reveals normal or minimally diseased coronary arteries, even when myocardial infarction is present, although coronary artery aneurysms have been documented in up to 30 percent of cocaine users. Electrocardiographic findings vary depending on the presentation: acute chest pain syndromes may show changes consistent with ischemia or infarction, while cardiomyopathy cases often display nonspecific features such as left ventricular hypertrophy, ST-T wave abnormalities, or arrhythmias, making continuous monitoring advisable.
Hypertension treatment
Patients who present with mild to moderate hypertension related to cocaine use often require no specific therapy beyond close observation and, when necessary, sedation with benzodiazepines. In situations where blood pressure elevation is more pronounced and consistent with a hypertensive crisis, intravenous vasodilators are typically indicated, with the addition of diuretics in select cases. Nitroglycerin is especially beneficial when there is evidence of myocardial ischemia. If sympathetic blockade is required to address arrhythmias or ischemic complications, beta blockers should not be administered as single agents, since this can result in unopposed alpha-adrenergic stimulation and worsening hypertension. Instead, beta blockers may be used in combination with alpha-adrenergic or ganglionic blockers to achieve safer hemodynamic control.
Myocardial Ischemia treatment
Chest pain is a frequent complaint among individuals who use cocaine and may result from myocardial ischemia or from musculoskeletal and other non-cardiac causes. An electrocardiogram is essential in all such cases to help distinguish between these possibilities. The use of beta blockers is contraindicated in patients with recent cocaine exposure who present with acute coronary syndrome, as this can increase the risk of coronary vasospasm. When myocardial ischemia is suspected without ST-segment elevation, intravenous nitroglycerin is the treatment of choice, with narcotic analgesics considered if pain persists despite nitrate therapy. In cases where ST-segment elevation is present, urgent cardiac catheterization should be pursued whenever possible. If catheterization is not immediately available, thrombolytic therapy may be considered, but clinicians must first rule out aortic dissection and intracranial hemorrhage, both of which have been associated with cocaine use.
Congestive heart failure treatment
A systematic review and meta-analysis published in 2020 highlighted that chronic cocaine use can induce structural and functional alterations in the myocardium, changes that are often more consistent with diastolic heart failure and may be reversible with beta-blocker therapy. Management of cocaine-related cardiomyopathy generally follows standard heart failure treatment protocols, including the use of diuretics and vasodilators when tolerated. In cases complicated by shock, inotropic support and vasopressors may be required. When ongoing myocardial ischemia is suspected, aggressive use of vasodilatory agents such as nitrates and calcium channel blockers is recommended to relieve coronary vasospasm. Advanced airway support, including endotracheal intubation, may be necessary in severe cases. Arrhythmias that compromise hemodynamic stability should be promptly addressed with appropriate therapy. Importantly, beta blockers should not be administered as sole agents, given the risk of unopposed alpha-adrenergic stimulation and worsening vasoconstriction.
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