Review Article

Cocaine-Induced Coronary Syndromes: Unraveling the Complex Pathophysiology and Clinical Implications

Nadia Nishat¹, Kevin J Lopez Romero², Jose C Rosario-Curcio³, Vianka Vanessa Yanez Montalvo⁴, Jean C Concepcion³, Kenol Clervil⁵, Nune Azaryan Dermenjian⁶, Krupa Ann Mathew⁷, Amir Bolous⁸, Marcela Garzon Olave⁹, Fátima Melissa Morales Navarro¹⁰, Jorge Mauricio Minero Reyes¹¹ and Maria Isabel Gomez Coral¹²*

¹Mandya Institute of Medical Sciences, India

²Universidad de El Salvador, El Salvador

³University of Medicine & Health Sciences, St. Kitts

⁴Universidad de Guayaquil, Ecuador

⁵Instituto Tecnologico de Santo Domingo, Dominican Republic

⁶Yerevan State Medical University, USA

⁷Tbilisi State Medical University, Georgia

⁸Minia School of Medicine, Egypt

⁹Universidad de los Andes, Colombia

¹⁰Hospital Médico Quirúrgico ISSS. El Salvador

¹¹Universidad Alberto Masferrer, El Salvador

¹²Universidad del Valle de México, México

Submission: March 25, 2024; Published: April 03, 2024

*Corresponding author: Maria Isabel Gomez Coral, Universidad del Valle de México, México

How to cite this article: Nadia N, Kevin J L R, Jose C R-C, Vianka Vanessa Yanez M, Jean C C, et al. Cocaine-Induced Coronary Syndromes: Unraveling the 002 Complex Pathophysiology and Clinical Implications. 2024; 19(2): 556009 DOI: 10.19080/JOCCT.2024.19.556009

Abstract

Cocaine-induced coronary syndromes represent a significant public health concern, with complex pathophysiology and high morbidity and mortality rates. This article provides a comprehensive overview of the epidemiology, pathophysiology, clinical manifestations, diagnosis, management strategies, prognosis, and complications associated with cocaine-induced coronary syndromes. Epidemiological data suggest a notable increase in cocaine use globally, with significant implications for cardiovascular health. The pathophysiology of cocaine-induced coronary syndromes involves multifaceted mechanisms, including vascular dysfunction, myocardial ischemia, atherosclerosis, and thrombosis. Clinical manifestations range from asymptomatic electrocardiographic changes to life-threatening acute myocardial infarction, posing diagnostic challenges for healthcare professionals. Management strategies encompass a multidisciplinary approach, including pharmacological interventions, revascularization procedures, and behavioral interventions aimed at addressing both acute cardiovascular events and underlying substance abuse disorders. Despite advancements in medical therapy and preventive measures, the burden of cocaine-induced coronary syndromes remains substantial, highlighting the need for collaborative efforts to mitigate the impact of cocaine-related cardiovascular complications on public health and clinical practice.

Keywords: Cocaine-induced coronary syndromes; Acute myocardial infarction; Coronary artery disease; Substance abuse coronary implications

Abbreviations: ACS: Acute Coronary Syndromes; ECG: Electrocardiography; PCI: Percutaneous Coronary Intervention; CABG: Coronary Artery Bypass Grafting; SAMHSA: Substance Abuse and Mental Health Services Administration; MI: Myocardial Infarction; CVD: Cardiovascular Disease; QT: QT Interval; ASA: Aspirin; P2Y12: P2Y12 Receptor; CK-MB: Creatine Kinase-MB; CT: Computed Tomography; ADHF: Acute Decompensated Heart Failure

Introduction

Coronary syndromes present a spectrum of conditions arising from acute myocardial ischemia, characterized by insufficient blood flow to the heart. This group of disorders ranges from unstable angina to myocardial infarction, known as a heart attack. The underlying pathology involves varying degrees of narrowing or blockage in one or multiple coronary arteries [1]. The severity of obstruction in the affected coronary artery, collateral perfusion, and myocardial oxygen demand influence the clinical manifestations. Acute myocardial infarction is distinguished from minimal injury based on clinical presentation, electrocardiographic changes, and varying levels of cardiac enzyme release. Unstable angina is characterized by non-occlusive thrombosis without significant enzyme release [2]. Acute coronary syndromes (ACS) are considered life-threatening conditions that require prompt medical intervention, given their significant impact on emergency healthcare services. Overall, coronary artery disease remains a predominant cause of mortality in the United States. As a result, understanding and managing cardiac conditions is of utmost importance [1].

Cocaine has been identified as a significant risk factor for ACS [3,4]. Chang et al. [3] highlighted that observational studies have shown an increased prevalence of coronary disease in patients with cocaine-induced myocardial infarction [3]. These findings surpassed the expected rates based on patient age. The pathological mechanisms behind the action of cocaine include increased myocardial oxygen demand, coronary vasoconstriction, platelet aggregation, and thrombus formation. Cocaine can induce myocardial ischemia, even in individuals with normal coronary arteries [3]. Cregler et al. [4] emphasized that cocaine abuse can lead to acute myocardial infarction even in young individuals without any cardiovascular risk factors [4]. Small and large doses of cocaine may cause this reaction. The study also discussed the multifactorial etiology of cocaine-related myocardial infarction. It involves vasoconstriction, spasms, and increased thrombotic potential in the coronary arteries. Cocaine abuse has been linked to conditions such as dilated cardiomyopathy, myocarditis, infective endocarditis, pulmonary edema, vascular thrombosis, and cerebrovascular accidents [4]. The relationship between cocaine and coronary syndromes is of high importance due to the significant cardiac complications. Understanding this connection is crucial in the medical field as it demonstrates the mechanisms by which cocaine exerts its adverse effects on the cardiovascular system [5].

The literature suggested that the risk of ACS following cocaine use is substantial. It was demonstrated by the high rates of acute myocardial infarction in patients presenting with cocaine-associated chest pain [3,4]. By recognizing the impact of cocaine on coronary arteries, vasospasm, thrombosis, and atherosclerosis, healthcare professionals can better treat and prevent the life-threatening consequences of cocaine use [5]. These insights highlight the importance of considering cocaine use in risk assessment of ACS in symptomatic emergency department patients [3,4]. Unraveling the relationship between cocaine and coronary syndromes can lead to the development of targeted therapeutic interventions that can alleviate the cardiovascular risks associated with cocaine abuse [5].

Epidemiology of Cocaine Use and Coronary Syndromes

The epidemiology of cocaine use and its association with coronary syndromes presents a complex landscape influenced by various factors. Globally, the prevalence of cocaine use has shown a notable increase over the past decade, with an estimated rise of around 2.5 million users, reaching approximately 22 million users by 2021 [5]. Despite this increase, recent years have witnessed a plateau in these figures, hovering around 22 to nearly 23 million users since 2014. Notably, the Americas account for more than half of all cocaine users, with a prevalence of 11.35 million in 2021, followed by Europe, Africa, and Asia [6]. However, due to the illicit nature of cocaine, these prevalence figures may be underestimated, with actual numbers potentially higher due to underreporting and fear of repercussions.

Assessing the incidence and prevalence of cocaine-induced coronary syndromes poses challenges due to the substance's illegality. However, studies suggest a correlation between cocaine use and increased cases of acute coronary syndrome (ACS) in hospital settings [7]. Typically, the age of incidence for cocaine-related coronary disease is observed in patients under 50 years old, with some studies reporting a range from 44 to 69 years old [8,9]. Across different populations, studies have found that cocaine-induced coronary syndromes occur in approximately 5% of patients, with chest pain being a common presenting symptom [7,8]. Additionally, there is evidence suggesting a relationship between the frequency of cocaine use and the likelihood of experiencing a nonfatal myocardial infarction (MI), with some studies reporting that around 25% of patients with nonfatal MIs had a history of frequent cocaine use [9,10].

Understanding the epidemiology of cocaine use and its association with coronary syndromes is crucial for informing public health interventions and clinical management strategies. Despite efforts to track prevalence and incidence, the clandestine nature of cocaine use presents inherent challenges in obtaining accurate data. Further research is warranted to explore the full extent of the relationship between cocaine consumption and cardiovascular health outcomes, enabling targeted interventions to mitigate the risks associated with cocaine-induced coronary syndromes [6].

Pathophysiology of Cocaine-Induced Coronary Syndromes

The pathophysiology of cocaine-induced coronary syndromes is multifaceted, encompassing various mechanisms that contribute to vascular dysfunction and myocardial injury. Cocaine exerts its effects on the cardiovascular system through multiple pathways, including sympathetic nervous system activation, inhibition of norepinephrine reuptake, and enhancement of catecholamine release, leading to vasoconstriction and increased blood pressure [11]. Additionally, cocaine impairs endothelial function by reducing nitric oxide bioavailability and promoting oxidative stress, thereby exacerbating vascular inflammation and endothelial dysfunction [12]. These vascular effects collectively contribute to increased myocardial oxygen demand and reduced oxygen supply, creating an imbalance predisposing individuals to ischemic events.

Moreover, chronic cocaine use has been implicated in the progression of atherosclerosis and thrombosis, further exacerbating the risk of coronary syndromes [13]. Cocaine promotes the formation of atherosclerotic plaques through various mechanisms, including endothelial injury, inflammation, and dyslipidemia, which contribute to the development of vulnerable plaques prone to rupture [14].

Furthermore, cocaine-induced platelet activation and aggregation enhance thrombus formation, exacerbating coronary artery occlusion and precipitating acute cardiovascular events such as myocardial infarction [15]. Understanding the intricate interplay between cocaine-induced vascular effects, myocardial oxygen imbalance, atherosclerosis, and thrombosis is essential for elucidating the complex pathophysiology of cocaine-induced coronary syndromes and informing targeted therapeutic strategies to mitigate their clinical consequences.

Clinical Manifestations and Diagnosis

Clinical manifestations of cocaine-induced coronary syndromes vary widely, ranging from asymptomatic electrocardiographic changes to life-threatening acute myocardial infarction. Patients may present with typical angina symptoms, such as chest pain or pressure, which can be indistinguishable from those of other causes of myocardial ischemia [16]. Moreover, cocaine use may mask underlying symptoms of coronary artery disease due to its sympathomimetic effects, leading to delayed recognition and diagnosis of myocardial ischemia [17]. Additionally, cocaine-induced vasospasm can result in transient ischemic events, presenting as angina pectoris or even acute coronary syndromes in the absence of significant coronary artery stenosis [18]. These clinical challenges underscore the importance of maintaining a high index of suspicion for cocaine-related myocardial ischemia in at-risk populations, particularly in young individuals with a history of substance abuse.

Diagnosing cocaine-induced coronary syndromes poses significant challenges due to the complex interplay between cocaine use and cardiovascular pathology. Differential diagnosis considerations include ruling out other causes of myocardial ischemia, such as atherosclerotic coronary artery disease, vasospastic disorders, and non-cardiac etiologies of chest pain [19]. Electrocardiography (ECG) remains a cornerstone in the initial evaluation, with findings ranging from ST-segment elevation or depression to T-wave abnormalities and QT prolongation. However, these changes may not be specific to cocaine-induced myocardial ischemia [20]. Cardiac biomarkers, including troponins and creatine kinase-MB, are crucial in confirming myocardial injury. In contrast, advanced imaging techniques such as coronary angiography and cardiac computed tomography can provide valuable information regarding the presence and severity of coronary artery disease [21].

Management Strategies

Management strategies for cocaine-induced coronary syndromes encompass a multidisciplinary approach aimed at addressing both acute cardiovascular events and underlying substance abuse disorders. In the acute setting, prompt recognition and treatment of cocaine-related coronary syndromes are paramount to minimize myocardial injury and improve outcomes. Pharmacological interventions play a crucial role, with antiplatelet agents such as aspirin and P2Y12 inhibitors utilized to mitigate thrombotic complications [22]. Nitroglycerin is commonly employed to relieve coronary artery spasms and alleviate chest pain. At the same time, beta-blockers may be administered cautiously to counteract cocaine-induced sympathetic stimulation and reduce myocardial oxygen demand [23]. However, the use of beta-blockers requires careful consideration due to the risk of unopposed alpha-adrenergic effects leading to severe hypertension and coronary vasoconstriction in some individuals [24].

Revascularization procedures, including percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG), may be indicated in select cases of cocaine-induced myocardial infarction or significant coronary artery disease [25]. PCI offers a minimally invasive option for restoring coronary blood flow and relieving ischemia, while CABG may be considered in patients with complex coronary anatomy or multivessel disease. Beyond acute management, addressing underlying substance abuse disorders is critical for long-term risk reduction and prevention of recurrent cardiovascular events. Behavioral interventions, including counseling, cognitive-behavioral therapy, and substance abuse treatment programs, play a pivotal role in promoting abstinence and supporting recovery from cocaine addiction [26]. Comprehensive management strategies that integrate acute cardiovascular care with substance abuse treatment are essential for optimizing outcomes and reducing the burden of cocaine-induced coronary syndromes.

Prognosis & Complications

Various factors, including the severity of myocardial ischemia, the extent of underlying coronary artery disease, and the presence of comorbidities, influence the prognosis of cocaine-induced coronary syndromes. Cocaine use in the setting of coronary syndromes is associated with worse outcomes compared to those without cocaine use, with higher rates of recurrent ischemic events, myocardial infarction, and mortality [27]. Recurrence rates of myocardial ischemia and adverse cardiovascular events are notably elevated among individuals with a history of cocaine use, underscoring the importance of aggressive risk factor modification and comprehensive secondary prevention strategies in this population [28]. Long-term outcomes are also impacted by continued cocaine use, with persistent substance abuse contributing to ongoing cardiovascular damage and a heightened risk of recurrent coronary events [29].

Complications of cocaine-induced coronary syndromes encompass a spectrum of cardiovascular manifestations, including arrhythmias, heart failure, and sudden cardiac death. Cocaine use can precipitate life-threatening arrhythmias such as ventricular tachycardia, ventricular fibrillation, and atrial fibrillation through various mechanisms, including myocardial ischemia, sympathetic hyperactivity, and alterations in cardiac ion channels [30,31]. Additionally, cocaine-induced myocardial ischemia can lead to acute decompensated heart failure, exacerbating hemodynamic instability and increasing the risk of cardiogenic shock [32]. Sudden cardiac death is a devastating complication associated with cocaine use, often attributed to fatal arrhythmias or acute coronary events, highlighting the importance of early recognition and aggressive management of cocaine-induced coronary syndromes to mitigate adverse outcomes [33].

Prevention and Public Health Implications

Evidence-based strategies for preventing substance abuse are diverse, involving coordinated efforts across schools, families, and communities, as highlighted by the Substance Abuse and Mental Health Services Administration (SAMHSA) [34]. These strategies include school-based programs that teach adolescents how to resist peer pressure, correct false beliefs about how common drug use is among their peers, and improve their coping skills [35]. Family-based programs focus on strengthening parenting skills, improving communication, and bonding within the family. Additionally, community targeting initiatives bring together educational programs, policy changes, and mass media campaigns to approach cocaine abuse in a holistic manner [36]. Education and awareness campaigns play a vital role in informing individuals about the harmful effects of cocaine use on the cardiovascular system and promoting cessation efforts to prevent further harm [37,11].

Cocaine ranks as one of the most widely used illegal drugs globally for recreational purposes, and even occasional consumption of cocaine can lead to immediate or long-term harm to the cardiovascular system [38]. Discontinuing cocaine consumption is crucial for preventing further harm, although addressing other risk factors like tobacco smoking could also be beneficial. Regrettably, about 60 percent of individuals with chest pain related to cocaine use continue to use cocaine within the year following a symptomatic incident [39]. Individuals who have received treatment for acute coronary syndrome (ACS) due to cocaine use should receive ongoing treatment to prevent atherosclerotic cardiovascular disease (CVD) [40,41]. Typically, this involves prescribing an antiplatelet medication (usually aspirin) and a statin drug (such as atorvastatin, rosuvastatin, etc.). Depending on the severity of ACS-related damage, patients may also need additional medical interventions, such as treatments for heart failure or reduced left ventricular systolic function. Moreover, patients should receive guidance on adopting a healthy diet, weight management (if overweight), regular physical activity, and quitting smoking [42].

Conclusion

Cocaine-induced coronary syndromes pose significant challenges to public health and clinical management due to their complex pathophysiology and high morbidity and mortality rates. Understanding the intricate interplay between cocaine use and cardiovascular health is essential for guiding preventive measures, early diagnosis, and effective management strategies. Despite advancements in medical therapy and behavioral interventions, the burden of cocaine-induced coronary syndromes remains substantial, emphasizing the need for comprehensive approaches that address both acute cardiovascular events and underlying substance abuse disorders. Collaborative efforts involving healthcare professionals, policymakers, and community stakeholders are essential for implementing evidence-based interventions and reducing the prevalence and impact of cocaine-related cardiovascular complications.

References

1. Torpy JM, Alison EB, Richard MG (2010) Acute coronary syndromes. JAMA 303(1): 90-90.
2. Fox KA (2000) Acute coronary syndromes: presentation-clinical spectrum and management. Heart 84(1): 93-100.
3. Anna MC, Kristy MW, Frances SS, Christine MM, Harold IL, et al. (2011) Relationship between cocaine use and coronary artery disease in patients with symptoms consistent with an acute coronary syndrome. Acad Emerg Med 18(1): 1-9.
4. Cregler LL (1991) Cocaine: the newest risk factor for cardiovascular disease. Clinical Cardiol 14(6): 449-456.
5. Talarico GP, Maria LC, Maria BG, Francesco S, Leonardo C, et al. (2017) Cocaine and coronary artery diseases: a systematic review of the literature. J Cardiovasc Med 18(5): 291-294.
6. Elflein J (2023) Number of people who use cocaine worldwide by region 2010-2021. Statista.
7. Carrillo X, Vilalta V, Cediel G, Fernandez NE, Rodriguez LO, et al. (2019) Trends in prevalence and outcomes of acute coronary syndrome associated with cocaine consumption: The Ruti-cocaine study. Int J Cardiol 283: 23-27.
8. DeFilippis EM, Singh A, Divakaran S, Gupta A, Collins BL, et al. (2018) Cocaine and marijuana use among young adults with myocardial infarction. J Am Coll Cardiol 71(22): 2540-2551.
9. Bosch X, Loma OP, Guasch E, Nogué S, Ortiz JT, et al. (2010) Prevalence clinical characteristics and risk of myocardial infarction in patients with cocaine-related chest pain. Revista Española de Cardiología (English Edition) 63(9): 1028-1034.
10. Qureshi AI, Suri MF, Guterman LR, Hopkins LN (2001) Cocaine use and the likelihood of nonfatal myocardial infarction and stroke: data from the Third National Health and Nutrition Examination Survey. Circulation 103(4): 502-506.
11. Lange RA, Hillis LD (2001) Cardiovascular complications of cocaine use. N Engl J Med 345(5): 351-358.
12. Bachi K, Mani V, Jeyachandran D, Fayad ZA, Goldstein RZ, et al. (2017) vascular disease in cocaine addiction. Atherosclerosis 262: 154-162.
13. O Neil M, Heller E, Rivera J (2012) The role of cocaine in atherosclerosis and peripheral vascular disease. Vasc Endovascular Surg 46(8): 592-599.
14. Wijetunga M, Bhan R, Lindsay J (2010) Cardiovascular manifestations of substance abuse: part 2: alcohol, amphetamines, heroin, cannabis, and caffeine. Heart Lung Circ 19(6-7): 391-401.
15. Chakrabarti A, Chen AW, Varon J (2007) Cocaine and cardiovascular disease: a systematic review of the literature. Am J Ther 14(5): 502-511.
16. Hollander JE, Hoffman RS, Gennis P, Burstein JL, Shih RD, et al. (1995) Cocaine-associated myocardial infarction: mortality and complications. Cocaine-Associated Myocardial Infarction Study Group. Arch Intern Med 155(10): 1081-1086.
17. Schwartz BG, Rezkalla S, Kloner RA (2010) Cardiovascular effects of cocaine. Circulation 122(24): 2558-2569.
18. Lange RA, Cigarroa RG, Yancy CW Jr, Willard JE, Popma JJ, et al. (1989) Cocaine-induced coronary-artery vasoconstriction. N Engl J Med 321(23): 1557-1562.
19. Levine GN, Lange RA, Bairey MCN (2007) Cocaine-induced acute coronary syndromes. Clin Cardiol 30(3): 80-84.
20. McCord J, Jneid H, Hollander JE (2008) Management of cocaine-associated chest pain and myocardial infarction: a scientific statement from the American Heart Association Acute Cardiac Care Committee of the Council on Clinical Cardiology. Circulation 117(14): 1897-1907.
21. Diercks DB, Kirk JD, Turnipseed SD (2005) Evaluation of chest pain in low-risk patients presenting to the emergency department: the role of immediate exercise testing. Ann Emerg Med 45(5): 402-410.
22. Honderick T, Williams D, Seaberg D, Wears R (2003) A prospective randomized, controlled trial of benzodiazepines and nitroglycerine or nitroglycerine alone in the treatment of cocaine-associated acute coronary syndromes. Am J Emerg Med 21(1): 39-42.
23. Richards JR, Johnson EB, Stark RW, Derlet RW (1999) Methamphetamine abuse and emergency department utilization. West J Med 170(4):198-202.
24. Brogan WC, Lange RA, Kim AS, Moliterno DJ, Hillis LD (1991) Alleviation of cocaine-induced coronary vasoconstriction by nitroglycerin. J Am Coll Cardiol 18(2):581-586.
25. Spatz ES, Chan PS (2017) Considerations in revascularization of patients with cocaine-associated myocardial infarction. Circ Cardiovasc Interv 10(11): e005571.
26. Kosten TR, Kosten TA (2013) Cocaine use disorders in DSM-5. Addiction 108(9): 1587-1588.
27. Kim ST, Park T (2019) Acute and Chronic Effects of Cocaine on Cardiovascular Health. Int J Mol Sci 20(3):584.
28. Maceira AM, Ripoll C, Cosin SJ, Igual B, Gavilan M, et al. (2014) Long term effects of cocaine on the heart assessed by cardiovascular magnetic resonance at 3T. J Cardiovasc Magn Reson 16(1): 26
29. Hale SL, Alker KJ, Rezkalla S, Figures G, Kloner RA (1989) Adverse effects of cocaine on cardiovascular dynamics, myocardial blood flow, and coronary artery diameter in an experimental model. Am. Heart J 118 (5 Pt 1): 927-933.
30. Pitts WR, Vongpatanasin W, Cigarroa JE, Hillis LD, Lange RA (1998) Effects of the intracoronary infusion of cocaine on left ventricular systolic and diastolic function in humans. Circulation 97(13): 1270-1273.
31. Hsue PY, Salinas CL, Bolger AF, Benowitz NL, Waters DD (2002) Acute aortic dissection related to crack cocaine. Circulation 105(13):1592-1595.
32. Restrepo CS, Rojas CA, Martinez S, Riascos R, Marmol VA et al. (2009) Cardiovascular complications of cocaine: Imaging findings. Emerg Radiol 16(1): 11-19.
33. Cooper CJ, Said S, Alkhateeb H, Rodriguez E, Trien R, et al. (2013) Dilated cardiomyopathy secondary to chronic cocaine abuse: A case report. BMC Res Notes 6: 536.
34. Substance Abuse and Mental Health Services Administration (SAMHSA). National Registry of Evidence-based Programs and Practices (NREPP web site). www.nrepp.samhsa.gov
35. Griffin KW, Botvin GJ (2010) Evidence-based interventions for preventing substance use disorders in adolescents. Child Adolesc Psychiatr Clin N Am 19(3): 505-526.
36. (2000) U.S. Department of Justice, Office of Justice Programs. Promising strategies to reduce substance abuse. Washington, DC. pp. 1-20.
37. Hollander JE, Hoffman RS, Gennis P, Fairweather P, Feldman JA, et al. (1995) Cocaine-associated chest pain: one-year follow-up. Acad Emerg Med 2(3): 179-184.
38. Waller BF. Chapter 55. Nonatherosclerotic Coronary Heart Disease. In: Hurst's The Heart, 13th, Fuster V, O'Rourke RA, Walsh RA, et al. (Eds), McGraw-Hill, 2010. Coronary Heart Disease. In: Hurst's The Heart, 13th, Fuster V, O'Rourke RA, Walsh RA, et al. (Eds), McGraw-Hil.
39. Maremmani I, Cibin M, Pani PP, Rossi A, Turchetti G, et al. (2009) Long-term outcomes of treatment-resistant heroin addicts with and without DSM-IV axis I psychiatric comorbidity (dual diagnosis). Eur Addict Res 15(4): 196-207.
40. Cheng C (2021) Assessing the risk factors of the recurrence of cocaine use disorder in a 3-year follow-up study. Psychiatry Res 298: 113789.
41. Yaramala SR, Grande A, Kalapatapu RK (2019) Cocaine Cardiotoxicity: A Review of Pathophysiology, Epidemiology, Clinical Features, Diagnosis, and Management. Am J Med 132(8): 904-909.
42. Pal R, Singh SN, Chatterjee A, Saurabh S, Lakhotia S, et al. (2018) Cocaine-induced cardiovascular complications: The role of beta-blockers in the acute setting. J Pract Cardiovasc Sci 4(1): 3-7.