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Abstract
Cocaine is a commonly abused drug that acts as a powerful stimulant. It accounts for over half of illicit drugrelated visits to the emergency room, with cardiovascular events being the most common cause of death. Few specific treatments for cocaine-related cardiovascular complications are available, but b-adrenergic receptor antagonists and lignocaine should be used with caution.
Background
Cocaine is associated with acute cardiovascular complications, but the long-term cardiovascular risks of cocaine use are poorly understood. We examined the association between cocaine use disorders and long-term cardiovascular morbidity in women.
Methods
We analyzed a longitudinal cohort of 1,296,463 women in Quebec, Canada between 1989 and 2020. The exposure included cocaine use disorders before or during pregnancy. The outcome was cardiovascular hospitalization up to 31 years later. We used adjusted Cox regression models to estimate hazard ratios (HR) and 95% confidence intervals (CI) for the association of cocaine use disorders with cardiovascular hospitalization.
Results
The cohort included 2,954 women with cocaine use disorders. Compared to women without an identified cocaine disorder, women with cocaine use disorders had 1.55 times greater risk of future cardiovascular hospitalization during three decades of follow-up (95% CI 1.37-1.75). Cocaine use disorders were strongly associated with inflammatory heart disease (HR 4.82, 95% CI 2.97-7.83), cardiac arrest (HR 2.93, 95% CI 1.46-5.88), valve disease (HR 3.09, 95% CI 2.11-4.51), and arterial embolism (HR 2.22, 95% CI 1.19-4.14). The association between cocaine use disorder and cardiovascular hospitalization was most marked after 5 to 10 years of follow-up (HR 2.15, 95% CI 1.70-2.72).
Conclusions
Women with cocaine use disorders have a high risk of cardiovascular hospitalization up to three decades later. Substance use reduction and cardiovascular risk surveillance may help reduce the burden of cardiovascular disease in women with cocaine use disorders.
Cocaine has become one of the most commonly abused recreational drugs, resulting in a significantly increased number of visits to the emergency department due to the acute symptoms caused by its intake. The acute onset of cardiovascular complications, such as myocardial infarction, arrhythmias, stroke, and kidney and spleen infarction, has been described in association with cocaine use, but aortic thrombosis has rarely been studied in this context. We report a case of acute aortoiliac thrombosis in a young male patient with no underlying medical records.
Cocaine remains highly prevalent and accessible in the general population, continues to represent one of the most commonly reported substances in drug-related presentations to emergency departments, and is frequently implicated in drug-related deaths. Fatal cardiac arrhythmias are often suspected in the latter cases. In spite of this, its complex effects on the human cardiac conduction system remain poorly elucidated. In this article we sought to systematically review the medical literature to identify the electrocardiographic findings that have been linked to cocaine use in humans in an effort to highlight what physicians can expect to encounter when managing patients using the drug. The evidence is discussed, common findings are emphasized and clinical recommendations are proposed.
The toxic effects of cocaine are enhanced in the presence of lidocaine.
Male Sprague-Dawley rats weighing 200 to 300 g.
Animals received intraperitoneal injections of cocaine (10, 20, 35, or 50 mg/kg), lidocaine (30 or 40 mg/kg), or a combination of all doses of cocaine given simultaneously with 30 or 40 mg/kg lidocaine. The incidence and time to seizure and death were recorded in these groups and compared by chi 2 and analysis of variance analyses, respectively.
At doses of 30 or 40 mg/kg, lidocaine does not induce seizures or death. The effect of simultaneous injection of both cocaine and lidocaine was to dramatically increase the incidence of both seizures and death over that of cocaine alone. The incidence of seizures in animals receiving 35 mg/kg cocaine alone was 10%; this increased to 50% and 80% with the addition of 30 and 40 mg/kg lidocaine, respectively (P less than or equal to .05; P less than or equal to .01). Death did not occur in animals receiving 35 mg/kg cocaine alone; the addition of 30 and 40 mg/kg lidocaine resulted in death in 30% and 60% of animals, respectively (P less than or equal to .01 each group). Similarly, in rats receiving 50 mg/kg cocaine, the incidence of death increased from 0% to 60% and 80% with 30 and 40 mg/kg lidocaine, respectively (P less than or equal to .01).
In the rat, overall toxicity of cocaine is significantly increased with simultaneous exposure to lidocaine.
Recent clinical studies suggest that certain betaadrenergic blocking drugs, such as timolol, may reduce sudden death in patients with ischemic heart disease, but the mechanism has not been established. To assess and compare antifibrillatory effects of beta-blocking drugs as a potential mechanism of sudden death prevention, the ventricular fibrillation (VF) threshold was measured in anesthetized, open-chest dogs before and after 3 minutes of coronary ischemia during intravenous administration of saline solution or 3-fold serial increments (0.003 to 1.0 mg/kg) of 5 beta-blocking drugs with various accessory properties. Ventricular fibrillation occurred in control studies after delivery of a current train of 11.7 ± 7.6 mA in the nonischemic state and 7.0 ± 7.4 mA during ischemia (n = 46). All 5 betablocking drugs but not saline solution caused substantial (average 6-fold) increases (p < 0.001) in the VF threshold under both nonischemic (to 67 ± 30 mA) and ischemic conditions (to 42 ± 31 mA). The maximal VF thresholds attained were similar for individual drugs: timolol, 71, 39 mA (nonischemic, ischemic conditions, n = 10): pindolol, 81, 46 mA (n = 7); propranolol, 58,36 mA (n = 7); metoprolol, 60, 40 mA (n = 7); and labetolol, 67,52 mA (n = 6). The effective doses (mg/kg) at which maximal effects first occurred, however, varied widely: timolol, 0.01 mg/kg; pindolol, 0.1 mg/kg; propranolol, 0.3 mg/kg; metoprolol, 1.0 mg/kg; and labetolol, 1.0 mg/kg. The antifibrillatory potency (mg/kg) generally paralleled known ratios of beta-blocking efficacy, except for timolol's apparently greater potency. Interruption of stellate ganglionic impulses accounted for part of the augmentation in VF threshold. Thus, a substantial antifibrillatory effect accompanies experimental blockade of beta-adrenergics timuli. An increase in VF threshold is suggested as a possible protective mechanism by which beta-blocking drugs reduce sudden death.
To evaluate the safety of lidocaine in the setting of cocaine-induced myocardial infarction (MI).
A retrospective, multicenter study.
Twenty-nine university, university-affiliated, or community hospitals during a 6-year period (total of 117 cumulative hospital-years).
Patients with cocaine-associated MI who received lidocaine in the emergency department.
Of 29 patients who received lidocaine in the setting of cocaine-associated MI, no patient died; exhibited bradydysrhythmias, ventricular tachycardia, or ventricular fibrillation; or experienced seizures after administration of lidocaine (95% confidence interval, 0% to 11%).
Despite theoretical concerns that lidocaine may enhance cocaine toxicity, the use of lidocaine in patients with cocaine-associated MI was not associated with significant cardiovascular or central nervous system toxicity.
Sudden, unexpected death due to cocaine in young otherwise healthy individuals occurs in an idiosyncratic manner and is commonly felt to be arrhythmogenic in nature, although the exact cause of death is rarely documented. In addition to indirect sympathomimetic actions, cocaine is a potent sodium channel blocking drug and, in this regard, most closely resembles agents such as flecainide. We suggest that sudden death due to cocaine is proarrhythmic in nature, occurring under similar circumstances as that due to specific antiarrhythmic drugs.
Recent increase in cocaine abuse and the supply of more potent “crack” cocaine has led to the recognition of a number of complications from its use. Cocaine induces generalized vasoconstriction, which could involve multiple organ systems. Cardiovascular involvement includes: myocardial ischemia and infarction, bradyarrhythmias and tachyarrhythmias, cardiomyopathy, aortic dissection, and endocarditis.1 Management of cocaine-induced complications, however, remains controversial. The present review discusses the recent developments in the management of cardiovascular complications of cocaine.
Cocaine use in the United States is widespread, affecting more than 30 million Americans. Although many of these persons do not seek healthcare, the overriding cause for hospitalization is cocaine-associated chest pain. Because only a minority of these patients suffer myocardial injury, it is important to exclude even rarer life-threatening causes for chest pain, such as aortic dissection or pneumothorax. Following that, a thorough knowledge of the pathophysiology and existing literature helps to provide cost-effective care, which focuses resources on those patients most likely to suffer complications. Regardless of the severity of complications, referral to cocaine detoxification programs, counseling, social support, and outpatient follow-up care for modification of cardiac risk factors is a fundamental component of long-term patient care.
The deaths of several celebrities in recent years in association with the nontherapeutic use of cocaine have focused widespread attention on the problem of cocaine abuse. In 1999, an estimated 25 million Americans admitted that they had used cocaine at least once; 3.7 million had used it within the previous year; and 1.5 million were current users. During the same year, cocaine was mentioned in 30 percent of all drug-related visits to emergency departments.1 Cocaine is the most commonly used illicit drug among subjects seeking care in hospital emergency departments or drug-treatment centers. In addition, it is the most frequent . . .
Cocaine-associated myocardial infarction (CAMI) is a well-reported entity. Most previous reports on CAMI have been limited to conservative care utilizing benzodiazepines, aspirin, nitroglycerin, calcium channel blockers, and thrombolytics. Current guidelines on CAMI advocate immediate use of angiography and angioplasty if available rather than routine administration of thrombolytics. However, based on literature search from 1966 to 2001 (using keywords "cocaine," "myocardial infarction," and "angioplasty"), there have been only two case reports of percutaneous coronary intervention (PCI) in patients with cocaine-associated myocardial infarction. Both were notable for complications either during or immediately after the procedure. We report a series of 10 patients with cocaine-associated myocardial infarction who were treated with percutaneous interventions, which included angioplasty, stenting, and AngioJet mechanical extraction of thrombus. Despite the different arteriopathic process involved, our findings suggest that PCI can be performed safely and with a high degree of procedural success in patients with CAMI.
ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias--executive summary : a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias).
Patients who have chest pain following the use of cocaine have become more common in emergency departments throughout the United States,with approximately 6% of these patients sustaining an acute MI. The authors have described the rationale for recommending aspirin, benzodiaze-pines, and nitroglycerin as first-line treatments and calcium-channel blockade or phentolamine as possible second-line therapies and have summarized the controversies surrounding the use of fibrinolytic agents. Admission for observation is one reasonable approach to the management of the low-risk cohort. Evaluation for underlying coronary artery disease is reasonable, particularly in patients who have acute MI. Patients who do not have infarction can undergo evaluation for possible coronary artery disease on an outpatient basis. Routine interventions for secondary prophylaxis as well as cocaine rehabilitation should be used in this patient population, because the long-term prognosis seems somewhat dependent upon the ability of the patient to discontinue cocaine use.
Habitual cocaine use can lead to dilated cardiomyopathy (DCM) and sudden cardiac death. Based on prior clinical observations, we hypothesized that prior habitual cocaine use is a strong predictor of high defibrillation threshold (DFT) during implantable cardioverter-defibrillator (ICD) implant.
We reviewed the medical records of 130 consecutive patients undergoing initial ICD implantation or revision at Parkland Hospital and the Dallas VA Hospital, Dallas, TX, from January 2002 to November 2005. Patient characteristics and DFT data were collected retrospectively.
The study group includes 11 patients (8.46%) who were identified as having a history of prior habitual cocaine use as demonstrated by history and urine toxicology; the rest (119 patients) form the control group. Cocaine-using patients tended to be younger (48.2 +/- 10 vs 60.1 +/- 12.3 years; P = 0.0026), were less likely to have coronary disease (36.3% vs 72.2%; P = 0.032), and had less comorbidity. The average DFT was 27.9 +/- 7.8 J for all cocaine-using patients and 14.5 +/- 4.1 J for noncocaine-using patients (P = 0.00018). In the cocaine-using group, three out of 11 patients required a subcutaneous array compared to none in the control group.
Our results suggest that patients with a history of habitual cocaine use may be at increased risk to have a high DFT during ICD implantation. This is the first study to demonstrate such association. ICD implantation in patients with this history should be planned with these findings in mind, as larger output generators or subcutaneous arrays might be required.
The goals of the present article are to provide a critical review of the literature on cocaine-associated chest pain and myocardial infarction (MI) and to give guidance for diagnostic and therapeutic interventions. Classification of recommendations and levels of evidence are expressed in the American College of Cardiology/American Heart Association (ACC/AHA) format as follows:
The Writing Committee conducted a comprehensive search of the medical literature concerning cocaine-associated chest pain and MI. The literature search included English-language publications on humans and animals from 1960 to 2007. In addition to broad-based searching concerning cocaine, specific targeted searches were performed on cocaine and the following topics: MI, chest pain, emergency department (ED), aspirin, nitroglycerin, calcium channel blocker, benzodiazepine, thrombolytics, phentolamine, heparin, primary angioplasty, ECG, and stress testing. Literature citations were generally limited to published articles listed in Index Medicus. The article was reviewed by 4 outside reviewers nominated by the AHA.
Cocaine is the second most commonly used illicit drug in the United States, with only marijuana …