Cardiovascular Effects of Cocaine
2010; Lippincott Williams & Wilkins; Volume: 122; Issue: 24 Linguagem: Inglês
10.1161/circulationaha.110.940569
ISSN1524-4539
AutoresBryan G. Schwartz, Shereif H. Rezkalla, Robert A. Kloner,
Tópico(s)Heart Rate Variability and Autonomic Control
ResumoHomeCirculationVol. 122, No. 24Cardiovascular Effects of Cocaine Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplementary MaterialsFree AccessResearch ArticlePDF/EPUBCardiovascular Effects of Cocaine Bryan G. Schwartz, MD, Shereif Rezkalla, MD and Robert A. Kloner, MD, PhD Bryan G. SchwartzBryan G. Schwartz From the Heart Institute, Good Samaritan Hospital, Los Angeles, Calif (B.G.S., R.A.K.); Department of Cardiology, Marshfield Clinic, Marshfield, Wis (S.R.); and Department of Internal Medicine, Division of Cardiovascular Medicine, Keck School of Medicine at the University of Southern California, Los Angeles (R.A.K.). , Shereif RezkallaShereif Rezkalla From the Heart Institute, Good Samaritan Hospital, Los Angeles, Calif (B.G.S., R.A.K.); Department of Cardiology, Marshfield Clinic, Marshfield, Wis (S.R.); and Department of Internal Medicine, Division of Cardiovascular Medicine, Keck School of Medicine at the University of Southern California, Los Angeles (R.A.K.). and Robert A. KlonerRobert A. Kloner From the Heart Institute, Good Samaritan Hospital, Los Angeles, Calif (B.G.S., R.A.K.); Department of Cardiology, Marshfield Clinic, Marshfield, Wis (S.R.); and Department of Internal Medicine, Division of Cardiovascular Medicine, Keck School of Medicine at the University of Southern California, Los Angeles (R.A.K.). Originally published14 Dec 2010https://doi.org/10.1161/CIRCULATIONAHA.110.940569Circulation. 2010;122:2558–2569The use of cocaine has evolved from chewing the leaves of the Erythroxylon coca bush thousands of years ago, to purification of cocaine hydrochloride over 100 years ago and its use in tonics and elixirs (at one time in popular cola drinks), to insufflating and injecting the fine, white, water-soluble, powder form, to a smokable freebase form called "crack," which became popular in the 1980s.1 In 2007, 2.1 million Americans had recent cocaine use; 1.6 million met criteria for cocaine dependence or abuse.1 Cocaine accounted for 31% of all visits to the emergency department related to drug misuse or abuse.1 From 1971 to 1987, the incidence of deaths caused by cocaine overdose increased 20-fold in Dade County, Florida.2 In a consecutive series of 233 emergency visits by cocaine-using patients, 56% presented with cardiovascular complaints, including 40% with chest pain.3 A minority of these patients have acute myocardial infarction (MI) (≈6%),4–7 and overall mortality is low (<1%).3–5,8–10 However, cocaine is associated with a number of cardiovascular diseases, including MI, heart failure, cardiomyopathies, arrhythmias, aortic dissection, and endocarditis. Identifying patients with acute disease is challenging. This review describes the relationship between cocaine and various cardiovascular diseases, as well as appropriate diagnostic evaluation and therapies.PathophysiologyMolecularCocaine stimulates the sympathetic nervous system by inhibiting catecholamine reuptake at sympathetic nerve terminals,11,12 stimulating central sympathetic outflow,11 and increasing the sensitivity of adrenergic nerve endings to norepinephrine (Figure 1).12 Cocaine also acts like a class I antiarrhythmic agent (local anesthetic) by blocking sodium and potassium channels, which depresses cardiovascular parameters.13 Of these 2 primary, opposing actions, enhanced sympathetic activity predominates at low cocaine doses, whereas the local anesthetic actions are more prominent at higher doses.12Download figureDownload PowerPointFigure 1. Acute effects of cocaine. Cocaine affects the cardiovascular system through 2 major pathways: increased sympathetic output and a local anesthetic effect. Through increased sympathetic tone and catecholamine levels, cocaine increases heart rate, blood pressure, and myocardial contractility, all of which increase myocardial oxygen demand. Myocardial oxygen supply is decreased through coronary vasoconstriction and enhanced thrombosis. Myocardial oxygen demand may exceed myocardial oxygen supply, leading to ischemia or infarction. Cocaine affects cardiac myocytes directly by blocking sodium channels, which decreases left ventricular (LV) contractility and is arrhythmogenic.In addition, cocaine stimulates the release of endothelin-1, a potent vasoconstrictor, from endothelial cells14 and inhibits nitric oxide production, the principal vasodilator produced by endothelial cells.15 Cocaine promotes thrombosis by activating platelets,16,17 increasing platelet aggregation,16,18 increasing platelet α-granule release,16,19 increasing plasminogen activator inhibitor activity,20 and increasing fibrinogen and von Willebrand factor levels.21 Calcification22 and aneurysms23 occur frequently in the coronary arteries of cocaine users. MI in non–cocaine-using patients with traditional risk factors typically results from plaque fissure or rupture with plaque hemorrhage, which precipitates thrombosis. In contrast, MI in cocaine-using patients involves intracoronary thrombosis superimposed on smooth muscle cell–rich fibrous plaques without plaque rupture or hemorrhage.24 Moreover, plaques in cocaine-using patients feature medial or intimal inflammation (primarily lymphocytes and plasma cells) and adventitial mast cells, whereas non–cocaine-using patients did not have arterial wall inflammation of this morphology.24ClinicalCocaine increases myocardial oxygen demand by increasing both heart rate and blood pressure (Table 1).25,26 The influence of cocaine on heart rate and blood pressure is dose dependent and is mediated through α-adrenergic stimulation.25,26 At the same time, cocaine decreases oxygen supply via coronary vasoconstriction.25 Cocaine-induced coronary vasoconstriction occurs in normal (nondiseased) coronary artery segments but is more pronounced in atherosclerotic segments.27 Combining cocaine use with cigarette smoking has additive effects on coronary vasoconstriction while markedly increasing the rate-pressure product.28 Long-term cocaine users demonstrate coronary endothelial dysfunction.29 Because endothelial dysfunction increases the sensitivity of a vessel to the constrictor effects of catecholamines,30 it may be particularly detrimental for cocaine users. Even in the absence of epicardial coronary disease, cocaine causes microvascular disease31,32 and is associated with thrombosis.24,33,34Table 1. Cardiovascular Effects of CocaineCauses Myocardial Oxygen Supply-Demand MismatchWorsens Myocardial PerformanceCauses Cardiovascular DiseaseCauses Clinical Cardiovascular End PointsIncreases heart rateDecreases ejection fractionArrhythmiasMyocardial infarctionIncreases blood pressureIncreases end-systolic volumeQT prolongationArrhythmiasDecreases coronary artery diameterIncreases end-diastolic pressureThrombosisCongestive heart failureDecreases coronary blood flowLengthens deceleration timeAtherosclerosisCardiomyopathyIncreases left ventricular hypertrophyEndothelial dysfunctionAortic dissectionMicrovascular diseaseEndocarditisSudden deathCocaine causes systolic and diastolic dysfunction, arrhythmias, and atherosclerosis. Cocaine decreases myocardial contractility and ejection fraction by blocking sodium and potassium channels within the myocardium.35 Intracoronary infusion of cocaine decreases left ventricular ejection fraction and increases left ventricular end-diastolic pressure and end-systolic volume (Table 1).36 Long-term cocaine use is associated with left ventricular hypertrophy37 and prolonged deceleration time.38 Cocaine prolongs the PR, QRS, and QT intervals.39,40 Cocaine is associated with coronary atherosclerosis even in young users with relatively few cardiac risk factors.41,42Chest PainCompared with nonusers of cocaine, cocaine users have a higher overall incidence of MI (odds ratio [OR], 3.8 to 6.9),43,44 and the risk of MI increases by 24-fold in the first hour after cocaine use.45 Cocaine contributes to ≈1 of every 4 MIs in persons between 18 and 45 years of age.44 MI occurs in ≈6% of all patients presenting to the emergency department with cocaine-associated chest pain (CACP).4–7Clinical Presentation and Patient CharacteristicsPatients presenting with CACP are typically young, male cigarette smokers with few other cardiac risk factors (Table 2). CACP is often substernal and pressure-like and may be associated with dyspnea and diaphoresis (Table 3). Atypical presentations, pleuritic pain, nausea, palpitations, syncope, and vomiting also occur. In patients with CACP, no historical or presenting features distinguish between patients with and those without MI.4,6,10,47 In a prospective cohort of 261 patients with CACP, the Thrombolysis in Myocardial Infarction risk score did not stratify patients into risk categories, and almost half of all adverse events occurred in patients with a Thrombolysis in Myocardial Infarction risk score of ≤1.51 Of patients with CACP, compared with patients without MI, patients with MI were slightly older,4,6 less often had a history of previous chest pain (21% versus 53%),4 and more often had known coronary artery disease.52 Any route of cocaine administration can precipitate MI, and no route is more predictive than another (Table 2).4,10,47Table 2. Demographics, Medical History, and Route of Cocaine Administration in Patients With Cocaine-Associated Chest PainCohort; No. of Cocaine-Using Patients and Clinical SettingMI, %*Age, Average, yMale, %Cigarette Smoker, %Hypertension, %Hyperlipidemia, %Diabetes Mellitus, %Family History, %History of CP, %History of MI, %Cocaine Route, %Nasal InsufflationSmoked (Crack)Intravenous246 Presented to ED with CP46337284195415514277311250 Presented to ED with CP563477772686344066852364 Presented to ED with CP67477390541522107812302 Presented to ED with CP8†038668417433145219774101 Hospitalized with CP903277310603049 Hospitalized with CP7629698004700653870 Hospitalized with CP10313480691403142441490 Angiography for CP4630426978543654393233 Angiography to rule out MI47363779731532720305091 With MI48100338887151031736493021136 With MI491003880913315738351330551597 With MI50100477386611924MI indicates myocardial infarction; CP, chest pain; and ED, emergency department. Data were not reported for items left blank.*Defined using creatine kinase-MB in all sources, except troponin was used in References 6, 8, and 50.†Excluded 42 high-risk patients hospitalized to rule out MI (10 of whom had an MI).Table 3. Presenting Symptoms and ECG Findings in Patients With Cocaine-Associated Chest PainCohort; No. of Cocaine-Using Patients and Clinical SettingMI, %*Substernal Pain, %Pressure/ Tightness, %Pleuritic Pain, %Shortness of Breath, %Diaphoresis, %Nausea, %Palpitations, %ECG, %AbnormalEarly RepolarizationIschemia/ Infarction246 Presented to ED with CP4671473659392733723112250 With CP5676551162482813733410364 Presented to ED with CP674432491622127772302 Presented to ED with CP8†07558236334301460101 Hospitalized with CP904618563228146832849 Hospitalized with CP76100100338433136 With MI49100916811595648188562ED indicates emergency department; CP, chest pain. Data were not reported for items left blank.*Defined using creatine kinase-MB in all sources, except troponin was used in References 6 and 8.†Excluded 42 high-risk patients hospitalized to rule out myocardial infarction (of whom 10 had MI).MI usually occurs within several hours of cocaine use but can be delayed. In a case-crossover study, the risk of MI increased by 24-fold in the first hour after cocaine use and decreased sharply thereafter to only a 4-fold increase in the second and third hours.45 Time elapsed from cocaine use to onset of chest pain has been as short as a median of 60 minutes4 and within 1 hour in 58% of patients9 or as long as a median of 18 hours.10Complications and PrognosisOf all cocaine-induced MIs, Q waves develop in approximately half, and the location is evenly distributed between the anterior and inferior territories (Table 4).4,5,7,10,47–49 Angiography in patients with cocaine-induced MI reveals 1- or 2-vessel disease in 31% to 66%, 3-vessel disease in 13% to 15%, normal coronary arteries in 18% to 45%, and thrombus without obstructive disease in as many as 24% (Table 5).48–50 In patients with CACP without MI, the spectrum of disease shifts toward more normal and nonobstructive disease.6,10,46,47Table 4. Acute Complications in Patients With CACPCohort; No. of Cocaine-Using Patients and Clinical SettingMI, %*Q Wave, %Anterior MI, %Inferior MI, %Death, %CHF, %Supraventricular Tachyarrhythmia,%Sustained VT, %Bradyarrhythmia, %sTotal No. of Stress Tests/No. of Stress Tests on Patients With MI/No. of Positive Stress Tests246 Presented to ED with CP4636215011.61.61.21.616/6/0250 With CP5660534000.41.20.80.4302 Presented to ED with CP8†000000158/0/4101 Hospitalized with CP900000070 Hospitalized with CP103150453201.404/3/091 With MI481005541371011/11/0136 With MI49100364544074419CHF indicates congestive heart failure; VT, ventricular tachycardia; ED, emergency department; and CP, chest pain. Data were not reported for items left blank.*Defined using creatine kinase-MB in all sources, except troponin was used in References 8.†Excluded 42 high-risk patients hospitalized to rule out myocardial infarction (of whom 10 had MI and 3 had CHF).Table 5. Angiographic Findings in Cocaine-Using Patients With Chest PainCohort; No. of Cocaine-Using Patients and Clinical SettingMI, %*Angiography, n PatientsAngiographic Findings, %NormalNonobstructive1-Vessel Disease2-Vessel Disease3-Vessel DiseaseThrombosis364 Presented to ED with CP6740621816470 Hospitalized with CP103183838121290 Angiography for CP46309050†3210633 Angiography to rule out MI47363340212112691 With MI48100544531‡24136 With MI491005233†25291397 With MI5010066184620156MI indicates myocardial infarction; ED, emergency department; and CP, chest pain Data were not reported for items left blank.*Defined using creatine kinase-MB in all sources, except troponin was used in Reference 8.†Study did not distinguish between normal and nonobstructive.‡Study did not distinguish between 1-, 2-, and 3-vessel disease.Death (<1%), congestive heart failure (<2%), and arrhythmias ( 12 hours after arrival in the emergency department, even in patients with MI.5,49 In 136 patients with cocaine-induced MI, congestive heart failure occurred in 7%, sustained ventricular tachycardia occurred in 4%, and 48% of all complications occurred by the time of arrival in the emergency department.49 Complications tended to occur more frequently in patients with ischemia or infarction indicated on the initial ECG (42% versus 26%; P=0.06) and occurred more frequently in patients with Q waves (57% versus 24%; P=0.0006).49In 261 patients with CACP followed up prospectively for 30 days, only elevated cardiac biomarkers increased the risk of the composite end point of all-cause mortality, MI, or revascularization (OR, 8.8), and almost half of all adverse events occurred in patients with a Thrombolysis in Myocardial Infarction risk score ≤1.51 Of 300 low-risk patients with CACP followed up prospectively for 30 days, 25% had recurrent chest pain, none had ventricular dysrhythmias or cardiovascular death (2 noncardiac deaths), and 4 (1.3%) developed nonfatal MI (all 4 continued to use cocaine and had at least 2 cardiac risk factors).8Of 203 patients with CACP (MI occurred in 5% during the initial presentation) followed up prospectively for a mean of 408 days, 2 patients (1%) developed a nonfatal MI and 6 patients (3%) died (5 noncardiovascular, 1 cardiac arrest).53 Of 130 patients, 78 (60%) continued to use cocaine (continued cocaine use unknown in 73). Both nonfatal MIs and 4 deaths occurred in patients who admitted continued cocaine use. No cardiovascular events occurred in patients who stopped using cocaine. Recurrent chest pain was more likely in persistent cocaine users (75% versus 31%; OR, 6.5). In contrast, outcomes did not differ in patients with versus without MI during the initial presentation.ElectrocardiogramInterpreting the ECG in patients with CACP is challenging because the initial ECG is "abnormal" in 56% to 84% of patients (Table 3).4–10 In 101 patients with CACP, 43% met ECG criteria for thrombolytic therapy despite 0% having elevated creatine kinase (CK)-MB.9 In 246 patients with CACP (acute MI in 6%), the ECG predicted acute MI with a sensitivity of only 36%, a specificity of 90%, a positive predictive value of 18%, and a negative predictive value of 96%.4 Eighteen of 97 patients (19%) with elevated cardiac troponin had normal ECGs.50 Many of the "abnormal" ECGs in patients with CACP were due to "normal" variants (ST-segment and J-point elevations) in patients 12 hours after arrival in the emergency department,5,49 Weber et al8 proposed a 12-hour observation period for patients with CACP. They prospectively categorized 344 patients with CACP into high-risk and non–high-risk groups. Forty-two patients were directly admitted and excluded because they were deemed high risk, defined as an "initial ECG suggested the presence of ischemia or acute MI, ST-segment elevation or depression of 1 mm or more that persisted for at least 1 minute; elevated serum levels of cardiac biomarkers; recurrent ischemic chest pain; or hemodynamic instability."8 Of the 42 high-risk patients, 10 had an acute MI and 10 had unstable angina. Patients not meeting criteria for high risk (n=302) were enrolled in a 12-hour observation protocol, during which patients underwent measurement of cardiac troponin I at the time of presentation and after 3, 6, and 9 hours and had continuous 12-lead ST-segment monitoring. None of the 302 non–high-risk patients developed MI, congestive heart failure, or arrhythmias in the observation unit, and all were discharged from the unit. At 30 days after presentation, none of the 302 patients sustained ventricular dysrhythmias or died of cardiovascular causes (1 died as a result of homicide, 1 as a result of heroin overdose). Twenty-five percent experienced recurrent chest pain, and 4 (1.3%) developed nonfatal MI (all 4 continued to use cocaine and had at least 2 cardiac risk factors).8 Hollander et al49 also described 130 patients with cocaine-associated MI: 90% of patients with complications developed their first complication within 12 hours, and the other 10% had either CK-MB elevation within 12 hours or an initial ECG indicating ischemia or infarction.Diagnostic TestingStress testing and myocardial imaging have been suggested to facilitate safe, rapid discharge of patients with CACP. Stress testing in patients with CACP rarely indicated ischemia (only 4 of 189 tests were positive), even in patients with MI (0 of 20 were positive; Table 4).4,8,10,48 Holter monitoring revealed frequent episodes of ST-segment elevation in 8 of 21 patients with cocaine addiction, yet only 1 of the same 20 patients had an exercise treadmill stress test that indicated ischemia.57 Computed tomography scanning identified coronary calcification in only 9.6% of persons 33 to 45 years of age, and coronary calcification was not related to cocaine use.58 Rest myocardial perfusion imaging indicated myocardial ischemia in only 5 of 216 patients with CACP, and only 2 of 5 patients with a positive test had MI.59 In 59 patients with CACP, coronary computerized tomography angiography indicated significant coronary artery disease in 6 patients (10%) but did not alter management in any patients.60Patients with CACP are at low risk for cardiovascular events,8,53 so an extensive diagnostic workup may not be cost-effective. The number needed to treat with computerized tomography coronary angiography to identify 1 case of clinically significant coronary artery disease was 59 in one study.61 Compared with a brief observation period, length of stay was only minimally shortened by diagnostic testing.61,62 Diagnostic testing has little influence on therapy because the benefit of percutaneous coronary intervention is unproven in cocaine-using patients and risk factors should be modified in all cocaine-using patients with chest pain or MI. Cessation of cocaine is the most important therapy.8,53,63Therapy for CACP and MIThe treatment of chest pain and acute coronary syndromes in cocaine-using patients is similar to that in patients with traditional risk factors but differs in the use of benzodiazepines and phentolamine and avoidance of β-blockers (Figure 2).Download figureDownload PowerPointFigure 2. Treatment algorithm for patients with cocaine-associated chest pain. β-Blockers (not included in the figure) should be avoided in the acute setting and initiated at discharge only in select patients. If hypertension persists after benzodiazepine administration, first-line treatment is nitrates; second-line treatment is phentolamine or calcium channel blockers. STEMI indicates ST-segment elevation myocardial infarction; NSTEMI, non-STEMI; and ACE I, angiotensin-converting enzyme inhibitor.BenzodiazepinesIn a dog model of acute cocaine toxicity, pretreatment with diazepam prevented the cocaine-induced increases in blood pressure, heart rate, acidemia, and hyperthermia.64 In a trial of 40 patients with CACP randomized to diazepam, nitroglycerin, or both, chest pain severity improved similarly in all 3 groups,65 whereas greater pain relief was observed with the combination of lorazepam plus nitroglycerin compared with nitroglycerin alone in a randomized study of 27 patients.66 Benzodiazepines are thought to relieve CACP though their antianxiety effects. Benzodiazepines should be administered intravenously to patients with CACP to relieve chest pain and to attenuate the hemodynamic manifestations of cocaine.67,68 If hypertension or tachycardia persists despite benzodiazepines or if the patient has evidence of myocardial injury, then additional therapies are indicated.NitroglycerinNitroglycerin relieves chest pain in approximately half of cocaine-using patients.65,69 Nitroglycerin reversed the coronary vasoconstriction induced by cocaine.70 Nitroglycerin abolished acetylcholine-induced coronary vasoconstriction in 8 of 8 long-term cocaine-users and dilated the coronary artery beyond baseline diameter in 7 of 8.29 If chest pain or hypertension does not resolve with benzodiazepines, then nitroglycerin should be administered.Calcium Channel BlockersIn mongrel dogs, verapamil prevented cocaine-induced ventricular fibrillation and attenuated the effects of cocaine on heart rate, blood pressure, and myocardial contractility.71 Verapamil abolished the effects of cocaine on blood pressure and coronary vasoconstriction in humans.72 Because calcium channel blockers have not benefitted important clinical end points in randomized trials involving traditional patients with MI, their role in cocaine-using patients with chest pain may be limited to second-line therapy for hypertension or coronary artery vasospasm.67 As in non–cocaine-using patients, short-acting nifedipine should not be used. In patients with heart failure, systolic dysfunction, bradycardia, or heart block, verapamil and diltiazem should be avoided.PhentolaminePhentolamine, an α-antagonist used predominantly in the treatment of hypertensive emergencies, appears to benefit cocaine-using patients with ischemia. In 45 patients undergoing cardiac catheterization for the evaluation of chest pain, phentolamine abolished the detrimental effects of cocaine on heart rate, blood pressure, coronary artery diameter, and coronary sinus blood flow.25 A case report describes the successful use of phentolamine in reducing chest pain and ST-segment elevation in a cocaine-using patient with normal coronary arteries.73 A short half-life and significant side effects limit the clinical utility of phentolamine in the general population, but its mechanism of action is ideal for the treatment of cocaine-induced vasoconstriction.Antiplatelet and Antithrombin AgentsCocaine promotes thrombus formation, so antiplatelet and antithrombin agents are probably beneficial, although they have not been well studied in cocaine-using patients. Aspirin should be routinely administered immediately for patients with CACP and continued indefinitely for patients with MI or coronary artery disease. Other agents, including clopidogrel, heparin, and glycoprotein IIb/IIIa inhibitors, should be administered as indicated by published guidelines.β-Blockersβ-Blockers are the most extensively studied and the most controversial drugs relating to cocaine-using patients. In non–cocaine-using patients, β-blockers benefit numerous end points, including mortality, during and after acute MI , and in patients with cardiomyopathy. In cocaine-using patients, however, β- blockade can potentially leave α-stimulation unopposed, resulting in pronounced systemic and coronary vasoconstriction. In animal studies of acute cocaine toxicity, propranolol worsened the seizure threshold and expedited death.64,74 In humans, cocaine-induced coronary artery vasoconstriction was exacerbated by propranolol.75 Esmolol increased blood pressure in 2 of 7 cocaine-using patients.76 In 1 instance, blood pressure increased after esmolol from 200/120 to 230/180 mm Hg.76 Labetalol and carvedilol offer the theoretical advantage of blocking both α- and β-receptors. Labetalol, however, did not reverse cocaine-induced coronary artery vasoconstriction.77 In pheochromocytoma, which features a hypersympathetic state similar to cocaine intoxication, labetalol caused severe hypertension.78 When combined with cocaine, carvedilol 25 mg tended to increase blood pressure consistent with unopposed α-stimulation, whereas carvedilol 50 mg decreased blood pressure and heart rate, suggesting that both α- and β-receptors were blocked.79 Recent, uncontrolled studies of β-blockers in patients with CACP report conflicting results. Death resulting from cocaine-induced MI is rare, which limits the benefit of β-blockers while they increase the risk of hypertension and coronary artery vasoconstriction. An anecdotal report of crushing chest pain, cardiac arrest, and death ensuing minutes after metoprolol administration illustrates the potential risk of mixing β-blockers with cocaine.80 All β-blockers should be avoided in cocaine-using patients in the acute setting. Because most patients continue to use cocaine after hospital discharge,53 postdischarge β-blocker therapy should be considered after careful risk-benefit assessment and perhaps should be withheld until cessation of cocaine has been proven. Patients should be educated on the potential hazards of combining cocaine with β-blockers.Other Pharmaceutical AgentsAngiotensin-converting enzyme inhibitors, angiotensin receptor blockers, statins, and diuretics have not been well studied in cocaine-using patients but are not expected to interact adversely with cocaine. Morphine reversed cocaine-induced coronary vasoconstriction.81 Dexmedetomidine, a potent central sympatholytic agent, abolished the cocaine-induced increases in blood pressure, heart rate, and sympathetic nerve activity.82 A cocaine antidote has been identified in the soil surrounding the coca plant: a bacterial cocaine esterase that hydrolyzes cocaine more efficiently than endogenous esterases.83 When administered to rats before or after cocaine, cocaine esterase prevented or reversed cocaine-induced QRS complex widening, QT prolongation, ST-segment elevation, bradycardia, hypertension, and troponin release.83Percutaneous Coronary Intervention and ThrombolysisCompared with non–cocaine-using patients with MI, percutaneous coronary intervention is even more desirable in cocaine-using patients. Two cases in which cocaine-using patients with ST-segment elevations, but without MI, suffered complications from fibrinolytic therapy illustrate that fibrinolytics should be used with caution because of safety concerns, lack of documented efficacy, and poor correlation of ECGs with MI.84 Ang
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