Hemodynamic and Arrhythmogenic Effects of Cocaine in Hypertensive Individuals

Abstract

J Clin Hypertens (Greenwich). 2011;13:744–749. ©2011 Wiley Periodicals, Inc. Despite the increased risk of myocardial infarction, aortic dissection, and arrhythmias in patients with hypertension who use cocaine, the hemodynamic and arrhythmogenic effects of cocaine use have not been well characterized in this population. The authors hypothesized that patients with hypertension demonstrate extreme, transient changes in arterial pressures as well as new arrhythmic activity during cocaine use. Ambulatory blood pressures, heart rates, and electrocardiograms (AECGs) were recorded for 48 hours in 10 patients with a history of hypertension who smoke cocaine. Active cocaine use was identified through patient diaries and manual activation of the blood pressure cuff. Of the 10 patients studied (6 men, 7 African Americans, age 49±8 years), 8 were taking antihypertensive medications. The mean blood pressure prior to cocaine use was 126/77 mm Hg and average increase in systolic, diastolic, and mean arterial pressure after use was 74 mm Hg, 30 mm Hg, and 45 mm Hg, respectively (P<.0001 for all). There was no significant change in heart rate. AECGs demonstrated arrhythmic activity during cocaine use, including 6 patients with increased atrial and ventricular ectopy, 2 patients with episodes of nonsustained atrial tachycardia, and 1 patient with 3 episodes of nonsustained monomorphic ventricular tachycardia. Cocaine use resulted in extreme elevations in arterial pressures in patients with hypertension taking medication. Cocaine use was also associated with an increase in arrhythmic activity. These findings may underlie the heightened risk of myocardial infarction, aortic dissection, and potentially lethal arrhythmias in patients with hypertension who use cocaine.

Electroacupuncture Reduces Cocaine-Induced Seizures and Mortality in Mice

“…As mentioned earlier, seizures are considered to be a major determinant of cocaine-related lethality in both humans [4] and animals [9]. However, the mechanism of sudden death in cocaine abuse also includes cardiac arrhythmia and intracerebral hemorrhage [10, 11]. Cocaine produces euphoria, elation, mood elevation, alertness, attention focusing, and fatigue reduction through interactions with monoamine transporters [80].…”

“…In addition to the central effects, cocaine also blocks norepinephrine uptake and increases sympathetic activity in the periphery [81]. Overstimulation of sympathetic activity may cause cardiac arrhythmia and intracerebral hemorrhage and hence may contribute to cocaine-induced fatality [10, 11]. EA frequency-specific differences observed in protection against seizures and death may be because the mechanism that induces death is more complicated than that involved in seizures.…”

“…Seizures are considered to be a major determinant of cocaine-related lethality in humans [4] and animals [9]. Sudden death in cocaine abuse may also be attributed to cardiac arrhythmia and intracerebral hemorrhage [10, 11]. Currently, no specific treatment modalities offer protection against cocaine-induced seizures and death in humans.…”

Hospital Admissions for Chest Pain Associated with Cocaine Use in the United States

“…Cocaine is a powerful sympathomimetic agent that results in coronary and peripheral arterial vasoconstriction, and its use is linked with cardiac arrhythmias. 1 The deleterious cardiovascular and prothrombotic effects of cocaine use have been well established and may underlie a wide range of clinical cardiovascular presentations. 2 Its acute and more chronic presentations encompass a myriad of pathologies that range from acute coronary syndromes, heart failure, cardiomyopathies, arrhythmias, aortic dissection, to others.…”

Acute Aortic Emergencies—Part 2 Aortic Dissections

“…Risk factors (see Table 1) relate to inherited and acquired weakening of the aortic media and intimal disease (Bonser et al, 2011;Braverman, 2010;Golledge & Eagle, 2008;Green & Kron, 2003;Hartnell & Gates, 2005;Hiratzka et al, 2010;Karthikesalingam, Holt, Hinchliffe, Thompson, & Loftus, 2010;Khoynezhad & Prestis, 2006;Landman & Torbati, 2012;O'Donnell et al, 2011;Secemsky, Lange, Waters, Goldsshlager, & Hsue, 2011;Stout, Scott, Stokes, & Panneton, 2010;Tilney, 2010;Upadhye & Schiff, 2012;Westover & Nakonezny, 2010;Wittels, 2011). Risk factors can be divided into two mechanisms:…”