Cocaine-Induced Coronary-Artery Vasoconstriction

Abstract

Intranasal cocaine is used frequently as a local anesthetic during many rhinolaryngologic procedures. Although its "recreational" use in high doses has been associated with chest pain and myocardial infarction, this association has not been established when cocaine is used in low doses as a topical anesthetic, and its effect on the coronary vasculature of humans is unknown. We studied the effects of intranasal cocaine (10 percent cocaine hydrochloride; 2 mg per kilogram of body weight) on the blood flow in and dimensions of the coronary arteries and on myocardial oxygen demand in 45 patients (34 men and 11 women, 36 to 67 years of age) who were undergoing cardiac catheterization for the evaluation of chest pain. Heart rate, arterial pressure, blood flow in the coronary sinus (measured by thermodilution), and the dimensions of the epicardial left coronary artery (measured by quantitative arteriography) were measured before and 15 minutes after the intranasal administration of saline (in 16 patients) or cocaine (in 29). No variables changed after the administration of saline. After cocaine was administered, the heart rate and arterial pressure rose, the coronary-sinus blood flow fell (from a mean [+/- SD] of 149 +/- 59 ml per minute to 124 +/- 53 ml per minute), and the diameter of the left coronary artery decreased by 8 to 12 percent (P less than 0.01 for all comparisons). No patient had chest pain or electrocardiographic evidence of myocardial ischemia after the administration of cocaine. Subsequently, the administration of the alpha-adrenergic blocking agent phentolamine caused all these values to return to base-line levels. There was no difference in response between the patients found to have disease of the left coronary artery (n = 28) and those without such disease (n = 17). We conclude that the intranasal administration of cocaine near the dose used for topical anesthesia causes vasoconstriction of the coronary arteries, with a decrease in the coronary blood flow, despite an increase in myocardial oxygen demand, and that these effects are mediated by alpha-adrenergic stimulation. It is reasonable to assume that these effects would be more pronounced at the much higher doses associated with the recreational use of cocaine.

Sudden death from superior mesenteric artery thrombosis in a cocaine user

“…It has been speculated that elevation of these markers is consistent with a cocaine-related pro-thrombotic state [23]. In addition to cocaine's pro-thrombotic properties, tissue ischemia may be potentiated by vasculature vasoconstriction via arterial alpha-adrenergic receptor stimulation [18,24]. Cocaine induced vasospasm may also be implicated [25,26].…”

“…Gastrointestinal complications occur less frequently and include mesenteric ischemia, ischemic colitis and perforation [3][4][5][6][7][8][9][10][11][12][13][14][15][16][17]. The mechanisms by which cocaine exerts its tissue-toxic effects are numerous and include arterial vasoconstriction, vasospasm, accelerated atherosclerosis and thrombosis [18][19][20][21][22][23][24][25][26][27][28]. We report a case of sudden death from superior mesenteric artery (SMA) thrombosis in a chronic cocaine user.…”

Cocaine-Induced Chest Pain and β-Blockade: An Inner City Experience

“…In small experimental studies cocaine has been shown to provoke coronary vasospasm in the catheterization laboratory. [11][12][13] This vasospasm in both diseased and nondiseased segments can be abolished by sublingual nitroglycerin and calcium channel antagonists and blocked by the adrenergic-receptor blocker phentolamine. 11,12 Labetalol in comparison reverses the cocaine-induced increase in arterial pressure but does not alleviate cocaine-induced coronary vasoconstriction.…”

Maternal cocaine abuse and fetal renal arteries: a morphometric study

“…Fetal renal vessels repeatedly exposed to cocaine may go into persistent vasospasm (decrease in lumen size), leading to hypertrophy and hyperplasia (increase in thickness) of the muscle layer of the vessel wall, as shown in our study. Animal experiments have suggested that cocaine may influence the vascular smooth muscle cell contraction both directly by its calcium-dependent vasoconstriction and indirectly by blocking norepinephrine uptake at the sympathetic terminals [12,13]. The vasoconstriction and interruption of the blood supply may be the cause of organ deformity in the fetus exposed to cocaine in utero [20,21].…”

“…However, the reports that document the outcome of the newborns and their subsequent development when exposed to cocaine in utero are limited [6,7,11]. The effects of cocaine on the vasculature are well documented in adults [12,13], particularly affecting the coronary and other systemic arteries and leading to fatal complications. Renal vascular changes in cocaine-addicted adults with its consequences have been reported also [14,15,16].…”