Coronary blood flow measurement by contrast echocardiography is limited by changes in intramyocardial blood content (original) (raw)
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Effect of cocaine on the coronary circulation and systemic hemodynamics in dogs
Journal of the American College of Cardiology, 1990
This study investigated the effect of intravenous cocaine (0.5 to 2 mg/kg body weight) on the coronary circulation and systemic hemodynamies in closed chest sedated dogs. The role of alpha. and beta-adeenoceptor stimulation in mediating these effects was aim investigated. Cocaine produced dose-dependent increases in mean arterial pressure and rate-pressure product. Although the lower doses of cocaine had no significant effect on the coronary ciccuiation, the 2 mg/kg dose produced a 55 ± 1 .1% increase in coronary vascular resistance (p < 0 .05 versus baseline) and a 19 m 3% reduction in diametor of the left anterior descending coronary artery (p < 0 .05 versus baseline). Despite these potentially deleterious effects on the coronary circulation (occurring at a time of markedly increased myocardial oxygen demand), the electrocardiogram did not demonstrate ischemic changes and there was no myocardial lactate production. Cocaine-induced coronary vasoconstriction was sholtshed by pretreatment with the alpha-adrenoceptor antag-The incidence of cocaine abuse has reached epidemic proportions in numerous communities throughout the United States. It is estimated that 30 million Americans have used cocaine at some time and 5 million use it regularly (1). Over the past 5 years, numerous cases of myocardial ischemia and infarction have been reported to be associated with the
Life Sciences, 1996
The effects of repeated cocaine administration on contractile responses were studied in adult rabbits. Repeated cocaine exposure caused a significant increase in the maximal response of the aorta to the agonists norepinephrine and serotonin as well as the receptor-independent stimulus KC1 when compared to the saline controls. Cocaine exposure caused a signiIicant increase in the wet weights of both the heart and aorta. When the contraction was normalized to the wet weight of the aorta there was no difIerence between rabbits administered cocaine and saline. Acute cocaine administration caused a time-dependent increase in immunoreactivity of the proto-oncogene c-Fos in the aorta. These results show that repeated cocaine administration leads to the development of cardiovascular hypertrophy.
Immediate Effects of Intravenous Cocaine on the Thoracic Aorta and Coronary Arteries
Chest, 1996
Cocaine use has been associated with a number of life-threatening cardiovascular complications, including dissection and rupture ofthe thoracic aorta and myocardial ischemia and infarction.' 5 Arterial vasoconstriction is thought to play a role in the etiology of these life-threatening cardiovascular complications, and this theory is supported by a number of studies documenting cocaine-induced vasoconstriction of the thoracic aorta6 and coronary arteries.7-10 Cocaine has been shown to cause vasoconstriction of *From the Cardiovascular Research Institute (Dr. Eisenber), the Cardiology Division of the Department of Medicine (Drs. risenber Redberg, and Foster),
Dichotomous cardiac and systemic vascular responses to cocaine in conscious rats
Life Sciences, 1993
This study examined the effects of cocaine on cardiac output in conscious freelymoving rats. Although pressor responses were similar at all doses, 14 of 32 rats had consistent declines in cardiac output (> 15%) and greater increases in systemic vascular resistance after administration of cocaine (5 mg/Kg, i.v.). Procaine (10 mg/Kg i.v.) did not mimic this effect in either subgroup. We propose that a subpopulation of rats exists with an enhanced susceptibility to cocaine-induced cardiac and systemic vascular alterations at higher doses.
Cocaine and Ethanol: Combined Effects on Coronary Artery Blood Flow and Myocardial Function in Dogs
Academic Emergency Medicine, 2009
Objectives: In combination, cocaine and ethanol are more cardiotoxic than is either substance alone. These substances together constitute a drug abuse combination that commonly results in fatality. Previously the authors have demonstrated that cardiotoxicity of cocaine and ethanol is in part due to synergistic myocardial-depressant effects. However, it remains unclear whether this myocardial depression is associated with concomitant adverse effects on coronary blood flow in relation to these substances. The aim of this study was to investigate combined effects of cocaine and ethanol on myocardial blood flow, in relation to indices of myocardial function. Methods: Anesthetized dogs were instrumented for hemodynamic monitoring with Doppler flow probes placed on the circumflex and left anterior descending (LAD) coronary arteries. Dogs were randomized to three groups (each n = 6): ethanol (E, 1.5 g ⁄ kg followed by placebo), cocaine (C, placebo followed by cocaine, 7.5 mg ⁄ kg IV), or cocaine plus ethanol (C + E). All measurements were made at control, after placebo or ethanol, and then at fixed time intervals after cocaine or placebo bolus over 3 hours. Results: In both the C + E and the C groups, circumflex blood flow (CBF) decreased by 71% (95% confidence interval [CI] = 56% to 85%) and 57% (95% CI = 43% to 72%, both p < 0.04 vs. baseline) immediately after cocaine bolus. This was associated with transient depression of cardiac output, myocardial contractile function, and rate-pressure product (RPP), all indices of myocardial oxygen demand. A subsequent rebound increase of coronary sinus blood flow (CSBF) of 56% (95% CI = 26% to 137%, p < 0.03) compared to baseline occurred only in the C group and was associated with increases of myocardial contractile function and RPP. In the C + E group, 2 hours after drug administration, there was a decrease in CSBF of 49% (95% CI = 32% to 67%; p < 0.01) compared to baseline, which was associated with concomitant numerical decreases of the indices of myocardial oxygen demand and accumulation of cocaethylene. Conclusions: Acute decreases in myocardial flow secondary to cocaine, and cocaine and ethanol in combination, were similar and temporally associated with cocaine's direct myocardial-depressant effects. Rebound increases in myocardial function and blood flow due to cocaine were attenuated by ethanol. Delayed myocardial depression and decreases in myocardial blood flow were observed only with coadministration of cocaine and ethanol.
Cocaine and coronary artery diseases
Journal of Cardiovascular Medicine, 2017
Cocaine is associated with important cardiac complications such as sudden death, acute myocarditis, dilated cardiomyopathy, life-threatening arrhythmias, and myocardial ischemia as well as infarction. It is well known that cocaine may induce vasospasm through adrenergic stimulation of the coronary arteries. Moreover, cocaine may promote intracoronary thrombosis, triggered by alterations in the plasma constituents, and platelet aggregation, leading to subsequent myocardial infarction. The long-term use of cocaine may stimulate atherosclerosis, probably through endothelial cell dysfunction. Significant and severe coronary atherosclerosis is common in young chronic cocaine users and there is probably a relationship between the duration and frequency of cocaine use and the extent of coronary disease.