Lange Richard A, Cigarroa Joaquin E, Hillis L David
Department of Internal Medicine, Cardiovascular Division, University of Texas Southwestern Medical Center, Dallas, Texas 75390-8837,, USA.
Trans Am Clin Climatol Assoc. 2004;115:99-111; discussion 112-4.
As cocaine abuse has become widespread, it has been associated with various cardiovascular complications, including angina pectoris, myocardial infarction, and sudden cardiac death. Cocaine's principal effects on the cardiovascular system are mediated via alpha-adrenergic stimulation and include (a) an increase in the determinants of myocardial oxygen demand (heart rate and systemic arterial pressure) and (b) a concomitant decrease in myocardial oxygen supply (caused by vasoconstriction of the epicardial coronary arteries). Cocaine-induced coronary arterial vasoconstriction is enhanced at sites of atherosclerotic narrowing. Delayed or recurrent vasoconstriction of the coronary arteries may occur hours after the serum cocaine concentration has declined and appears to be caused by cocaine's major metabolites. Beta-adrenergic blocking agents may exacerbate cocaine-induced coronary arterial vasoconstriction, thereby increasing the magnitude of myocardial ischemia. Concomitant cigarette smoking exacerbates the deleterious effects of cocaine on myocardial oxygen supply and demand substantially.
随着可卡因滥用变得普遍,它已与各种心血管并发症相关联,包括心绞痛、心肌梗死和心源性猝死。可卡因对心血管系统的主要作用是通过α-肾上腺素能刺激介导的,包括(a)心肌需氧量决定因素(心率和体循环动脉压)增加,以及(b)心肌氧供应同时减少(由心外膜冠状动脉血管收缩引起)。可卡因诱导的冠状动脉血管收缩在动脉粥样硬化狭窄部位会增强。血清可卡因浓度下降数小时后,冠状动脉可能会出现延迟或反复的血管收缩,这似乎是由可卡因的主要代谢产物引起的。β-肾上腺素能阻滞剂可能会加剧可卡因诱导的冠状动脉血管收缩,从而增加心肌缺血的程度。同时吸烟会显著加剧可卡因对心肌氧供需的有害影响。