Infarto agudo do miocárdio relacionado ao uso de cocaína / Acute myocardial infarction related to cocaine use

Esta revisão discute o estado atual da fisiopatologia e do tratamento do infarto agudo do miocárdio relacionado ao uso de cocaína. O abuso de drogas ilícitas, em especial, da cocaína é cada vez mais frequente, com o aumento consequente da quantidade de consultas de emergências relacionadas a suas complicações, incluindo o infarto do miocárdio. Os principais mecanismos fisiopatológicos que contribuem de forma aguda ou crônica para causar o infarto relacionado ao uso de cocaína são: vasoespasmo, aterosclerose, trombogenese mediada por aumento dos níveis de fatores pró-trombóticos associada com a elevação da agregação plaquetária, aumento da demanda de oxigênio pelo miocárdio. O tratamento do infarto agudo do miocárdio relacionado ao uso de cocaína é semelhante ao do infarto na população em geral, com ácido acetilsalicílico, nitratos e oxigênio. As diferenças estão no uso de benzodiazepínicos e na contraindicação do uso de beta-bloqueadores. Existe controvérsia quanto ao uso do labetalol e da terapia trombolítica. Está sob investigação o uso de novos medicamentos como a fentolamina para reverter os efeitos de vasoconstrição e dos inibidores plaquetários para evitar a progressão do trombo.

This article aims to review current pillars of the pathophysiology and treatment of acute myocardial infarction related to cocaine use. Cocaine use has become increasingly frequent, and consequently the number of medical emergencies has increased related to its complications, including myocardial infarction. Four seems to be the pathophysiological mechanisms that contribute acutely or chronically, to cause infarction related to cocaine use: vasospasm, atherosclerosis, thrombus formation mediated by increased levels of prothrombotic factors and increased platelet aggregation, and increased demand for myocardial oxygen. The cocaine related infarction treatment is similar to infarction in general population with aspirine, nitrates and oxigen therapy. The differences are based on the use of benzodiazepines and the non indication of beta blockers, in the first case. Labetalol and trombolitic therapy use are controversial. The patophisiology knowledgement plays an important role in the introduction of new medications specific to cocaine related infarction, like phentolamine and platelets inhibitors.

Effect of atenolol and labetalol on serum lipids.

Adverse alterations in lipid profile suggesting higher atherogenicity were observed following 12 weeks treatment with atenolol in patients of hypertension. No significant alterations in lipid profile were observed with labetalol therapy.

Effects of maternal labetalol on the newborn infant.

Forty eight neonates, born to mothers suffering from pregnancy induced hypertension and receiving labetalol for control of blood pressure, were studied for the possible adverse effects of the drug. These were compared with eighty one neonates matched for gestation and weight and born to mothers with pregnancy induced hypertension treated with drugs other than labetalol. Incidence of birth asphyxia and intrauterine growth retardation (IUGR) in the study population was 10.4 and 22.9%, respectively and in the control group 5 and 19.7%, the difference between two groups was not statistically significant (p > 0.05). However, the incidence of hypoglycemia was significantly higher (p < 0.01) in the study group (47.9%) as compared to the control group (17.2%). Two-thirds of the hypoglycemic babies in the study population were asymptomatic and they were managed with sugar-fortified milk feeds. In the study population, the symptomatic hypoglycemic babies had hypoglycemia for prolonged duration of 43.3 +/- 23.3 hours as compared to 11.5 +/- 6.3 hours in symptomatic hypoglycemic babies of the control group (p < 0.01). The mothers of the symptomatic babies in the study group received higher doses of labetalol in the range of 287.6 +/- 142.3 mg/day while rest of the mothers in the same group whose babies had either asymptomatic hypoglycemia or normal blood glucose levels, received 239.5 +/- 118.5 mg/day, though the difference was not statistically significant. It is concluded that maternal labetalol therapy is associated with increased risk of neonatal hypoglycemia.