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.

[Neurological manifestations in critically ill patients]. / Manifestaciones neurologicas del paciente en estado critico.

AIMS: To describe the pathophysiology, diagnosis and clinical manifestations of the neurological complications that critically ill patients often develop in intensive care units, and to discuss their treatment and prognosis, in the light of the most significant contemporary literature. DEVELOPMENT: The most frequent complication suffered by critically ill patients is sepsis, with encephalopathy as the main manifestation, and this has a direct effect on their prognosis. Polyneuropathy of the critically ill patient is linked to sepsis, as the main precipitating factor, as well as to the presence of high levels of glucose, which plays an important role in deciding whether mechanical ventilation can be withdrawn or not. Myopathy of the critically ill patient is related to the use of fluorinated steroids and neuromuscular blockers, which are frequently administered to these patients. All these entities represent a significant diagnostic challenge for the physician and are accompanied by important sequelae that continue after the patient's discharge from hospital, as well as myopathies and neuropathies associated to the use of drugs that are commonly administered to critically ill patients. It is therefore necessary to be familiar with the pathophysiology of the damage and with the associated factors, if a suitable diagnostic approach is to be employed. CONCLUSIONS: The incidence of these pathologies and their complications makes them important conditions that require a swift, accurate diagnosis so that treatment can be established early on and a prognosis can also be determined.

Use of glucagon to treat neonatal low-output congestive heart failure after maternal labetalol therapy.

Labetalol is used to treat hypertensive crisis in women with preeclampsia. Glucagon was used as a nonselective beta-adrenergic agonist to treat a preterm infant with symptomatic beta-blockade caused by maternal labetalol therapy.

Combined alpha/beta-blockade versus beta 1-selective blockade in essential hypertension in black and white patients.

The purpose of this multicenter investigation was to determine the efficacy and safety of the alpha/beta-blocker labetalol versus the beta 1-selective beta-blocker atenolol in white and black patients with essential hypertension. Equal numbers of black and white patients were enlisted to form four treatment groups (white patients taking either labetalol or atenolol and black patients taking either labetalol or atenolol). Two hundred ninety-two patients (152 white and 140 black patients) with essential hypertension characterized by a standing diastolic blood pressure of 105 to 119 mm Hg (inclusive) were recruited for this trial. Patients were randomized to either labetalol (dosage titrated from 200 to 1600 mg/day) or atenolol (dosage titrated from 50 to 100 mg/day). The therapeutic goal was achievement of a standing diastolic blood pressure of 90 mm Hg or less or a fall of 15 mm Hg in diastolic pressure from baseline value at the end of the placebo run in period. At the end of the study there were no significant differences in blood pressure or heart rate changes in the supine position between the labetalol and atenolol groups. In contrast, labetalol produced greater reduction in both the standing systolic and diastolic blood pressure (-12/-13 mm Hg, respectively) compared with atenolol (-7/-9 mm Hg; p less than 0.05; p less than 0.005, respectively). The greatest decrease in blood pressure was observed in white patients receiving labetalol. In black patients the decrease in blood pressure was greater in those treated with labetalol compared with atenolol, particularly with respect to the systolic blood pressure. We conclude that the alpha 1-blocking property of labetalol provides an additional lowering of the blood pressure over that seen with beta 1-blockade alone, especially in the standing position, and this enhanced efficacy is not confined to one radical group.

Comparison of dilevalol and enalapril administered once daily for mild hypertension.

This was a multicenter, randomized, double-blind, parallel-group study of the efficacy and safety of dilevalol, 200 mg (n = 86), compared with enalapril, 20 mg (n = 92), administered once daily to patients with mild hypertension. Three weeks of placebo washout were followed by 4 weeks of comparative treatment. Beginning with the first week of treatment, both drugs substantially decreased blood pressure from baselines of approximately 160/100 mm Hg. Decreases in systolic pressure were comparable throughout treatment, but dilevalol tended to have a greater effect on diastolic pressure. At the end of double-blind treatment, average decreases in blood pressure with dilevalol and enalapril were 16/13 and 16/11 mm Hg supine and 15/13 and 15/10 mm Hg standing (p = 0.03 for between-group comparisons of standing diastolic pressure). More dilevalol- than enalapril-treated patients achieved a diastolic pressure less than 90 mm Hg; 73 vs 55% (p = 0.02) supine, and 69 vs 43% (p less than 0.01) standing. The safety profiles of the 2 drugs were comparable. The incidence of adverse effects was low, and few patients discontinued treatment. Headache and gastrointestinal discomfort were reported in both groups. Average postural changes in blood pressure were similar to baseline. Electrocardiographic changes were rare and not treatment related. Changes in laboratory test results were minor. Heart rate decreased modestly with dilevalol relative to enalapril (6 vs 2 to 3 beats/min; p less than 0.01), but no bradycardia was observed.

A study of labetalol in patients of European, West Indian and West African origin.

1 Hypertension in West Indians and Africans is common and has an unacceptably high mortality in the younger patients. 2 Fifty-three patients received labetalol (a combined alpha- and beta-adrenoreceptor antagonist) as part of an open evaluation of its anti-hypertensive effect. Ten non-caucasian patients were included. 3 Significant reductions in systolic and diastolic pressures were obtained in the caucasian patients, the African and West Indian patients remaining refractory to therapy.