Levels of serum cortisol, plasma free fatty acids (FFA), and urinary catecholamines were collected in 31 patients with acute myocardial infarction on the day of admission to the coronary care unit (samples obtained from 15 patients with diseases other than myocardial infarction were considered as controls). These values were correlated with the presence or subsequent development of left ventricular failure, arrhythmias, shock, or death. Sixteen of 17 infarction patients without the above complications had cortisol levels less than 20 µg%; 10 of 12 patients with complications had higher cortisol levels. All of the infarction patients without complications had plasma FFA levels less than 1100 µEq/liter, while six of nine patients with complications had levels of 1100 µEq/liter or higher. Fourteen of 16 patients without complications had urinary catecholamines less than 12.5 µg%, while seven of 10 patients with complications had levels greater than this. Of interest were a few patients without complications on admission, but with elevated cortisol or FFA levels, who developed complications on the following day. The results of the present study suggest that the generalized metabolic stress of acute myocardial infarction results in elevations of cortisol, FFA, and catecholamines as measurable biochemical indicators and/or predictors of the severity of the infarction.

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Eleven patients with arteriographically confirmed coronary artery disease and normal arterial oxygen saturation were studied. The angina threshold was determined first by successive elevation of heart rate at increments of 10 and 5 beats/min by right atrial pacing while the patients were breathing air via a close-fitting mask. The mask was then connected to an oxygen tank without the patient's knowledge. After 5 min of oxygen breathing, the heart rate was again raised to the previously determined threshold level. In nine of 11 patients angina did not recur. The absence of angina was associated with improvement in myocardial lactate extraction from -17 ± 15 to +18 ± 10% ( P < 0.025), in S-T abnormalities in six of seven patients, and in pulsus alternans in three of five patients. The pacing rate was then raised at increments of 5 beats/min until angina recurred. With oxygen breathing, angina developed at higher pacing rates (129 ± 7 beats/min with air and 137 ± 6 beats/min with oxygen, on the average; P < 0.005), at higher rate-pressure product (18.0 ± 0.8 and 19.5 ± 0.9 x 10 3 mm Hg/min, respectively; P < 0.01), and at higher left ventricular oxygen consumption (21.3 ± 1.1 and 24.6 ± 1.1 ml/min, respectively; P < 0.005). The results indicate that oxygen breathing permits the heart to do more work before coronary insufficiency develops.

Accidental inhalation of helium under high pressure can cause symptomatic cerebral and coronary artery gas embolism.

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We caution against possible isoniazid neurotoxicity in healthy individuals using recommended preventive doses.

The first dose of angiotensin-converting enzyme (ACE) inhibitors may trigger a considerable fall of blood pressure in chronic heart failure. The response may be dose-related. To determine hemodynamic and systemic oxygenation effects of low-dose enalaprilat, we administered intravenous enalaprilat (0.004 mg/kg) as bolus (group B) or continuous 1-hour infusion (group C) in 20 patients with congestive heart failure due to ischemic heart disease with acute decompensation refractory to inotropic, vasodilator and diuretic therapy. Hemodynamic and systemic oxygenation variables were recorded at baseline (+0 min), +30, +60, +120, +180, and +360 min after the start of intervention. Mean arterial pressure (MAP) (p < 0.001), mean pulmonary artery pressure (MPAP) (p < 0.001), pulmonary artery occlusion pressure (PAOP) (p < 0.001), oxygen extraction ratio (ER) (p < 0.026) decreased regardless of enalaprilat application. Compared to group B, there was in group C prolonged decrease of MAP, MPAP, PAOP, ER and increase of pulmonary artery oxyhemoglobin saturation in regard to baseline values. Cardiac index, heart rate, central venous pressure and oxygen consumption index did not change. A low dose of intravenous enalaprilat (0.004 mg/kg) can be used to safely improve hemodynamics and systemic oxygenation in congestive heart failure due to ischemic heart disease with acute refractory decompensation.