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The increased morning frequency of cardiovascular disease onset has created concern that morning exertion promotes greater risk than evening exertion. The physiologic responses to isometric exercise (handgrip) in the morning (9 A.M.) versus the evening (6:30 P.M.) were compared in 15 subjects with mild hypertension. Isometric exercise produced similar increases at both times of the day (morning vs evening) in systolic arterial pressure (31 [+ or -] 4 vs 35 [+ or -] 4 mm Hg, p = NS) and heart rate (7 [+ or -] 1 vs 8 [+ or -] 1 bents/min, p = NS). It also produced similar increases in fibrinolytic activity (reduction in euglobulin clot lysis time) at both times of the day (-53 [+ or -] 27 vs -53 [+ or -] 21 minutes). However, because basal fibrinolytic activity was lower in the morning than in the evening (euglobulin coat lysis time 364 [+ or -] 45 vs 220 [+ or -] 33 minutes, p

Although [Beta]-adrenergic blocking agents are known to reduce the risk of myocardial infarction, the mechanism of this protective effect is not well understood. The recent demonstration that [Beta] blockers selectively blunt the increased morning risk of myocardial infarction suggests that these agents block the pathophysiologic consequences of stressors concentrated in the morning. We determined the effect of nadolol on the hemodynamic and hemostatic responses to mental stress and isometric exertion (handgrip), 2 patential triggers of infarction. The study was conducted in 15 subjects with mild systemic hypertension, using a placebo-controlled, double-blind, crossover design. Nadolol reduced systolic pressure and heart rate after mental stress. Poststress systolic pressure was 139 [+ or -] 4 mm Hg during therapy with nadolol versus 161 [+ or -] 4 mm Hg during placebo administration (p

The clinical course of 363 patients with acute myocardial infarction who did not complete high school education was compared with that of 453 who completed at least high school. Both the in-hospital and 4-year mortality rates were markedly greater for the less educated than for the more educated patients (13 vs 5% [p

The recent demonstration of aspirin's ability to prevent and reduce the severity of myocardial infarction has led to a marked increase in its use and to a need for information regarding the time-course of onset and offset of its antiplatelet effect. A study of healthy men was conducted to determine (1) the rapidity of onset of inhibition of platelet aggregation in response to adenosine diphosphate, and thromboxane [A.sub.2] production after chewed enteric-coated aspirin (325 mg, n = 10); and (2) the duration of platelet inhibition after cessation of enteric-coated aspirin (325 mg) every other day for 14 days (n = 10). When chewed, enteric-coated aspirin greatly inhibited platelet aggregation response to adenosine diphosphate and thromboxane [A.sub.2] production within 15 mintues. Complete recovery of platelet aggregation occurred in half of the subjects by day 3, and in 80% of the subjects by day 4; the platelet response was not affected by exercise. This study demonstrates a rapid onset of aspirin's antiplatelet effect and provides information relevant for optimal timing of initiation of aspirin for acute conditions such as myocardial infarction and unstable angina, and cessation of aspirin before surgery.

Several studies have observed an increased occurrence of acute myocardial infarction (AMI) in the morning based on subjective self-reports and objective confirmation. Evidence has also been collected to suggest a circadian variation in the onset of sudden cardiac death and silent myocardial ischemia. No published reports have examined the time of onset of AMI in relation to time after awakening. The present study examines the times of onset of AMI in relation to awakening in 137 patients with confirmed AMI. Information concerning time of awakening on the day of AMI revealed a marked increase in the onset of initial AMI symptoms within the first hour after awakening. Of the patients studied, approximately 23% reported onset of the initial symptoms of AMI within 1 hour after awakening. An increased onset of symptoms of AMI soon after awakening was also observed when patients in whom the acute cardiac symptoms were known to or may have caused awakening were excluded from consideration. This was also noted in subgroups of AMI patients classified according to age, order and location of AMI. These results extend previous observations of the circadian morning increase of AMI onset and assist in narrowing the search for potential triggers of the circadian variation of onset of AMI to physiologic changes that may occur soon after awakening. (Am J Cardiol 1990;66:140-144), Acute myocardial infarction (AMI) or sudden heart attack is the deterioration of heart tissue due to cessation of blood supply to the heart. Previous studies have revealed certain facts about the timing of AMI. For example, heart attacks occur more often in the morning than at other times of the day. In addition, sudden cardiac death and silent myocardial ischemia (insufficient blood supply to the heart) occur according to a circadian or 24-hour pattern. The relation between the onset of AMI symptoms and the time after awakening was evaluated in 137 heart attack patients. The results indicate that there was an increase in the onset of symptoms within the first hour after waking. Twenty-three percent of the patients reported the onset of symptoms of AMI within the first hour after waking. When patients with heart attack symptoms that caused awakening were excluded, an increased onset of symptoms soon after waking was still apparent. This observation was noted in groups of patients classified according to age, order, and location of AMI. These findings are consistent with previous studies reporting a circadian morning increase in the onset of AMI. In addition, this study provides knowledge about important factors, such as physiologic changes that occur after awakening, which influence the circadian variation in the onset of AMI. (Consumer Summary produced by Reliance Medical Information, Inc.)

Although many new drugs useful in the treatment of congestive heart failure have been introduced during the past 25 years, spironolactone continues to have an important role in the management of this condition. Spironolactone adds to the activity of the thiazide and loop diuretics to enhance the elimination of sodium and water. Furthermore, unwanted electrolyte disturbances such as hypokalemia and hypomagnesemia, associated with the administration of other classes of diuretics, can be minimized with spironolactone. (Am J Cardiol 1990;65:51K-53K), Congestive heart failure (CHF) is the inability of the heart to pump blood, leading to congestion or fluid accumulation in the lungs. Therapy for CHF includes the use of diuretics, agents that increase sodium and water excretion and thereby relieve congestion; digitalis, a drug that increases the contractility of the heart; and recently, vasodilators, which dilate blood vessels and reduce the pressures against which the heart must pump blood. However, thiazide-type diuretics lose their effectiveness after long-term use and have been associated with the development of potassium and magnesium deficiencies. Potassium deficiency may directly cause the development of arrhythmias, or abnormal heart rhythms, and enhance the ability of digitalis to cause arrhythmias. Hence, more interest has focused on diuretics which are potassium-sparing or do not cause potassium depletion. The drug spironolactone antagonizes or prevents the actions of the adrenal hormone aldosterone, which regulates the metabolism of potassium, sodium, and chloride. This aldosterone antagonist mildly increases sodium excretion without causing losses of potassium and magnesium from the kidney. Spironolactone, a potassium-sparing diuretic, was shown to be both safe and effective in treating hypertension and CHF. It may be given alone or combined with thiazide diuretics. Spironolactone enhances the ability of thiazides to eliminate sodium and water, and reduces the loss of potassium and magnesium associated with the use of thiazides alone. (Consumer Summary produced by Reliance Medical Information, Inc.)