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In general, continued resuscitation efforts in the emergency department for victims of cardiopulmonary arrest in whom prehospital resuscitation has failed are not worthwhile, and they consume precious institutional and economic resources without gain.

We performed a multicenter, double-blind, randomized study to evaluate the effect of diltiazem on reinfarction after a non-Q-wave myocardial infarction. Nine centers enrolled 576 patients: 287 received diltiazem (90 mg every six hours) and 289 received placebo. Treatment was initiated 24 to 72 hours after the onset of infarction and continued for up to 14 days. The primary end point, reinfarction, was defined as an abnormal reelevation of MB creatine kinase in plasma within 14 days. Reinfarction occurred in 27 patients in the placebo group (9.3 percent) and in 15 in the diltiazem group (5.2 percent)--a 51.2 percent reduction in cumulative life-table incidence (P = 0.0297; 90 percent confidence interval, 7 to 67 percent). Diltiazem reduced the frequency of refractory postinfarction angina (a secondary end point) by 49.7 percent (P = 0.0345; 90 percent confidence interval, 6 to 73 percent). Mortality was similar in the two groups (3.1 and 3.8 percent, respectively, in the placebo and diltiazem groups), but adverse drug reactions (most of which were mild) were more common in the diltiazem group. Nevertheless, the drug was well tolerated, despite concurrent treatment with beta-blockers in 61 percent of the patients. We conclude that diltiazem was effective in preventing early reinfarction and severe angina after non-Q-wave infarction and that it was also safe and generally well tolerated.

SUMMARYPatients with severe congestive heart failure (CHF) have been found to have a diminished response to the metabolic arteriolar dilator stimulus of ischemia. In order to evaluate a more physiologic stimulus and the possible metabolic consequences of this vascular abnormality, 22 normal subjects (N) and seven patients with severe CHF performed rhythmic forearm exercise by squeezing a rubber bulb to 25, 50, or 100 mm Hg for 5 sec, four times/min, for 5 min. During the last half of the 10 sec relaxation phases, forearm blood flow (FBF) was measured plethysmographically. Not only was FBF reduced at rest in CHF (CHF: 2.00 i 0.31; N: 3.10 ± 0.27 ml/min 100 ml, P < 0.02) but it was reduced at each level of exercise as well (CHF: 4.05 0.71, 5.57 + 0.71, 6.68 + 3.09; N: 7.10 ± 0.76, 11.15 ± 1.24, 20.32 ± 1.93 ml/min. 100 ml, P < 0.01). Forearm oxygen extraction, calculated from brachial venous and systemic arterial blood, was consistently increased in CHF and was sufficient to maintain a normal forearm oxygen consumption at rest (CHF: 0.14 ± 0.04; N: 0.12 + 0.01 ml 02/min 100 ml, P < 0.5). During exercise the calculated index of oxygen consumption was reduced at all levels of exercise (CHF: 0.30 0.04, 0.48 + 0.09, 0.54 + 0.14; N: 0.51 ± 0.05, 0.89 i 0.08, 1.63 + 0.13 ml 02/min 100 ml, P < 0.01). These differences persisted despite alpha-adrenergic blockade with phentolamine and suppression of skin flow in N by epinephrine iontophoresis. Therefore, at comparable levels of dynamic forearm exercise patients with CHF DURING DYNAMIC EXERCISE patients with congestive heart failure (CHF) appear to have an exaggerated sympathoadrenal response which results in a decreased perfusion of regional circulations that have low metabolic requirements and adequate alpha-adrenergic receptor sites.'`6 A similar increase in alpha-adrenergic tone also occurs in exercising skeletal muscle. However, these constrictor impulses are offset by the local accumulation of metabolites and a vasodilation occurs.7' 8 Therefore, in exercising muscle, vascular resistance falls and oxygen delivery increases. It is important to note that patients with CHF demonstrate a reduced metabolic arteriolar dilator response following restoration of flow to an ischemic limb (reactive hyperemia) which is considerably reduced when compared with that of normal subjects.9 This relative arteriolar stiffness has been postulated to be a possible protective mechanism for

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The signal-averaged ECG predicts serious arrhythmic events in the first year after infarction better than do clinical, ejection fraction and ventricular arrhythmia variables, and QRSD-40 Hz > or = 120 ms provides the best predictive criterion in this clinical setting.

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