The relationship of anticoagulation level and complications after successful percutaneous transluminal coronary angioplasty.

The degree of anticoagulation and its effect on the frequency of abrupt coronary artery closure, coronary ischemia, bleeding complications requiring transfusion, and death were examined in 336 patients after elective percutaneous transluminal coronary angioplasty (PTCA). All patients received a bolus of 10,000 U of heparin at the beginning of the procedure followed by a continuous infusion of 2000 U/hr. At the conclusion of the procedure the infusion was reduced to 1000 U/hr and continued for 18 to 24 hours at which time the heparin infusion was suspended to allow removal of arterial and venous access sheaths. Partial thromboplastin time (PTT) was examined while patients continued to receive the heparin infusion. There was a variable degree of PTT prolongation in response to a standard dose of heparin with a range of 34 seconds to "greater than 150 seconds." Patients were divided into two groups according to the degree of heparin-induced PTT prolongation: group A included 271 patients with PTT greater than or equal to 3 times the control value, and group B comprised 65 patients with PTT less than 3 times the control value. Ischemic complications were analyzed on day 1 after PTCA and at hospital discharge. Bleeding complications and mortality were examined only at hospital discharge. There was a significant reduction in the incidence of abrupt coronary artery closure in group A on day 1 (1.5% vs 10.7%, p less than 0.001) and at hospital discharge (2.6% vs 10.7%, p less than 0.003).(ABSTRACT TRUNCATED AT 250 WORDS)

Anatomic and prognostic implications of an early positive treadmill exercise test.

Eighty men (group A) with clinical coronary artery disease underwent coronary angiography regardless of symptoms and previous therapy because they had a positive treadmill exercise test in stage I or II of the Bruce protocol. Thirty-four other men (group B) who also had an early positive treadmill test underwent coronary angiography because they had disabling angina pectoris despite medical therapy. We found left main coronary artery stenosis of 50% or greater of the vessel diameter in 28% of group A and 35% of group B (p greater than 0.3). In contrast, only 10% of 93 other catheterized patients who had treadmill tests that were not early positive had left main coronary disease (p less than 0.001). Fifty-four patients from group A who did not have left main stenosis of 50% or greater were treated medically. In this subgroup, 85% had 2 or 3 major coronary vessels with 75% or greater stenosis. These patients had a 36 month survival rate of 89.2%. We conclude that an early positive treadmill test identifies patients who have an increased likelihood of having left main coronary stenosis, even if they are minimally symptomatic. To identify left main coronary stenosis, catheterization may be justified in patients whose angina pectoris has been mild or not intensively treated when they have an early positive treadmill response. After left main coronary stenosis has been excluded, these patients may be treated medically with a low mortality.

Myocardial infarct extension: incidence and relationship to survival.

Myocardial infarct extension, defined as reelevation or reappearance of creatine phosphokinase-MB (CK-MB) 48 hours after the onset of symptoms, was evaluated prospectively in 56 consecutive patients with acute myocardial infarction. Myocardial infarct extension occurred in eight patients (14%). The sensitivity, specificity and predictive accuracy in the diagnosis of myocardial infarct extension were 63%, 85% and 42%, respectively, for recurrent chest pain requiring morphine; 50%, 65% and 19% for recurrent ST-segment elevation on routine 12-lead ECGs; and 88%, 63% and 28% for reelevation of total CK. Three of the eight episodes of extension were clinically silent. Four of eight patients (50%) with extension died, compared with one of 46 patients (2%) without extension (p = 0.0009). CK-MB persisted for 72 hours or longer in 16 patients and identified seven of eight patients who subsequently had infarct extension. We conclude that myocardial infarct extension is an infrequent complication of acute myocardial infarction and is associated with a very high mortality rate. Persistence of CK-MB for 72 hours or more identifies a subgroup of patients at high risk for subsequent infarct extension and death.

Autonomic mechanisms of training bradycardia: beta-adrenergic receptors in humans.

To address the autonomic mechanisms underlying the bradycardia of physical training in human subjects, we performed a cross-sectional study comparing the heart-rate responses to graded doses of isoproterenol in 7 elite marathon runners and 7 age-matched controls, and a longitudinal study in 12 normal volunteers of the effects of 6 wk of intense physical training on lymphocyte beta-adrenergic receptors identified by l-[3H]dihydroalprenolol. We observed no significant differences between marathoners and controls in the dose of isoproterenol that produced a 25-beat/min increment in heart rate, either in the absence (1.9 +/- 0.6 vs. 2.5 +/- 0.6 microgram; P, 0.509) or in the presence of cholinergic blockade (4.4 +/- 1.3 vs. 3.1 +/- 0.4 microgram: P, 0.320). Likewise, we observed no effects of physical training on lymphocyte beta-adrenergic receptors in terms of receptors number (53 +/- 11 vs. 56 +/- 10 fmol/mg protein) or receptor affinity (Kd 4.0 +/- 0.7 vs. 3.6 +/- 0.7 nM) (P, 0.9178). Although our data cannot exclude reduced chronotropic sensitivity to catecholamines as contributing to lowered heart rate in some highly conditioned individuals, these results are consistent with the hypothesis that altered neuronal input to the sinus node is usually a more important mechanism of training bradycardia.

Cholesterol metabolism in non-obese women--Failure of physical conditioning to alter levels of high density lipoprotein cholesterol.

The effects of a 6-week program of vigorous exercise were studied in 14 non-obese females aged 22--26. Preceding and following a regimen consisting of 30--45 min of jogging 5 days per week, treadmill performance, body weight, total plasma cholesterol, and plasma high density lipoprotein (HDL) cholesterol were assessed. Aerobic performance improved markedly after training as demonstrated by a reduced heart rate at each submaximal treadmill workload, and by an increase in maximal attainable workload. In the absence of a significant change in body weight, total cholesterol fell significantly after training (171 +/- 6 vs 161 +/- 5 mg/dl, P less than 0.05) whereas HDL cholesterol was not significantly altered (63 +/- 5 vs 58 +/- 3 mg/dl). The ratio of total cholesterol to HDL cholesterol fell insignificantly (2.92 +/- 0.19 vs 2.86 +/- 0.14). Our findings differ from prior reports of elevations of high density lipoprotein levels following physical conditioning in men. We suggest that hormonal or other factors leading to higher baseline levels of HDL in women counteract the expected alterations in lipoprotein metabolism induced by physical training.

Persistence of MB isoenzyme of creatine phosphokinase in the serum after minor iatrogenic cardiac trauma. Absence of postmortem evidence of myocardial infarction.

The specificity of serum CPK-MB for acute myocardial infarction was examined by retrospective analysis of 401 consecutive patients admitted to Coronary Care Unit over a three and one-half year period with suspected infarction in whom the isoenzyme was subsequently detected. Four patients (1 per cent) who died during the hospital admission had no autopsy evidence of acute myocardial infarction. All four had experienced mild iatrogenic cardiac trauma, following which serum CPK-MG persisted for at least 24 hours. In one patient, a permanent pacemaker had been inserted by the transmediastinal approach. Two patients had been subjected to closed chest cardiac massage and intracardiac puncture, and one to external cardiac massage alone. The findings suggest that persistent identification of serum CPK-MB, although specific for myocardial necrosis, cannot be regarded as diagnostic of myocardial infarction. The implications of this are important to treatment of patients after cardiopulmonary resuscitation and operative trauma to the heart.