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Biomedical subjects

G Jablonsky

Publications and source records attributed to G Jablonsky.

24 records · Page 2Linked to original sources

Aspirin, sulfinpyrazone, or both in unstable angina. Results of a Canadian multicenter trial.

We performed a randomized, double-blind, placebo-controlled trial in 555 patients with unstable angina who were hospitalized in coronary care units. Patients received one of four possible treatment regimens: aspirin (325 mg four times daily), sulfinpyrazone (200 mg four times daily), both, or neither. They were entered into the trial within eight days of hospitalization and were treated and followed for up to two years (mean, 18 months). The incidence of cardiac death and nonfatal myocardial infarction, considered together, was 8.6 per cent in the groups given aspirin and 17.0 per cent in the other groups, representing a risk reduction with aspirin of 51 per cent (P = 0.008). The corresponding figures for either cardiac death alone or death from any cause were 3.0 per cent in the groups given aspirin and 11.7 per cent in the other groups, representing a risk reduction of 71 per cent (P = 0.004). Analysis by intention to treat yielded smaller risk reductions with aspirin of 30 per cent (P = 0.072), 56 per cent (P = 0.009), and 43 per cent (P = 0.035) for the outcomes of cardiac death or nonfatal acute myocardial infarction, cardiac death alone, and all deaths, respectively. There was no observed benefit of sulfinpyrazone for any outcome event, and there was no evidence of an interaction between sulfinpyrazone and aspirin. Considered together with the results of a previous clinical trial, these findings provide strong evidence for a beneficial effect of aspirin in patients with unstable angina.

Angina Pectoris↗

Changes in the ratio of lactate dehydrogenase isoenzymes 1 and 2 during the first day after acute myocardial infarction.

It is known that the ratio of isoenzyme 1 to total lactate dehydrogenase (LD, EC 1.1.1.27) in serum is increased in all patients with acute myocardial infarction within 24 h of the infarct. We now show that the LD-1/LD-2 ratio for serum more promptly indicates acute myocardial infarction, being for most patients equivalent to measurement of creatine kinase (EC 2.7.3.2) isoenzyme 2 (CK-2, CK-MB) in serum. Of 128 patients with a confirmed diagnosis of myocardial infarction, 66 had normal values for all "cardiac" enzymes at the time of admission, but greater than 75% of them showed a parallel increase in values for CK-2 and the LD-1/LD-2 ratio. Of the 26 patients who had one or more abnormal values for cardiac enzymes on admission, 95% showed a parallel increase in CK-2 and the LD-1/LD-2 ratio, the median time for the beginning of these changes being 9 h from the onset of chest pain. The remaining 36 patients were excluded from the study because CK-2 decreased after admission or because the time of onset of chest pain was uncertain.

Adult↗

Clinically unrecognized ventricular dysfunction in young diabetic patients.

Left ventricular function at rest and during supine bicycle exercise was assessed by gated radionuclide angiography in 20 diabetic patients and 18 normal control subjects without clinical evidence of heart disease. The diabetic patients were aged 21 to 44 years and all except one used insulin. No subject developed chest pain or electrocardiographic changes during exercise. Both groups had a similar rest and exercise heart rate and blood pressure, and both achieved similar work loads. The control group had an ejection fraction at rest of 65.4 +/- 6.2% (mean +/- SD) and only 1 of 18 showed a decrease with exercise; peak exercise ejection fraction averaged 77.1 +/- 7.8%. The diabetic group had a mean ejection fraction at rest of 63.7 +/- 6.5%, similar to that of the control group, but 7 of 20 showed a decrease during exercise; the exercise ejection fraction averaged 67.7 +/- 9.7%, significantly lower than that of the control group (p less than 0.01). The diabetic patients varied widely in ejection fraction response to exercise, ranging from an increase of 25% to a decrease of 21%. This response did not correlate with age, sex, duration of diabetes, smoking, retinopathy, exercise heart rate, blood pressure or rate-pressure product, work load attained or ejection fraction at rest. These data suggest that approximately one-third of patients with diabetes have subclinical left ventricular dysfunction without correlation to risk factors for atherosclerosis or other diabetic complications. Whether this is due to unrecognized coronary artery disease or primary myocardial disease remains unknown.

Adult↗

Rest and exercise ventricular function in adults with congenital ventricular septal defects.

Rest and exercise right and left ventricular function were compared using equilibrium gated radionuclide angiography in 19 normal sedentary control subjects (mean age 28 years, range 22 to 34) and 34 patients with hemodynamically documented congenital ventricular septal defect (VSD) (mean age 27 years, range 20 to 40). The 34 patients with VSD were divided into 3 groups: those in Group 1 (17 patients) had pulmonary to systemic blood flow ratios of less than 2 to 1; those in Group 2 (12 patients) had prior surgical closure of VSD (mean interval from surgery 17 years, range 9 to 22), and those in Group 3 (5 patients) had Eisenmenger's complex. Gated radionuclide angiography was performed at rest and during each level of graded supine bicycle exercise to fatigue. Heart rate, blood pressure, maximal work load achieved, and right and left ventricular ejection fractions were assessed. The control subjects demonstrated an increase in both the left and right ventricular ejection fractions with exercise (0.70 +/- 0.07 to 0.79 +/- 0.05 and 0.46 +/- 0.06 to 0.57 +/- 0.04; p less than 0.001 for left and right ventricles, respectively). All study groups failed to demonstrate an increase in ejection fraction in either ventricle with exercise. Furthermore, resting left ventricular ejection fraction in Groups 2 and 3 was lower than that in the control subjects (0.59 +/- 0.09 and 0.54 +/- 0.06 versus 0.70 +/- 0.07; p less than 0.001) and resting right ventricular ejection fraction was lower in Group 3 versus control subjects (0.30 +/- 0.07 versus 0.46 +/- 0.06; p less than 0.001). Thus (1) left and right ventricular function on exercise were abnormal in patients with residual VSD as compared with control subjects; (2) rest and exercise left ventricular ejection fractions remained abnormal despite surgical closure of VSD in the remote past; (3) resting left and right ventricular function was abnormal in patients with Eisenmenger's complex; (4) lifelong volume overload may be detrimental to myocardial function.

Adult↗

Left ventricular function in trained and untrained healthy subjects.

Left ventricular function was compared in 18 normal sedentary controls (mean age 28 years, range 22 - 34 years) and nine endurance-trained athletes (mean age 19 years, range 15 - 25 years) at rest and during supine bicycle exercise. Gated radionuclide angiocardiograms were performed at rest and at each level of graded maximal supine bicycle exercise. Heart rate, blood pressure, left ventricular ejection fraction and the relative changes in left ventricular end-diastolic and end-systolic volumes were assessed. Athletes attained a much greater work load than controls (mean 22.1 kpm/kg body weight vs 13 kpm/Kg body weight). Both groups achieved similar increased in heart rate, blood pressure and ejection fractions. In the controls, the mean end-diastolic volume increased to 124% of that at rest (p less than 0.02) during exercise and the mean end-systolic volume decreased to 81% of the rest level (p less than 0.02). In contrast, the mean end-diastolic volume did not significantly change during exercise in the athletes, and the mean end-systolic volume decreased to 64% of rest (p less than 0.05). Thus, although trained and untrained healthy subjects had similar increases in the left ventricular ejection fraction during exercise, different mechanisms were used to achieve these increases. Untrained subjects increased end-diastolic volumes, whereas trained subjects decreased the end-systolic volumes. The ability of athletes to exercise without increasing preload may be an effect of training amd might have important implications in reducing myocardial oxygen demand during exercise.

Adult↗

The hemodynamic and metabolic response to pacing after aortocoronary bypass.

Long-term follow-up of aortocoronary bypass has shown good preservation of ventricular function. However, myocardial reserve in the immediate postoperative period may not be optimal. Nineteen patients who underwent elective aortocoronary bypass protected with cold potassium cardioplegia were studied in the early postoperative period at rest and during the stress of atrial and ventricular pacing. Performance was assessed by hemodynamic, metabolic and nuclear angiographic measurements. In the first 2--6 hours after aortic cross clamping, myocardial performance was preserved at rest and there was no evidence of ischemic metabolism. Atrial pacing at a rate of 119 beats/min caused a significant increase in cardiac index (p less than 0.01) without deterioration in hemodynamics, ejection fraction or metabolic status. At the same rate, ventricular pacing did not change the cardiac index and there was a decrease in hemodynamic function. Ejection fraction decreased from 56% to 44% (p less than 0.05) without a change in end-diastolic volume. Lactate, pyruvate and beta hydroxybutyrate extractions were changed to net production. Ventricular performance was preserved at rest immediately after aortocoronary bypass done with multidose cold potassium cardioplegia, with adequate reserve to meet the stress of atrial but not ventricular pacing. We conclude that the therapeutic implications of the type of pacing selected in the immediate postoperative period may be important.

Atrial Function↗