Biomedical subjects
Publications and source records attributed to V A Gebhardt.
A case of adult onset angina in a patient with previously undiagnosed childhood Kawasaki disease is presented. Evidence to support the diagnosis--such as clinical presentation and pertinent positive and negative laboratory data to rule out other conditions--is provided. The patient was successfully treated with coronary artery bypass surgery.
To determine if intrinsic sympathomimetic activity (ISA) is associated with a hemodynamic advantage over non-ISA beta blockade, 17 patients with ischemic heart disease underwent resting echocardiography and symptom-limited stress radionuclide angiography on three occasions: control, pindolol (with ISA), 10 mg twice a day, and propranolol, 40 mg four times a day, in a nonrandomized design. In six patients with normal resting ejection fraction (EF) (mean = 57 +/- 4%), neither drug was associated with a significant hemodynamic improvement over control. In 11 patients with reduced resting EF (mean = 37 +/- 9%), pindolol was associated with a higher EF and peak velocity of circumferential fiber shortening at rest compared with propranolol but not control. On maximal exertion, pindolol was associated with a higher EF than that during control but was similar to propranolol. These observed beneficial effects on pindolol appear primarily to be related to the partial beta agonist activity which this agent possesses.
As an agent potentially capable of inducing ischemia in patients with coronary artery disease, dopamine administered intravenously was evaluated as a pharmacologic stress agent by supine radionuclide angiography, and the results were compared with ergometer exercise. In a preliminary group of 11 subjects (4 normal subjects and 7 patients with coronary disease), dopamine alone was administered in increments of 2.5 micrograms/kg per min to a maximum of 15 micrograms/kg per min. There were significant differences between exercise and dopamine in maximal stress heart rates, 129.3 +/- 30.0 versus 88.0 +/- 35.8 beats/min (p less than 0.05) in normal subjects and 118.9 +/- 21.1 versus 87.6 +/- 22.6 beats/min (p less than 0.05) in patients with coronary disease, as well as in maximal stress rate-pressure products, 213.3 +/- 51.4 versus 155.0 +/- 52.5 mm Hg/min X 10(2) (p less than 0.02) in normal subjects and 216.0 +/- 45.6 versus 161.0 +/- 48.6 mm Hg/min X 10(2) (p less than 0.003) in patients with coronary disease. As a result, in these patients the ejection fraction response was significantly different: -3.3 +/- 4.5% with exercise versus + 6.3 +/- 4.6% with dopamine (p less than 0.05). In a second group of 41 subjects (9 normal subjects and 32 patients with coronary disease), atropine (0.6 mg) was administered intravenously before and after every second dopamine dose increment. This produced statistically similar maximal stress heart rates as compared with exercise in all subjects, rate-pressure products in normal subjects and slightly higher values with dopamine in patients with coronary disease: 200.3 +/- 47.2 versus 183.1 +/- 43.0 (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
The left ventricular (LV) volume response to supine exercise (EX) was studied in 15 normal volunteers (mean age 44, asymptomatic, with normal resting ECG and treadmill stress test) and 28 coronary artery disease patients (CAD, documented by cardiac catheterization) with no previous myocardial infarction. Each individual underwent stress gated equilibrium radionuclide angiography (RNA) and was on no medication. A nongeometric count based LV volume programme developed in our laboratory (correlation to biplane cineangiography R = .98), was used to calculate end diastolic volume index (EDI), end systolic volume index (ESI), stroke volume index (SVI), cardiac index (CI), and ejection fraction (EF). In normal individuals, end diastolic volume did not change from rest to exercise, while end systolic volume decreased by an average of 16%. In the patients with coronary artery disease, however, both end diastolic volume and end systolic volume increased (14% and 15% respectively). Furthermore, our preliminary data suggest that the extent of the changes may be dependent upon the extent of the underlying CAD. While all the CAD patients had an increase in their end diastolic volumes, there was no change in the end systolic volume in those with single vessel disease, an 11% increase in patients with double vessel disease and a 19% in patients with triple vessel disease.