Biomedical subjects

K Zmudka

Publications and source records attributed to K Zmudka.

At least 37 records · Page 2Linked to original sources

PubMed1992

[Subendocardial blood flow index in relation to selected parameters of left-ventricular function in patients with aortic valve stenosis].

The aim of our studies was to estimate the relation between the reduction of the subendocardial blood flow, expressed by DPTI/TTI ratio and the grade of aortic stenosis determined by the maximal systolic aortic gradient. Additionally the influence of subendocardial blood flow reduction of left ventricular function and ECG alterations was assessed. The analyzed data were obtained during the cardiac catheterizations in a group of 30 patients (average age 32 years). The mean value of DPTI/TTI ratio was decreased (0.49 +/- 0.2) and associated with the elevated mean value of AGmax (72.2 +/- 38.1 mmHg). Negative correlation between DPTI/TTI and AGmax (r = -0.73; p less than 0.003), DPTI/TTI and LVEDP (r = -0.53; p less than 0.005) occurred. Depression of ST-T segment in EEG and episodes of anginal pain accompanied the reduction of subendocardial blood flow. We concluded that reduction in subendocardial blood flow in patients with SA-may lead subendocardial ischaemia of the left ventricular wall with subsequent of its function.

Adolescent↗

PubMed1991

[Comparative study of acute and chronic effects of nifedipine in patients with secondary pulmonary hypertension].

The effects of nifedipine in a single dose of 10 mg on the pulmonary circulation and the selected right and left ventricular function indices were studied in a group of 10 patients with secondary pulmonary hypertension (mean systolic pressure 55.2 mm Hg). In 8 patients hemodynamic studies were repeated after seven days treatment (3 x 10 mg). Acute treatment with nifedipine resulted in a reduction in mean systolic arterial pressure by 21.8%, diastolic by 12.2% and systemic resistance by 25.5%, and in an increase in cardiac index by 14.3%. After 7 days a similar pattern of changes was observed, however with less intensity: systolic pressure was reduced by 10.3% diastolic by 5.5%, and systemic resistance by 17.1%. Pulmonary artery wedge pressure did not change after a single dose, and mean pulmonary artery pressures showed a tendency toward lower levels: systolic by 8.9% and diastolic by 8.6%, whereas total pulmonary resistance decreased markedly (by 22.7%), as well as pulmonary vascular resistance. Right ventricular filling pressure was reduced. After chronic treatment we found a further slight fall in the pulmonary arterial pressure. Although per cent changes were similar to those in the arterial pressure, alterations in the mean values were not statistically significant. The total pulmonary resistance remained reduced. While analysing the changes in the pulmonary circulation and right ventricular indices it should be noted that they were less intense and less homogeneous than the left ventricular function parameters. Some of the patients showed certain similarities in the direction and intensity of changes in the hemodynamic indices of the pulmonary circulation in the acute and chronic experiment.

Adult↗

PubMed1989

Effect of prolonged inhibition of angiotensin converting enzyme by captopril on some hemodynamic parameters of pulmonary circulation in patients with secondary pulmonary hypertension.

The effect of prolonged treatment with captopril on some parameters of pulmonary circulation was studied in a group of 17 patients with secondary pulmonary hypertension due to mitral stenosis. Each patient received 25 mg of captopril four times daily for mean time of means = 12.5 +/- 2.1 days. A drop in pulmonary artery mean pressure of at least 20% was observed in 5 patients (29.4%). In 4 patients (23.5%) captopril had adverse effect on the hemodynamics of the pulmonary circulation, and in 8 patients no effect of captopril on the pulmonary hypertension was noticed. Our model of the experiment did not allow us to select before the treatment the group of patients in whom positive effects of captopril could be expected.

Adult↗

PubMed1988

Influence of a single dose of captopril on pulmonary haemodynamics and right ventricular function in mitral stenosis with pulmonary hypertension.

The response of the pulmonary circulation to captopril 75 mg has been examined in 21 patients with pulmonary hypertension secondary to mitral stenosis. The effects of captopril were measured every 15 min up to 2 h by recording pressures in the pulmonary and systemic circulations and by measuring cardiac output. Pulmonary artery systolic pressure fell significantly by 21.6% (from means = 54.6 to 42.8 mm Hg), pulmonary artery diastolic pressure by 23.3% (from 26.2 to 20.1 mm Hg), and the pulmonary artery mean pressure by 23.2% (from 36.9 to 28.3 mm Hg). Right ventricular end-diastolic pressure also fell significantly by 7% (8.1 to 7.5 mm Hg). Heart rate decreased by 6.5% (from 76.3 to 71.3 beats.min-1). Cardiac index and stroke volume index did not change. The total and vascular pulmonary resistance dropped significantly by 23.2% (from 721 to 553.7 dyn.s.cm-5) and 40% (from 287.2 to 172 dyn.s.cm-5), respectively. The right ventricular stroke work index fell by 33% (from 15.1 to 10.1 g/beat/m2). Systemic systolic pressure decreased by 10.5% (from 124.5 to 111.4 mm Hg). Thus, captopril lowered pulmonary pressures and resistances and no deterioration in right ventricular function was observed.

Blood Pressure↗

PubMed1988

Pulmonary artery pressure changes in primary pulmonary hypertension after verapamil and oxygen.

A comparison of verapamil (V) and oxygen (O) effect on pulmonary artery pressures (PAP) was carried out in 7 patients with primary pulmonary hypertension (PPH). The changes of PAP were examined, first, after O breathing, then after 10 mg of V infused into the pulmonary artery and, finally, after a second oxygen test repeated at the peak of V action. A 15% decrease in PA systolic and diastolic pressures and total pulmonary resistance after V was used as the criterion of a positive effect. The same increase in these parameters was called a negative effect and the remaining changes were considered absence of an effect. The fact of different reactivity of pulmonary vessels to V was confirmed. In 2 patients with a positive response to V, a decrease in pulmonary pressure after O was observed. In 3 patients, the effect of V on PAP was negative and, in the remaining 2, there was no effect at all. In these 5 patients with PAP and total pulmonary resistance values higher than those of the other 2, oxygen did not decrease PAP either. The comparable in magnitude response of PAP on O and V was observed in individual patients with PPH.

Adult↗

PubMed1988

Influence of verapamil and oxygen on pulmonary hypertension and right ventricular function.

The study was designed to elucidate verapamil action on the pulmonary vascular bed and right ventricular function and to compare it with the effect of oxygen in view of the fact that calcium antagonists can attenuate hypoxic pulmonary vasoconstriction. 16 patients with secondary, and 4 with primary, pulmonary hypertension and with a mean pulmonary artery systolic pressure of 68.6 +/- 28.7 mmHg were examined. After determination of initial haemodynamic values, the oxygen test (OT) was performed; later on, when the values returned to the initial ones, verapamil was infused into pulmonary artery. Measurements were carried out in the 10th min of OT and until the 30th min after verapamil. While verapamil decreased statistically significantly pulmonary artery pressures and resistances, it did not deteriorate right ventricular systolic function, although it lowered its stiffness significantly. The effect of oxygen was comparable with that of verapamil though the magnitude of changes was smaller.

Humans↗

PubMed1987