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Biomedical subjects

M Van Kuyk

Publications and source records attributed to M Van Kuyk.

5 recordsLinked to original sources
PubMed1986

Predictors of early death after acute myocardial infarction: two months follow-up.

Clinical variables and the results of non-invasive tests (exercise test, echocardiogram, gated equilibrium radionuclide ventriculography and 24 h ECG) were recorded in a series of 202 patients who left the hospital alive after an acute myocardial infarction. The short term (two months) predictive value of all these data was prospectively assessed by uni- and multi-variate analysis. The best correlation with early death was observed with the variables related to the extent of infarction and left ventricular dysfunction, namely: early clinical signs of heart failure, high peak CK-MB level, complete bundle branch block, increased cardiothoracic ratio on chest X-Ray, number of Mets reached during the stress test, echocardiographic dyskinesia index, and decreased left ventricular ejection fraction as measured by radionuclide ventriculography. Using multi-variate stepwise discriminant analysis, the following independent prognostic factors appeared by order of entry: early clinical signs of heart failure, peak CK-MB level and cardiothoracic ratio on chest X-Ray. These results highlight the short-term predictive value of the data related to left ventricular dysfunction and especially of simple clinical data for patients surviving an acute myocardial infarction.

Acute Disease↗
PubMed1984

Hemodynamic effects of vasopressin, alone and in combination with nitroprusside, in patients with liver cirrhosis and portal hypertension.

We have investigated the effects on systemic, pulmonary, hepatic, and renal hemodynamics, and on blood gases of vasopressin, 0.4 U/min I.V. first alone, then in combination with nitroprusside 1-5 micrograms/kg/min I.V., in 12 patients with liver cirrhosis and portal hypertension. Portal pressures were estimated by the gradient between occluded and free hepatic vein pressures, hepatic blood flow was measured by indocyanine green infusion, renal blood flow by an isotopic method, and cardiac output by thermodilution. Vasopressin alone reduced cardiac output (-23%) and O2 delivery to the tissues (-25%), increased mean arterial pressure (+20%) and filling pressures of the heart (+136%), reduced portal pressures (-36%) (from 19 +/- 1 to 12 +/- 1 mmHg, mean +/- SEM), hepatic blood flow (-35%) (1.33 +/- 0.2 to 0.87 +/- 0.1 l/min), and renal blood flow (-16%) (0.77 +/- 0.07 to 0.65 +/- 0.05 l/min). Adding nitroprusside restored cardiac output, preload and afterload, and renal blood flow to pretreatment values. Oxygen delivery remained depressed (-12%) because of a negative effect on pulmonary gas exchange (physiologic shunt increased from 16 +/- 2 to 28 +/- 4%). Portal pressures remained reduced by 31% and hepatic blood flow by 25%. These results suggest that small doses of I.V. nitroprusside minimize the deleterious hemodynamic effects of vasopressin while maintaining the therapeutic benefit of portal pressure reduction in cirrhotic patients.

Adult↗