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Biomedical subjects

W Kupper

Publications and source records attributed to W Kupper.

At least 55 records · Page 3Linked to original sources
PubMed1988

Anti-ischemic effects of slow-release formulations of nifedipine, isosorbide-5-mononitrate and their combination in patients with coronary heart disease.

Eighteen patients (2 females, 16 males) with coronary artery disease and a positive bicycle exercise test were treated with 50 mg slow-release isosorbide-5-mononitrate (ISMN SR) once daily, 20 mg nifedipine SR twice daily and a combination of both drugs during 2 weeks in a randomized double-blind sequence. Fifteen patients completed the study. The efficacy of each therapy was assessed by ECG stress testing after each treatment period. Both substances were equally effective in the reduction of ischemic ST depression: 0.40 +/- 0.22 mV with placebo, 0.31 +/- 0.16 mV during nifedipine SR and 0.31 +/- 0.29 mV during ISMN SR, 0.28 +/- 0.21 mV during the combination. However, during monotherapy with either nifedipine SR or ISMN SR 6 patients did not improve. The alternative monotherapy was effective in 3 out of 6 patients. Combination treatment gave further advantage only to one third of the patients. We conclude that both nifedipine and ISMN in slow-release formulations are equally effective in the treatment of myocardial ischemia. In the individual patient, however, therapy failure may occur. These patients should be switched to another monotherapy. If both monotherapies are ineffective, combination treatment should be considered.

Coronary Disease↗
PubMed1987

[Intracoronary thrombus in patients with unstable angina pectoris].

Intracoronary thrombi were found in 20 of 52 patients (38%) who had coronary angiography because of treatment-resistant unstable angina. Unrelated to the angiographic finding, eight patients (15%) sustained a myocardial infarction, and two died during their hospital stay. Only one patient (5%) with and six patients (19%) without intracoronary thrombi were stabilized and discharged from hospital. The remaining patients either had an aortocoronary bypass (n = 31) or transluminal balloon angioplasty (n = 13). These findings underline the importance of intracoronary thrombus formation in the pathogenesis of treatment-resistant unstable angina.

Adrenergic beta-Antagonists↗
PubMed1987

Biochemical evidence of platelet activation in patients with persistent unstable angina.

Thromboxane released from activated platelets and prostacyclin of the vessel wall may act as potent antagonistic modulators of platelet aggregability and coronary vascular tone. Therefore, urinary excretion of their major metabolites, 2,3-dinor-thromboxane B2 and 2,3-dinor-6-ketoprostaglandin F1 alpha, was studied in 16 patients presenting with prolonged angina at rest. The 10 patients whose condition did not improve under vigorous antianginal treatment within 48 hours exhibited higher thromboxane metabolite excretion than did the 6 patients who responded to therapy (2,208 +/- 1,542 versus 609 +/- 312 ng/g creatinine; p less than 0.001). Elevated values were also found in four of eight patients with sustained postinfarction angina. Enhanced thromboxane metabolite excretion was frequently associated with angiographic evidence of thrombus formation. When nine patients were restudied in a stable phase after 11 +/- 5 months, thromboxane metabolite excretion was consistently normal or high normal. Excretion of prostacyclin metabolites was not depressed in any patient but correlated weakly with thromboxane (r = 0.41). Thus, enhanced thromboxane production as an index of platelet activation may identify patients with active thrombus formation who could benefit most from platelet inhibitory treatment.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

[Left ventricular diastolic function in PTCA: a Doppler echocardiographic study].

The measurement of left ventricular inflow by Doppler echocardiography provides a continuous, non-invasive assessment of parameters of diastolic function. We studied changes in left ventricular diastolic function during percutaneous transluminal coronary angioplasty (PTCA) of the left anterior descending coronary artery (LAD). In ten patients, the diastolic flow velocity profile across the mitral valve was measured by Doppler echocardiography, before and 60 s after inflation and 60 s after deflation of the balloon. The peak velocity of early diastolic filling (VE) significantly decreased during angioplasty, from 68 +/- 12 to 56 +/- 10 cm/s (p less than 0.001), while the peak velocity of late diastolic filling caused by atrial contraction (VA) showed no change. This resulted in a significant decline in the diastolic velocity ratio (VE/VA) from 1.11 +/- 0.47 to 0.92 +/- 0.35 (p less than 0.01). The total area under the diastolic flow velocity profile representing the total filling volume fell from 14.3 +/- 4.1 to 10.9 +/- 3.6 cm (p less than 0.001). The early diastolic filling fraction decreased from 68 +/- 5% to 64 +/- 7%, in favor of the filling fraction due to atrial contraction, which increased from 32 +/- 5%, to 36 +/- 7% (p less than 0.01). 60 s after deflation of the balloon, the parameters of diastolic filling returned to baseline values. We conclude from our results that diastolic dysfunction caused by angioplasty of the LAD results in a decrease in early diastolic left ventricular filling, which is completely reversible after 60 s.

Adult↗
PubMed1987

[Lung hemorrhage as a sequela of heart catheterization study].

We report a case of pulmonary hemoptysis induced by a balloon-tipped catheter. The bleeding ceased spontaneously. Factors known to be associated with pulmonary artery rupture such as pulmonary hypertension, anticoagulant therapy, and advanced age were absent in our patient. Bleeding occurred despite careful consideration of the guidelines for right heart catheterization suggested by Swan and Ganz in 1974. We conclude that hemoptysis may be a complication of balloon-tipped right heart catheterization even in the absence of risk factors for this procedure. Therefore the indication for this intervention should be considered carefully.

Cardiac Catheterization↗
PubMed1986

[Tolerance development during a 1-week course of dobutamine treatment].

UNLABELLED: Eleven patients with chronic heart failure (NYHA stage III or IV) were given dobutamine infusions over 7 days, mean dose 6.2 +/- 2.2 micrograms/kg X min. The patients were pretreated with digitalis, diuretics, and vasodilators. Haemodynamic parameters were measured prior to infusion, 30 minutes and 7 days thereafter as well as 24 hours after the end of therapy. Before and after the 7-day therapy a two-dimensional echocardiogram was taken. In four patients, the protocol had to be discontinued prematurely for technical or medical reasons. RESULTS: Arterial blood pressure, body weight, fractional shortening and end-diastolic diameter of the left ventricle were not changed significantly. Cardiac index rose acutely and returned to initial values after 7 days. Total peripheral resistance, which was initially significantly reduced, again rose after infusion over 7 days. Permanent reduction in pulmonary artery wedge pressure, even one day after the end of therapy, was observed in three patients showing a left-ventricular end-diastolic wall thickness greater than 7 mm. However, in patients whose wall thickness was less than 7 mm, there was a rise in pulmonary artery wedge pressure accompanied by a fall in cardiac index even below initial values.

Adult↗
PubMed1986

[Anti-angina action and tolerance of isosorbide-5-mononitrate or nifedipine in retard form].

Twelve patients with stable angina and reproducible depression of the ST-segment during bicycle exercise of at least 0.15 mV were assessed in a double-blind randomized cross-over study. Patients were treated either with 50 mg isosorbide-5-mononitrate (IS-5-MN) daily or 2 X 20 mg nifedipine retard daily or the combination of both drugs for 2 weeks. The sum of ST-segment depression at maximal exercise was reduced by nifedipine and IS-5-MN to the same amount, while ST-segment reduction was highest during treatment with the combination of both drugs. The best exercise duration and maximal working capacity were also recorded during combination treatment. However, patient appreciation concerning efficacy and side-effects was best with nifedipine, slightly worse with IS-5-MN, and only one patient judged the combination of both drugs as good.

Angina Pectoris↗
PubMed1986

[Pleural and mediastinal fibrosis with involvement of the external pericardium as a cause of decompensated heart failure].

Symptoms of cardiac failure were observed in a 60-year-old man 38 years after the therapy of cavernous tuberculosis of the right upper lobe with a paraffin oil plomb. The irritation by the paraffin oil induced a pleural and mediastinal fibrosis involving the pericardium. The rigid pericardium enclosed the heart and caused biventricular cardiac failure by the impaired diastolic filling. Possibilities of medical and surgical treatment are discussed.

Fibrosis↗
PubMed1983

Haemodynamic and cardiac metabolic effects of the new beta 1 agonist prenalterol in patients with cardiac failure.

Prenalterol, a beta 1 selective agonist, exerts a positive inotropic action in animal studies as well as in human volunteers and is effective when administered orally. To assess its immediate haemodynamic and myocardial metabolic effects, we studied the response to prenalterol (50 and 100 micrograms kg-1 given intravenously by cardiac catheterization) in 15 patients with congestive heart failure secondary to coronary artery disease or non-ischaemic cardiomyopathy. At peak effect, cardiac index increased from 2.6 +/- 0.5 to 3.2 +/- 0.8 l min-1 m2 (mean +/- S.D.) (P less than 0.001); peak rate of left ventricular pressure development rose from 963 +/- 242 to 1335 +/- 411 mmHg s-1 (P less than 0.001); left ventricular end-diastolic pressure fell from 25 +/- 6 to 17 +/- 7 mgHg (P less than 0.001); coronary sinus blood flow increased from 113 +/- 39 to 148 +/- 55 ml min-1 (P less than 0.01); myocardial oxygen consumption was augmented from 12.7 +/- 3.9 to 16.4 +/- 5.8 ml min-1 (P less than 0.001); and heart rate increased slightly (from 76 +/- 12 to 86 +/- 14 beats min-1; (P less than 0.05)). No significant changes occurred in left ventricular systolic pressure, stroke volume index, myocardial lactate extraction rate and myocardial arteriovenous oxygen difference, and no patients developed angina, ECG changes or ventricular arrhythmias. Infusion of prenalterol effectively improved haemodynamic function and cardiac metabolism in cardiomyopathy. Therefore this agent deserves further investigation to evaluate its possible role for the long-term therapy of patients with chronic heart failure.

Adrenergic beta-Agonists↗
PubMed1982

Effect of intravenous prenalterol on haemodynamics and myocardial lactate extraction in patients with left ventricular failure.

To assess the immediate haemodynamic and myocardial metabolic effects of the beta 1-agonist prenalterol, we studied by cardiac catheterisation the response to 50 and 100 micrograms/kg given intravenously in 16 patients with congestive heart failure secondary to coronary artery disease or non-ischaemic cardiomyopathy. At peak effect, cardiac index increased from 2.6 +/- 0.5 to 3.2 +/- 0.8 1/min/m2 (mean +/- SD) p less than 0.001); peak rate of left ventricular pressure development rose from 963 +/- 242 to 1355 +/- 411 mm Hg per second (p less than 0.001); left ventricular end-diastolic pressure fell from 27 +/- 6 to 13 +/- 7 mm Hg (p less than 0.001); coronary sinus blood flow increased from 120 +/- 39 to 147 +/- 55 ml/min (p less than 0.01); myocardial oxygen consumption was augmented from 12.9 +/- 3.9 to 15.7 +/- 5.8 ml/min (p less than 0.001); and heart rate increased slightly (76 +/- 12 to 86 +/- 14 beats per minute, p less than 0.05). No significant changes occurred in left ventricular systolic pressure, stroke volume index, myocardial lactate extraction rate, myocardial arteriovenous oxygen difference and no patient developed angina, ECG-changes or ventricular arrhythmias. Infusion of prenalterol effectively improved the haemodynamic function and cardiac metabolism in congestive cardiomyopathy.

Adrenergic beta-Agonists↗
PubMed1982

The effect of pindolol on myocardial blood flow, metabolism and function during rest and pacing in patients with coronary heart disease.

1 The study was designed to elucidate further the mechanism by which beta-adrenoceptor antagonism with pindolol relieves the symptoms of angina pectoris in patients with coronary heart disease. 2 Pindolol administration was associated with an elevated threshold for angina pectoris and improved myocardial lactate metabolism during supraventricular pacing. 3 This beneficial effect of pindolol was independent of changes in myocardial blood flow and was not mediated by haemodynamic effects. 4 The results suggest that in angina pectoris, in addition to the recognized beneficial effects of beta-adrenoceptor blockade, the actions of pindolol also result from, as yet, poorly described phenomena such as redistribution of myocardial blood flow or metabolic effects.

Adult↗