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Biomedical subjects

W Kupper

Publications and source records attributed to W Kupper.

At least 37 records · Page 2Linked to original sources
PubMed1991

[Loading-induced ST-interval elevations in the case of normal coronary arteries. The angiographic demonstration of loading-induced coronary artery spasm].

In a 60-year-old man with exercise-dependent anginal symptoms, reversible ST segment elevations of maximally 0.8 mV occurred in the anterior chest leads during ergometric exercise at 75 W. Angiography excluded coronary artery stenoses. To demonstrate whether he had exercise-dependent vasospastic angina, angiography was performed during bicycle ergometry. At 75 W the typical symptoms recurred, accompanied by ST elevations in the ECG. At the same time, spasm in the region of the anterior interventricular branch was demonstrated angiographically; it disappeared at once after intracoronary injection of 200 micrograms nitroglycerin. The patient subsequently remained free of symptoms while taking isosorbide dinitrate (120 mg daily) and nifedipine (80 mg daily).

Angina Pectoris↗
PubMed1991

Comparison of hormonal and haemodynamic changes after long-term oral therapy with pimobendan or enalapril--a double-blind randomized study.

Twenty-four patients (one female, 23 male) with mild to moderate heart failure were randomly and double-blindly assigned to an oral treatment with 5 mg enalapril twice daily or 5 mg pimobendan (UDCG 115) twice daily. After the first tablet intake, blood pressure and heart rate were measured for 6 h. Therapy continued over 6 months. Systolic arterial blood pressure dropped from 126 +/- 20 mmHg to 111 +/- 14 mmHg (P less than 0.05) after the first enalapril tablet and from 123 +/- 16 mmHg to 112 +/- 13 mmHg (P less than 0.05) after the first pimobendan tablet. After 6 months, no important changes in blood pressure were observed in the pimobendan group and only a minor decrease in the enalapril group. There was no significant change in heart rate either after the first dose or after long-term therapy with either medication. After 6 months, cardiac index increased from 2.73 +/- 0.75 l.min-1.m-2 to 3.38 +/- 0.69 l.min-1.m-2 (P less than 0.01) after pimobendam, but did not change after enalapril (2.95 +/- 0.75 l.min-1.m-2 to 2.96 +/- 0.89 l.min-1.m-2, NS). Pulmonary capillary wedge pressure decreased during pimobendan long-term therapy from 16 +/- 8 mmHg to 14 +/- 8 mmHg (NS) and during enalapril from 21 +/- 7 to 14 +/- 7 mmHg (P less than 0.01). Exercise capacity increased in the pimobendan group from 17.2 +/- 5.4 kJ to 23.0 +/- 9.6 kJ (P less than 0.05), and in the enalapril group from 20.4 +/- 11.9 kJ to 24.8 +/- 18.5 kJ (NS) during long-term therapy over 6 months. Plasma renin activity increased from 0.96 to 3.6 ng.ml-1.h-1 (P less than 0.05) during enalapril long-term therapy, but remained unchanged (1.38 vs. 1.32 ng.ml-1.h-1, NS) during pimobendan. The new inotrope, pimobendan, exerted favourable long-term effects without haemodynamic or humoral signs of tolerance development.

Aged↗
PubMed1990

Recanalization of chronic, totally occluded coronary arteries by new angioplasty systems.

The benefit and safety of new angioplasty equipment as compared with the conventional guidewire approach was evaluated in 154 consecutive patients. with chronic, totally occluded coronary arteries. The protocol followed a stepwise design: first, conventional guidewires and low-profile balloons were used, followed by "balloon-on-the-wire" systems (Probe, Ace) or by a shaft-enforced, tip-deflecting catheter (Omniflex). In 97 patients with occlusions of 2 to 12 weeks' duration, recanalization was achieved in 51 patients (53%) with the conventional approach and in 29 patients with the new devices (balloon-on-the-wire [n = 5], Omniflex [n = 24]), thereby raising the success rate to 82%. In 57 occlusions of greater than 12 weeks' duration, the recanalization attempt was successful in 58%, mediated in 16 patients (28%) by the Omniflex catheter and in 5 patients by balloon-on-the-wire systems. There were no life-threatening complications and only 1 (0.6%) emergency bypass operation was necessary. New angioplasty devices are therefore of considerable value in the attempt to improve the results of coronary angioplasty in chronic total occlusions.

Angioplasty, Balloon, Coronary↗
PubMed1990

Acute haemodynamic and neurohumoral effects of intravenous nisoldipine in patients with severe congestive heart failure.

Twenty patients (5 females, 15 males) with severe heart failure (NYHA IV), due to coronary artery disease in 14, and congestive cardiomyopathy in 6, received an intravenous bolus of the calcium blocker nisoldipine 0.2 mg followed by a continuous infusion of 0.2 micrograms.kg-1.min-1. Haemodynamic measurements were performed at baseline and after 30 min. The mean arterial pressure fell from 91 to 73 mmHg, pulmonary capillary wedge pressure from 31 to 26 mm Hg and systemic vascular resistance from 1695 to 1040 dyn.s.cm-5. The cardiac index (2.2 to 2.71.min-1.m-2, and stroke volume index (25 to 33 ml.m-2) were markedly increased. There was no reflex tachycardia as the heart rate dropped from 92 to 85 beats.min-1. Plasma renin activity and norepinephrine concentration did not change significantly. The findings indicate that nisoldipine acts as a strong vasodilator and that it has a beneficial acute haemodynamic effect in patients with severe left heart failure irrespective of its aetiology.

Adult↗
PubMed1990

Exercise capacity, arrhythmias, humoral and chemical parameters during long-term therapy with xamoterol.

In order to assess potential harmful effects of the partial beta-1 agonist xamoterol during long-term therapy, we randomly assigned 30 patients with coronary arterial disease and heart failure in classes II and III of the classification of the New York Heart Association to 200 mg of xamoterol twice daily or placebo during a treatment period of 3 months. A supine bicycle exercise test was performed at baseline and after three months in order to assess changes of exercise capacity. Blood samples for determination of creatinine, electrolytes, renin and norepinephrine were withdrawn simultaneously. Twenty-four hour ambulatory Holter electrocardiograms were performed before study, at the end of the study and 72 hours after withdrawal of study medication. On xamoterol, exercise capacity increased from 21.9 +/- 9.7 to 27.8 +/- 14.8 kilojoule (P = 0.032) compared to baseline levels. Exercise duration increased from 340 +/- 115 to 400 +/- 144 seconds (P = 0.043). Heart rate decreased by 10% (P = 0.05) at the 50 watt level and by 10% (P = 0.024) on maximum exercise compared to the baseline values. The rate pressure product was unchanged at rest and dropped by 11% (P = 0.038) on maximum exercise. In contrast, on placebo no significant changes occurred. During xamoterol therapy no changes of blood pressure, electrolytes, renal function and the time-intervals of electrocardiogram were observed. Xamoterol did not enhance arrhythmias during 24-hour ambulatory Holter monitoring. No serious side effects were observed. Xamoterol would appear to be a suitable and safe drug in the therapy of mild to moderate heart failure.

Adrenergic beta-Agonists↗
PubMed1990

Sympathetic modulation in practice: the German clinical experience.

Xamoterol is a beta 1-selective adrenoceptor partial agonist. The acute effects of xamoterol were studied in 30 patients with ischaemic heart failure. Haemodynamic data were assessed at baseline, at rest and after supine bicycle exercise (50 W for 3 min), and repeated 15 min after xamoterol (0.2 mg kg-1) given by infusion over 5 min. At rest, xamoterol increased heart rate, mean blood pressure and cardiac index, and reduced pulmonary wedge pressure. On exercise, heart rate fell while cardiac index was maintained and pulmonary wedge pressure fell slightly but significantly. There was a tendency for plasma renin activity and plasma noradrenaline to fall both at rest and on exercise. The clinical relevance of these haemodynamic and neurohumoral changes were examined in conjunction with the German-Austrian Xamoterol Group's study, screening 443 patients with mild to moderate heart failure and giving xamoterol or placebo for 3 months as part of a randomized, double-blind study. The German experience was then placed in context of the pooled world-wide database of efficacy and safety in three other large (greater than 100 patients) studies with xamoterol in mild to moderate heart failure. In brief, this overview demonstrated a 2.98 +/- 0.68 kJ improvement in work done over placebo, equivalent to 14% (xamoterol) and 6% (placebo) improvements over baseline (P less than 0.0001). Xamoterol is thus a promising new approach to the treatment of mild to moderate heart failure.

Adrenergic beta-Agonists↗
PubMed1990

Lack of tolerance development after long-term administration of the partial beta-adrenoceptor agonist xamoterol.

Xamoterol is a selective partial beta-adrenoceptor agonist. In a double-blind randomized placebo-controlled study, 30 patients (1 female, 29 male) with mild to moderate heart failure were treated with 200 mg of xamoterol twice daily or placebo during 3 months. At baseline and 72 h after the last tablet intake, the hemodynamic and humoral effects of a single intravenous dose of xamoterol (0.2 mg/kg) were assessed by right heart catheterization. At baseline, intravenous xamoterol raised resting heart rate by 3% (NS) in the placebo and by 6% (NS) in the xamoterol group. On exercise, heart rate was reduced by 10% (p = 0.015) and 7% (p = 0.016), respectively. Pulmonary capillary wedge pressure (PCWP) dropped in both groups: at rest by 4 mm Hg (p = 0.0004) in the placebo group and by 6 mm Hg (p = 0.0002) in the xamoterol group; on exercise by 1 mm Hg (NS) in the placebo and by 6 mm Hg (p = 0.0001) in the xamoterol group. Similar changes of all variables were obtained after long-term therapy in both groups. Mean arterial blood pressure, cardiac index and systemic vascular resistance did not change importantly. Norepinephrine levels did not change, but plasma renin activity decreased at baseline as well as after long-term therapy in both groups by similar amounts. Thus, no signs of tolerance development were observed after an oral treatment with 200 mg of xamoterol twice daily during 3 months. However, xamoterol as a partial agonist exerted only weak changes of cardiac index and PCWP compared to full beta-adrenoceptor agonists. The drug was well tolerated, and serious side effects were absent.

Administration, Oral↗
PubMed1990

[Hemodynamic and humoral changes following intravenous administration of xamoterol in patients with heart failure and coronary heart disease].

Xamoterol is a beta-1 selective partial adrenoceptor agonist. Thirty patients (one female, 29 male, mean age 56 +/- 8 years) with coronary artery disease and mild to moderate heart failure, according to NYHA classes II and III, were studied before and 15 min after intravenous administration of 0.2 mg/kg xamoterol, at rest and during standard, supine bicycle exercise. At rest, the pulmonary capillary wedge pressure fell by 39% (p = 0.0001) and the cardiac index increased by 7% (p = 0.0084); heart rate increased only slightly. With exercise, cardiac index did not change and the pulmonary capillary wedge pressure decreased by 11% (p = 0.0003). In addition, the heart rate dropped from 115 to 105 bt/min (p = 0.0001) which resulted in a decrease of the rate pressure product by 9% (p = 0.0041). Arterial blood pressure remained unchanged. Norepinephrine plasma levels did not change at rest or during exercise, whereas at rest plasma renin activity dropped by 18% (p less than 0.05) and by 20% (p less than 0.05) during exercise. No untoward side effects were observed and the drug was well tolerated. In conclusion, xamoterol, given acutely to patients with heart failure NYHA classes II or III exerted advantageous hemodynamic effects at rest and during exercise.

Adrenergic beta-Agonists↗
PubMed1989

[Effects of low-dose acetylsalicylic acid on thrombocytes in health subjects and in patients with coronary heart disease].

The effects on platelet function of a four-week administration of aspirin at a low dosage (100 mg daily) were compared in two groups, 14 healthy young volunteers and 14 patients with coronary heart disease. In both groups there occurred a clear inhibition of platelet aggregation with collagen (1 and 5 micrograms/l) and arachidonic acid (1 mmol/l) during the aspirin period. The inhibitory effect reached its maximum after three days, remaining at maximum for the remainder of the four weeks. Platelet functions returned to normal within eight days of discontinuing aspirin. The inhibitory effects went together with a definite in-vitro decrease in thromboxane synthesis. In both groups there was no change in aggregation velocity with adenosine diphosphate (ADP) as aggregation-inducing substance, while the frequency of irreversible aggregation decreased with submaximal concentrations of ADP (0.5 and 1.0 mumol/l). The results indicate that low-dose aspirin causes a definite inhibition of platelet function, in a similar manner, in both healthy subjects and patients with coronary heart disease.

Adenosine Diphosphate↗
PubMed1989

Effects of aspirin and prostaglandin E1 on in vitro thrombolysis with urokinase. Evidence for a possible role of inhibiting platelet activity in thrombolysis.

The formation of thrombi in vivo includes the activation of both platelets and the coagulation cascade. Conventional thrombolytic therapy is primarily directed toward the dissolution of fibrin. To evaluate the possibility that platelet activity impairs the lysis of thrombi, we studied the effects of aspirin and platelet-deaggregating prostaglandin E1 on thrombolysis with urokinase. Combined platelet and fibrin thrombi were produced in vitro by adding CaCl2 and collagen (1 microgram/ml) to citrated platelet-rich plasma (250,000 platelets per microliters). Urokinase (500-10,000 units/ml) caused a dose-dependent weight loss of the thrombi that was maximal at 2,000 units/ml. The addition of aspirin (10-200 micrograms/ml) to platelet-rich plasma before thrombus formation markedly enhanced thrombolysis with urokinase. This effect was most pronounced at 20 micrograms/ml aspirin. However, when aspirin was added after completion of thrombus formation, no significant effect on thrombolysis was noted. Prostaglandin E1 (1-100 mumol/l) improved the lysis with urokinase of the combined platelet and fibrin thrombi. This effect was maximal at 20 mumol/l prostaglandin E1. When pure fibrin thrombi were produced in platelet-free plasma, prostaglandin E1 was without effect on lysis. Thus, in vitro lysis with urokinase of combined platelet and fibrin thrombi was enhanced by the addition of platelet-deaggregating prostaglandin E1 and by pretreatment with aspirin.

Adult↗
PubMed1989

[Lipid-lowering and anti-aggregating effect of low-dose therapy with fish oil].

Fifteen healthy volunteers were treated for 30 days with 5 g daily fish oil in capsule form (MaxEPA). After that time, serum triglycerides had decreased by a mean of 26% (p less than 0.05). This relative decrease in triglycerides was the larger the higher were the baseline levels before the start of therapy (p less than 0.01). Total cholesterol remained unchanged with fish oil. HDL-cholesterol showed a small mean increase by 12% (p less than 0.10). The rate of platelet aggregation after induction with collagen 1 microgram/ml was reduced after 30 days of therapy (p less than 0.05), while no effect on platelets was observed with collagen 5 micrograms/ml or ADP (0.5, 1 and 10 mumol/l) as aggregating agents. In vitro thromboxane synthesis after stimulation with collagen (1 microgram/ml) or arachidonic acid (1 mmol/l) was inhibited cumulatively by fish oil and, after 30 days, reached 56% (p less than 0.02) and 44% (p less than 0.05) of the initial values, respectively. Both the basal and prostaglandin E1 stimulated concentrations of c-AMP in platelet rich plasma remained uninfluenced. Thus, the ingestion of a low dose of fish oil by young and healthy subjects led to significant changes in serum triglycerides and platelet function.

Administration, Oral↗
PubMed1989

[Sudden heart death in a long distance runner during a marathon].

Sudden cardiac death during running is mainly caused by an acute myocardial infarction and coronary artery disease. Other diseases like myocarditis are rarely documented. Before a marathon a 37-year-old, well-trained long-distance runner had normal findings at a sports medical consultation. During the race he collapsed after 41 km and died despite of immediate resuscitation attempts. At autopsy a 50% stenosis of the descending branch of the left coronary artery, and histologically an active myocarditis were observed (Dallas-classification). The endured extreme stress of the marathon probably resulted in arrhythmias and in sudden cardiac death.

Adult↗
PubMed1988

[Thrombocyte function in unstable angina pectoris].

In a prospective study, platelet aggregation in platelet-rich plasma after ADP stimulation (0.5, 1.0 and 10 mumol/l) and collagen (1 and 5 micrograms/ml) was measured in 36 patients with coronary heart disease, 18 with angina at rest during the eight hours preceding the time of blood sampling, and 18 patients with stable, exercise-dependent angina, matched for age and sex. In addition, c-AMP was determined, before and (as a measure of platelet adenylate cyclase activity) after stimulation of this enzyme by prostaglandin E1 (10 mumol/l for 30 sec). There were no differences between all the tested ADP and collagen concentrations with regard to platelet aggregation. c-AMP levels were also similar. Thus, in patients with unstable angina there was no evidence for generalized hyperaggregation of platelets in comparison with control subjects who had stable exercise-dependent angina.

Adenosine Diphosphate↗
PubMed1988

Quantitation of coronary venous adenosine in patients: limitations evaluated by radioimmunoassay.

Experimental studies have shown that adenosine is rapidly released in response to myocardial ischaemia. To evaluate whether coronary venous adenosine release is a metabolic characteristic of myocardial ischaemia in patients, adenosine concentrations were measured by a highly sensitive and specific radioimmunoassay. In three patients with normal coronary arteries and in seven with obstructive coronary artery disease coronary venous adenosine content was measured at rest and during atrial pacing. When whole blood or plasma were extracted immediately with perchloric acid the adenosine content was found to be lower than that previously reported. Recovery studies showed that the importance of time and temperature at low adenosine concentrations had been underestimated in preceding studies. In patients with coronary artery disease coronary venous adenosine concentration increased from 106.3(48.8) nmol.litre-1 to 114.9(57.0) nmol.litre-1 (NS) during pacing and was 130.4(63.3) nmol.litre-1 (NS) 2 min after pacing. Even in the presence of lactate production enhanced adenosine release was not consistently evidenced. Furthermore, venous adenosine content did not increase in five patients undergoing coronary artery occlusion during angioplasty of the left anterior descending coronary artery. The extremely short half life of coronary venous adenosine appears to preclude its use as an index of myocardial ischaemia in patients.

Adenosine↗