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Biomedical subjects

W D Bussmann

Publications and source records attributed to W D Bussmann.

At least 109 records · Page 6Linked to original sources
PubMed1983

[Therapy of cardiogenic shock with dobutamine and nitroglycerin].

Pulmonary artery, right atrial and systemic arterial pressures, cardiac output and total peripheral resistance were measured in 12 patients with the clinical picture of cardiogenic shock. The patients were then given dobutamine alone or in combination with various high doses of nitroglycerin. In seven patients with severe valvar malfunction, cardiac output rose significantly after dobutamine from 4.0 to 4.5 l/min . 1.73 m2, without changes in systemic arterial pressure and left and right-ventricular filling pressures. Additional intravenous infusion of nitroglycerin (1.5-3.0 mg/h) raised cardiac output to 4.7 l/min (P less than 0.01), reduced filling pressure, and stabilized systemic arterial pressure. Further increase in nitroglycerin dose (3.0-6.0 mg/h) reduced the filling pressures considerably, but cardiac output and systemic arterial pressure fell. In the five patients with severe myocardial damage, cardiac output rose after dobutamine (P less than 0.05), but could not be further enhanced by nitroglycerin. When the dose was increased, left and right-ventricular filling pressures fell clearly, but at the same time there was also a fall in systemic arterial pressure. The optimal left-ventricular filling pressure is unexpectedly high (28 mm Hg) in cardiogenic shock. It is concluded that the treatment of cardiogenic shock with dobutamine (7 micrograms/kg . min) in combination with low nitroglycerin dose (1.5-3.0 mg/h) causes definite improvement in haemodynamics, symptoms and prognosis.

Adult↗
PubMed1983

[Reduction in CK- and CKMB-measured infarct size by verapamil].

In a prospective, randomized and controlled study, 29 patients received i.v. verapamil, 5-10 mg/h for two days, at a mean of eight hours after onset of myocardial infarction. In a control group, 25 patients received no specific treatment. In all patients, left ventricular end-diastolic pressure was initially less than 15 mm Hg. The two groups were comparable as to age, infarct site and haemodynamics (measured via Swan-Ganz catheter). CK and CKMB peaks were significantly lower in the verapamil than the control group (CK 547 vs 703 U/1, P less than 0.05; CKMB 51 vs 68 U/1, P less than 0.025), as well as infarct weight (CK = 48 vs 65 g-equivalent; P less than 0.03; CKMB = 31 vs 49 g-equivalent; P less than 0.005). Arterial blood pressure was lower by 10 mm Hg than in the control group. Peripheral resistance and filling pressure remained unchanged. In patients without left ventricular failure verapamil reduces the infarct size by about 30%. The most prominent haemodynamic change is a reduction in blood pressure.

Blood Pressure↗
PubMed1983

[Possible evidence for a reduction of early and late mortality during nitroglycerin therapy in acute myocardial infarction].

60 patients with acute myocardial infarction were randomized in two groups to examine the influence of intravenous nitroglycerin on early and late prognosis. 31 patients received intravenous nitroglycerin in the first 2-3 days. One cardiac death following an emergency bypass operation occurred in the early phase during the first 14 days (3%). 5 of the 29 patients in the control group died during the same period (17%), however, cardiac cause was not entirely clear in one case.--In the late phase on the average 1 1/2 years later 3 deaths were registered in 27 treated patients (11%) compared to 7 of 23 patients in the control group (30%). For this difference in mortality reduced infarct size as well as possibly the higher dose of nitrates (38 versus 21 mg/die) were responsible. Sudden deaths and the incidence of reinfarction with and without death during the early and late observation period were significantly lower in the nitroglycerin group (11% - 3 patients) compared to the control group (39% - 11 patients, p less than 0.01).--This pilot result seems to indicate a beneficial influence of nitroglycerin therapy in the acute phase for prognosis for the short term and long term follow up. The result should simulate trials in larger patient groups.

Aged↗
PubMed1983

[Does long term treatment with high dose nitrates affect prognosis in coronary heart disease?].

The daily dose of nitrates was determined in 293 patients who had undergone coronary angiography seven years earlier. A questionnaire was filled out by those still living; medical records and information provided by family physicians were used for those who had died during the intervening period. The dose could be ascertained in a total of 168 patients. Patients were divided into two groups: in group I were those with a daily isosorbide dinitrate dose of less than 40 mg (n = 46), in group II those with a dose greater than 40 mg (n = 72). 56 patients had died. Two-thirds of them had been on the low-dose regimen, whereas only one-third were in the high-dose group. The extent of ventricular impairment was comparable in both groups. Seven-year mortality in group I was 39% with a mean daily nitrate dose of 14 mg. In group II, however, only 26% died with a mean daily dose of 55 mg. The difference can already be seen during the first year. Age, extent of coronary sclerosis, degree of ventricular damage, and cardiac size were identical in both groups. Thus mortality rate in group II was reduced by 30-40%. A causal relation to the height of the nitrate dose should be considered.

Aged↗
PubMed1983

Nitroglycerin therapy in acute myocardial infarction--an overview.

Nitroglycerin and nitrates have long been contraindicated in the treatment of acute myocardial infarction. Beneficial effects, however, are reported in patients with left ventricular failure. In this report the available data from the literature are reviewed with respect to the influence of the drug on myocardial ischemia, infarct size and necrosis as well as on ventricular arrhythmias and prognosis. All authors have confirmed a beneficial influence of nitroglycerin on myocardial ischemia and QRS signs of necrosis. Some authors have demonstrated a reduction in CK and CKMB activity. Ischemia-related ventricular dysrhythmias were also effectively reduced. Some promising data are available on prognosis.

Arrhythmias, Cardiac↗
PubMed1983

Sustained antianginal efficacy of oral high-dose isosorbide dinitrate in patients with coronary heart disease.

Ten patients with angiographically proven coronary heart disease, stable exercise-induced angina pectoris, and reproducible ST-segment depression were treated with ISDN tablets in daily doses of 240 mg (6 X 40 mg) and placebo for 28 days each on the basis of a randomized double-blind protocol with intraindividual crossover. On the 1st, 7th and 28th days of each treatment cycle an exercise stress test was performed 1 h after the second dose of the day. ISDN treatment resulted in a sustained reduction of anginal attacks, with a weekly rate ranging from 1.4 to 3.9 (mean values) as compared to 10.5 to 11.7 attacks during placebo treatment (2 p less than 0.001). Exercise-induced ST-segment depression during ISDN-therapy (constant work-load) was found to be significantly improved as compared to placebo: day 1, ISDN: 5.3 +/- 1.5 mm vs. placebo: 12.1 +/- 2.2 mm (2p less than 0.01); day 7, ISDN: 7.6 +/- 2.0 mm vs. placebo: 10.8 +/- 2.1 mm (2p less than 0.05); day 28, ISDN: 5.7 +/- 1.2 mm vs. placebo: 11.2 +/- 2.1 mm (2p less than 0.01). Heart rate in the upright position (tilting table) was significantly different between ISDN and placebo on day 7: ISDN 92 +/- 3 bpm vs. placebo 85 +/- 4 bpm (2p less than 0.001), but not on day . 28.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1983

[Pharmacokinetics and Antiarrhythmic effects of Prajmalium Bitartrate].

8 patients with ventricular premature contractions were treated with prajmalium bitartrate (Neo-Gilurytmal) 20 mg q.i.d. The electrocardiograms were continuously monitored by a computerized arrhythmia monitoring system. For definition of the drug's pharmacokinetic properties plasma concentrations were determined. 7 patients showed a marked arrhythmia reduction. Mean ventricular premature contraction frequency was significantly reduced 6 h after onset of treatment, maximum arrhythmia suppression to 34% of control was observed after 24 h of treatment. The correlation of antiarrhythmic response and plasma concentrations was good. Mean plasma concentrations during steady state conditions were 218 ng/ml. Plasma half-life was determined 7.3 h. The lower limit of therapeutic plasma concentrations was between 43 and 145 ng/ml. A mean total clearance of 344 ml/min indicates a low hepatic extraction of prajmalium bitartrate. Moreover, the distribution volume of 204 l suggests a high tissue affinity of the drug.

Adult↗
PubMed1982

[Dose-effect relationship of isosorbide dinitrate in the treatment of angina pectoris (author's transl)].

Fifteen males with angiographic evidence of coronary heart disease and stable, exercise-induced angina pectoris were given placebo or isosorbide dinitrate (ISDN) in a dialy dose of 30 mg, 120 mg, 240 mg and 480 mg in a randomized single-blind trial. The daily doses were given as a single oral dose of 5 mg, 20 mg, 40 mg and 80 mg tablets. Each dose and placebo was given for seven days. On the seventh day an exercise ECG of standardized level and duration of exercise was recorded. The ischaemia response in the ECG revealed a dose-dependent reduction by 28% (5 mg ISDN), 43% (20 mg), 60% (40 mg) and 73% (80 mg). The number of anginal attacks similarly fell parallel to dose. Plasma level of ISDN and the mononitrates, measured one and four hours after drug intake, rose almost linearly in relation to dose. Oral ISDN thus has a dose-dependent effect on the frequency of angina and ischaemia parameters during ergometric exercise. The protracted anti-anginal effect of ISDN is largely due to its metabolites. At high doses there is presumably an added effect of the high blood level of the basic substance.U

Adult↗
PubMed1982

[Effect of molsidomine on hemodynamics and myocardial ischemia in patients with acute myocardial infarction (author's transl)].

The effect of molsidomine on hemodynamics and myocardial ischemia were studied in 48 patients with acute myocardial infarction. Between 8 and 12 mg of orally and intravenously administered molsidomine led to a significant reduction in left ventricular filling pressure. In response to 2 x 4 mg p.o., diastolic pulmonary arterial pressure fell from 12.1 to 8.8 mm Hg in patients with filling pressure below 20 mm Hg. Patients with left heart failure and left ventricular filling pressure above 20 mm Hg (Group 2) displayed a decline in filling pressure from 23.8 to 17.4 mm Hg following 12 mg i.v. In addition, right atrial pressure dropped significantly across the entire range of dosages. Although patients without left ventricular failure (Group I) showed a decline in cardiac output (5.7 to 4.7 l/min), this parameter remained unchanged in Group 2. Heart rate in Group 2 fell from 85 to 81 per min. Arterial blood pressure was reduced by a mean of only 10 mm Hg at high dosages and remained unchanged at lower dosages. No change was observed in peripheral resistance. The maximum effect was seen 30 min after oral administration. Three hours later, the effect was reduced by half. Only minimal activity could be observed after 8 h. The incidence of side effects was low, with transient headaches occurring in 8% of the patients. An intraindividual comparison with 1.6 mg of sublingually administered nitroglycerin demonstrated no significant difference in hemodynamic effectiveness (n = 11). Molsidomine, not unlike nitroglycerin, exerts a favorable effect on hemodynamics and myocardial ischemia. It acts primarily to reduce preload. The additional moderate effect on afterload with a slight decline in arterial pressure at high dosages may also be considered advantageous.

Administration, Oral↗