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Biomedical subjects

M Kaltenbach

Publications and source records attributed to M Kaltenbach.

At least 397 records · Page 22Linked to original sources
PubMed1976

[Treatment of hypertrophic obstructive cardiomyopathy with verapamil, a calcium antagonist (author's transl)].

Cardiac catheterisation with pressure measurements, left-ventricular cine-angiography and selective coronary angiography confirmed the diagnosis of hypertrophic obstructive cardiomyopathy in 20 patients. After a mean observation period of 20 months during which most of them were treated with beta-blockers, verapamil, 480 mg by mouth, was given for an average of 12 months. There was an impressive improvement in symptoms, compared with the state under beta-blocker treatment. There was a significant reduction in the ECG signs of left-ventricular hypertrophy and of the radiologically measured heart volume. Treatment of this condition with verapamil appeared to be superior to that with beta-blockers.

Adrenergic beta-Antagonists↗
PubMed1976

[Coronary arteriography in patients with Prinzmetal's angina associated with ST elevations (author's transl)].

Among 1000 patients with coronary heart disease studied at rest and on exercise and by coronary arteriography, 17 had ST elevations during the anginal episodes. ST changes during exercise occurred in 16 patients, 12 of whom had spontaneous angina. One patient had ST changes only during spontaneous attacks at rest. Critical proximal lesions in the descending branch of the left anterior coronary artery were revealed by coronary arteriography in all 17 patients. Biplane ventricular cine-angiography revealed slight abnormalities in 12, normal pattern in the other five. It is thought that ST elevation during anginal attacks is caused by severe transmural ischaemia. Spontaneous attacks are thought to be due to additional functional narrowing, probably resulting from an increased vascular tone within the area of obstruction.

Angina Pectoris↗
PubMed1976

[Surgical treatment of ventricular aneurysm: an analysis of post-resection haemodynamic changes (author's transl)].

Of 500 patients with angiographically proven myocardial infarction 75 had a left ventricular aneurysm. 25 of them subsequently had resection of the aneurysm. Postoperative studies revealed marked improvement of symptoms. Pulmonary arterial pressure was significantly decreased at rest (from 28 to 20 mm Hg) and on exercise (from 58 to 35 mm Hg). There was a reduction in left ventricular end-diastolic volume (from 247 to 1.54 ml/1.73 m2) and a raised ejection fraction (from 36 to 59%). Good results were obtained especially in those patients who had congestive heart failure due to paradoxical systolic expansion of the ventricular wall and (or) secondary reversible damage in the remaining viable myocardium. Left ventricular aneurysms should be suspected after myocardial infarction when there is left ventricular failure and an increase in heart size.

Adult↗
PubMed1976

[Effect of nitroglycerin in acute myocardial infarction. II.Intravenous infusion of nitroglycerin in patients with or without left-heart failure, and its effect on infarct size (author's transl)].

Twenty-four patients with acute myocardial infarction were divided into two groups according to left-ventricular filling pressure (LVFP): group I (n = 13) with LVFP less than 20 mm Hg, group II (n = 11) with LVFP greater than 20 mm HG. After infusion of 3 mg nitroglycerin in the first and 6 mg in the second hour there was a highly significant decrease in the filling pressure (from 15 to 9 mm Hg in group I, 28 to 16 mm Hg in group II). Mean arterila pressure fell in both groups by an average of 9 mm Hg. There were only slight changes in heart rate. Cardiac output fell from 4.4 to 3.9 1/min in group I, while it rose significantly (from 3.5 to 4.0 1/min) in group II from an initially markedly decreased level. In patients of group II the subjective symptoms improved with positive changes in the haemodynamic variables. Electrocardiographic precordial mapping indicated that nitromapping indicated that nitroglycerin at a dose of 3 mg/h diminished the zone of ischaemia, while at a dose of 6 mg/h S-T elevations and depressions increased again.

Acute Disease↗
PubMed1976

[The effect of nitroglycerin in patients with acute myocardial infarction. IV. Myocardon in patients with and without left ventricular failure (author's transl)].

Myocardon (1 tablet=0.5 mg Nitroglycerin, 100 mg Euphyllin, 29.7 mg Papaverin-hydrochlorid and 0.3 mg Atropinmethylnitrat, without phenobarbital) was given in a dosis of 3 and 6 tablets in patients with acute myocardial infarction. According to the initial value of left ventricular filling pressure (LVFP) the patients were divided into 2 groups: Group I with a LVFP below 20 mm Hg and group II with a LVFP above 20 mm Hg. In group II there was clinical evidence of left ventricular failure. In both groups a decrease in pulmonary artery pressure and especially in left ventricular filling pressure was observed (in group I from 13 +/- 4 to 8 +/- 3 mm Hg and in group II from 26 +/- 7 to 16 +/- 4 mm Hg). Heart rate and mean arterial pressure did not change. In group II cardiac output increased from 3.5 +/- 0.6 to 4.3 +/- 1.31/min, whereas in group I it decreased from 5.1 +/- 0.9 to 4.6 +/- 0.91/min. Like isosorbid dinitrate Myocardon is useful in the management of left ventricular failure in patients with acute myocardial infarction. Side effects were observed: in two patients vomiting and in one patient sickness. The main effect of Myocardon is probably due to nitroglycerin, which is part of the substance. In higher dosis Myocardon has to be given without phenobarbital. Myocardon is especially useful if in the case of headache after nitrates the drug has to be changed.

Acute Disease↗
PubMed1976

[Effect of prajmalium bitartrate and procaine amide on ventricular extrasystoles (author's transl)].

Prajmalium bitartrate (Neo-Gilurytmal) was given to 19 patients, who had either runs of ventricular extrasystoles or frequent extrasystoles. The E. C. G. was continuously monitored on magnetic tape. At a dosage of 80 mg/d (20 mg every six hours) a significant reduction in ventricular extrasystoles was demonstrated on 20 separate occasions. After two hours extrasystoles decreased to 63% of the initial level. After six hours practically the full effect of the drug had been reached; the reduction in extrasystoles stabilized after 12 hours at an average of 30% of initial level. Ten hours after the last tablet had been taken the frequency of extrasystoles had risen to 57% of initial level. Comparison with procaine amide (3 g/d) in 14 patients revealed no significant difference between the two drugs. Prajmalium bitartrate was well tolerated, while three patients receiving procaine amide complained of nausea and gastrointestinal symptoms, so that treatment had to be discontinued in two. In one patient, receiving procaine amide by continuous drip, there were reversible joint pains, resembling lupus erythematodes.

Adult↗
PubMed1976

[Volume parameters of the right and left ventricles in coronary disease with and without myocardial infarct].

In 58 patients (pts) with coronary heart disease volume parameters of both ventricles were determined from two angiograms . Four groups of pts were formed according to localization of left ventricular damage: group I (24 PTS) without myocardial infarction, group II (17 pts) with anterior wall infarction (AWI), group III (9pts) with inferior wall infarction (IWI), and group IV (8 pts) with AW and IWI. In group I enddiastolic volume (EDV) of the left ventricle (LV) was 135 +/- 61 ml/1.73 m2, of the right ventricle (RV) 145 +/- 62 ml/1.73 m2, the ejection fraction (EF) 74% (LV) and 66% (RV). In group II EDV of LV increased significantly (194 +/- 88) and EF decreased to 50%, whereas EDV and EF of RV remaine unchanged. In group III EDV (LV 160 +/- 46, RV 172 +/- 95) of both ventricles was increased and EF (LV 57%, RV 58%) decreased, In group IV a more pronounced increase in EDV (LV 218 +1- 58, RV 181 +/- 30) and decrease in EF (LV 46%, RV 48%) was seen. A disturbance in contraction of RV was observed only in cases with IWI of LV. In contrast to LV, a diffuse impairment of RV occured. It was assumed that in RV disturbances in contraction exceeded the extent of scarred areas which might be explained by partially reversible ischemic disturbances of function.

Cardiac Catheterization↗
PubMed1976

[Nitroglycerin in the therapy of coronary insufficiency and heart failure].

In the treatment of angina pectoris nitroglycerin is still the most important drug. Its mechanism of action is described in reference to the lowering of preload and afterload as well as to the question of redistribution of regional myocardial blood flow. It is shown that after oral administration of issosorbide dinitrate effects on myocardial ischemia and left ventricular filling pressure can be seen lasting over more than four hours. In the treatment of acute myocardial infarction and left ventricular failure nitroglycerin can be used with favourable results and without undesired side effects if the hemodynamic is carefully observed. Under these conditions the intravenous infusion seems the most appropriate way of administration.

Administration, Oral↗
PubMed1976

Sublingual nitroglycerin in the treatment of left ventricular failure and pulmonary edema.

In 15 patients with left heart failure due to coronary heart disease (10 acute and 5 old infarcts) the enddiastolic pressures in the pulmonary artery (left ventricular filling pressure) were elevated to 25 +/- 8 mm Hg and signs of pulmonary congestion were present. After nitroglycerin sublingually (0.8-1.6 mg) the left ventricular filling pressure fell to 17 +/- 8 mm Hg and caridac output tended to increase. Mean arterial pressure did not change significantly. In 6 patients with pulmonary edema, clinically an impressive improvement was observed within 5-15 min after administration of the drug. In 1 case the left ventricular filling pressure decreased from 50 to 27 mm Hg within 5 min. In left heart failure, especially in the presence of pulmonary edema, sublingual nitroglycerin is a potent drug with a favorable influence on hemodynamic and clinical parameters.

Blood Pressure↗