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Biomedical subjects

W D Bussmann

Publications and source records attributed to W D Bussmann.

At least 163 records · Page 9Linked to original sources
PubMed1978

[Contractile and relaxation reserve of the left ventricle. III. Patients with cardiomyopathy (author's transl)].

Seven of 22 patients with cardiomyopathy increased maximal rate of left ventricular pressure rise (max dP/dt) above 3200 mm Hg/s and dP/dt/P above 60/s. Relaxation reserve was normal with an increase of min dP/dt above 2400 mm Hg/s.--In 15 patients contractile and relaxation reserve was reduced. In congestive cardiomyopathy, contractility and relaxation reserve were equally reduced. Left ventricular enddiastolic pressure increased during exercise slightly or not (grade 1). Enddiastolic volume was elevated to 173 +/- 50 ml/1.73 m2 and endsystolic volume to 63 +/- 22 ml/1.73 m2; ejection fraction and mean circumferential fiber shortening were reduced (61 +/- 17%; 1.3 +/- 0.9 circ/s). In hypertrophic cardiomyopathy without obstruction, contractile and relaxation reserve and ejection phase parameters could be found to be normal. Enddiastolic pressure at rest was elevated. In severe cases, contractile and relaxation reserve were markedly reduced and enddiastolic pressure increased to a greater extent than in congestive cardiomyopathy. In addition, relaxation reserve was reduced, especially in patients with excessive hypertrophy of the myocardium. These had abnormal (grade 2) and pathological reaction to exercise: contractile and relaxation reserve were decreased and enddiastolic pressure (grade 3) increased. Left ventricular contractility was found to be almost normal in patients with hypertrophic obstructive cardiomyopathy. This was the case despite increases in enddiastolic pressure. Contractile reserve was reduced, however, in patients with excessive hypertrophy. Diastolic filling was impeded during exercise.--Measuring left ventricular function during exercise, different types of cardiomyopathy correlate with typical hemodynamic alterations.

Adult↗
PubMed1978

[Contractile and relaxation reserve of the left ventricle. IV. Patients with coronary heart disease (author's transl)].

51 patients with coronary heart disease had exercise tests on a bicycle ergometer (86 +/- 32 watts). Compared to a normal control group, only 13 patients had normal contractile reserve (group 4.1). In 32 patients the increase in contractility during exercise was reduced (max dP/dt below 3200 mm Hg/s, group 4.2). Patients with reduced contractile reserve were graded according to the height of left ventricular enddiastolic pressure during exercise: In patients with grade 1, enddiastolic pressure was normal. In patients with grade 2, enddiastolic pressure increased between + 4 and + 15 mm Hg and in the patients with grade 3a a above + 15 mm Hg. Contractile and relaxation reserve decreased along with a rise in enddiastolic pressure and an increase in the complaints of the patients. Severe chest pain led to termination of exercise in patients of grade 3b. Enddiastolic pressure increased above + 15 mm Hg. During ischemia, peak-measured velocity of contractile elements (dP/dt/P) and the maximal rate of left ventricular pressure fall (min dP/dt) decreased. In conclusion, with increasing chest pain a decrease of contractile reserve was observed. Left ventricular enddiastolic pressure rose excessively. This has to be taken as a sign of myocardial failure due to ischemic dyskinesia and impeded relaxation.

Adult↗
PubMed1978

Effects of intravenous nitroglycerin on hemodynamics and ischemic injury in patients with acute myocardial infarction.

In 24 patients with acute myocardial infarction intravenous nitroglycerin in 2 different dosages was administered and the effect on hemodynamics and extent of myocardial ischemia was investigated. According to the initial left ventricular filling pressure (LVFP) the patients were divided in Group I: LVFP below 20 mm Hg (13 patients) and in Group II: LVFP above 20 mm Hg (11 patients). Following an infusion of 3 mg of nitroglycerin in the first and 6 mg in the second hour, a significant decrease (P less than 0.0001) in the filling pressure (in Group I from 15 +/- 4 to 9 +/- 3 (+/-1 SD) and in Group II from 28 +/- 11 to 16 +/- 7 mm Hg) was observed. The mean arterial pressure decreased in both groups by an average of 9 mm Hg. The changes in the heart rate were minimal. The cardiac output decreased in Group I from 4.4 +/- 1.0 to 3.9 +/- 0.8 1/min (P less than 0.005) whereas in the group with left ventricular failure it increased significantly from a lowered initial value (3.4 +/- 1.0 to 4.0 +/- 1.1 1/min) (P less than 0.001). By using precordial mapping for estimation of ischemic injury in 12 patient sigma ST elevation decreased from 14.6 +/- 11.9 to 12.2 +/- 9.8 mV at a dose of 3 mg/h (P less than 0.03). The dose of 6 mg/h, however, was less effective on the extent of myocardial ischemia than 3 mg/h. Thus, the dosage of nitroglycerin may be critical in respect to infarct size, despite the beneficial hemodynamic effects of the drug.

Adult↗
PubMed1977

[Effect of nitroglycerin sublingually in the emergency management of "classical" pulmonary oedema (author's transl)].

Of 22 patients with the classical clinical signs of pulmonary oedema (orthopnoe, cyanosis, sweating and rales heard at a distance) 15 (Group A) were observed clinically, while seven (Group B) underwent haemodynamic studies. Those in Group A were given 0.8-2.4 mg nitroglycerin sublingually one to six times at 5--10 minute intervals. Within five minutes of nitroglycerin administration 7 of the 15 had their first signs of clinical improvement. In 11 patients the rales had disappeared after 15--20 minutes or had regressed. In the remainder the dyspnoea had decreased so that at this point in 14 of the 15 patients various degrees of improvement had occurred. Four patients were completely without clinical signs after 30 minutes. The increased arterial blood pressure and heart rate had fallen markedly. In the seven patients of Group B mean left ventricular filling pressure fell within ten minutes of nitroglycerin administration (1.6 mg) from 33 +/- 10 to 24 +/- 8 mmHg, cardiac output rising sifnificantly from 3.3 +/- 0.8 to 3.7 +/- 0.8 1/min. Such favourable results with nitroglycerin are to be expected only if the pulmonary oedema is of cardiac origin.

Aged↗
PubMed1977

Orally administered isosorbide dinitrate in patients with and without left ventricular failure due to acute myocardial infarction.

The oral effectiveness of 10 mg followed by 20 mg of isosorbide dinitrate in 21 patients with acute mycardial infarction was studied over a period of 13 hours. The patients were grouped according to initial left ventricular filling pressure: group I, pressure less than 20 mm Hg, and group II, pressure more than 20 mm Hg. Patients in group II had left ventricular failure. In both groups isosorbide dinitrate resulted in a significant decrease in pulmonary arterial pressure. The left ventricular filling pressure decreased in group I from 13.6 +/- 4.0 to 7.1 +/- 2.6 mm Hg (mean +/- 1 standard deviation) and in group II from 26.9 +/- 4.6 to 19.0 +/- 3.6 mm Hg (P less than 0.001). Cardiac output decreased in group I from 5.1 +/- 1.0 to 4.5 +/- 0.9 liters/min, whereas in group II it increased significantly from 3.5 +/- 0.8 to 4.1 to 0.9 liters/min (P less than 0.001). In both groups, peripheral arterial blood pressure decreased (P less than 0.60). Heart rate remained constant. Whether cardiac output increased or decreased was found to be dependent on the initial left ventricular filling pressure. In patients with an initially high value (above 20 mm Hg), the increase in cardiac output is probably due to the reduction of afterload. An additional factor may be the decrease in left ventricular filling pressure, which leads to an improved blood supply in the affected mural segments as a result of the decrease in the extravascular component of the coronary resistance. Significant changes in cardiac output and left ventricular filling pressure were achieved 3 to 5 hours after oral administration of isosorbide dinitrate. Clinical signs of failure were less pronounced. Isosorbide dinitrate is, therefore, a therapeutic agent in the treatment of left ventricular failure due to acute myocardial infarction.

Administration, Oral↗
PubMed1977

[Left ventricular contraction reserve in coronary heart disease. Evaluation, quantification and prognostic value (author's transl)].

Regional and overall left ventricular contraction reserve was studied in 14 patients with coronary heart disease, in 5 healthy subjects and in 4 patients before and after aorto-coronary bypass surgery. Quantification of overall contraction was based on ventricular volumes and ejection fraction. Regional contraction reserve was calculated with the hemiaxis method and a ventricular score. Contraction reserve under nitroglycerin and in postextrasystolic beats was compared. For routine quantification of contraction reserve the ventricular score is recommended. For research purposes the hemiaxis method is to be preferred. Postextrasystolic beats are better suited for analysis of contraction reserve than are angiograms following administration of nitroglycerin. This is due to the minor expense of the procedure, furthermore, postextrasystolic beats allow better differentiation between contracting and non-contracting areas. Left ventricular contraction reserve is larger in patients with coronary heart disease, angina pectoris and ischemic reactions in the exercise ECG than in control patients. These findings are based on overall and on regional volume parameters. A quantitatively greater improvement in contraction could be provoked in the anterior wall than in the posterior wall. Regional contraction improved significantly in most cases either in the anterior wall or in the posterior wall; rarely it improved simultaneously in both left ventricular regions. In a few cases contraction deteriorated in one area with a simultaneous improvement in the opposite area. Overall and regional ventricular function, as assessed preoperatively by contraction reserve determinations could not be completely regained in normal beats after successful bypass surgery. Differences in the regional contraction reserve seemed to be mainly due to varying degrees of ischemia and scarring.

Angina Pectoris↗
PubMed1977

[Right and left ventricular volume parameters in cardiomyopathy (author's transl)].

In 41 patients with different types of cardiomyopathy (19 congestive = COCM, 6 hypertrophic obstructive = HOCM, and 16 hypertrophic non-obstructive = HCM) ventricular enddiastolic volume (EDV), endsystolic volume (ESV), and ejection fraction (EF) were determined angiographically and values of both ventricles were compared. In the mean, volume parameters increased significantly and EF of both ventricles decreased as compared to control values of patients with coronary heart disease without myocardial infarction. In COCM volume parameters reached pathologic values as in the total patient group whereas in HOCM and in HCM values did not differ significantly from control. Left ventricular function was reduced more often and, in the mean, more severely than right ventricular function. This became evident e.g. from the incidence of enddiastolic volume increase and the course of the regression line. A similar finding can be derived from the reversal of the normal relation of volume parameters of both ventricles. Only in rare cases right ventricular function was more severely impaired than left ventricular function. These findings indicate a simultaneous impairment of both ventricles in cardiomyopathy. The more pronounced left ventricular function disturbance may be attributed to the higher left ventricular work load. Thus, left ventricular biopsies might be of greater diagnostic significance than right ventricular biopsies.

Cardiac Catheterization↗
PubMed1977

[Contractile and relaxation reserve of the left ventricle. I. Normal left ventricle (author's transl)].

The validation of parameters of left ventricular contractility at rest is pure. Therefore, the contractile function of the left ventricle was measured during exercise. The reserve in contractility and relaxation was obtained in a group of 13 patients with normal left ventricle (ergometer). The maximal rate of left ventricular pressure rise (max dP/dt) increased from 1721 +-378 to 4954 +- 1246 mmHg/s and the peak measured velocity of contractile elements (dP/dt/P) from 38 +- 9 to 76 +- 11 s-1 at a mean load of 112 +- 43 (+-SD) watts. The parameter of the isovolumic relaxation phase, the maximal rate of left ventricular pressure fall (min dP/dt) increased from 1862 +- 343 to 3128 +- 445 mmHg/s. Left ventricular enddiastolic pressure was unchanged. All patients reached at least 3200 mmHg/s (max dP/dt) 60 s-1 (dP/dt/P) and 2400 mmHg/s (min dP/dt). The difference between rest- and exercise values was at least 1800 mmHg/s (max dP/dt), 22 s-1 (dP/dt/P) and 1000 mmHg/s (min dP/dt).

Adolescent↗
PubMed1977

[Contractile and relaxation reserve of the left ventricle. II. Patients with rheumatic valvular disease (author's transl)].

The function of the left ventricle is important for the success of surgery. To differentiate between normal and abnormal ventricular function, the contractile and relaxation reserve was measured. In 19 patients, 10 with mitral and 9 with aortic valve disease, max dP/dt and min dP/dt were measured at rest and during exercise (ergometer). Max dP/dt increased in 7 patients above 3200 mm Hg/s and dP/dt/P above 60 s-1 (normal contractile reserve). Only 3 of these patients reached a normal increment of relaxation velocity (min dP/dt above 2400 mm Hg/s). In 12 patients the contractile and relaxation reserve was decreased. All patients with mitral stenosis had abnormal relaxation reserve despite normal contractile function in 4 cases. Left ventricular enddiastolic pressure did not correlate well with myocardial dysfunction. Isovolumic contractility during exercise was decreased in patients with aortic valve disease. Enddiastolic pressure increased from 18 +- 8 to 22 +- 14 mm Hg during exercise.

Adolescent↗
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↗