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Biomedical subjects

H Kreuzer

Publications and source records attributed to H Kreuzer.

At least 271 records · Page 15Linked to original sources
PubMed1983

Hemodynamic effects of nisoldipine in chronic congestive heart failure.

The hemodynamic effects of 10 and 20 mg isobutyl methyl 1,4-dihydro-2,6-dimethyl-4-(2-nitrophenyl)-3,5-pyridinecarboxylate (nisoldipine, Bay k 5552) p.o. were studied in 15 patients with chronic congestive heart failure due to ischemic heart disease or cardiomyopathy. The dose of 10 mg elicited only a decrease of pulmonary wedge pressure during exercise, all other parameters remained unaffected. After 20 mg nisoldipine arterial blood pressure was reduced already at rest. During exercise, arterial as well as pulmonary artery and wedge pressures were significantly reduced. Heart rate remained unaffected and cardiac index increased slightly. It is concluded, that nisoldipine improves the hemodynamic situation in chronic congestive heart failure by simultaneously reducing cardiac pre- and afterload.

Adult↗
PubMed1983

[Ventricular septal defect as a complication of myocardial infarct].

Between 1978 and 1982 emergency closure of postinfarction ventricular septal defect was performed in 4 patients (51--74 years) on the 3rd-7th day after acute myocardial infarction. All patients had a large left-to-right shunt and were in intractable acute heart failure; all of them survived the operation (3 patients had additional aortocoronary bypass grafts), and follow-up (0.5--4.5 years) was uncomplicated. The favorable clinical and functional results of surgical therapy indicate that postinfarction ventricular septal defects should be operated on even in patients over 70 years of age.

Aged↗
PubMed1983

[Effect of the calcium antagonist nisoldipine on electrophysiologic parameters in the human].

We investigated the influence of nisoldipine, a new calcium antagonist, on sinus node function, intracardiac conduction times, and the refractoriness of different compartments of the heart. Three catheters were placed in the right heart: a quadripolar one in the high right atrium, a bipolar one in the His position, and one in the apex of the right ventricle. Nisoldipine given i.v. in a dose of 1.5 microgram/kg body weight shortened the sinus node cycle length and the sinus node recovery time by 10%. The rate corrected sinus node recovery time, the sinoatrial conduction time, and the intracardiac conduction times remained unaffected. The effective refractory period of the right ventricle decreased slightly but significantly. The refractoriness of the other compartments did not change significantly. Systolic blood pressure decreased by 6%, whereas diastolic blood pressure remained constant. Nisoldipine thus exhibits no major effects on electrophysiological parameters in man. The increase in heart rate is regarded as a sympathetic reflex mechanism due to the decrease of systemic resistance.

Aged↗
PubMed1982

Comparative study of the haemodynamic effects of oral molsidomine and isosorbide dinitrate in man.

The haemodynamic effects of oral molsidomine 4 mg and sustained-release isosorbide dinitrate (ISDN) 40 mg have been compared in 10 patients recovering from acute myocardial infarction. After both drugs pulmonary arterial, pulmonary capillary wedge and systemic arterial blood pressure were reduced to about the same extent. The maximum effect was reached 1.5 to 2 h after ingestion of both drugs, but the effect of molsidomine declined during the following 2 h and control values were almost reached after 4 h. After ISDN there was no rebound during the observation period of 6 h. Unlike molsidomine, ISDN reduced total peripheral resistance, so cardiac output and stroke volume index remained constant despite the reduction in cardiac preload. It is concluded that sustained release ISDN 40 mg and molsidomine 4 mg are about equieffective doses in terms of reduction of cardiac preload, but that the effect of molsidomine is of shorter duration. Since molsidomine alone causes venous pooling, cardiac output and stroke volume index are reduced, which may be an untoward side effect in patients with severe heart failure.

Cardiac Output↗
PubMed1982

[Left ventricular contraction and relaxation in patients with congestive cardiomyopathy during exercise].

UNLABELLED: Left ventricular (LV) contraction and relaxation were analysed in 16 patients with congestive cardiomyopathy (COCM) at rest (R) and during supine bicycle ergometer exercise (E), and were compared with 10 normals (N). In patients with COCM, left ventricular ejection fraction (EF) was significantly reduced at rest, but during exercise like in the normal patients there were no significant changes (EFCOCM: 34 +/- 12% (R) and 35 +/- 10% (E);EFN: 72 +/- 5% (R) and 74 +/- 5% (E). LV-enddiastolic volume in COCM was more than 100% larger than in N. Left ventricular filling pressures (PLVed) were elevated already at rest, the increase during exercise was very similar to that of the normal group (COCM: 20.5 +/- 9.0 (R), 33.3 +/- 7.6 (E) mm Hg, p less than 0.001; normal group: 11.1 +/- 2.2 (R), 18.7 +/- 5.9 (E) mm Hg, p less than 0.001). The increase of maximum dP/dt during exercise as an index of contractility reserve was distinctly lower in COCM (delta means COCM: + 51%; delta means N: + 105%). Left ventricular relaxation as measured from minimal dP/dt was significantly impaired already at rest in COCM (COCM: -1109 +/- 329; N: -1832 +/- 468 mm Hg X s-1, p less than 0.001), the increase of dP/dtmin during exercise (COCM + 37%) was similar to that of normal patients (+ 35%). The time constant T of isovolumic pressure fall was significantly prolonged at rest in COCM, and there were no changes during exercise. After correction for the right atrial pressure rise during exercise, the time contant T' was significantly shortened to the same extent in the normal group (COCM: (R) 44 +/- 9, (E) 36 +/- 10 ms; N: (R) 33 +/- 5, (E) 25 +/- 5 ms, p less than 0.001). CONCLUSIONS: In patients with COCM, changes of left ventricular ejection fraction during exercise are inconsistent; in the individual patient, changes in global LV function during exercise cannot be predicted from EF at rest. At rest, LV relaxation is prolonged, the lack of shortening of the time constant T during exercise is thought to be mainly due to the pressure rise in the pericardial space.

Adult↗
PubMed1982

[Changes of global and regional left-ventricular function by reperfusion in acute myocardial infarction].

UNLABELLED: Biplane ventriculography was performed during the acute and chronic stage (3 weeks) of myocardial infarction in 54 patients. Early recanalisation was attempted by intravenous streptokinase in 33, by intracoronary streptokinase in 15 and by catheter manipulation in 6 patients. In patients with successful recanalisation (n = 37) biplane LV ejection fraction (EFbi) increased slightly from 53 +/- 10 to 56 +/- 9% on the average, with late recanalisation or permanent occlusion EFbi decreased significantly from 47 +/- 11 to 39 +/- 8% (p less than 0.001). Correspondingly the akinetic segment length (AKS) and the number of akinetic radians (Sak) (semiautomated system) decreased with early recanalisation and increased with permanent occlusion. Comparing global and regional LV function, EF and Sak correlated closely (r = 0.81) while EF and AKS revealed only a loose correlation (r = 0.59). Biplane and RAO single plane EF correlated with an r-value of 0.88, Sy,x however was 9.9%. There was a considerable scatter in the relation between the parameters of regional wall motion, AKS and Sak (r = 0.80; Sy,x = 10.6). CONCLUSIONS: On the average there is a slight improvement in LV function after successful early reperfusion, which seems to be independent of the method of recanalisation. Changes of regional akinesis after reperfusion cannot be assessed accurately by angiographic determination.

Coronary Circulation↗
PubMed1981

[Myoglobinuric renal failure in hyperosmolar diabetic coma (author's transl)].

Acute rhabdomyolysis with myoglobinuric renal failure occurred in a 66-year-old woman who was in hyperosmolar non-ketotic diabetic coma. No previous description of such a case has been found. The clinical picture was characterized by the typical findings of hyperosmolar coma, in addition to excessive serum creatine kinase and myoglobin levels and massive myoglobinuria with acute renal failure. The rhabdomyolysis became fully manifest only under insulin treatment, possibly the result of insulin-induced hypophosphataemia, which seems to be of importance in the causation of the rhabdomyolysis.

Acute Kidney Injury↗
PubMed1981

[Elevated serum myoglobin in renal failure (author's transl)].

In 44 patients with chronic renal failure of varied etiology serum immunoreactive myoglobin was measured and compared to values obtained in patients with normal renal function. Irrespective of the underlying disease a highly significant linear correlation was found between serum immunoreactive myoglobin and serum creatinine concentration. In patients with serum creatinine concentrations above 550 mu mol/1 (6.2 mg%) serum myoglobin was as a rule elevated above the range found in the controls with normal renal function. This was also true in dialysis patients. These result demonstrate that serum myoglobin may only be used with restrictions in the diagnosis of myocardial infarction in patients suffering from advanced chronic renal failure.

Humans↗
PubMed1981

[The effect of molsidomin on the arterial windkessel (author's transl)].

The antianginal effect of Molsidomin is due to a reduction of preload. The decrease of aortic pressure is interpreted by the diminuation of the cardiac output. It is not yet known whether there is an additional primary reduction of afterload, caused by a change of the elastic properties of the arterial windkessel. Therefore in ten patients the effects of Molsidomin were investigated. After Molsidomin the pulmonary capillary pressure decreased by 58%, and the cardiac index by 12%. Mean aortic pressure was diminished by 12%, too, The capacity of the windkessel C was determined from the diastolic pressure decay in the thoracic descending aorta. After Molsidomin there was a decrease of C by 21%. This decrease was due to a reduction in the filling-state but not to altered elastic properties of the arterial windkessel.

Angina Pectoris↗
PubMed1981

[Virological and morphological results in patients with congestive cardiomyopathy (author's transl)].

In 30 patients with congestive cardiomyopathy, right ventricular biopsies were performed. The biopsy material was investigated by virological and morphological methods. In all cases it was impossible to isolate viruses from the right ventricular myocardium, corresponding to the lack of infiltrative changes as shown by morphology. Results point against a direct causative role of viruses in the genesis of congestive cardiomyopathy.

Adult↗
PubMed1981

[Left ventricular volumes by cross-sectional echocardiography in the dog: a comparison with biplane angiocardiography (author's transl)].

Using apical long axis and precordial short axis views, left ventricular end-diastolic and end-systolic volumes and ejection fraction were determined by cross-sectional echocardiography and compared with biplane angiocardiography. 10 anesthetized, closed chest dogs were first studied in the control state. Inferior vena cava was occluded by a balloon-inflated catheter, measurements were repeated. Descending aorta was blocked, with measurements retaken. Finally 8 dogs were studied after left coronary artery occlusion. For enddiastolic volumes correlation coefficients were 0.89, 0.93, 0.89, and 0.90 respectively (n = 10, 10, 10, 8; p less than 0.01). End-systolic volumes correlated with r 0.94, 0.92, 0.83, 0.92 (p less than 0.01). Left ventricular volumes were systematically underestimated by echocardiography (p less than 0.05). Ejection fraction corresponded less favourably, overall r was 0.85 (n = 38; p less than 0.01). Thus, cross-sectional echocardiography appears suitable for quantifying left ventricular volumes, less ejection fraction in the dog, during acute interventions as well as in the presence of regional dysfunction.

Angiocardiography↗
PubMed1981

[Early prediction of infarct size by serial determination of serum myoglobin (author's transl)].

40 patients with acute myocardial infarction had serial determinations of CK, CKMB and an addition of serum myoglobin (SMb) by radioimmunoassay. In 10 patients with normal values on admission SMb rose earlier than CK and CKMB. In another 20 patients SMb was pathologically increased while CK and CKMB were normal and in 10 patients all parameters were elevated on admission. In all 40 patients SMb was significantly elevated in between 10 hrs after beginning of angina, and peak myoglobin occurred 10 hrs before CK and CKMB. In 10 patients peak SMb correlated with infarct size as determined by angiocardiography in the chronic stage (r = 0.863; p less than 0.01). Peak SMb also correlated with infarct size as estimated by CK release (r = 0.73; p less than 0.001). Thus determination of SMb is a sensitive method in diagnosing early myocardial infarction, and peak serum myoglobin allows early prediction of infarct size.

Acute Disease↗
PubMed1980

[Oestrogen as a risk factor for the vascular system (author's transl)].

Plasma oestradiol and testosterone concentrations were measured in 44 men with angiographically proven coronary heart disease, 66 men without evidence of coronary heart disease serving as control. Another group consisted of 28 men with renal failure. Those with coronary heart disease had a significantly higher oestradiol concentration than the control group. This increased value also was present in patients with renal failure. There was a relationship between the level of oestradiol on one hand and glucose tolerance, ratio of beta to alpha-lipoproteins and blood pressure, on the other, in both the patients with coronary heart disease and the healthy controls. These results indicate the oestradiol may in males be an indicator of a risk constellation of vascular damage. Perhaps, it may be the cause of an abnormal carbohydrate and fat metabolism, which then leads to hypertension and degenerative vascular lesions.

Adult↗