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Biomedical subjects

G Liebau

Publications and source records attributed to G Liebau.

At least 19 recordsLinked to original sources
PubMed1993

[Left cerebral ischemia in mitral valve aneurysm].

An anterior mitral leaflet aneurysm was detected by two-dimensional echocardiography using the transesophageal approach in a 53-year-old patient with cerebral ischemic event. The transesophageal examination allowed a clear description of the aneurysm which was confirmed during surgery. This case demonstrates that transesophageal echocardiography is the method of choice in evaluation of distinct valvular lesions. The importance of TEE examination in patients with a neurological history is evident.

Aneurysm↗
PubMed1986

Effectiveness of converting enzyme inhibition (enalapril) for mild congestive heart failure.

The present study investigates the effectiveness of converting enzyme inhibition (CEI) on cardiac performance of patients with congestive heart failure (New York Heart Association functional class II). Outpatients (n = 12) were treated with enalapril, 5 to 10 mg twice daily, in addition to stable doses of digitalis and diuretic drugs. Before and after 4 and 12 weeks of treatment a treadmill exercise test and echocardiography were performed. Maximal oxygen uptake and exercise tolerance increased significantly and mean arterial pressure at rest and on exertion decreased significantly. Heart rate did not change. Left ventricular end-diastolic diameter decreased significantly. Serum angiotensin converting enzyme activity was reduced to nearly 0; plasma renin concentration, which was already elevated, increased further. Plasma norepinephrine levels did not change significantly. Treatment was tolerated well by all patients. CEI decreased preload and afterload, suggesting that they might have had an inappropriately elevated arteriolar and venous tone owing to a moderately stimulated renin angiotensin system and sympathetic nervous system. These conditions may lead to further deterioration of cardiac performance. By means of CEI one may be able to interrupt these pathogenetic mechanisms, relieving the already damaged heart from inappropriate elevations of preload and afterload and delaying or even preventing further deterioration of cardiac performance.

Adult↗
PubMed1985

Coronary hemodynamic and metabolic effects of nifedipine in patients with coronary artery disease treated with beta-blocking drugs.

In humans, reflex sympathetic nerve activation modulates the direct cardiac action of nifedipine after systemic administration and results in a positive chronotropic and inotropic response. The coronary hemodynamic and metabolic effects of nifedipine were evaluated after propranolol-induced acute beta-receptor blockade in 12 patients with angiographically documented coronary artery disease. The intravenous injection of propranolol led to a decrease in heart rate, coronary blood flow and myocardial oxygen consumption and an increase in coronary vascular resistance and the coronary arteriovenous oxygen difference. Mean aortic pressure did not change. The subsequent intravenous administration of nifedipine resulted in a transient increase in coronary blood flow and a reduction in coronary vascular resistance and the coronary arteriovenous oxygen difference and a sustained decrease in mean aortic pressure and myocardial oxygen consumption without significant changes in heart rate. Thus, in the presence of beta-receptor blockade, the positive chronotropic response to nifedipine is attenuated and nifedipine reduces myocardial oxygen consumption significantly. The vasodilatory effect of nifedipine is maintained and a potential propranolol-related inappropriate vasoconstriction may be reversed. The combination of nifedipine and beta-receptor blocking agents may be useful in the treatment of patients with both effort-induced angina and angina related to changes in coronary vasomotor tone.

Adult↗
PubMed1985

Four years of experience in endomyocardial biopsy--an immunohistologic approach.

Left ventricular biopsies from 376 patients (including 78 patients undergoing bypass surgery) were analyzed by light microscopy (necrosis, infiltration with or without fibrosis) and by immunohistology (bound antibodies). Circulating antisarcolemmal antibodies (ASA) were determined at the time of biopsy using a double-sandwich technique. Circulating antimyolemmal antibodies were assessed in intact rat and human cardiocytes. Histologic findings, heart catheterization, and echocardiography together with the patient's history established the diagnosis of perimyocarditis, myocarditis, postmyocarditic dilated cardiomyopathy, healed myocarditis, and healed perimyocarditis. Both bound and circulating ASA were found in up to 100% of cases in acute inflammatory heart disease and postmyocarditic cardiomyopathy, indicating a secondary immunopathogenesis of the myocardial disease. Analysis of immunoglobulin subclasses revealed: IgG-binding does not discriminate between acute/healing/healed carditis and postmyocarditic dilated heart disease (61.1%-91.7% positive); IgM binding is diagnostic for acute or healing perimyocarditis but has a relatively low incidence (33.3%); IgA binding occurs in acute or healing myocarditis (45.5%), perimyocarditis (33.3%), and in postmyocarditic heart disease (39.4%), but not in controls; complement fixation was never seen in controls, but was seen in acute myocarditis (45.4%), perimyocarditis (25%), and postmyocarditic heart disease (46%). Pretreatment of cryostat sections with collagenase to avoid "nonspecific" binding of antibodies to collagen considerably reduced the sensitivity but increased the specificity. Thus, endomyocardial biopsy proved a safe and valuable method for the further analysis of patients with carditis and myocardial disease of unknown origin.

Acute Disease↗
PubMed1985

[Therapy of dilated cardiomyopathy with digitalis, diuretics and vasodilators].

The treatment of dilated cardiomyopathy is primarily concerned with that of congestive heart failure. Digitalis is widely use in dilated cardiomyopathy but an improvement in the prognosis has not yet been demonstrated. Furthermore, the effects of digitalis in patients with sinus rhythm are debatable. If dilated cardiomyopathy induces atrial fibrillation and tachyarrhythmia, digitalis should be used. Diuretics are helpful in the treatment of congestive heart failure associated with dilated cardiomyopathy. By reducing hypervolemia and by venous dilatation, diuretics lower preload and afterload. This leads to relief of congestion and termination of the vicious cycle of congestive heart failure. Accordingly, the prognosis of dilated cardiomyopathy might be improved by diuretics. There are numerous diuretics acting differently on the renal tubules, the choice of which depends on the renal function and serum electrolyte concentrations. Reduction of preload and afterload improves congestive heart failure as has been demonstrated repeatedly. Many substances have therefore been used for arterial and venous dilation with differing results. At least for short-term periods, congestion is reduced and cardiac output increases. Especially inhibitors of angiotensin II converting enzyme are very effective since they act both in the arterial and venous systems. Additionally, inhibition of the action of angiotensin may be regarded as causal therapy since the renin-angiotensin system is the trigger for vasoconstriction and fluid retention in congestive heart failure. Unlike other substances, ACE inhibitors have been demonstrated to improve prognosis of patients with congestive heart failure. At present, combined diuretic therapy and angiotensin conversion enzyme inhibition would seem the most reasonable treatment for patients with dilated cardiomyopathy and sinus rhythm. If atrial fibrillation and tachyarrhythmia develop, additional digitalis therapy is effective.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1985

Muzolimine therapy in patients with congestive heart failure in comparison with furosemide pretreatment. Effect on digoxin plasma concentration.

Eight patients suffering from congestive heart failure (NYHA III-IV) and pretreated with digoxin received muzolimine over 14 days in an open clinical study. The muzolimine dose was adjusted to 3/4 of the daily furosemide dose necessary to keep the body weight constant at least three days prior to the onset of muzolimine treatment. Plasma concentrations of epinephrine, norepinephrine, aldosterone, renin and digoxin were determined on the last day of the furosemide treatment period and on the last day of the muzolimine period. No significant changes were observed in plasma concentrations of epinephrine, aldosterone, renin, creatinine, and potassium. After muzolimine treatment, however, body weight and sonographically determined liver size decreased further and plasma norepinephrine concentrations were significantly lower. The digoxin concentrations did not change after muzolimine treatment. The results demonstrate the beneficial effect of muzolimine in heart failure patients. Since plasma concentration of digoxin does not change despite marked diuretic effects of muzolimine no relevant interaction between both substances has to be expected.

Adult↗
PubMed1984

[Effect of nifedipine and nitroglycerin on epicardial vessels in coronary heart disease].

The effect of nifedipine and nitroglycerin on the diameter of epicardial coronary arteries, the stenosis diameter, as well as arterial blood pressure and heart rate were recorded in 20 patients with coronary-heart disease. Nifedipine (20 mg sublingually) caused a significant fall in arterial pressure and a significant rise in heart rate. Additional administration of nitroglycerin (0.8 mg sublingually) caused a further fall in arterial pressure while heart rate remained constant. A definite relaxation (vasodilatation) of the epicardial vessels was demonstrated after nifedipine and a further increase after nitroglycerin. While nifedipine on average led to a significant increase in the diameter at the site of stenosis, response of individual stenoses was highly variable. In one patient with subtotal stenosis of the anterior interventricular branch a complete, transitory occlusion at the site of the stenosis occurred during nifedipine medication. This paradoxical reaction was not noted after nitroglycerin. Relaxation of the epicardial coronary arteries by nifedipine with suppression of phasic tone thus seems to be the major part of its anti-anginal effect. This effect is potentiated by nitroglycerin so that the combination of nitrate and calcium-antagonist appears to be therapeutically reasonable. In individual patients, however, there may be a paradoxical reaction to nifedipine.

Adult↗
PubMed1984

Role of the renin-angiotensin system in the development of congestive heart failure in the dog as assessed by chronic converting-enzyme blockade.

Hormonal factors may be important in the regulation of peripheral vascular resistance (PVR) in congestive heart failure (CHF). The role of the renin-angiotensin system in the development of CHF was studied in 16 unanesthetized dogs. CHF was induced by rapid right ventricular pacing, with and without chronic converting-enzyme inhibition (CEI) by captopril. The hemodynamic changes and the activity of renin, aldosterone, norepinephrine and vasopressin were studied. The control dogs showed a greater decrease in cardiac output and a greater increase of mean pulmonary artery pressure than the captopril-treated group. In the group with CEI, only a small, transient increase in PVR was observed during the development of CHF; in the control group, there was an increase of 94% of basal values. The control group showed a continual increase of renin, aldosterone and norepinephrine. Four control dogs showed an inappropriately high secretion of arginine vasopressin. The increase of sympathetic nervous activity was only insignificantly attenuated by angiotensin II inhibition and was without a considerable influence on PVR except for an early transient increase in vascular tone. In our animal model, the renin-angiotensin system plays an important role in the regulation of PVR in CHF. In this kind of CHF the sympathetic nervous system appears to be of minor importance for the long-term regulation of PVR. Plasma arginine vasopressin levels were increased in control dogs; this increase may contribute to the increased vascular tone.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1984

[Acute hemodynamic effects of alifedrine in patients with heart failure].

The newly synthesized cardiotonic agent alifedrine (1-cyclohexyl-3-[(1S, 2R)-2-hydroxy-methyl-2-phenylethylamino]-propan-1-one) was shown to have vasodilating and positive inotropic effects in experimental animals. The effectiveness was tested in 8 patients with congestive heart failure already receiving digitalis and diuretics. After the intravenous administration of 40 mg alifedrine, cardiac output and stroke volume index increased and systemic vascular resistance and left ventricular filling pressure decreased. Left ventricular ejection fraction improved and there were no significant changes in heart rate and mean aortic pressure. Alifedrine, therefore, improves left ventricular performance in patients with congestive heart failure treated with digitalis and diuretic agents.

Adult↗
PubMed1983

Diagnostic relevance of humoral and cytotoxic immune reactions in primary and secondary dilated cardiomyopathy.

Circulating muscle-specific antimyolemmal antibodies (AMLAs) were found in 18 of 61 patients with secondary dilated cardiomyopathy (DC). All 18 patients had clinical or histologic evidence of previous perimyocarditis. AMLAs were found both in patients' serum samples and bound to the sarcolemmal sheath of the autologous myocardial biopsy specimen. Only AMLAs in postmyocardiac DC induced cytolysis of vital cardiocytes in the presence of complement, whereas hepatocytes remained unaffected. Titers of AMLAs correlated with the degree of cardiocytolysis. In contrast, antiinterfibrillary antibodies were found in 49% patients with primary DC (n = 79) and in 61% of patients (n = 30) with alcoholic DC. The incidence of antifibrillary antibodies of the antimyosin type was 23 and 24%, respectively. Incidence of both antibodies increased according to the severity assessed by New York Heart Association functional classes. Circulating immune complexes assayed by a new Clq-solid phase fluorometric assay were present in 30% of patients with postmyocarditic DC only. Lymphocyte-mediated cytotoxicity against heterologous cardiac target cells (K-cell activity) was measured in 33% of patients each with primary and secondary alcoholic DC but not postmyocarditic DC. There were no blocking factors in primary but were some in alcoholic heart disease.

Antibodies↗
PubMed1983

Effect of intravenous and intracoronary nifedipine on coronary blood flow and myocardial oxygen consumption.

The effect of intravenous and intracoronary nifedipine on coronary sinus blood flow, coronary vascular resistance, and myocardial oxygen consumption was studied in 20 patients with coronary artery disease. An intravenous infusion of 1.0 mg nifedipine resulted in a decrease in mean aortic pressure, an increase in heart rate and coronary blood flow, and no significant change in myocardial, oxygen consumption. In contrast, the intracoronary injection of 0.1 mg nifedipine led to a moderate reduction in mean aortic pressure, no change in heart rate, an increase in coronary blood flow, and a significant reduction in myocardial oxygen consumption. During rapid atrial pacing before and approximately 6 minutes after the intracoronary nifedipine injection, coronary blood flow and myocardial oxygen consumption reached identical levels. Thus, only intracoronary injection of nifedipine increases coronary flow in the presence of reduced myocardial oxygen consumption. After intravenous administration, reflex tachycardia counteracts the direct myocardial effect of nifedipine and the potential oxygen-saving effect of afterload reduction. There is no evidence of a prolonged oxygen-sparing effect after cessation of the immediate effects.

Adult↗
PubMed1982

Captopril in the long-term treatment of essential hypertension: changes in the renin-angiotensin-aldosterone system.

We investigated changes in the renin-angiotensin-aldosterone system in seven patients with essential hypertension during treatment with captopril (SQ 14225) (300 to 450 mg/day) for 12 months. While blood pressure decreased, the plasma-renin concentration increased to 700 percent of the initial value (6.1 +/- 2.5 ng angiotensin l/ml . h) and angiotensin I increased to about 300 percent of the basal value (179 +/- 32 pg/ml). Converting enzyme inhibition resulted in a 30 percent decrease in plasma angiotension II levels from a basal level of 66 +/- 21 pg/ml. Plasma aldosterone decreased 52 percent from 63 +/- 13 pg/ml initially. These changes in hormone levels were maintained throughout the study. There was no significant change in serum sodium and serum potassium concentration.

Aldosterone↗
PubMed1982

[Captopril in congestive heart failure (author's transl)].

Captopril (Lopirin, Squibb, von Heyden) is an inhibitor of the angiotensin-I converting enzyme. In congestive heart failure angiotensin mediated vasoconstriction and aldosterone secretion is reversed by captopril. Both effects of captopril induce reduction of cardiac preload and afterload. The clinical state of patients with congestive heart failure therefore improves since cardiac output increased and pulmonary pressures decrease. Captopril acts orally and the dosage used for the treatment of congestive heart failure ranges from 50 to 150 mg daily. After oral ingestion of a single dose the maximum haemodynamic effect is observed after 45-90 min. No tolerance induction or tachyphylaxis has been observed during maintenance therapy over a period of 18 months. There are some reversible adverse reactions like pruritus, skin rash and partial or complete taste loss which are dose related. Serious side effects include leucopenia, agranulocytosis, renal failure and membranous glomerulonephritis. Therefore regular urinary and blood analysis is necessary during captopril therapy.

Acute Kidney Injury↗