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Biomedical subjects

K Kochsiek

Publications and source records attributed to K Kochsiek.

At least 55 records · Page 3Linked to original sources
PubMed1991

[Lipid status and basal steroid hormone level following 16 weeks of lovastatin therapy in primary hypercholesterolemia].

We examined the effect of a 16 week therapy with the HMG CoA reductase inhibitor lovastatin in 29 patients (mean age 43 years) with primary hypercholesterolemia. All patients had cholesterol levels above 250 mg/dl (mean 348 +/- 96 mg/dl) inspite of a lipid lowering diet and a therapy with conventional lipid lowering drugs during a three month screening period. After 4 weeks on placebo 20 mg lovastatin was given orally for 4 weeks. If total cholesterol exceeded 200 mg/dl the dose of lovastatin was increased monthly by 20 mg up to the maximal dose of 80 mg/day. After 16 weeks lipid values changed compared with the placebo period: total-cholesterol -25%, triglycerides -8.6%, LDL-cholesterol -31%, APO B -25%, HDL-cholesterol +5.8%, APO AI +0.8%, total-cholesterol/HDL-cholesterol -25%. There was a significant improvement of lipid parameters after lovastatin therapy compared with conventional lipid lowering drugs at the end of the screening period. Lovastatin was well tolerated. A small and reversible rise of transaminases and/or creatinine kinase was observed in 6 patients. Basal levels of ACTH in the morning increased significantly during lovastatin therapy within the normal range. This observation was more frequent in females (10/12) than in males (10/17).

Adrenocorticotropic Hormone↗
PubMed1991

[Effects of high and low doses of acetylsalicylic acid on the restenosis rate after initially successful coronary angioplasty].

A comparison was made in 79 patients (63 men, 16 women: mean age 52 +/- 9 years) of the effect of high and low doses of aspirin on restenosis rate during the first six months after originally successful percutaneous transluminal coronary angioplasty (PTCA), 39 patients (group 1) received 1000 mg aspirin daily, while 40 (group 2) received 100 mg daily. All patients took 1000 mg aspirin as loading dose on the day before PTCA, and additionally calcium antagonists and slow-release nitrates in the post-PTCA period. Both groups were comparable with respect of localization of the dilated coronary artery stenosis and the morphological changes after dilatation. Intimal lesions after PTCA were demonstrated in 9 patients of group 1 and 10 of group 2. Within six months clinically significant restenosis had occurred in 8 patients of group 1 and 7 of group 2. 33 patients in group 2 and 31 in group 1 were free of symptoms and had no ischaemic reaction on the exercise ECG six months after the initial successful PTCA. These results demonstrate that high aspirin dosage does not reduce the restenosis rate more than low dosage.

Adult↗
PubMed1991

Are antisarcolemmal (ASAs) and antimyolemmal antibodies (AMLAs) "natural" antibodies?

Antisarcolemmal (ASAs) and in particular antimyolemmal antibodies (AMLAs) are a serologic hallmark of inflammatory heart muscle disease and its sequelae. Since they may also occur to a much lesser incidence with increasing age, it was examined whether they also possess properties of "natural antibodies". As natural antibodies, AMLAs and ASAs have specificity for conserved structures on the membrane. They possess cross-reactivity and increase with age. In contrast to natural antibodies, however, they occur most frequently after viral stimulation, and are more often of the IgG- and IgA- than of the IgM-isotype and fix complement in the acute stage of the disease. They also exhibit cytolytic and cytotoxic properties when incubated in vitro with isolated heart muscle cells. In addition, antigenic mimicry has been demonstrated to be operative, since they are cross-reactive to viral proteins.

Adult↗
PubMed1991

Compensatory mechanisms for cardiac dysfunction in myocardial infarction.

Loss of contractile myocardial tissue by myocardial infarction would result in depressed cardiac output if compensatory mechanisms would not be operative. Frank-Straub-Starling-mechanism and increased heart rate and contractility due to sympathetic stimulation are unlikely to chronically compensate for cardiac dysfunction. Structural left ventricular dilatation may be compensatory, but results in increased wall stress and, ultimately, in progressive dilatation and heart failure. In patients with myocardial infarction, we have shown left-ventricular dilatation in dependence of infarct size and time after infarction. Dilatation is compensatory first and normalizes stroke volume. However, left ventricular dilatation progresses without further hemodynamic profit and, thus, may participate in development of heart failure.

Animals↗
PubMed1991

Effect of mediators on coronary circulation.

A number of vasoactive mediators have been identified in plasma and in the heart. Some of them may be liberated in inflammatory heart disease. The action of mediators on coronary vasculature in various animal models and their potential role in inflammatory heart disease is reviewed. Their role in patients remains to be determined.

Adrenal Glands↗
PubMed1991

Prognostic determinants in conventionally treated myocarditis and perimyocarditis--focus on antimyolemmal antibodies.

In this study from two specialized centres 85 patients with histologically proven myocarditis (n = 10) and clinically ascertained perimyocarditis (pericardial effusion and cardiomegaly or segmental wall motion abnormality; n = 75) were followed up for 4.5 + 1.9 years. Immunosuppressive treatment was not applied. After a mean follow-up period of 4.5 + 1.9 years 55% of patients had improved clinically and 35% of patients were completely free of symptoms. Relapses had occurred up to three times. Chronic forms were found in 20% of patients, mostly in those with pericarditis and effusions. Eighteen percent of the patients deteriorated gradually. In 20% of the chronic or deteriorating patients congestive heart failure developed (postmyocarditic heart muscle disease). Fifteen percent of the patients died, mainly from bacterial perimyocarditis and to a lesser extent from inflammatory heart disease from enteroviruses. Patients who succumbed after more than 6 months died either suddenly or from progressive heart failure. A favourable outcome was often accompanied by a decrease in titre, but this decrease was less impressive in those who had antimyolemmal and antisarcolemmal antibodies. The persistence of these antibodies in high titres predominated in patients with poor prognosis and postmyocarditic dilated heart muscle disease, as did cytolytic serum activity.

Autoantibodies↗
PubMed1991

[Possibilities of ACE inhibitor therapy in acute myocardial ischemia].

Acute myocardial ischemia results from an increased cardiac workload in presence of a critical coronary stenosis (demand ischemia), coronary occlusion (supply ischemia) or a combination of both. It is complicated by cardiac arrhythmias and deterioration of function of ischemic myocardium and results in an increased load and dilatation of non-ischemic myocardium. Cardiac protection in acute myocardial ischemia can be related to preservation of coronary blood flow, function of ischemic and non-ischemic myocardium or prevention of cardiac arrhythmias. In control animals and humans, ACE-inhibitors have no major effect on coronary blood flow. Myocardial ischemia raises plasma-renin-activity, angiotensin I-conversion by passage through coronary circulation, and plasma-angiotensin-II-concentrations. ACE-inhibitors and angiotensin-II-receptor blockers increase coronary blood flow during myocardial ischemia. Other mechanisms (bradykinin potentiation) may be involved. We found a potentiation of the coronary dilatory effect of the neuropeptide neurotensin (which is probably mediated by prostaglandins) by ACE-inhibitor. ACE-inhibitor may delay infarct development in animal experiments and improve function of ischemic myocardium. The importance of early dilatation of non-ischemic myocardium is unknown and it is unclear whether it may be prevented by an ACE-inhibitor as was shown for late dilatation. Studies on the effect of ACE-inhibitors in exercise-induced angina pectoris are controversial. An antiischemic and coronary dilatory effect has been shown by invasive studies in patients. A preliminary study in unstable angina pectoris was positive. Beneficial hemodynamic and antiarrhythmic effects (as well as excessive hypotension, however) have been shown in patients with acute myocardial infarction.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1991

Effects of acetylsalicylic acid on renal function in patients with chronic heart failure.

PURPOSE: We conducted a double-blind, placebo-controlled trial to determine whether the administration of acetylsalicylic acid has adverse effects on renal function in patients with moderate chronic congestive heart failure with and without stimulation of the renin system. PATIENTS AND METHODS: Forty patients were randomly assigned to one of the following four groups: Group 1, low sodium diet and placebo; Group 2, low sodium diet and acetylsalicylic acid; Group 3, normal sodium diet and placebo; or Group 4, normal sodium diet and acetylsalicylic acid. Patients were studied over 8 days. After Day 5, patients in Groups 2 and 4 received acetylsalicylic acid (500 mg three times a day). The low sodium diet consisted of 13.6 mmol of sodium per day and the normal sodium diet consisted of 136 mmol of sodium per day. RESULTS: The low sodium diet resulted in a highly significant increase in the plasma renin (2p = 0.0001), aldosterone (2p = 0.0006), and urinary prostaglandin E2 (2p = 0.01) concentrations and the renal potassium excretion (2p = 0.0009), whereas renal sodium excretion was significantly reduced (2p = 0.0001). Severe sodium depletion led to a reduction of the glomerular filtration rate (2p = 0.007), which was independent from cyclooxygenase inhibition. In patients on the low sodium diet, acetylsalicylic acid reduced the elevated urinary prostaglandin E2 levels to normal values without changing the renal sodium excretion rate. In patients with a normal sodium intake, acetylsalicylic acid significantly reduced the renal sodium excretion rate by 29% (2p = 0.04). CONCLUSION: We conclude that severe sodium depletion has adverse effects on kidney function in patients with heart failure due to a reduction in the glomerular filtration rate. Administration of acetylsalicylic acid in doses that reduce the synthesis of renal prostaglandin E2 significantly reduces renal sodium excretion.

Aspirin↗
PubMed1991

[Experimental and clinical possibilities of MR spectroscopy of the heart].

MR-spectroscopy of the heart is a relatively new technique for the study of various aspects of cardiac metabolism. The majority of results has so far been obtained with the isolated perfused heart. Here, 31P-MR spectroscopy can be employed to measure high-energy phosphate metabolism and intracellular pH repeatedly and non-invasively. Using a technique called saturation transfer, velocities of enzymatic reactions, such as the creatine kinase reaction, can be measured. Intra- and extracellular Na+ and K+ concentrations can be registered with 23Na- and 39K-MR in conjunction with shift reagent. 13C-MR can be used to tackle carbohydrate metabolism. In-situ-R-spectroscopy allows determination of high-energy phosphates in intact large mammals. Clinical applications of MR-spectroscopy remain to be defined; preliminary results indicate high diagnostic and prognostic potential for patients with coronary artery disease and congestive heart failure.

Animals↗
PubMed1990

Influence of angiotensin-converting enzyme inhibition on cardiac function in myocardial infarction.

Cardiac function in myocardial infarction (MI) depends on the extent of damage in ischemic myocardium and the compensatory response of residual myocardium. Because thrombolytic therapy is performed in many patients, reperfusion of ischemic myocardium may take place at various stages of progression of the ischemic insult. If perfusion is reestablished before necrosis occurs, myocardium may recover immediately or after hours to weeks ("stunned myocardium"). If coronary occlusion persists, necrosis develops in the subendocardium, propagates transmurally and forms a scar after the healing phase. Residual myocardium responds to loss of contractile tissue and material properties of the ischemic zone by hypertrophy and dilatation. This study shows that left ventricular dilatation is accompanied by an increase in stroke volume from 4 days to 4 weeks; however, left ventricular dilatation progresses while stroke volume remains constant from 4 weeks to 6 months, suggestive of noncompensatory left ventricular dilatation. Angiotensin-converting enzyme (ACE) inhibitors have been shown to reduce lactate production after 60 seconds, and infarct size after 6 hours of coronary occlusion in dogs. Stunned myocardium recovers faster in animal experiments and pacing-induced myocardial ischemia may be prevented by ACE inhibitors. Left ventricular dilatation and mortality is reduced by ACE inhibitors in rats after MI. Several potential mechanisms are discussed to establish a favorable action of ACE inhibitors at various stages of MI. Clinical evidence is still pending; however, large studies are ongoing to clarify potential indications of ACE inhibitors in ischemic heart disease in humans.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1990

Exercise capacity, hemodynamic, and neurohumoral changes following acute and chronic administration of flosequinan in chronic congestive heart failure.

We evaluated the responses to 90 minutes and 8 days of therapy with a new long-acting vasodilator flosequinan in ten patients with moderate chronic congestive heart failure in an open, uncontrolled study. Acute administration of 100 mg orally resulted in a decrease of preload, with a reduction of left ventricular end-diastolic volume, left ventricular end-diastolic pressure, pulmonary capillary wedge pressure, and right atrial pressure. Following the acute administration, we found no significant changes of heart rate, cardiac index, stroke volume, peripheral vascular resistance, ejection fraction, and dp/dt. Chronic application for 8 days (100 mg/day) showed persistent effects on preload, with a significant decrease of pulmonary capillary wedge pressure, right atrial pressure, and pulmonary arterial pressure. After 8 days of treatment, cardiac index was significantly increased from 2.2 +/- 0.2 l/min/m2 to 2.8 +/- 0.2 l/min/m2 (p = 0.013) and stroke volume from 57 +/- 10 ml to 74 +/- 9 ml (p = 0.022). Peripheral vascular resistance decreased by ml (p = 0.022). Peripheral vascular resistance decreased by 28%. After 8 days, bicycle exercise capacity increased significantly from 383 +/- 44 sec to 422 +/- 43 sec (p = 0.01) and the patients were able to increase their walking distance over a 6-minute exercise test from 426 +/- 46 m to 477 +/- 33 m (p = 0.007), with a concomitant decrease of dyspnea (p = 0.013). Plasma renin concentration showed only a rise 90 minutes after the acute administration on day 8 of the study, and atrial natriuretic peptide and 6-keto-prostaglandin F1-alpha decreased significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic Disease↗
PubMed1990

Immunological features in a case of hypereosinophilic syndrome and myocarditis.

The clinical and immunological follow-up of a 38-year-old female patient with hypereosinophilic syndrome and classical cardiac involvement, but without demonstrable degranulation of eosinophils and lacking binding of a specific antibody for activated eosinophils, is presented. Instead, the patient demonstrated all the immunological features of autoreactive myocarditis: cytolytic, complement-fixing antimyolemmal antibodies and increased concentrations of circulating immune complexes were present over 3 years.

Adult↗