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Biomedical subjects

K Kochsiek

Publications and source records attributed to K Kochsiek.

At least 19 recordsLinked to original sources
PubMed1992

Effects of long-term treatment with lovastatin on the clotting system and blood platelets.

In a study of 20 patients with hypercholesterolemia (type IIa) the effects of lovastatin (20-80 mg/day) on various clotting and thrombosis parameters were monitored for 12 months. On 11 occasions various cholesterol fractions and clotting parameters were determined in each patient. In addition, the clotting inhibitors AT III, protein C, protein S, and C1-esterase inhibitor and the fibrinolysis parameters plasminogen and alpha 2-antiplasmin were examined. Platelet function was monitored on the basis of spontaneous and induced (collagen, ADP, epinephrine, ristocetin) aggregation. Lovastatin in the above dosage brought about a 66 mg/dl (from 320 +/- 12.6 to 254 +/- 12.0 mg/dl) reduction in the total cholesterol level and a 56 mg/dl (from 244 +/- 11.4 to 188 +/- 12.1 mg/dl) reduction in LDL cholesterol at the end of the study. Fibrinogen showed a significance decrease during the study period, whereas PT and aPTT remained unaffected. The initial slopes of the ADP-induced platelet aggregation revealed a significant decrease. C-reactive protein and platelet count remained within the normal range, indicating no significant change. Thrombin clotting time, AT III, C1-esterase inhibitor, plasminogen, and alpha 2-antiplasmin were not modified. Protein C and S behaved in a contradictory way, but remained within the normal range. Long-term treatment with lovastatin was associated with a significant reduction of fibrinogen levels and platelet aggregation induced by ADP in type-IIa hypercholesterolemic patients. These alterations, as well as their role in cardiovascular disease, should be the subject of further investigations.

Adolescent↗
PubMed1992

Compensatory and noncompensatory left ventricular dilatation after myocardial infarction: time course and hemodynamic consequences at rest and during exercise.

Survival after myocardial infarction decreases with left ventricular dilatation, although dilatation at 4 weeks was found to be compensatory. To study this apparent discrepancy, prospective simultaneous volume and hemodynamic measurements at rest were extended in 39 patients with small and 37 with large myocardial infarctions from 4 (range 2 to 6) days and 4 (range 3 to 5) weeks to 6 (range 5 to 8) months after myocardial infarction and were repeated during exercise. In small myocardial infarctions, end-diastolic volume index (EDVI) decreased from 4 days to 6 months; ejection fraction, stroke volume index (SVI), and end-systolic volume index (ESVI) remained unchanged. SVI increased during exercise at 4 weeks and at 6 months. In large myocardial infarctions (n = 37) ESVI (4 days = 38 +/- 3, 4 weeks = 47 +/- 3,* 6 months = 52 +/- 3*; *p less than 0.05 versus 4 days) and EDVI (4 days = 72 +/- 3, 4 weeks = 86 +/- 5,* 6 months = 92 +/- 5* ; *p less than 0.05 versus 4 days and p less than 0.05 versus 4 weeks) increased at constant wedge pressure. SVI remained unchanged beyond 4 weeks (4 days = 35 +/- 2, 4 weeks = 42 +/- 2*, 6 months = 42 +/- 2*; *p less than 0.05 versus 4 days) and increased during exercise at 4 weeks (rest = 45 +/- 2, exercise = 55 +/- 3; p less than 0.05) but not at 6 months (rest = 42 +/- 3, exercise = 45 +/- 3; p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Catheterization↗
PubMed1992

Determinants of coronary effects of atrial natriuretic factor in dogs.

The direct vascular action of atrial natriuretic factor (ANF) is unclear. In coronary vasculature, vasodilation has been reported as well as vasoconstriction. Doses of ANF, baseline plasma ANF levels and interference with the renin-angiotensin system might account for the controversy. We tried to further analyse determinants of the effect of ANF on coronary blood flow in anaesthetized dogs. The chest was opened and the left anterior descending coronary artery cannulated and perfused at constant normal (= 76 +/- 5 mmHg, n = 10) or reduced (= 37 +/- 3 mmHg, n = 10) pressure from the femoral arteries. At normal coronary perfusion pressure, ANF (1 ng kg-1 i.c.) reduced coronary flow from 30.7 +/- 4.2 to 26.9 +/- 4.0 ml min-1 (P less than 0.05). This effect was no longer significant at reduced coronary perfusion pressure (4.9 +/- 0.8 vs. 4.6 +/- 0.7 ml min-1). ANF (1 ng kg-1 i.c.) reduced coronary blood flow in correlation with baseline plasma ANF levels (r = 0.77, P less than 0.001). However the large variability of the constrictor effect of ANF in the rather small range of baseline plasma ANF, weakens the importance of this result and suggests other additional determinants. ANF (100 ng kg-1 i.c.) significantly increased coronary blood flow by 16-23% (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Reverse use dependence of antiarrhythmic class Ia, Ib, and Ic: effects of drugs on the action potential duration?

UNLABELLED: The prolongation of the action potential duration (APD) induced by sotalol has been shown to be diminished with increasing heart rate. This phenomenon is called "reverse use dependence." We examined the Ia, Ib, and Ic effects of different Class I drugs on the APD under normal and fast stimulation rates (1.0 and 2.5 Hz) in isolated rabbit atrial and ventricular muscles by means of intracellular microelectrodes. Results (n = 98): With 1.0 Hz lidocaine (Ib, 4.3 x 10(-5) M) shortened the APD at 90% repolarization (APD90) in the atrium by 9% and in the ventricle by 8% (NS), whereas quinidine (Ia, 2.2 x 10(-5) M) and prajmaline (Ia, 10(-6) M) prolonged the APD90 in the atrium (quinidine +45%; prajmaline +10%, P < 0.001) and in the ventricle (+42%, P < 0.001; +17%, P < 0.05). Propafenone (Ic, 2.6 x 10(-6) M) showed this effect only in the atrium (APD90 +33%; P < 0.01). With the faster stimulation rate of 2.5 Hz we could not find a significant influence of any drug on the APD90 in the ventricle and only quinidine prolonged the APD90 in the atrium by 16% (P < 0.05). CONCLUSIONS: The subclassification of Class I antiarrhythmic drugs that is based on APD modifying influences is only valid under normal heart rates (1.0 Hz). During tachycardia these actions are absent and the phenomenon of "reverse use dependence" is found in Class I drugs. Therefore, an additional antiarrhythmic effect due to APD modification by the examined drugs should not be expected at rapid heart rates.

Action Potentials↗
PubMed1992

New concept in activity-controlled pacemakers: clinical results with an accelerometer-based rate adaptive pacing system.

An accelerometer-based rate adaptive generator (EXCEL VR) has been introduced. A preclinical group of 22 subjects with strap-on devices was observed and reported. A clinical protocol including observation of rate adaptive response to typical daily activities and incremental exercise on a treadmill was administered in seven implanted patients. Indications for implantation in these patients was either second- or third-degree atrioventricular block (five patients, VVIR pacing mode) and sick sinus syndrome (two patients, AAIR pacing mode). Mean pacing rates were 50 ppm (supine), 56 ppm (standing), 77 ppm (descending the stairs), 81 ppm (slow walk), 83 ppm (slow stair climb), 91 ppm (fast walk), and 92 ppm (fast stair climb). When the arm proximal to the pulse generator was exercised, the rate rose to 92 ppm. When the distal arm was strained, the rate was 63 ppm. During treadmill testing, rates between 82 ppm (2 km/hour) and 104 ppm (5 km/hour) were observed. This accelerometer-based rate adaptive pulse generator provided a proportional response to graded activities of treadmill exercise and daily living in these groups of preclinical and clinical subjects.

Acceleration↗
PubMed1992

[Indium-111 or Tc-99m-HMPAO marked granulocytes as specific markers of florid stage endocarditis--results comparing clinical, histological and scintigraphic findings in 30 patients with suspected endocarditis].

Thirty patients with clinically suspected infective endocarditis were scanned with Indium-111- or Tc-99m-HM-PAO-labeled granulocytes. The scans were correlated with the clinical course, and in 20 cases with the results from histologic examination of the valves. In six cases the scintigraphic examination gave correct positive results, in three cases false negative, in one case a false positive, and in 20 cases correct negative results. If we limit the analysis to only the histologically proven cases, our data suggest a specificity of the method of 86% and a sensitivity of about 67%.

Abscess↗
PubMed1991

Serial changes in left ventricular size after acute myocardial infarction.

The prognosis is poor for patients with left ventricular enlargement associated with large infarcts. We studied 78 patients using gated single-photon emission computed tomography (SPECT, to assess left ventricular volumes), right heart catheterization (to measure pulmonary wedge pressure and cardiac output), and conventional planar radionuclide ventriculography (to estimate ejection fraction), 2-6 days, 3-5 weeks, and 5-8 months after their first myocardial infarction. Patients were assigned to a large or small infarct-size group based on creatine kinase analysis. In 37 patients with large infarcts, left ventricular volume increased and was greater than 27% after 5-8 months than after 2-6 days (p less than 0.05). Although ejection fraction remained significantly depressed, stroke volume, which initially declined, was restored as a result of dilation and thus returned to normal by 3-5 weeks, indicating that enlargement of the left ventricle compensated for the loss of contractile myocardium and depression of global ejection fraction. The progressive nature of left ventricular dilation suggested that this process is of major pathophysiologic importance and that it plays an etiologic role in the genesis of heart failure and perhaps of sudden death following myocardial infarction. Dilation preceded hemodynamic deterioration, which became evident on exercise after 5-8 months in patients with large infarcts.

Cardiac Volume↗
PubMed1991

[Primary coronary stent implantation in complex morphology of stenosis or unsatisfactory results of angioplasty].

Early and late results of coronary angioplasty are influenced by the morphology of the coronary artery stenosis. Primary implantation of a balloon-expandable Palmaz-Schatz stent was indicated in 37 patients (31 men and 6 women; mean age 57 +/- 2 years) with symptomatic coronary heart disease and complex morphology of the stenosis. Intracoronary stents were successfully placed in 30 of 37 patients, without complications in all but one. This patient developed a thrombotic occlusion of the vessel 3 days after the procedure which, despite high-dosage thrombolysis treatment, resulted in an anterior wall myocardial infarction. A repeat angiography has since been performed (3-7 months after the procedure) in 25 of the 29 patients with a complication-free course. In 19 of the 25 patients the site of implantation was smooth, while a silent re-occlusion had occurred in one after successful recanalization of a chronic occlusion. Two patients had a subtotal restenosis (12% angiographic restenosis rate). These data indicate that intracoronary stent implantation improves the morphological results after balloon dilatation and reduces the restenosis rate.

Angiography↗
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↗