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Biomedical subjects

K Kochsiek

Publications and source records attributed to K Kochsiek.

At least 37 records · Page 2Linked to original sources
PubMed1994

[Indications for ACE inhibitors in the postinfarct period].

Prognosis of patients post-myocardial infarction depends largely on the degree of left ventricular dysfunction, which results from loss of contractile tissue and remodeling of infarcted and surviving myocardium. This remodeling process may result in chronically progressive dysfunction and ultimately in heart failure. Next to mechanical determinants humoral control of hypertrophy, dilatation and qualitative changes of surviving myocardium are discussed. A major determinant of the extent of remodeling is infarct size. Efficacy of angiotensin-converting enzyme (ACE) inhibitors on infarct size was tested in animal experiments with conflicting results. Recent clinical studies also report beneficial (GISSI-3 and ISIS-4) or no (CONSENSUS II) effects on survival post-myocardial infarction when ACE-inhibitors were used in the acute phase. Up to date it remains unsettled which patients may benefit from acute therapy with ACE-inhibitors. Three days after myocardial infarction hemodynamically stable patients with heart failure may be treated with ACE-inhibitors (AIRE study). Prognosis may be improved and manifestation of heart failure prevented or delayed also in patients without heart failure treated in this phase of myocardial infarction with ACE-inhibitors (SAVE study). Prevention of heart failure may also be observed in patients treated later (at least 4 weeks) after myocardial infarction (SOLVD prevention arm). It is essential for this indication that patients are carefully selected for treatment depending on left ventricular function. Duration of treatment in patients with severe left ventricular dysfunction probably has to be lifelong, the doses of ACE-inhibitors used have to be relatively high (e.g. 3 x 50 mg captopril or 2 x 10 mg enalapril).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

[Acute pancreatitis and stomach wall necrosis caused by cholesterol embolisms].

A 60-year-old man was hospitalized because of a sudden onset of severe pain in the epigastrium and haematemesis. Acute pancreatitis was diagnosed on the basis of an increased serum amylase concentration (642 U/l). Abdominal ultrasound and computed tomography demonstrated a necrotic zone with central liquefaction in the tail of the pancreas adjoining the stomach wall. Gastroscopy revealed as source of the bleeding an extensive mucosal necrosis at the greater curvature of the stomach. At laparotomy, partial resection of the pancreas, gastrectomy and splenectomy were performed. Histological examination of the resected specimens showed multiple cholesterol emboli in the small arteries of the pancreas and the gastric submucosa.

Acute Disease↗
PubMed1993

Clinical and prognostic effect of a positive granulocyte scan in infective endocarditis.

Thirty patients with clinical signs of infective endocarditis and pathologic echocardiographic findings indicating vegetations underwent scanning with In-111 or Tc-99m hexamethylpropylene amineoxime (HMPAO) labeled granulocytes. Blood cultures were positive in 60% of the patients. The other cases were negative as a result of antibiotic pretreatment. The results of scintigraphy were correlated with the subsequent clinical course, and in 20 cases with data obtained by histologic examination of the valves. With regard to the degree of the inflammatory process, the nuclear medical procedure provided the following results: true-positive in 6 cases, false-positive in 1 case, true-negative in 19 cases, and false-negative in 3 cases. In this study, positive granulocyte scans correlate with high activity of the inflammatory process and predict a poor prognosis for the patients concerned.

Echocardiography↗
PubMed1993

[Epidemiology and prognosis of myocardial infarct and chronic heart failure].

The incidence of coronary heart disease and myocardial infarction fell gradually during the seventies. Reasons for this decline are not well understood. Speculations include changes of life style and health care. However, cardiovascular disease is still the leader of mortality in Western developed countries. Mortality of myocardial infarction has also declined. The major benefit was associated with broad establishment of coronary care units, smaller steps were achieved by various progresses in medical treatment. In contrast, the incidence of heart failure has increased. The major etiology of heart failure nowadays is coronary heart disease, especially large or recurrent myocardial infarction. The incidence of heart failure in patients having recovered from myocardial infarction is dramatically higher than in normal population. The Framingham Study showed an incidence of 14% in five years following a myocardial infarction. Prognosis of patients with manifestation of symptoms of heart failure is very poor. Patients with heart failure had an overall six years mortality of 55%. These observations suggest that coronary care units, thrombolysis and modern treatment as developed so far, suppressed in-hospital mortality and improved survival for the first year after a myocardial infarction. Thus, patients with larger infarcts who had succumbed early under previous regimens, survived. They carry, however, the burden of severely impaired left ventricular function, high probability to develop heart failure, and of a dubious long-term prognosis. Large efforts have put upon development of scores to estimate long-term prognosis after a myocardial infarction. With the development of techniques, composition of scores changed. However, residual ischemia, major left ventricular dysfunction, and ventricular arrhythmias are the basis of most scores indicating an adverse prognosis after an infarction. This review will be limited to the prognostic impact of left ventricular dysfunction and development of heart failure post myocardial infarction. A hypothetic cascade of events which may lead from myocardial infarction to heart failure and death is schematically outlined in Figure 1. Loss of contractile myocardium results in left ventricular dysfunction which may induce dilatation of the left ventricle, heart failure and ultimately death. This paper focuses on the evidence for the prognostic impact of the single steps and the whole cascade. Figure 1 shows in parenthesis the variables which were frequently measured to assess loss of contractile tissue, left ventricular dysfunction, and dilatation. Since heart failure is understood as a clinical syndrome of symptoms, it may only be semi-quantitated according to the classification of the New York Heart Association (NYHA).(ABSTRACT TRUNCATED AT 400 WORDS)

Cause of Death↗
PubMed1993

Cytolytic cross-reactive antibodies directed against the cardiac membrane and viral proteins in coxsackievirus B3 and B4 myocarditis. Characterization and pathogenetic relevance.

BACKGROUND: Coxsackievirus B3 and B4 (CVB) myocarditis was assessed by a more than twofold change in titer of the microneutralization tests against enteroviruses within 3 weeks in all patients, by an endomyocardial biopsy indicative of active myocarditis in eight cases, and by pericardial effusion and acute cardiomegaly in two patients. In all endomyocardial biopsies, immunoglobulin binding to the sarcolemma and to the interstitial tissue was demonstrated irrespective of an infiltrate being at the same focus or not. IgG binding was found in nine, IgM and IgA in seven, C3 in C1q in three, and C5b9 in three of 10 patients. In addition, circulating antimyolemmal antibodies (AMLAs) were demonstrated regularly. METHODS AND RESULTS: In this study, for the first time adult human myocytes isolated from atrial appendages during open-heart surgery were used as antigen in the indirect immunofluorescence test: nine of 10 sera of patients with CVB myocarditis demonstrated AMLAs of the homologous type in titers of 1:40-1:320, whereas eight of 10 reacted with rat myocytes (heterologous type) only. Circulating AMLAs fixed complement component C4 in the majority of cases. During the in vitro assay of antibody-mediated cytolysis with vital heart cells, fixation of components C3, C4 to the myolemma in all, of C1q in seven, and of the C3b9 complex in eight of 10 sera was demonstrated after addition of a fresh complement source, indicating the potential of a complement-mediated cytolysis being operative. In vitro cardiocytolysis of isolated adult rat heart cells is present in the untreated sera of patients with enteroviral myocarditis and is abolished after adsorption of sera with CVB and with isolated rat heart cells. This indicates functional cross-reactivity of the antimembrane antibodies. To analyze further the cross-reactive epitopes, sodium dodecyl sulfate gel electrophoresis of human and rat sarcolemma and consecutive immunoblots were performed. Cross-reactivity between viral (CVB) and sarcolemmal epitopes could be demonstrated to bands of 220 kd in 10%, 110 kd in 50%, 48 kd in 40%, 35 kd in 40%, and 31 and 28 kd in 30% each. Cardiospecific non-cross-reactive epitopes for antisarcolemmal antibodies or AMLAs were membrane proteins of 90 kd and 78 kd in 50%, 72 kd in 90%, 67 kd in 40%, and 45 kd in 50%. Virus-specific antibody binding sites for sera included proteins of 33 and 34 kd. CONCLUSIONS: Western blot analysis of sera incubated with cardiac membranes or enteroviral proteins demonstrated that the antibodies are directed to defined epitopes of the sarcolemma. Some antibodies were cross-reactive to enteroviral proteins, indicating that enteroviral infection may be the etiological trigger of an autoreactive myocarditis. The cytolytic property of the patients' sera in vitro suggests in addition that humoral autoreactivity and antigenic mimicry are major pathogenetic principles operative in human enteroviral myocarditis and its sequelae.

Adsorption↗
PubMed1993

Adaptation to cardiac dysfunction after myocardial infarction.

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 days (range, 2-6 days) and 4 weeks (range, 3-5 weeks) to 6 months (range, 5-8 months) after infarction and were repeated during supine bicycle exercise at 50 W. In patients with small infarction, end-diastolic volume (mL/m2) decreased from 4 days to 6 months; ejection fraction (%), stroke volume (mL/m2), and end-systolic volume (mL/m2) remained unchanged. Stroke index rose during exercise at 4 weeks and 6 months. In patients after large infarction (n = 37), left ventricular end-systolic volume index (4 days, 38 +/- 3; 4 weeks, 47 +/- 3*; 6 months, 52 +/- 3*; *p < 0.05 versus 4 days) and end-diastolic volume indexes (4 days, 72 +/- 3; 4 weeks, 86 +/- 5*; 6 months, 92 +/- 5*; *p < 0.05 versus 4 days, +p < 0.05 versus 4 weeks) increased at constant wedge pressure. Stroke index remained restored beyond 4 weeks after infarction (4 days, 35 +/- 2; 4 weeks, 42 +/- 2*; 6 months, 42 +/- 2*; p < 0.05 versus 4 days) and rose during exercise at 4 weeks (rest, 45 +/- 2; exercise, 55 +/- 3; p < 0.05) but not at 6 months (rest, 42 +/- 3; exercise, 45 +/- 3; p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
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↗