Biomedical subjects

F Burkart

Publications and source records attributed to F Burkart.

At least 19 recordsLinked to original sources

PubMed1992

[Anti-arrhythmia treatment using L-carnitine in acute myocardial infarct].

Carnitine, a quaternary amine (3-hydroxy-4-N-trimethylaminobutyric acid), plays an important physiologic role in fatty acid transport and metabolism as well as in energy production of the myocardial cell. L-carnitine in high doses has been postulated to have an antiarrhythmic effect and this has also been clinically proven. We studied 20 patients with acute myocardial infarction (AMI), 4-12 hours after onset of pain. The patients were randomized and treated double-blind with 5 g L-carnitine (n = 12) or placebo (n = 8) at hours 0, 12, 24, 36, and with 2 x 3 g on days 3 to 7 by intravenous infusion over 2 hours. The two groups were similar for age, sex, infarct site, maximum CPK and conventional antiarrhythmic therapy. 24-hour Holter-ECG was performed on days 1, 2 and 7 and showed no significant difference between the two groups with respect to incidence of ventricular premature beats (VPB) per hour. On the second day following AMI, however, only 4 of 12 carnitine-treated patients showed high-grade VPB (Lown IVa and IVb), in comparison with 7 of 8 patients in the placebo group. The difference is significant: p = 0.028 (Fisher's Exact Test). Carnitine was well tolerated and the efficacy demonstrated on the second day following AMI must be interpreted with caution.

Aged↗

PubMed1992

Beneficial effect of amiodarone on cardiac mortality in patients with asymptomatic complex ventricular arrhythmias after acute myocardial infarction and preserved but not impaired left ventricular function.

To determine whether the beneficial effect of low-dose amiodarone on survival in patients with complex ventricular arrhythmias after myocardial infarction was dependent on left ventricular (LV) function, results of the Basel Antiarrhythmic Study of Infarct Survival were analyzed. Two hundred twelve patients after acute myocardial infarction with asymptomatic complex arrhythmias were randomly assigned to receive amiodarone 200 mg/day or to a control group and followed up for 1 year. Results of mortality and arrhythmic events were related to baseline radionuclide LV ejection fraction. With preserved (greater than or equal to 40%) LV ejection fraction, there was a significantly lower 1-year cardiac mortality in patients treated with amiodarone (1 of 68 or 1.5%) versus control subjects (5 of 56 or 8.9%; p less than 0.03). This was not the case for patients with LV ejection fraction less than 40%. Similarly, arrhythmic events were significantly reduced only in patients with preserved LV function. These results suggest an interaction between the effects of amiodarone on survival and LV dysfunction in patients after acute myocardial infarction. Because of 2 other small studies with similar results, this finding may be of clinical relevance and should be addressed in ongoing and future research with this drug.

Aged↗

PubMed1992

[Mechanisms of myocardial ischemia and circadian fluctuations of ischemic episodes].

The circadian variation of angina pectoris, myocardial infarction and sudden death, with a first peak in the early morning and a second one in the late afternoon, suggests that physical activity plays an important role in triggering ischemic events by an increase of cardiac oxygen demand. But there is also evidence of decreased oxygen supply related to a paradoxical catecholamine-induced vasoconstriction which reflects the endothelial dysfunction of atherosclerotic coronary arteries. Elevated blood pressure during daytime and other mechanical factors can facilitate a plaque-rupture which triggers formation of coronary thrombosis. Hypercoagulability in the early morning hours by increased platelet aggregability and by elevated levels of plasminogen-activator inhibitors may contribute to this fatal mechanism.

Catecholamines↗

PubMed1992

Anticardiolipin antibodies and coronary heart disease.

Arterial or venous thrombotic events have been described as complications in patients with positive anticardiolipin antibodies (aCL), affecting various organs including the heart. In order to see whether aCL could be, among others, a predisposing factor for coronary artery occlusions and whether it could serve as a prognostic marker for coronary heart disease, 232 patients enrolled in the European Concerted Action on Thrombosis Angina Pectoris Study were studied. aCL and various other haemostatic parameters were determined at time of admittance in order to see whether a relationship existed between haemostasis at baseline and extent or prognosis of the cardiovascular disease. A follow-up at 12 and 24 months after angiography included information about relapsing coronary or other thrombotic events, treatment and outcome of the disease. aCL were not found to be a marker of either progressive cardiovascular disease or recurrent thrombotic events. No correlation was found, either in aCL positive or in aCL negative patients, between high levels of haemostasis activation markers, such as beta-thromboglobulin, platelet factor 4 or fibrinopeptide A and recurrent cardiovascular disease.

Aged↗

PubMed1992

Clinical risk assessment after first myocardial infarction--is additional noninvasive testing necessary?

In order to assess whether the outcome of MI can be predicted by clinical data alone or whether and how much noninvasive testing is necessary to predict cardiac events or death, 361 patients were prospectively evaluated and followed for up to five years. A recursive partitioning analysis indicated that high-risk patients can be identified clinically after MI with a high degree of accuracy; to separate low-risk patients who need no further investigation or therapy, however, one additional noninvasive test is necessary which allows quantification of myocardial damage as well as exercise-induced ischemia. Additional tests added little to this risk prediction, indicating that multiple noninvasive testing should not be performed.

Adult↗

PubMed1992

Secondary and tertiary prevention with calcium antagonists in coronary artery disease.

Recent multicentre studies evaluating the therapeutic value of calcium antagonists in reducing the incidence of cardiovascular complications after myocardial infarction (secondary prevention) and in retarding the development of atherosclerosis in coronary artery disease (tertiary protection) are reviewed. The prognosis of patients after acute myocardial infarction can be improved not only by interventional measures such as aortocoronary bypass surgery or percutaneous transluminal catheter angioplasty, but also by various drugs. Numerous studies have shown that beta-blockers and platelet aggregation inhibitors can reduce mortality and reinfarction rates. Calcium antagonists in secondary prevention trials after acute myocardial infarction, however, have produced variable results. Whereas the Secondary Prevention Reinfarction Israeli Nifedipine Trial (SPRINT) [Israeli SPRINT Study Group 1988] with nifedipine showed no beneficial effect of the drug, studies with verapamil in the Danish Verapamil Infarction Trial II (DAVIT II) [Danish Study Group on Verapamil in Myocardial Infarction 1990] and diltiazem in the Multicentre Diltiazem Postinfarction Trial (MDPIT) [Multicenter Diltiazem Postinfarction Trial Research Group 1988] as secondary prevention have demonstrated improvements in survival and cardiovascular complications, but these improvements were restricted to patients without heart failure. In view of the ability of calcium antagonists to reduce atheroma progression in coronary artery disease in animal models, the antiatherosclerotic effects of these agents in clinical studies have generally been disappointing. In the International Nifedipine Trial on Antiatherosclerotic Therapy (INTACT) [Lichtlen et al. 1990], however, nifedipine treatment was associated with a 28% reduction in new lesion development, but did not affect the development of severe lesions. Similar results have been obtained with nicardipine.

Arteriosclerosis↗

PubMed1991

Circulatory abnormalities and compensatory mechanisms in heart failure.

Knowledge of the basic alterations of central hemodynamics in congestive heart failure has failed to explain many aspects of this important syndrome. Increasing attention has recently been paid to compensatory and adaptive mechanisms occurring after the initial insult. Thus, new insights have been gained into the pathophysiology of contraction of hypertrophied myocardium and changes of adrenergic receptors in the myocardium due to chronically increased cardiac sympathetic tone. The role of the renin-angiotensin-aldosterone system in early and advanced congestive heart failure has been further elucidated, and the role of the vasodilating atrial natriuretic peptide is undergoing further definition. New results further clarify the mechanisms leading to breathlessness and muscular fatigue in congestive heart failure, with emphasis shifting from the traditional concept of the importance of increased filling pressures to changes to the peripheral circulation and exercising muscles. Although progress has been made in understanding of the pathophysiology of congestive heart failure, many aspects are still poorly understood and await clarification.

Blood Circulation↗

PubMed1991

Coronary vasodilatation and improved myocardial lactate metabolism after angiotensin converting enzyme inhibition with cilazapril in patients with congestive heart failure.

The effects of angiotensin converting enzyme inhibition on systemic and coronary hemodynamics and on myocardial lactate metabolism were investigated before and 2 and 6 hours after cilazapril at rest and during supine submaximal exercise in 10 patients with New York Heart Association class II or III chronic congestive heart failure. Angiotensin converting enzyme inhibition, indicated by a significant increase in plasma renin activity, resulted in significant reductions in blood pressure and systemic vascular resistance. Myocardial oxygen demand decreased (resting double product 10.9 +/- 3.7 vs 12.2 +/- 3.8 mm Hg beats/min 10(-3); p less than 0.05), but coronary sinus blood flow remained unchanged and calculated coronary resistance decreased (0.45 vs 0.5 units, rest 6 hours; p less than 0.05) suggesting coronary vasodilatation. Changes in coronary vascular resistance were directly related to changes in systemic vascular resistance (r = 0.75, p less than 0.5). Myocardial lactate extraction increased at rest (47 +/- 60 vs 134 +/- 132 mumol/min; p less than 0.5) and during exercise (27 +/- 54 vs 491 +/- 317 mumol/min; p less than 0.05) both in patients with coronary artery disease (n = 5) and idiopathic dilated cardiomyopathy (n = 5). Resting lactate production was converted to lactate extraction in two patients with coronary artery disease. Neither plasma catecholamine nor atrial natriuretic peptide concentrations changed significantly. The results suggest coronary vasodilation and improved aerobic myocardial metabolism by angiotensin converting enzyme inhibition in patients with congestive heart failure.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1991

Prolonged myocardial stunning after thrombolysis: can left ventricular function be assessed definitely at hospital discharge?

To assess whether myocardial dysfunction after acute reperfusion ('stunning') may show delayed recovery, 33 patients of the European Cooperative Study (rtPA vs placebo) had radionuclide angiocardiography on day 9 and after 3-6 months. Sixteen patients (13 inferior, three anterior infarcts) had a normal left ventricular ejection fraction (LVEF) which remained unchanged (55.4 vs 53.9%). In contrast, LVEF of 17 patients (10 inferior, seven anterior infarcts) with depressed values on day 9 improved during follow-up from 38.8 to 45.2% (P less than 0.01). Improvement was only observed in patients with early reperfusion defined a priori as peak creatine kinase value less than or equal to 15 h of pain onset (from 40.9 to 49.3%; P less than 0.05) in contrast to patients without reperfusion (from 34.0 to 35.2%; ns). Accordingly, LVEF increased in patients with open infarct-related arteries at hospital discharge (n = 8; P = 0.053) but not with persistent occlusion (n = 7; P = 0.11). Thus, a depressed LVEF observed 9 days after reperfusion may show delayed recovery due to prolonged stunning. Therefore, after thrombolysis, left ventricular function may not be evaluated definitively at hospital discharge; results of such studies should be interpreted with caution.

Adult↗

PubMed1991

Cilazapril in congestive heart failure. A pilot study.

The haemodynamic effects of a single dose of cilazapril 2.5 or 5 mg were studied in 33 patients with stable chronic congestive heart failure who were receiving digitalis and diuretics. Subsequently, a double-blind comparison of the haemodynamic and clinical effects of 3 months' treatment with cilazapril 1.25 to 5 mg daily or placebo in 24 evaluable patients revealed that the acute haemodynamic improvement produced by a single dose of cilazapril was maintained in patients receiving repeated administration of the drug, but not in those randomly allocated the placebo. Acute cilazapril significantly decreased mean arterial pressure, systemic vascular resistance, pulmonary capillary wedge pressure, pulmonary artery pressure and right atrial pressure, while cardiac index and stroke volume index increased at rest and during submaximal exercise. After 3 months' treatment 11 of 13 cilazapril recipients improved their New York Heart Association (NYHA) class compared with 2 of 11 patients treated with placebo. This functional improvement was paralleled by a patient-perceived improvement in general well-being.

Adult↗

PubMed1991

Effect of antiarrhythmic therapy on mortality after myocardial infarction.

In an attempt to improve survival of patients with coronary artery disease and high-grade ventricular ectopic activity, several studies using different antiarrhythmic drugs were undertaken. A meta-analysis of all randomized controlled trials using type I antiarrhythmic agents showed that the treatment effect was much more likely to be adverse than beneficial. In contrast to these studies, the pooled results of major secondary prevention trials using beta-blocking agents could demonstrate a significant reduction in the sudden death rate by an average of 24% during observation periods of 9-36 months. In the beta-blocker trials, however, patients with contraindications for this type of drug, such as overt congestive heart failure or chronic obstructive lung disease, were excluded. In these patients a type III antiarrhythmic drug, such as amiodarone, may have a place, and in fact, the Basel Antiarrhythmic Study of Infarct Survival, a prospective, controlled, randomized trial using low-dose amiodarone as an antiarrhythmic agent, could demonstrate a 60% reduction in sudden death rate and a 74% reduction in arrhythmic events incidence during the first year after myocardial infarction. Therefore, in patients with repetitive ventricular ectopic activity after myocardial infarction and adequate left ventricular function, a therapeutic attempt with beta-blockers without intrinsic sympathomimetic activity seems advisable. Beside beta-adrenergic blockade, low-dose amiodarone is an alternative, especially in patients with impaired left ventricular function or other contraindications for beta-blockers.

Anti-Arrhythmia Agents↗

PubMed1991

[Diagnostic procedures in patients with known coronary heart disease].

Patients with coronary artery disease can be stratified by noninvasive techniques into risk-groups for further diagnostic and therapeutic management. The prognostic impact of the patient's history, physical examination and ECG are discussed. With this clinical assessment a high-risk group of patients, who should undergo coronary angiography, can be identified. In a low-risk group, further evaluation depends on results of exercise-stress testing. The relative value of exercise ECG, thallium-201-scintigraphy and radionuclide ventriculography in this special clinical setting are discussed in detail.

Algorithms↗

PubMed1991

[Percutaneous transluminal coronary angioplasty].

Since its first application in a patient, PTCA has undergone a tremendous evolution: Based on growing experience and due to technical developments, indications have been markedly extended. Despite the fact that PTCA has been used in more risky situations, the primary success rate has risen and the rate of severe complications has dropped. This evolution is shown based on the Basel experience and on data from Switzerland. The problem of restenosis, however, has not been solved and remains the main problem to be looked for during follow-up of these patients.

Aged↗

PubMed1990

Prevention of aortocoronary vein bypass graft occlusion: which antithrombotic treatment and for how long?

The effects of 50 mg aspirin combined with 400 mg dipyridamole were compared with those of standard anticoagulant therapy, in the prevention of aortocoronary vein bypass graft occlusion. Early graft occlusion in 249 patients, with 749 distal vein graft anastomoses, were angiographically assessed 11.5 +/- 2 days after surgery and were almost equal in both treatment groups. In half of the patients in each group, active treatment was replaced by placebo after 3 months. Repeat angiography after 1 year (360 +/- 24 days) showed that more new late graft occlusions occurred in patients with only 3 months active medication (either regimen). The incidence of major complications was significantly higher in patients treated with anticoagulants, with minor side-effects more common in the antiplatelet group. Thus, this antiplatelet drug regimen was as effective as standard anticoagulant therapy in the prevention of early and late bypass graft occlusion, but carried a significantly lower risk of severe complications. In addition, as replacement of active treatment by placebo after 3 months resulted in significantly more graft occlusions, antithrombotic treatment should be continued for at least one year after coronary artery bypass graft surgery.

Adult↗

PubMed1990

Prevalence and extent of right ventricular dysfunction after myocardial infarction--relation to location and extent of infarction and left ventricular function.

In view of today's efforts to preserve myocardial function in acute myocardial infarction, the prevalence and extent of persistent right ventricular dysfunction was analysed in a prospective study of 127 patients admitted with a first myocardial infarction without thrombolysis. Right ventricular ejection fraction measured at hospital discharge by radionuclide angiocardiography was related to the location of infarction as judged electrocardiographically, its size as estimated enzymatically, and by the simultaneously measured left ventricular ejection fraction. Two opposite patterns of right and left ventricular function were observed in relation to the location of infarction: the right ventricular ejection fraction was significantly depressed in inferior, but not in anterior, infarction and the reverse was true for left ventricular ejection fraction (P less than 0.001 between infarct locations for both right ventricular ejection fraction and left ventricular ejection fraction). There were significant correlations between peak levels of creatine kinase and left ventricular ejection fraction for anterior (r = 0.76, P less than 0.001) and inferior (r = 0.57, P less than 0.001) infarction, while peak levels of creatine kinase and right ventricular ejection fraction correlated only in inferior infarction (r = 0.45, P less than 0.01). There was no overall correlation for left ventricular ejection fraction and right ventricular ejection fraction (r = 0.28, P NS), despite the fact that right ventricular ejection fraction was lower in patients with severely reduced left ventricular ejection fraction than in those with normal left ventricular function (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1990

Cardiac evaluation of candidates for kidney transplantation: value of exercise radionuclide angiocardiography.

In view of the high incidence and mortality of coronary artery disease (CAD) in patients with kidney transplantation, a systematic cardiac evaluation was prospectively performed in 103 uraemic patients eligible for transplantation. After clinical examination, 28 patients with symptoms of CAD or diabetes mellitus were referred directly for coronary angiography, whereas the remaining 75 patients had rest and exercise radionuclide angiocardiography for evaluation of possible asymptomatic CAD. Among them, left ventricular ejection fraction was below 40% at rest or fell during exercise by at least 5 EF% in 12 patients; coronary angiography in nine showed CAD in four and hypertensive heart disease in five. In the remaining 63 (of 75) patients without severe resting left ventricular dysfunction or exercise ischaemia, the follow-up of 28 +/- 7 months revealed no clinical manifestation of CAD. Overall incidence of CAD in symptomatic and asymptomatic patients during a follow-up of 27 months after cardiac evaluation was 20 and 25% in nondiabetic and diabetic candidates for kidney transplantation, respectively (P = n.s.). Thus, clinical examination combined with exercise radionuclide angiocardiography in patients without signs or symptoms of heart disease had a high predictive accuracy for presence or absence of late manifestations of CAD. Exercise radionuclide angiocardiography is therefore a useful method for screening kidney transplantation candidates for asymptomatic CAD.

Adult↗

PubMed1990

[The long-term management of heart transplant patients].

The long-term care of patients following heart transplantation is characterized by the problems associated with long-term immunosuppression. In addition, a specific form of coronary atherosclerosis develops within years in many patients requiring coronary angiography on a yearly basis. The examination of patients after heart transplantation does not reveal characteristic findings, as long as the transplanted heart functions properly and a normally functioning graft allows a functionally almost normal life. The dependence on a specialized center, which may be more or less depending on the clinical course, and the ever present knowledge of the potentially lethal consequences of a graft failure present a severe psychic stress to the patient. This stress is handled more or less well and requires special attention by the treating physicians and, ideally, an intact social environment. The care of patients in a center close to their place of living is less time consuming for the patient and relieves the burden of the transplanting center.

Follow-Up Studies↗

PubMed1990

Relations between sympathetic activation and plasma atrial natriuretic factor in man.

To study the relationship between sympathetic activation and cardiac release of atrial natriuretic factor in man, plasma concentrations of norepinephrine, epinephrine and atrial natriuretic factor were measured in 20 patients before and after dynamic exercise (16 subjects) or the application of venous occlusion cuffs to the thighs (4 subjects). Plasma concentrations of norepinephrine, epinephrine and atrial natriuretic factor all increased during exercise, whereas venous occlusion produced a fall in plasma atrial natriuretic factor. There was no relation between basal plasma concentrations of atrial natriuretic factor and either norepinephrine or epinephrine. However, there was a linear relation between the changes in plasma atrial natriuretic factor induced by exercise or thigh cuffs and both plasma norepinephrine (r = 0.829, p less than 0.0001) and epinephrine (r = 0.733, p less than 0.001). We conclude that, in man, acute changes in sympathetic activity and release of atrial natriuretic factor are closely related. Further studies are required to determine whether this association is due wholly to the hemodynamic effects of sympathetic activation, or whether the latter has a direct effect on the release of atrial natriuretic factor.

Atrial Natriuretic Factor↗