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Biomedical subjects

F Burkart

Publications and source records attributed to F Burkart.

At least 73 records · Page 4Linked to original sources
PubMed1988

["Ambulatory" monitoring of left ventricular function using a scintillation detection system. Evaluation of a new method].

To validate a new portable scintillation probe (VEST) for determination of LV function, 68 patients were studied after standard radionuclide angiography (RNA). Reproducibility of VEST LV-ejection fraction was good (rest r = 0.93; exercise r = 0.96) with unchanged probe position, somewhat less good after probe repositioning (r = 0.84) and correlated with RNA (rest r = 0.79; exercise r = 0.83). Long term measurements in 7 patients showed valid data for up to 12 hours. Combined with simultaneous two lead ECG recording VEST seems suitable for detection of transient changes of LV function such as occur during ischemia or due to drug treatment.

Exercise Test↗
PubMed1988

[The treatment of heart infarct in comparison: attempt at quality control].

Treatment of patients with acute coronary artery disease in a medium-sized hospital (with multidisciplinary intensive care unit) is compared with treatment in a university hospital. Two groups of 68 patients (under 70 years of age, without preexisting infarction) are comparable in history, physical findings, infarct size and localization, and complications. Quality or care is assessed on the basis of the findings at discharge and the length of hospital stay. We conclude that the quality of care in a medium-sized community hospital (in collaboration with the university hospital) is satisfactory.

Adult↗
PubMed1988

Effects of vasodilators on the coronary circulation in congestive heart failure.

Pressure or volume overload of the myocardium increases the wall stress, particularly of the subendocardium, and leads to hypertrophy. Even though cardiac hypertrophy is viewed as a beneficial compensatory process that normalizes wall stress, the increased muscle mass carries with it the need of increased blood supply. Overall flow per unit mass is similar at rest in hypertrophic and normal hearts but a reduction of flow to the subendocardium and an increase in minimal coronary vascular resistance have been described. Thus, the potential exists for a vasodilator-induced steal mechanism shunting blood away from potentially ischemic areas. Angiotensin-converting enzyme inhibitors reduced myocardial oxygen consumption and coronary blood flow in parallel manner in some studies, indicating preserved coronary autoregulation, but there is also some evidence of a coronary vasodilator effect. Calcium antagonists reduce coronary vascular resistance and improve the myocardial demand-supply ratio, but the clinical usefulness of the newer compounds with supposedly little or no negative inotropic effects remains to be established. Hydralazine improved the myocardial oxygen demand-supply ratio in patients with dilated cardiomyopathy, but metabolic function may deteriorate more often after hydralazine than after angiotensin-converting enzyme inhibitors in patients with coronary heart disease. Similar observations have been made using alpha-adrenergic blockers. Although progress has been made in the understanding of the coronary circulation and the influence of vasodilators in congestive heart failure, many questions await clarification using refined or new methodology.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1988

Ambulatory scintigraphic assessment of transient changes in left ventricular function: a new method for detection of silent myocardial ischaemia.

Demonstration of ischaemic left ventricular dysfunction in the absence of chest pain should provide important confirmation of silent myocardial ischaemia in patients with asymptomatic ST segment changes. For this purpose, a new portable scintillation probe (VEST) similar to a miniaturized nuclear stethoscope combined with a Holter ECG was evaluated. After standard equilibrium radionuclide angiocardiography with technetium-99m labelled red blood cells, the VEST was positioned under gamma-camera control and data were recorded from 1-12 h in 61 unselected patients. Ejection fraction (LVEF), relative changes in volumes, heart rate and ST segment changes were determined. Reproducibility of LVEF at rest (r = 0.91; variability 3.8 +/- 3%, N = 19) and during exercise (r = 0.98; variability 3.2 +/- 2%, N = 19) was good. In 15 asymptomatic exercise tests four different patterns of LVEF and ST segment responses were identified: (1) decrease in LVEF followed by significant ST depression (five times); (2) ST depression followed by decrease in LVEF (three times); (3) decrease in LVEF without significant ST changes (three times); and (4) ST depression without significant LVEF change (four times). In this still small series, patterns (1) to (3) corresponded to patients with documented coronary artery disease, which was not the case for pattern (4). For detection of silent ischaemia at rest, a decrease in LVEF of greater than 5% lasting for greater than 1 min was defined as ischaemic LV dysfunction. Using this definition, four spontaneous episodes of silent LV dysfunction could be demonstrated in two of three CCU patients with unstable angina during 160-680 min of data recordings without simultaneous ST changes.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Hemodynamic effects of penticainide (CM 7857), a novel class I antiarrhythmic drug--comparison with disopyramide.

Penticainide (CM 7857) is a new class I antiarrhythmic agent, which has been shown to suppress ventricular arrhythmias by a specific effect on repolarization, shortening the action potential duration. To assess acute hemodynamic effects of penticainide and to compare them to those of disopyramide, 20 patients with normal left ventricular function were studied by simultaneous left and right heart catheterization before as well as 5 and 30 min after intravenous drug administration (1.5 mg/kg for both compounds) in a randomized fashion. After penticainide, a maximal negative inotropic effect was noted at the end of the 5 min infusion, as reflected by reductions in stroke index and parameters of contractility despite increases in vascular resistances. These changes returned to baseline after 30 min except for ejection fraction, which was still lower than at baseline. After disopyramide, similar hemodynamic drug effects were observed that were greater than after penticainide, leading to a moderate tachycardia immediately after drug infusion. In addition, all parameters of contractility as well as stroke index were still significantly reduced 30 min after disopyramide, but not after penticainide. Thus, the hemodynamic profiles of both drugs tested were similar, but the negative inotropic effect of penticainide was less marked and of shorter duration than that of disopyramide in an equipotent antiarrhythmic dose. Penticainide may therefore be used in treatment of acute ventricular arrhythmias, but it should be administered with caution in patients with depressed left ventricular function.

Adult↗
PubMed1988

Prospective controlled randomized trial of prophylactic antiarrhythmic therapy in postmyocardial infarction patients with asymptomatic ventricular arrhythmias--study design and initial results.

In order to assess the effect of prophylactic antiarrhythmic therapy in asymptomatic patients with persistent complex ventricular ectopic activity after myocardial infarction, a prospective controlled trial was started in 1981 and is still ongoing. Until August 1986, 965 consecutive patients less than or equal to 70 hospitalized for acute myocardial infarction were screened without antiarrhythmic drugs by 24-h ECG before discharge from the hospital. In this group, 238 patients (28%) had ventricular arrhythmias Lown class III-IVb during at least 2 of 24 hours; they were randomly assigned to three treatment groups: (1) individualized antiarrhythmic therapy based on efficacy in multiple 24-h ECGs and drug level determinations (starting with mexiletine or quinidine; n = 79), (2) treatment with low-dose amiodarone (200-400 mg/day after a loading phase; n = 73), and (3) no antiarrhythmic therapy (n = 86). The three groups were comparable regarding age, gender, previous infarction, Q-wave infarction, ejection fraction, as well as incidence and severity of ventricular ectopic activity. Follow-up, including 24-h ECGs, was performed after 3, 6, and 12 months. Based on the results of this study which will be completed by the end of June 1988, it should be possible to estimate the benefit--or harm--of antiarrhythmic drug therapy as well as its cost in postmyocardial infarction patients with asymptomatic ventricular ectopic activity and to decide whether such treatment may improve survival.

Aged↗
PubMed1988

Heart valve replacement with St. Jude Medical valve prosthesis. Long-term experience in 743 patients in Switzerland.

Between November 1978 and June 1986, 828 St. Jude Medical valves were implanted in 743 patients whose mean age was 57 years (range, 1-83 years) and who had been admitted to the University Hospitals in Basel, Berne, and Lausanne, Switzerland. Aortic valve replacement was performed in 456 patients, mitral valve replacement in 200, tricuspid valve replacement in six, double valve replacement in 77, and triple valve replacement in four. In 187 patients, additional surgical interventions were performed. Operative mortality was 1.6%, and the 4-week postoperative mortality was 4.0%. During a mean follow-up period of 2.6 years, the annual mortality rate was 3.1%, and the annual cardiac mortality rate was 2.1%. The thromboembolic rate per 100 patient-years was 1.3 after aortic valve replacement, 3.0 after mitral valve replacement, and 1.0 after multiple valve replacement. The incidence of major bleeding was 1.3 per 100 patient-years. Valve dysfunction attributable to thrombotic obstruction occurred in three patients, and that attributable to leaflet dislocation in one (annual dysfunction rate, 0.2%). Twelve patients developed infectious endocarditis, six of whom died. However, in four patients, reoperation and, in two patients, antibiotic treatment alone were successful in treating the infection. A paravalvular leak necessitating reoperation developed in 10 patients. In three patients, the leak was caused by infectious endocarditis. Reoperation had no operative mortality. In three patients (0.4%), a mild hemolytic anemia was found.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

[Swiss statistics on the use of cardiac pacemakers in 1986].

The 1986 annual pacemaker survey covers the data from all centers implanting cardiac pacemakers in Switzerland. The number of centres has increased from 34 to 36 while the number of first implants remains unchanged with 226 per million population. Clinical indications, ECG indications and etiology have undergone no significant changes in the last 3 years. Within the pacing system used, however, 13% of VVI pacemakers were now rate responsive, whereas the percentage of physiological pacemakers remained unchanged at 7%.

Humans↗
PubMed1987

[Dipyridamole and low-dose aspirin in patients with aortocoronary bypass--comparison with anticoagulation].

The effects of antiplatelet therapy (AP; dipyridamole 400 mg [beginning 2 days preoperatively] + aspirin 50 mg/day) and anticoagulation (AC) were compared prospectively in 251 patients with coronary artery bypass grafting (CABG). Two weeks postoperatively, 85.2% of AP and 81% of AC patients had all grafts patent with graft patency rates of 93.6% and 91.3% respectively (p = n.s.) Significant differences in favour of AP therapy were found in subgroups with multiple grafts and with low intraoperative graft flow. Up to 3 months postoperatively, severe complications occurred in 22 AC patients (11 bleedings) but only in 9 patients on AP therapy (p less than 0.01). Overall, AP therapy should therefore be preferred to AC in patients with CABG surgery.

Anticoagulants↗
PubMed1987

Arterial vasodilator, systemic and coronary hemodynamic effects of nisoldipine in congestive heart failure secondary to ischemic or dilated cardiomyopathy.

The systemic and coronary hemodynamic and neurohumoral effects of nisoldipine, a calcium antagonist drug with high vascular specificity, were investigated in 17 patients with chronic congestive heart failure (CHF). Brachial artery infusions (n = 9) decreased forearm vascular resistance in a dose-dependent manner, attesting to its powerful arterial vasodilator properties. A dose of 3 micrograms/kg intravenously decreased mean blood pressure 16% and systemic vascular resistance 33%, while increasing stroke index 19% and ejection fraction 21% at rest and similarly during exercise. Pulmonary capillary wedge pressure decreased significantly during exercise. Intravenous infusion of nisoldipine increased rest coronary sinus flow 10% (p less than 0.05, n = 7), decreased rest and exercise coronary vascular resistance 28% and 19% (p less than 0.01) and rest myocardial oxygen consumption 14% (p less than 0.05). In 13 patients similar systemic hemodynamic results were found after treatment with oral nisoldipine, 2 X 20 mg for 4 weeks. Stroke index and stroke work index increased long-term more than acutely (31% and 12.4% vs 19% and 4.5% at rest, both p less than 0.05), which may indicate a compensated mild cardiodepressant effect of intravenous nisoldipine. Changes in forearm vascular resistance after intra-arterial administration did not correlate with changes of systemic vascular resistance after intravenous administration, suggesting that factors other than vascular calcium entry blockade importantly influence hemodynamic responses. Elevated control plasmas norepinephrine and renin levels, on average, did not change during chronic therapy but individual changes were compatible with a reduction of sympathetic activity in patients with hemodynamic improvement.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Paradoxical inhibition of atrial natriuretic peptide release during pacing-induced hypotension.

1. To determine the influence of loss of atrioventricular synchrony on release of atrial natriuretic peptide (ANP), plasma ANP concentrations were measured by radioreceptor assay in 16 patients during sequential and ventricular cardiac pacing at normal heart rates. 2. Ventricular pacing induced an increase in plasma ANP concentrations (means +/- SEM) from 44 +/- 3 to 104 +/- 4 pmol/l (P less than 0.01) in 11 patients in whom systemic blood pressure was maintained. 3. In contrast, when ventricular pacing was associated with a fall in blood pressure (five patients), ANP levels (means +/- SEM) fell from 68 +/- 6 to 14 +/- 4 pmol/l (n = 5, P less than 0.05) within 5 min, despite an increase in atrial pressure. Plasma catecholamines also rose significantly in these latter patients. 4. We conclude that when loss of atrioventricular synchrony is well tolerated haemodynamically, cardiac release of ANP is increased in keeping with elevation in atrial pressure. However, the fall in plasma ANP concentration observed when ventricular pacing produces a fall in blood pressure suggests that in addition to atrial pressure, ANP release may be influenced by negative feedback mechanisms, possibly involving the baroreflex and autonomic nervous system.

Aged↗
PubMed1987

Acute hemodynamic effects of MDL 19205 in mild congestive heart failure.

MDL 19205 4-ethyl-1-,3-dihydro-5-(4-pyridinylcarbonyl)-2H-imidazol-2-one, a new cardioactive agent, has been shown to increase myocardial contractile force in animals. It is effective by both oral and intravenous routes. We studied 11 patients with congestive heart failure--in 10 cases owing to coronary artery disease, and in one to cardiomyopathy. All patients had symptoms of NYHA class II or III, left ventricular ejection fractions (LVEF) less than 55%, and left ventricular end-diastolic pressures (LVEDP) greater than 15 mm Hg. Following routine coronary angiography and ventriculography, 0.5 mg/kg MDL 19205 was administered intravenously over 5 min to six patients. Thirty minutes after injection, hemodynamic measurements and ventriculography were repeated. Mean LVEF increased from 42 to 49% (p less than 0.05 for baseline vs. 30 min). In five patients ventriculography was repeated 60 min after placebo administration: LVEF decreased from 45 to 40%. LVEDP decreased from 29 +/- 8 to 16 +/- 8 mm Hg after MDL 19205 administration (p less than 0.05) and remained constant at 24 mm Hg in the placebo group. The small although nonsignificant increase of LVdP/dt after MDL 19205 administration (10 +/- 33%), together with a considerable decrease in LVEDP, was consistent with a positive inotropic effect. LVdP/dt/total pressure developed (VPM), a measure of contractility relatively independent of changes in pre- and afterload, increased from 1.0 +/- 0.3 to 1.3 +/- 0.3 s-1 (p less than 0.05). Neither parameter of contractility (LVdP/dt and VPM) changed significantly in the placebo group.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiotonic Agents↗
PubMed1987

Electrocardiographic changes during antihypertensive therapy in the International Prospective Primary Prevention Study in Hypertension.

In the International Prospective Primary Prevention Study in Hypertension, electrocardiographic changes before and during 3- to 5-year antihypertensive treatment were investigated in a cohort of 5819 men and women aged 40 to 64 years with entry diastolic blood pressures of 100 to 125 mm Hg. They were randomly allocated to treatment regimens that either included or excluded the slow-release beta-blocker oxprenolol. Electrocardiograms (ECGs) were assessed using the Minnesota Code and assigned to groups of normal ECGs or ECGs with pressure-related, ischemic, "intermediate," or "other" abnormalities. Antihypertensive treatment was associated with a decrease (mainly in men) of pressure-related and (mainly in women) of intermediate abnormalities. Ischemic abnormalities increased, particularly in men. Inclusion of the beta-blocker resulted in a greater reduction in intermediate abnormalities and in a lesser increase in ischemic abnormalities. Better blood pressure control was associated with a lesser increase in ischemic abnormalities and in a regression of pressure-related abnormalities. The presence of ST segment depression and of a complete left bundle branch block in the entry ECG was associated with a significant risk for sudden death and myocardial infarction. Optimal blood pressure control prevents pressure-induced cardiac target organ damage and, hence, heart failure, and may delay the progression of ischemic abnormalities. This tallies with the lower critical cardiac event rate associated with lower blood pressure that was observed in the same study.

Antihypertensive Agents↗