[Long-term results of vasodilator therapy with prazosin in severe refractory cardiac insufficiency].
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Biomedical subjects
Publications and source records attributed to F Burkart.
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To assess the relation between stress-induced perfusion defects and wall motion abnormalities (WMA), 20 patients were studied by thallium-201 (201Tl) scintigraphy and cineventriculography at rest and during exercise. Of 100 analyzed segments, 63 were normal while 13 showed constant (scar) and 24 reversible (ischemia) perfusion defects. At peak exercise, 85% of the scar and 80% of the ischemic segments corresponded to abnormally contracting wall segments. There was a marked correlation between the extent of ischemia and the degree of WMA. The increase in abnormal scintigraphic and angiographic segments from rest to exercise was parallel by a significant deterioration in left ventricular function. It is concluded that (1) ischemic perfusion defects detected by 201Tl scintigraphy correlate well with exercise induced wall motion abnormalities, and (2) the localization, extent and degree of WMA can be predicted by non-invasive 201Tl scintigraphy.
The relationship between clinical findings and invasively measured hemodynamic data was investigated in a prospective trial of 70 patients with acute myocardial infarction. In 26 out of 27 consecutive patients without clinical signs of disturbed myocardial function, normal hemodynamic values were also found invasively. In 43 patients, depressed myocardial function was diagnosed on the basis of the clinical findings. These findings were verified in 38 patients (88%) by means of cardiac catheterization; 5 patients (12%) had normal hemodynamic values. In 26 patients with clinical signs of congestive heart failure, an attempt was made to identify non-invasively those with a low output (cardiac index less than 2/min/m2). Only 3 of the 6 patients with a low output could be identified by clinical examination alone. In one patient a low output was clinically diagnosed despite normal cardiac function measured invasively. In 16 patients, 48 subsequent clinical examinations were performed during treatment of congestive heart failure to identify either persistent elevated left ventricular filling pressure or low output; 15 (31%) were found to be incorrect when compared with the cardiac catheterization data. Patients with acute myocardial infarction and normal ventricular function can be identified with high accuracy by means of clinical examination alone. The clinical diagnosis of congestive heart failure was incorrect in 12% of the patients. A low output state in acute myocardial infarction is often overlooked in clinical examination alone. Of the clinical examinations on patients during therapy, 30% were incorrect. Invasive hemodynamic monitoring in acute myocardial infarction therefore appears to be unnecessary in patients with normal clinical findings, but in those with clinically diagnosed congestive heart failure it is mandatory for precise indication and evaluation of therapy.
Cardiac function is regulated by four parameters: heart rate, preload, contractility and after-load. In the treatment of heart failure cardiac function is influenced by way of these parameters. The longterm pacemaker can normalize heart rate in patients with bradycardia; diuretics and volume load influence the filling pressure of the heart, while glycosides and sympathomimetic drugs increase contractility. If these mechanisms fail, peripases cardiac work. Vasodilators reduce this peripheral constriction was well as the elevated preload, and can therefore improve cardiac performance. The use and limitations of these pharmacological agents are discussed.
Combined ECG/myocardial perfusion szintigraphy (MPS) exercise tests were performed in 82 out-patients with suspected CAD who eventually underwent left heart catheterization. The sensitivity of MPS as compared to ECG was higher in patients with angina (86% vs. 67%) as well as in patients with atypical symptoms (63% vs. 25%). Here MPS was also more specific than ECG (86% vs. 68%). Combination of both tests improved sensitivity even more. The comparison of radionuclide and contrast ventriculography in 20 patients studied at rest revealed an excellent correlation (r = 0.90). Changes in radionuclide ejection fraction during exercise in 60 subjects showed significant differences between normals (increase of greater than 10% above resting level) and patients with CAD (decrease in patients with angina, no significant change without angina). Methods and indications are briefly discussed in the light of this experience.
With the Swan-Ganz catheter it has become possible to measure the hemodynamics repeatedly in patients with acute myocardial infarction. It was shown that the majority of these patients have an elevated filling pressure but cardiac output and stroke volume remain normal. The clinical signs of a third sound, rales and elevated venous pressure are therefore due to the initial backward failure but are not signs of depressed cardiac output. However, in a small group of patients with clinical signs of flow output, treatment with diurectis and vasodilators is necessary. The mean filling pressure of the left ventricle in this subgroup was 26.2 +/- 2 mm Hg at entrance and could be effectively lowered with both treatments. On the other hand, the cardiac index at entrance (2.3 +/- 0.21/min/m2) did not change significantly under vasodilation but in some cases fell dangerously under furosemide. It is therefore considered that in patients with a low output syndrome hemodynamic monitoring is necessary not only when they are treated with vasodilators but also under furosemide.
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A unique case of 'variant' angina pectoris has been observed in a patient with normal coronary arteries and typical chest pain appearing spontaneously at rest, and repeatedly provoked by ergonovine maleate (0.1 mg iv) associated with large transmural perfusion defects on 201Tl-imaging (after ergonovine) and a marked increase in T wave voltage despite no demonstrable spasm of a major coronary artery after the same doses of ergonovine. While saline solution could not provoke chest pain and treatment with a beta-blocking agent increased the frequency of ischemic attacks, a calcium antagonist therapy reduced and eventually eliminated the attacks. Thus, this case provides evidence for yet another aspect of a 'variant' form of angina pectoris: small vessel coronary artery spasm.
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Furosemide was administered intravenously to 11 patients with cardiac failure after acute myocardial infarction. After an initial loading dose furosemide was given four-hourly if the pulmonary capillary wedge pressure (PCW) was not normalized, i.e. less than or equal to 15 mm Hg. The comparison of the hemodynamic results with the results of a previous study with nitrates was as follows: like the nitrates furosemide lowered the PCW early, i.e. within 15 minutes from 22 +/- 3 to 18 +/- 5 mm Hg, but the therapeutic objective (PCW less than or equal to 15 mm Hg) was reached later than with nitrates. During the 24-hour observation period PCW and total peripheral resistance decreased steadily. The decrease of cardiac index to critical low values in some patients after a mean of 7.5 hours of therapy, and of the mean arterial pressure from 100 +/- 13 to 91 +/- 14 mm Hg, may limit the use of furosemide alone in these patients. During nitrate therapy PCW started to rise again after 12 hours in some patients, necessitating higher doses of nitrates with a corresponding decrease of diuresis. A combination of both forms of therapy may be of value and needs further investigation.
The spontaneous variability of ventricular arrhythmias was investigated in 8 patients with chronic coronary heart disease. In each patient 6 eight-hour long-term ambulatory ECG recordings were made. During the first three periods patients were without medication and during the following three periods they received a placebo b.i.d. Hour to hour variability was high in all patients. When compared with the first hour of an eight-hour period the number of ventricular premature beats (VPB) per hour in four patients declined by more than 90%, in two patients by more than 70% and in only two by less than 50%. On the other hand, increments of several hundred percent were often observed. Day to day variability of VPBs was also high. When compared with the first documented eight-hour period VPBs either decreased or increased substantially (-84% to +940%). A spontaneous reduction of VPB's for several hours may simulate an antiarrhythmic drug effect. For the group as a whole placebo had a significant effect on the number of VPBs (p less than 0.001). Beside variations of quantity, the complexity of ventricular arrhythmias (Lown classification) spontaneously changed several classes in one patient. Therefore, high spontaneous variability renders it very difficult to estimate the behaviour of ventricular arrhythmias in the individual patient with the Holter-ECG.
The influence of ACB on cardiac arrhythmias was examined in 27 patients. Eight-hour Holter monitoring was performed 8 days preoperatively and 100 days postoperatively. Arrhythmias were divided into 3 groups (Class I: NSR +/- occasional APBs; Class II: less than five unifocal VPBs per minute; Class II: more than five VPBs per minute, multifocal VPBs, VPBs in a row or VT). Preoperative classification disclosed that 13 patients (48.1 per cent) were in Class I, six patients (22.2 per cent) were in Class II, and eight patients (29.6 per cent) were in Class III. The corresponding values after surgery were 10 patients (37.0 per cent), 13 patients (48.1 per cent), and four patients (14.8 per cent). These differences were not statistically significant (p less than 0.1). In view of the tendency of arrhythmias of Class III to improve after ACB, we feel that further investigations in this area are needed. At the present time ventricular arrhythmias alone constitute no indication for bypass surgery.
Ten patients with severe congestive heart failure after acute myocardial infarction were treated with 40 mg isosorbiddinitrate-retard every 4 hours and additional sublingual nitroglycerine. There was a prompt improvement of hemodynamic parameters which was maintained for 24 hours: pulmonary capillary wedge pressure (PCW) decreased within 10 min from 26 +/- 5 (X +/- SEM) to 17 +/- 2 mm Hg (p less than 0.01) and mean arterial pressure from 109 +/- 7 to 98 +/- 6 mm Hg. The heart rate remained constant, and the cardiac index improved from 2.3 +/- 0.2 to 2.5 +/- 0.21/min/m2. The fall in blood pressure was dependent on the pretreatment pressure: it was significantly greater in patients with elevated blood pressure and only slight in those with a low pretreatment blood pressure. In the presented series of patients neither adverse effects or symptoms nor a critical reduction of blood pressure were observed. Combined oral treatment with isosorbiddinitrate and nitroglycerine can therefore be carried out without invasive blood pressure monitoring.
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