[Acute coronary heart disease].
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Biomedical subjects
Publications and source records attributed to F Burkart.
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The unipolar pulse generator systems were tested in 220 patients (96 VVIM, 97 VVIO, 27 physiological systems) to determine the incidence of sensing interference with muscle potentials. 23% exhibited oversensing, with a sex distribution of 32% for males and 15% for females. The interference was observed more often in VVIM pacemakers at nominal setting (35%) than in VVIO pacemakers (11%). In DDD pacemakers both inhibition and triggering of ventricular stimulation was observed. Among the 23 patients with persisting syncope or dizziness after implantation of the pacemaker, the symptoms were observed during physical activity only in 5. In these 5 the underlying arrhythmia was tachycardia in 3 and inhibition of the pacemaker by muscle potentials in only one patient.
To assess acute hemodynamic effects of combined oral nifedipine (10 mg) and acebutolol (100 mg), 21 patients with angiographically documented coronary artery disease and stable angina pectoris were studied (three groups of seven randomized patients). Simultaneous hemodynamic and equilibrium radionuclide ejection fraction measurements were performed at rest and during exercise before treatment, 1 hour after administration of nifedipine, acebutolol or a combination of the two and again 1 hour after combined nifedipine and acebutolol. At the same exercise level achieved without drugs, angina, subjectively scored by the patients, decreased significantly after nifedipine, acebutolol and a combination of the two in association with a significant improvement in left ventricular ejection fraction (p less than 0.01). There was an additive effect of both drugs on heart rate, systolic blood pressure and therefore the double product (p less than 0.01 each). The negative effects of acute beta receptor blockade on cardiac index, resting ejection fraction and total peripheral resistance were balanced by the vasodilatory action of nifedipine. In patients with borderline heart failure no untoward effects were seen after combined therapy. Thus, acute combined acebutolol/nifedipine therapy in patients with stable angina proved to be hemodynamically superior to therapy with either drug alone and safe even in patients with moderately depressed left ventricular function. This finding provides a basis for appropriately designed long-term studies.
A new transdermal therapeutic system (TTS) for the administration of nitroglycerin (NTG) was tested in human pharmacological studies in 26 healthy volunteers. Plasma concentrations and haemodynamic responses were determined after the application of the system in different dosages. The concentrations of NTG reached in the plasma were uniform and dose-related, i.e. dependent on the drug-release area, and showed only minor inter-individual variation. They remained almost constant as long as the system was in contact with the skin. Renewal of the system caused no appreciable change in the plasma concentration. The haemodynamic effects, like those of all nitrates, were not clearly related to the dose administered, and were not always dependent on the plasma concentration. Upon repeated application, NTG-TTS was well tolerated locally and systemically and led to no alteration in blood chemistry or haematological parameters. The typical nitrate headaches disappeared after a few days. The presence of the system on the skin caused no discomfort or inconvenience.
Eleven of 12 patients with severe congestive heart failure who were pretreated with diuretics and digitalis benefited from long-term therapy with prazosin which was titrated to the individual's maximally tolerated dose. Nine of the 11 patients improved their functional state by one (n = 4) or two (n = 5) New York Heart Association (NYHA) classes. Within 4 weeks the stroke volume index increased from 23 +/- 10 to 29 +/- 9 SD (ml/beat/m2) while pulmonary capillary pressure decreased from 29 +/- 8 +/- 9 mm Hg (p less than 0.05 for both) and peripheral vascular resistance fell from 2,245 +/- 792 to 1,603 +/- 355 dyn/s cm-5 (p less than 0.01). Hemodynamics results were similar on the same regimen in eight patients assessed for 6 months. Death of three patients (week 5 and week 17) was unrelated to prazosin therapy. Prazosin resulted in improved cardiac performance during leg-up-tilt or supine ergometry. Increase in stroke volume index was related to the fall in peripheral vascular resistance (r = -0.79, p less than 0.01). Plasma adrenaline (301 +/- 480 pg/Ml), noradrenaline (1,312 +/- 1,382 pg/ml), and renin activity (22 +/- 30 ng/ml/h) were in the range observed with pheochromocytoma; variables did not change on prazosin. This reflects an important role of alpha-adrenoceptor-mediated vascular regulation in patients with heart failure in whom long-term treatment with prazosin produces a sustained and well-tolerated vasodilator effect without further rise in catecholamines and renin.
26 patients who had undergone right heart catheterization were enrolled in the study. The average age was 51.7 +/- 15 years. Half the patients showed coronary artery disease at selective coronary angiography. His bundle recordings and atrial pacing were performed before and 10 min after 1 or 1.5 mg/kg i.v. tiapamil. In addition, arterial blood pressure was recorded. P-R interval increased from a mean value of 153 +/- 36 to 168 +/- 49 ms (p less than 0.05) due to an increase in the A-H time from 88 +/- 19 to 97 +/- 23 ms (p less than 0.05). Arterial blood pressure and heart rate decreased significantly. These changes were more pronounced in patients with coronary artery disease. In the groups with the higher dosage, the differences from the control values were greater than in the patient groups receiving 1.0 mg/kg. Sinus node recovery time tended to increase in all groups but the differences did not reach significance. Patients with the 'sick sinus syndrome' were not studied.
57 patients were admitted to the study, 3-6 weeks after acute myocardial infarction. They received either placebo or 1 mg/kg tiapamil intravenously according to a randomized, double-blind procedure. The study had two objectives: (a) to assess the effect of tiapamil on work tolerance and exercise-induced myocardial ischemia: (b) to demonstrate possible antiarrhythmic effects against exercise-induced arrhythmias. The duration of exercise and physical work capacity increased slightly in both groups, these effects, however, not reaching statistical significance. On the other hand, the number of exercise-induced extrasystoles did not change significantly under placebo but decreased from 30.9 to 14.8 beats/min after tiapamil (p less than 0.01). No side effects were observed. While the hemodynamic effects of tiapamil in patients with coronary artery disease are yet to be elucidated, our findings confirm the efficacy of this calcium antagonist against exercise-induced ventricular premature beats in patients with coronary artery disease.
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To assess the accuracy of serial myocardial perfusion scintigraphy with thallium-201 (201Tl) to predict graft patency early and late coronary artery bypass surgery, rest and exercise 201Tl and coronary arteriography were performed preoperatively and 2 weeks and 1 year after operation. The scintigraphic results were compared with graft patency, symptoms, left ventricular function and physical work capacity in a consecutive series of 55 patients with a total of 154 grafts. Serial 201Tl had an 80% sensitivity, 88% specificity and 86% overall accuracy in detecting or excluding graft occlusion, which was predicted by reversible ischemia as well as persistent "new scar" segments. Occluded grafts were correctly localized by 201Tl scintigraphy in 61%. Postoperative apical 201Tl defects were frequent (two-thirds of cases), and were the result of intraoperative transapical venting of the left ventricle. After coronary bypass graft surgery, ejection fraction at rest was unchanged. Left ventricular end-diastolic pressure and physical work capacity improved significantly. In the presence of new perfusion defects detected postoperatively, physical work capacity was reduced significantly. New 201Tl defects in addition to typical or atypical angina provided a high probability of graft occlusion, while in the absence of new 201Tl defects all grafts were patent in more than 90% of patients, all of whom had no or only atypical chest pain. We conclude that serial 201Tl imaging after coronary artery bypass surgery is an accurate noninvasive method that can be used routinely to assess graft function, to localize spatially occluded grafts and to identify patients with a high likelihood of graft occlusion who may need invasive studies.
Plasma adrenaline (A) and noradrenaline concentrations (NA) were determined in 41 patients admitted to the coronary care unit (CCU). Eleven with suspected acute myocardial infarction (AMI), subsequently excluded as a diagnosis, had significantly elevated A and NA compared with 20 normal resting subjects. Patients with proven infarcts but no ventricular fibrillation had even higher levels of A and NA. Nine patients with ventricular fibrillation as a complication of AMI showed the highest plasma catecholamine values on admission. Patients with AMI and congestive heart failure exhibited substantially increased A, while NA was only slightly elevated compared with that of AMI patients without congestive heart failure. High plasma catecholamines and the relationship between adrenaline and the severity of ventricular arrhythmias suggest that the sympathetic nervous system plays an important role in sustaining a vicious circle of increased myocardial damage and increased irritability during the acute phase of AMI.
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Prior to diagnostic left heart catheterization, 22 patients with atypical chest pain underwent thallium scintigraphy and radionuclide ventriculography at rest and during exercise. Combining both noninvasive tests, 6/8 patients with coronary artery disease, 3/4 with cardiomyopathies, and 9/10 patients without heart disease were correctly identified. From detailed analysis of the results it is concluded that left heart catheterization should not be necessary if the radionuclide findings are typical of either coronary artery disease (localized perfusion defect and abnormal left ventricular function) or absence of heart disease (normal perfusion and function studies).
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Twelve patients with severe chronic congestive heart failure (CHF) (NYHA class III and IV) resistant to digitalis and diuretics were treated with the postsynaptic alpha-blocking agent prazosin (PZ) (3 to 20 mg/day). In 11 patients oral PZ treatment was well tolerated; the agent was discontinued in the remaining patient because of orthostatic dizziness. After 4 weeks of PZ, total systemic vascular resistance decreased from 2245 +/- 792 to 1603 +/- 355 dyn sec cm-5, mean blood pressure declined from 100 +/- 15 to 90 +/- 14 mm Hg, and pulmonary capillary wedge pressure decreased from 29 +/- 8 to 25 +/- 9 mm Hg. Cardiac index increased from 1.92 +/- 0.63 to 2.30 +/- 0.41 l/min/m2. The increase of stroke volume index correlated with the fall in peripheral vascular resistance (r = --0.79, p less than 0.01) and the decline in pulmonary capillary wedge pressure (r = --0.75, p less than 0.05). In parallel, exercise tolerance increased significantly. Four patients improved from functional class IV to II, four from class IV to III, and one from class III to II, while two patients were unchanged. In the eight patients followed for 6 months, the beneficial effects of ambulatory PZ were maintained throughout the expansive observation period. Three patients died as their disease process progressed during the study (sudden death, pneumonia, and post-PZ withdrawal pump failure). Prazosin is a valuable vasodilator for long-term treatment of otherwise refractory congestive heart failure with the agent given in sufficient individualized dosage.
We analysed a group of 35 consecutive patients with acute myocardial infarction-23 of the inferior, 12 of the anterior wall-who needed temporary pacing for bradycardiac arrhythmias. We observed in three patients ventricular tachycardias induced by pacemaker stimuli falling onto the vulnerable part of the cardiac cycle due to improper sensing. All three had an inferior myocardial infarction involving the right ventricle. Because the pacemaker electrode in this condition lies in the vicinity of the infarcted myocardium sensing problems occur more frequently and re-entry tachycardias can be triggered more easily. It represents a possible risk of pacemaker treatment in his group of patients who, on the other hand, often need cardiac pacing in the acute phase following the development of transient AV-block.
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