Ventricular arrhythmias in rehabilitated and nonrehabilitated post-myocardial infarction patients with left ventricular dysfunction.

The incidence of ventricular arrhythmias in rehabilitated post-myocardial infarction (MI) patients with left ventricular dysfunction included in a long-term rehabilitation program was assessed and compared with that in similar patients who were not in such a program. Thirty-eight post-MI patients (2 to 19 years after the acute event) with ejection fraction < 40% were investigated by 48-hour Holter monitoring. They were divided into the following 3 groups: group I, 11 patients who underwent arm training for 60 months; group II, 11 patients who underwent calisthenics for 36 months; and group III, 16 patients who were not in any rehabilitation program; the age of the patients was 61 +/- 7, 61 +/- 6 and 61 +/- 9 years, respectively, (p = not significant). Ejection fraction at rest was 31 +/- 9 for group I, 29 +/- 7 for group II, and 29 +/- 7 for group III (p = not significant). There were no significant differences concerning the location of MI, and antiarrhythmic treatment received by patients from all groups. At the conclusion of 48-hour Holter monitoring, 2 blood samples were obtained for assessment of norepinephrine (at rest and after postural change). Quality of life was determined by a detailed questionnaire, including questions concerning social activity, life satisfaction and sexual function. After 36 and 60 months, an improvement in hemodynamic condition of patients in group I was noted. Quality of life was higher in the rehabilitated patients, with enhanced emotional stability, satisfaction with work and social life, and a high percentage of return to work (82 vs 40%).(ABSTRACT TRUNCATED AT 250 WORDS)

Exercise dependent complete left bundle branch block.

Eleven patients with an exercise dependent complete left bundle branch block (CLBBB) were followed-up over a period of 2-13 years (mean 6.5 +/- 3.8). Their ages ranged from 19 to 62 years (mean 48). Four patients complained of chest pain on effort and one of palpitations. All patients underwent a clinical examination, 12 lead ECG, routine blood tests, chest X-ray, a multistage exercise test, echo Doppler, radionuclide ventriculography with TC99 and 48-h Holter monitoring. Ten were submitted to a coronary angiography with left ventriculography. The ECG at rest displayed a normal ECG in seven patients and an incomplete left bundle branch block (ILBBB) in four patients. The onset heart rate (HR) of CLBBB ranged from 95-146 beats.min-1 (mean 123) and the offset HR75-135 (mean 102 beats.min-1). Coronary angiography showed three-vessel disease in two patients and an obstruction of the left anterior descending coronary artery (LAD) in the third. In the other seven patients all the investigations (including coronary angiography) were normal. During the follow-up period the HR at onset of CLBBB decreased from 145 beats.min-1 to 100 beats.min-1 in four patients but no coronary artery disease (CAD) could be proven at coronary angiography. In our series chest pain did not always signify the presence of CAD. We conclude, that in patients with exercise-dependent CLBBB the prognosis is good if no underlying heart disease can be detected. It appears from our limited experience that an exercise-dependent CLBBB at heart rate below 125 beats.min-1 does not by itself constitute a sign of CAD.

Bopindolol and atenolol in patients with stable angina pectoris. Double-blind randomized comparative trial.

32 patients with stable angina and a positive symptom-limited exercise test (SLET) were investigated in a double-blind randomized trial in order to assess the therapeutic efficacy of bopindolol or atenolol on the incidence of angina pectoris and on angina pectoris threshold heart rate (ATHR). After a washout and placebo period of 2 weeks, each of the two drugs were applied in dosages of 0.5 mg bopindolol and 50 mg atenolol. The dosage was increased every month up to 2 mg bopindolol and 200 mg atenolol. At the end of every period, the patients were retested by SLET. After 3 months of active treatment, we noticed that the incidence of anginal attacks was lower in the bopindolol group (2.45 vs. 3.29). The resting heart rate was also lower in the bopindolol group (55.89 vs. 63.38). No statistical significance was found between the peak work rate, ATHR, exercise duration and S-T depression. The rate-pressure product was lower in the bopindolol group. We concluded from this that bopindolol and atenolol are active in decreasing the incidence of angina, the former being more effective. Exercise performance and cardiocirculatory parameters did not differ between the two groups.

Prolonged PR interval associated with an abnormal frontal plane QRS axis as an electrocardiographic criterion of left ventricular function.

The aim of this study was to investigate whether, in patients who had had one or more myocardial infarctions, the electrocardiographic appearances of prolonged PR interval associated with an abnormal frontal plane QRS axis are correlated with the value of left ventricular ejection fraction. Seventy-three consecutive patients all of whom had had at least one myocardial infarction, were divided into 3 groups: Group A, 22 patients having on their electrocardiogram a prolonged PR interval and an abnormal frontal plane QRS axis; Group B, 15 patients having an abnormal QRS axis as a solitary conduction disturbance; and Group C, 36 patients without conduction abnormalities. The ejection fraction, determined in all patients by gated blood pool imaging, was found to be 30% +/- 8 (mean +/- 1 SD) in Group A, 53% +/- 21 in Group B, and 52% +/- 14 in Group C (P less than 0.001). An ejection fraction of less than 40% was found in 91% of patients in Group A, in 33.33% in Group B, and in 8.33% in Group C (P less than 0.01). Multiple segment ventricular wall contraction abnormalities were found in 50, 6.66, and 11.11%, respectively (P less than 0.001). It can be presumed, therefore, that in patients after one or more myocardial infarctions, this association of conduction abnormalities signifies a severe impairment of ventricular contractility and may identify a subgroup with a high prevalence of severely depressed ejection fraction.

Correlation between arrhythmias and abnormal systolic blood pressure response to exercise in mitral valve prolapse patients.

A wide variety of arrhythmias as well as exercise induced hypotension were described in some Mitral Valve Prolapse (MVP) patients. The aim of our study was to evaluate the correlation between the incidence of arrhythmias and the decrease of Systolic Blood Pressure (SBP), ST-T changes and prolonged QTc interval. 50 MVP patients (diagnosis confirmed by M-mode and 2-D echocardiography) underwent a complete clinical evaluation, 12 lead standard ECG, 24 hr. monitoring ECG and a submaximal exercise test. On the basis of the SBP response to effort, the patients were divided into 2 groups (gr.): gr. A, 18 patients with a decrease of the SBP during effort, mean 135 +/- 16.5 mmHg and gr. B, 32 patients with a normal increase of the SBP at the end of the effort, mean 168 +/- 14.7 mmHg (p less than 0.001). Arrhythmias were found in 83.33% among patients in gr. A and in 50% in gr. B (p less than 0.05). We did not find a significant difference concerning the types of arrhythmias between the 2 groups. Exercise induced ST-T changes, appeared in 55.55% in gr. A and in 25% in gr. B (p less than 0.05) but the incidence of arrhythmias in patients with ST-T changes was not significantly different between the 2 groups (5.55% and 6.25% respectively). Rhythm disturbances were found in 3 out of 4 patients with prolonged QTc in gr. A and in 2 out of 4 patients in gr. B (p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Holter monitoring for dizziness and syncope in old age.

Among 509 patients referred to our Institute for Holter monitoring, between 1st September, 1982-30th October, 1983, 28 patients aged 65-90 (mean 76) were referred for dizziness and syncope. There were 17 men and 11 women. Seven patients had a M.I. in their past, 4 angina pectoris, 5 hypertension, 4 aortic stenosis or aortic insufficiency or both, hemodynamically significant, one had mitral valve prolapse (MVP) and one transient ischemic attacks (TIA). In our series 16 out of 28 patients received digoxin and antiarrhythmic drugs (quinidine, propranolol, procainamide, Neo-gilurythmal, amiodarone), 2 of them digoxin and quinidine in full doses and one digoxin and amiodarone. Other drugs administered to our patients included Aldomin, Isordil, Lasix, aminophylin, cromoglycate etc. In 10 patients (35.7%) we found complex ventricular arrhythmias (7 with M.I., 3 patients of 4 with significant aortic valve lesion, 2 patients of 2 with left anterior hemiblock (LAH), 1 patient with MVP, 1 patient with TIA). In another 5 patients (17.8%) we found atrial fibrillation, fast rhythm (2 with chronic obstructive lung disease, 2 with hypertension and 1 in post M.I.) which explained their symptomatology. From our data we conclude that the pluripathology found in old age as well as the multimedication administered, cause a plurietiology of syncope, arrhythmias playing an important role in its determination, in this particular age group.

Cardiac tamponade in Dressler's syndrome. Case report.

A case of Dressler's syndrome with cardiac tamponade is presented. 19 days after an acute lateral myocardial infarction, the patient, 46 years old, was admitted the second time with a characteristic clinical picture of cardiac tamponade. The patient did not receive at any time during his admission an anticoagulant treatment. The clinical diagnosis was supported by fluoroscopic and echocardiographic findings. A pericardiocentesis performed immediately revealed a hemorrhagic pericardial fluid. After withdrawal of 60 ml, the patient's clinical condition improved dramatically and this improvement continued further under treatment with corticosteroids. At the best of our knowledge this is the second case in the literature of Dressler's syndrome with cardiac tamponade and hemorrhagic fluid in a patient not treated with anticoagulants.

Usefulness of myoglobin radioimmunoassay determintion in CCU.

In 112 patients with an acute coronary event, admitted to the CCU of Assaf-Harofeh Hospital, myoglobin radioimmunoassay was determined at 0 (time of admission), 12 and 24 hours. In 77 patients with acute myocardial infarction (M.I.) (64 patients with acute transmural and 13 with acute subendocardial M.I.), the myoglobin values were significantly increased. Appearing in blood 3-4 hours after the onset of chest pains, myoglobin represents the earliest marker of acute M.I. known until know. In 12 of 23 cases diagnosed at first as acute coronary insufficiency according to clinical, biological and E.C.G. criteria, significantly increased values of myoglobin were found, as an expression of micro-necroses which were not detected by conventional methods (SGOT, CPK, LDH). This finding has important practical, prognostic and therapeutical implications, showing that myoglobin radioimmunoassay may detect myocardial micronecroses which are not discovered by usual methods. Myoglobin radioimmunoassay assessment offers a valuable indication of necrosis extent. Values above 800 ng/ml were accompanied in 65% of our cases with symptoms and signs of left heart failure, the highest values of myoglobin being found in extensive anterior M.I. associated with acute pulmonary edema. In 9 non cardiac patients with repeated intra-muscular injections with antibotics, the myoglobin was at the upper normal limit, demonstrating that intra-muscular injections, at least with antibiotics, have no influence on myoglobin values. From our experience it appears that the myoglobin radioimmunoassay determination is a useful tool for the early establishment of M.I. diagnosis and the assessment of myocardial necrosis extent.

Right myocardial infarction with predominant right ventricular dysfunction.

Two patients with right ventricular myocardial infarction are described. In both cases, the hemodynamic criteria established for this diagnosis were fulfilled, namely, right-side pressure values (central venous pressure and right atrial pressure) equal to or higher than left-side pressure values (pulmonary capillary wedge pressure and left ventricular end-diastolic pressure). ECG tracings showed acute diaphragmatic myocardial infarction. The lungs were clear both clinically and radiologically. The diagnosis of right ventricular myocardial infarction was confirmed in the first patient by hemodynamic studies and at autopsy, and in the second patient, by hemodynamic and echocardiographic studies. Only in the second care was the administration of massive quantities of fluids and dopamine followed by good results. The importance of establishing a precise diagnosis of right ventricular myocardial infarction is emphasized, since therapy for this condition is different than that for left ventricular myocardial infarction.

Holter monitoring in dizziness and syncope.

Holter monitoring was used to detect the underlying mechanism among 53 patients referred for dizziness, fainting and/or syncope. The complaints were unexplained on clinical grounds in 38, suggestive of SSS in 11, and of pacemaker dysfunction in 4 patients who underwent pacemaker implantation for symptomatic A-V block. Occult dysrhythmias were revealed in 24 of 38 (61%) of the first group; the clinical impression of SSS was confirmed in 8 of 11 (72%) in the second, and ineffective pacing confirmed in 2 of 4 in the third group. Thus, the diagnosis was clarified in 34 of 53 (64%) of patients. It is concluded that Holter monitoring is most useful for detecting the underlying mechanism in the above mentioned conditions, especially in elderly subjects whose syncopal attacks remained unexplained despite routine cardiological and neurological examination. Holter monitoring should be carried out for at least 36 hours before ruling out dysrhythmias as a cause of dizziness and/or syncopal attacks.

Left ventricular aneurysm of unusual aetiology: report of two cases.

Two young patients aged 14 and 25 with left ventricular aneurysms are described. In both, a clinical picture initiated by attacks of supraventricular tachycardia led to the discovery of the condition. In the first patient the clinical picture clearly suggested a traumatic aetiology. In the second, the angiographic and histological findings strongly favoured a congenital origin. Both patients underwent successful aneurysmectomy. The literature on the incidence and aetiology of traumatic or congenital ventricular aneurysms is discussed.