Charles K. Friedberg

Arrhythmias in the Wolff-Parkinson-White syndrome

Summary The incidence of the WPW anomaly in adults ranges from 0.1 to 3.1 per thousand and in children from 0.77 to 4.8 per thousand. Acquired heart disease as well as many congenital cardiac defects are associated with the WPW anomaly. Sixty to 70 per cent of patients demonstrating this pattern are males. Arrhythmias occur in about 40 to 80 per cent of patients, and tend to reoccur. The most common arrhythmia is atrial tachycardia. Atrial fibrillation and flutter are also seen. There is a high incidence of rapid ventricular rate with aberration in conduction in response to these arrhythmias (30 per cent). This rapid aberrant ventricular response may be confused with ventricular tachycardia and the criteria for diagnosis are described. Quinidine has been used to terminate the arrhythmias associated with the WPW syndrome. Although the use of digitalis in these arrhythmias has not achieved widespread acceptance, it should be employed as it is in situations not complicated by the WPW anomaly. Combination therapy with digitalis and quinidine has been successful in refractory cases. Electrical cardioversion has also been employed. There should be no deley in instituting therapy since several instances of death have been reported during the acute attacks. Prophylactic use of quinidine is indicated when attacks tend to recur and are severe. The prognosis of the individual patient is affected by the presence or absence of underlying heart disease, age at onset of tachycardia, tendency for recurrence and duration and severity of the single episodes.

UNUSUAL FORMS OF SECOND-DEGREE ATRIOVENTRICULAR BLOCK, INCLUDING MOBITZ TYPE-II BLOCK, ASSOCIATED WITH THE MORGAGNI-ADAMS-STOKES SYNDROME.

Abstract Several unusual forms of second-degree atrioventricular block associated with the Morgagni-Adams-Stokes (M-A-S) syndrome are discussed. Three out of 100 patients with the M-A-S syndrome demonstrated a transient Mobitz Type-II block. Seven additional cases are reviewed from the literature. All of the patients had frequently changing degrees of heart block, and in only 1 patient did the Mobitz Type-II block persist. In all cases in which a clinical history is available, Mobitz Type-II block was associated with an Adams-Stokes syndrome. Although a particularly poor prognosis has been indicated for this type of block, the outlook appeared to be no different from that in other cases of M-A-S syndrome in our series. On the other hand, Mobitz Type-II block is of prognostic importance if it indicates that the M-A-S syndrome is likely to develop. Two patients who had 2:1 A-V block with A-V interference dissociation presented with the M-A-S syndrome. Neither of these cases was caused by excessive administration of digitalis. Eight patients had advanced or high-grade A-V block related to their M-A-S syndrome. All of them subsequently developed complete heart block. Although odd-numbered ratios of advanced heart block are said to be rare, such forms were present in all 8 cases, whereas 4:1 block was present in only 2 cases. This may indicate that M-A-S syndrome is more likely to occur in the odd-ratio type of advanced heart block. Awareness that these unusual forms of second-degree block are associated with M-A-S syndrome may enable the prediction of later development of complete heart block and M-A-S syndrome.

Computer diagnosis of electrocardiograms. IV. A computer program for contour analysis with clinical results of rhythm and contour interpretation

Abstract The logic for the contour analysis programs and the results of a comparison of computer and physician diagnosis for over two thousand cases are described. A detailed breakdown of the patient population and nature of the errors made by the program is given. The effectiveness of the program as a screening tool is also considered.

The Two-Step Exercise Electrocardiogram A Double-Blind Evaluation of Its Use in the Diagnosis of Angina Pectoris

A double-blind study was made to evaluate the two-step exercise electrocardiographic test (Master) as a means of differentiating between anginal and nonanginal chest pain in 100 consecutive patients. A high percentage of false-positive results in nonanginal cases and a number of false negatives in anginal cases greatly impaired the usefulness of the test for this purpose. When Masters criterion of an ST depression of 0.5 mm. or more was employed, there were 39 per cent false positives and 12 per cent false negatives. Stricter criteria progressively diminished the number of false positives, but resulted in increasing numbers of false negatives. Even if 1 mm. or more of ST depression was required, there were 8 per cent false positives and 43 per cent false negatives. There were no false positives only when the ST segment was depressed 2 mm. or more. Although an ischemic type of ST depression may be more significant for angina pectoris than the J type, in our series ischemic ST depressions also occurred more frequently than the J type in false-positive tests in nonanginal patients. The new criteria of Master and Rosenfeld were not more satisfactory than the previous criteria recommended. There are relatively few cases in which an objective two-step test is necessary to aid in the differentiation of anginal and nonanginal pain, since an unequivocal diagnosis of angina pectoris or nonanginal pain was made in 86 per cent of cases independently by at least two observers, on the basis of a single interview, and since this percentage could undoubtedly have been increased by further interviews concerning the effect of effort and of nitroglycerin. Insofar as confirmation of a clinical diagnosis of angina pectoris by an objective exercise test is desirable, an ST-segment depression of at least 1 mm. usually offers such confirmation. However, this degree of ST-segment depression is often absent in unequivocal cases of angina pectoris and conversely may be occasionally present in patients with nonanginal pain.

Bilateral Bundle-Branch Block Clinical and Electrocardiographic Aspects

The electrocardiograms and salient clinical features of seven patients with electrocardiographic evidence of various types of bilateral bundle-branch block (BBBB) have been presented. When the complexes change in form and the P-R interval varies, the mechanisms are usually best interpreted by using the concepts of first degree, second degree, and third degree bundle-branch block with or without block in the higher conduction system. The etiology of BBBB in many cases is idiopathic fibrosis of both bundles. The diagnosis of BBBB by ECG is important because of its relation to the subsequent development of complete heart block or Adams-Stokes syndrome, or both. In this series five of seven patients with BBBB had Adams-Stokes syndrome and three of seven had complete heart block.

PRODUCTION OF CHRONIC ELEVATION OF LEFT VENTRICULAR END DIASTOLIC PRESSURE IN DOGS: HEMODYNAMIC AND RENAL STUDIES.

In an effort to produce a preparation for the study of sodium excretion in chronic left heart failure a graft anastomosis was created between the left subclavian artery and the left atrium in five dogs. This resulted in chronic progressive elevation of left ventricular end diastolic and left atrial pressures. Maximal left ventricular end diastolic pressures ranged between 18 and 30 mm Hg, 10 to 20 weeks postoperatively. There was only a slight rise in right ventricular diastolic pressure and no clinical evidence of right heart failure. Cardiac outputs remained within normal limits in all animals. Serial electrocardiograms disclosed the development of left ventricular hypertrophy and left ventricular hypertrophy and dilatation were observed at postmortem examination. One dog which survived with a patent shunt for more than a year had right as well as left ventricular hypertrophy but no right heart failure. Glomerular filtration rates, renal plasma flow and excretion of rapidly infused isotonic saline remained unaltered even at the highest levels of left ventricular end diastolic pressure. Although the development of left and eventually right ventricular hypertrophy, the chronic and progressive elevation of left ventricular end diastolic, mean left atrial and pulmonary arterial pressure, with only slight elevation of right ventricular end diastolic pressure, were regarded as characteristic features of isolated left ventricular failure, the propriety of this term may be questioned in view of the unaltered cardiac output and renal hemodynamics. But the observations do indicate that marked elevation of left ventricular end diastolic and presumably pulmonary venocapillary pressure, such as occur in left heart failure, do not impair renal excretion of sodium.

Ventricular arrhythmias after precordial electric shock

Abstract New cardiac arrhythmias occurred 43 times in 50 patients who underwent 55 elective precordial applications of synchronized D.C. shock for the control of cardiac arrhythmias. Ventricular arrhythmias were seen after 27 procedures. There were unifocal ventricular premature systoles in 11, multifocal ventricular premature systoles in 15, and ventricular bigeminy in 17. Three of these patients developed runs of ventricular tachycardia, and 2 developed ventricular fibrillation. One patient with ventricular fibrillation received additional D.C. shock to control this arrhythmia. Except for this one patient, all arrhythmias were transient and self-limited. All patients survived the procedure, and there were no complications due to the new arrhythmias. Although there were only 7 patients who were not receiving digitalis, 3 of these 7 patients developed new ventricular arrhythmias (bigeminy, unifocal and multifocal premature systoles). This suggests that, in these patients, electric shock acted to increase ventricular irritability, even though there were no cases of ventricular fibrillation or tachycardia in this small group. Furthermore, in those patients who were not receiving toxic doses of digitalis, the dose of digitalis being used did not appear to be an important factor in determining which patients would develop new ventricular arrhythmias. Ventricular arrhythmias were more frequent after multiple shocks and high levels of energy. This may have been due either to a dose-dependent pro-arrhythmic effect of electric shock or to the severity of the underlying heart disease that necessitated multiple shocks of high energy, or to both.

Reflex Circulatory Effects Elicited by Hypertonic and Hypotonic Solutions Injected into Femoral and Brachial Arteries of Dogs

Rapid injection of 40 ml. of 5 per cent saline into the femoral or brachial arteries of 24 dogs resulted in an average elevation of arterial blood pressure of +42/+20 mm. Hg, an increase in the heart rate of +20 beats/min., and an acceleration of the respiratory rate of +140 per cent. The response began 6 to 10 seconds after the onset of injection and lasted for 5 to 30 minutes. It occurred with the injection of hypertonic solution of saline, dextrose, and urea. The magnitude of the response was related to the degree of hypertonicity. Responses could be provoked by 10 ml. of 1.25 per cent saline. Rapid intra-arterial injection of isotonic saline, dextrose, and urea solutions, and of whole blood in volumes up to 80 ml. had no circulatory effect. Rapid injection of distilled water, 0.225 per cent and 0.45 per cent saline into the femoral or brachial arteries resulted in a slight degree of hypotension and a rise in the respiratory rate. The appearance of circulating catechol amines following the response to intra-arterial injection of hypertonic solutions was suggested by the demonstration of hypotensive response to intravenous injection of phentolamine. These responses to injection of hypertonic and hypotonic solutions in the femoral artery were abolished by section of the sciatic nerve in animals with an ipsilateral partially-transected hind limb, a preparation which left intact only the femoral artery, femoral vein, and femur. Sciatic section in the intact limb reduced but did not abolish the response. Removal of the sympathetic chain from the eleventh thoracic through the third lumbar ganglia had no apparent effect. It is concluded that the response to femoral aud brachial intra-arterial injection of hypertonic and hypotonic solutions is initiated by peripherally located “osmoreceptors” in the distribution of these arteries and is mediated via a reflex whose afferent fibers travel in the peripheral somatic nerves and enter the spinal cord without passing through the sympathetic chain. The efferent are is the sympathetic nervous system.

Nonrheumatic calcific aortic stenosis

1. 1. A study was made of fifteen cases of calcific aortic stenosis in which detailed pathologic examination (previously reported) had shown that the lesion was nonrheumatic. In four of the cases there was an associated syphilitic aortitis. 2. 2. While in most cases of calcific aortic stenosis there is considerable evidence that the etiology of the lesion is rheumatic, this evidence does not preclude the existence of a nonrheumatic form of the disease. 3. 3. The cases in our series fell into three groups. The first, consisting of six cases, was characterized by the development of left- and right-sided heart failure. The history of these patients revealed the typical symptoms of calcific aortic stenosis, including angina pectoris, dizziness, and syncope. Electrocardiograms frequently showed varying degrees of heart block, such as bundle branch block and intraventricular conduction disturbances, and abnormalities of the T-waves and RST transitions. In occasional cases death occurred suddenly. In the second group, consisting of five cases, the valvular lesion was discovered accidentally in patients who died of some unrelated disease. Neither the characteristic symptoms of the valvular abnormality nor evidences of heart failure were present. The third group, containing four cases, resembled the first, both in the occurrence of cardiac failure and in the appearance of the other characteristic symptoms. These cases were segregated because there was associated syphilitic aortitis and aortic valvular disease. 1. 4. Seven cases typifying these three groups were presented in moderate detail. 2. 5. The occurrence and pathogenesis of angina pectoris, conduction disturbances, dizziness and syncope, and sudden death were discussed. 2.1. A. Angina pectoris is believed to be caused by myocardial ischemia due to coronary insufficiency. When the patient is at rest, coronary insufficiency is due partly to the increased demand for blood made by a greatly hypertrophied heart, and partly to the diminished coronary flow. The coronary flow is reduced by the increased peripheral coronary resistance resulting from the extremely high systolic pressure within the left ventricle. During exertion the coronary insufficiency becomes more marked. Verification of the existence of coronary insufficiency in these cases is furnished by the occasional instances of myocardial infarction without acute coronary occlusion and by the electrocardiograms, which may resemble those of coronary occlusion. 2.2. B. The conduction disturbances, as well as the changes in T-waves and RST transitions, were similarly explained as being caused by myocardial ischemia due to coronary insufficiency. Occasionally, heart block is due to extension of the calcific process to the septum, but the nature of some of the conduction disturbances, their occurrence in some patients on effort, and their transience suggested that they were due predominantly to myocardial ischemia. 2.3. C. Dizziness and syncope occur almost always on effort. They are thought to be due to cerebral ischemia. The already high left intraventricular pressure necessary to compensate for extreme aortic stenosis can be further elevated only with difficulty when there is a demand for increased cerebral blood flow. Occasionally, a hypersensitive carotid sinus also may play a role. 2.4. D. Sudden death in this disease may have various causes. It may be due to coronary thrombosis, or to myocardial infarction resulting from severe ischemia without acute occlusion (i.e., from coronary insufficiency). Occasionally it may be due to severe cerebral ischemia, obstructing thrombi on the stenotic aortic valve, a hypersensitive carotid sinus reflex, cardiac standstill, or ventricular fibrillation. 3. 6. A summary was given of the means of diagnosing calcific aortic stenosis, of differentiating it from the diseases with which it is ordinarily confused, and of distinguishing the rheumatic from the nonrheumatic cases.

Effects of Propranolol on Patients with Complete Heart Block and Implanted Pacemakers

The effects of beta-adrenergic blockade with propranolol were studied in 10 patients with complete heart block and fixed rate internal pacemakers. The patients were grouped according to the absence or presence of premature systoles before propranolol was given. In the patients with premature systoles propranolol was uniformly effective in abolishing the premature systoles. Propranolol was found to increase the systemic venous pressure, to decrease the cardiac output, and to lower myocardial contractility both at rest and during exercise in both groups. Since the heart rate was fixed, it was concluded that beta-adrenergic blockade has a significant negative inotropic effect, in addition to the chronotropic effect.