Development Of Complete Heart Block Research Articles

Dissociation of atrioventricular conduction and refractoriness following application of radiofrequency energy to the canine atrioventricular node: acute and chronic observations.

The electrophysiology of AV nodal modification induced by radiofrequency energy (n = 5) or a sham procedure (n = 5) was studied in ten dogs. The five dogs that received radiofrequency energy had an AH prolongation > 100% from baseline values and this prolongation persisted throughout the 2-month study. The AV nodal functional refractory period was prolonged only acutely. These data indicate a dissociation between the effects on AV nodal conduction and refractoriness that was induced by this procedure. The five sham treated controls showed no acute or chronic electrophysiological changes. In the dogs that received radiofrequency energy, there was fibrosis of the approaches to the AV node and the region of the AV node itself. It is concluded that chronic modification of AV nodal conduction without concomitant changes in refractoriness can be induced by radiofrequency energy delivered in the proximal portion of the AV node. It would be anticipated that this procedure would not decrease the ventricular response to atrial fibrillation or flutter, may be effective in preventing AV nodal reentrant tachycardia by interfering with conduction either in the AV node or perinodal region. Since the AV node itself suffers at least moderate pathological damage, there may be an appreciable incidence of the late development of complete heart block after this procedure.

Adult Acute Rheumatic Fever: A Rare Case Presenting with Left Bundle Branch Block

In contrast to the more common electrocardiographic patterns seen in acute rheumatic fever, such as first-degree heart block, the appearance of left bundle branch block is rare. An adult patient with acute rheumatic fever presented with left bundle branch block on admission, subsequently had sudden cardiac arrest. She was resuscitated successfully and required temporary pacing. An echocardiogram and radionuclide ventriculography were compatible with interventricular septal involvement in the rheumatic carditis. After 20 days of steroid therapy, the left bundle branch block pattern of the electrocardiogram disappeared. A possible mechanism for the development of complete heart block in acute rheumatic fever is discussed. It is suggested that patients with acute rheumatic carditis who have electrocardiographic manifestations of prolonged P-R interval and left bundle branch block should be managed with prophylactic pacing.

Complete heart block during retrograde left-sided cardiac catheterization

Transient rhythm disturbances have been noted in 0.5 to 1.3% of patients undergoing cardiac catheterization, 1–3 and the most frequent are atrial or ventricular tachycardia or fibrillation. Complete heart block is not often observed, occurring in only 7 of the 12,367 catheterizations reported in the Cooperative Study on Cardiac Catheterization. 1 When complete heart block occurs, it usually appears during right-sided cardiac catheterization in patients with left bundle branch block. 4–6 We report the development of complete heart block during retrograde left-sided cardiac catheterization in a patient with preexisting conduction abnormalities.

15- to 30-Year Follow-up of Patients Undergoing Repair of Ruptured Congenital Aneurysms of the Sinus of Valsalva

Rupture of a congenital aneurysm of the sinus of Valsalva is a rare congenital cardiac malformation. Between 1956 and 1971, we operated on 14 patients aged 9 to 36 years (median, 20 years) for repair of a ruptured aneurysm of the sinus of Valsalva, and have followed each patient to the present. Two operative and 4 late deaths occurred, 3 following a second cardiac operation and the other from dysrhythmia. Late complications have included development of complete heart block in 2 patients (necessitating permanent pacemaker insertion 11 and 24 years after initial repair), progression of aortic regurgitation in 2 (necessitating valve replacement 9 and 13 years after initial repair), and endocarditis in 1 patient 20 years after repair. Four of the 8 remaining long-term survivors (followed for 15 to 30 years [mean, 23.6 years]) are in New York Heart Association (NYHA) Class 1, and the other 4 are in NYHA Class II. Three of the 5 patients with suture closure (no pledgets or adjacent ventricular septal defect repair) of the ruptured aneurysm of the sinus of Valsalva sustained recurrent rupture and required repeat closure. Whether the lack of prosthetic material to bolster the repair or inadequate resection of redundant aneurysmal fibrous tissue was responsible for these recurrences cannot be stated. Operative management of patients with ruptured congenital aneurysms of the sinus of Valsalva is discussed.

Cryosurgical Modification of Atrioventricular Conduction for Treatment of Atrioventricular Node Reentrant Tachycardia

Cryosurgical modification of atrioventricular (AV) node conduction was performed in five patients with AV node reentrant tachycardia that used dual AV nodal pathways and was refractory to drug therapy. The procedure alleviated the tachycardia in all patients without the development of complete heart block and without any associated surgical morbidity or mortality. These results suggest that cryosurgical modification of AV node conduction is a promising and potentially curative method of treating AV node reentrant tachycardia.

Histopathologic studies of the conduction system in marked left-axis deviation

The histopothologic changes of the left ventricular (LV) conduction system were studied in 11 autopsy cases with, marked left-axis deviation (LAD). In all cases the LV conduction system was fanlike and spread broadly over the left septal surface. However, the sizes and sites of the histopathologic lesions varied. In 2 cases the lesions were small and localized at, the initial portion of the LV conduction system, wereas in 9 cases the lesions were located more peripherally and were more extensive, especially in 2 cases in which the lesions were mainly localized in the apical third of the LV conduction system. These differences in the sizes of lesions were believed to be due to the anatomic structure of the conduction system. At the initial portion of the LV conduction system, cells were oriented longitudinally with collagen partitions, which presumably resulted in functionally longitudinal dissociation. The variability in the lesions in these patients may explain why prognosis in terms of development of complete heart block is not always poor in patients with LAD and right bundle branch block.

Clinical and electrophysiologic course of sinus node disease: Five-year follow-up study

Thirty patients with symptomatic sinus node disease (SND) who 5 years previously had undergone a clinical investigation including intracardiac electrophysiologic studies with pharmacologic inhibition of autonomic tone were followed up with respect to development of arrhythmias and cardiac conduction abnormalities. In 17 of these patients a reinvestigation, including a second intracardiac study, was performed. Stable atrial fibrillation developed in five patients, paroxysmal supraventricular tachycardia occurred in one patient, and complete heart block appeared in another patient. Paroxysmal atrial arrhythmias and radiographic atrial enlargement were more common at the initial investigation in patients who during follow-up developed either stable atrial fibrillation or paroxysmal supraventricular tachycardia. Development of complete heart block was associated with signs of severe conduction defects at the initial study. General progression of conduction dysfunction as evaluated by intracardiac techniques was not a finding in this study. Conduction abnormalities limited to the atrioventricular (AV) node did not in this context predict a clinically important progression. The results indicate that those patients with SND who are predisposed to develop high-grade AV block and atrial arrhythmias can be identified by Holter monitoring, chest x-ray examination, and an intracardiac electrophysiologic study. These possibilities improve the selection of patients suitable for pacing modes preserving atrial transport.

Bundle branch block and sudden death

It is clear from the available data that the prognosis for patients with chronic BBB depends to a large extent on the presence and etiology, as well as the severity, of the associated heart disease. In most patients, the terminal event is usually one of heart failure or the complication of coronary artery disease. In the absence of clinically detectable heart disease, the long-term prognosis for this group of patients is good. Patients with chronic bundle branch block Have been shown to have an incidence of ventricular arrhythmias greater than that found in a normal population. The mechanism of sudden death in any single unmonitored patient is speculative. Most patients dying suddenly, especially those with coronary artery disease, probably do so from ventricular fibrillation. Patients with documented transient high-degree AV block are at a substantial risk of sudden death. No clinical variable (such as age, syncope, angina, shortness of breath), or physical finding (such as S 3 gallop, cardiomegaly, heart failure), or electrocardiographic finding (such as RBBB with LAD, RBBB with RAD, P-R interval prolongation), or electrophysiologic variable (such as A-H or H-V interval prolongation) is useful in predicting progression to complete heart block. All the above variables occur frequently in patients with BBB and yet the progression to CHB is relatively infrequent. One might single out His-Purkinje block with normal AV nodal conduction during atrial pacing as a possible marker for development of complete heart block. However, the opposite, namely a normal H-V interval, does not rule out progression to complete heart block. The data available on the use of pacing in patients with unexplained recurrent syncope or dizziness suggests that this approach is reasonable provided an effort has been made to exclude noncardiac cause for the symptoms. Some suggest that documentation of bradyarrhythmia or measurement of H-V interval is essential prior to institution of pacing. Further studies are needed to clarify this point. BBB complicating acute myocardial infarction places the individual at significant risk of developing congestive heart failure, with mortality usually secondary to myocardial failure or refractory ventricular arrhythmias. The pressence of high-degree AV block per se does appear to increase the mortality in patients without pump failure. Recent data suggest that immediate survival may be enhanced by prophylactic pacing in patients at high risk for abrupt complete heart block complicating acute myocardial infarction, but who do not manifest evidence of heart failure. The assumption that prophylactic pacing will improve survival of patients with bundle branch block and significant heart failure complicating acute myocardial infarction is purely speculative. Insufficient and conflicting data prevent a definitive statement regarding the usefulness of the P-R and H-V intervals as guidelines for the management of patients with recent-onset bundle branch block and acute myocardial infarction. Permanent pacing appears to benefit survivors of acute myocardial infarction complicated by BBB and transient high-degree AV block. However, the evidence is far from convincing. Little information is available on the influence of antiarrhythmic therapy on sudden death in patients with BBB. All currently used antiarrhythmic agents have a potentially high risk when administered to patients with BBB. Since there is no convincing prospective study as to the efficacy of drugs in preventing sudden death in patients with BBB, drug selection and its use in this group of patients remains at the discretion of the individual physician. It is based on the individual physician's experience with the drug in question and his perception of the benefit-to-risk ratio of the agent to be used.

Acute myocardial infarction in hospitalized patients over age 70

The history and clinical course of 175 patients aged 70 and older (Group A) with acute myocardial infarction (MI) was studied to determine the hospital mortality rate in this population group and to determine the clinical factors that influenced the hospital mortality rate. The mortality rate of a second group of 772 patients below age 70 years (Group B) admitted during the same time period was determined for comparison with the mortality rate in Group A. The hospital mortality rate in Group A (32%) was 3.9 times the hospital mortality rate in Group B (8.2%). Advanced age was associated with a significantly higher mortality rate, even when so called “good risk” patients from Group A were compared with patients in Group B. The major causes of death in this hospitalized group of patients aged 70 and older were shock (33.9%) and cardiac rupture (28.6%). Factors that significantly influenced hospital mortality rate in the elderly group were the development of shock, pulmonary edema on chest x-ray, a clinical diagnosis of congestive heart failure, and the development of complete heart block or new bundle branch block during the hospital course.

Reversible Heart Block Following Nonpenetrating Chest Trauma

Blunt chest trauma, if sustained selectively to the midchest or precordium, can result in a variety of cardiac injuries (3, 7). These lesions may involve separately or together all structures of the heart, including pericardium, myocardium, valves, and coronary arteries. Depending on the extent of trauma, such injuries can cause varying amounts of mechanical or electrical dysfunction. The incidence and nature of cardiac dysrhythmias following trauma are largely unknown clinically, but have been extensively documented in several animal studies (2, 4, 5). Disturbances in both impulse generation and transmission were noted, usually beginning immediately after impact with the development of complete heart block and progressing quickly through several other electrical patterns to either sinus rhythm or ventricular fibrillation. High-grade atrioventricular (A-V) block has rarely been recognized clinically in association with nonpenetrating heart trauma (1), perhaps because of its rapid replacement by other dysrhythmias. It was, therefore, of interest when a patient presented to this institution in third-degree heart block following a blunt chest injury. Specifics of her illness are discussed.

Prognosis for patients with congenital heart disease and postoperative intraventricular conduction defects.

Intraventricular conduction defects are common following repair of various forms of congenital heart disease. Such defects may affect adversely the long-term prognosis of patients in whom cardiac hemodynamics were adequately restored. Review of previously published studies suggests that the site of the conduction defect may be the reason for the different prognoses reported for patients from different institutions. The so-called "trifascicular block" pattern which sometimes occurs following open heart surgery is probably due to a more extensive lesion to the branching and penetrating parts of the His bundle rather than additional injury to the posterior left bundle branch fibers. Transient complete heart block in the immediate postoperative period seems to be a predictor for late development of complete heart block or sudden death at least as powerful as right bundle branch block and left anterior hemiblock.

Histologic observations of the cardiac conduction system in a patient with postoperative bilateral bundle branch block

It has been suggested that the postoperative development of a right bundle branch block pattern is due to injury of peripheral rather than proximal parts of the right bundle branch and does not affect the prognosis for the later development of complete heart block. However, the occurrence of complete heart block in a patient with postoperative right bundle branch block who later has left bundle branch block has not previously been documented. The entire specialized cardiac conduction system of a patient who had two operations for repair of double outlet right ventricle and multiple ventricular septal defects was serially sectioned. In the first operation, which resulted in a right branch block pattern, a subaortic ventricular septal defect was repaired through a right ventriculotomy. In the second operation complete heart block occurred after multiple muscular ventricular septal defects were repaired with a patch inserted through a left ventriculotomy. Examination of the conduction system showed that the right bundle branch was completely interrupted by the patch used to repair the subaortic ventricular septal defect and the left bundle branch was completely severed by the patch used to repair the muscular ventricular septal defects. This case proves that some patients who have a right bundle branch block pattern after repair of a ventricular septal defect may later have complete heart block if left bundle branch block develops as a result of sclerodegenerative or atherosclerotic heart disease or other cause.

The conducting tissues in congenitally corrected transposition.

The histopathological findings are reported in 11 cases of congenitally corrected transposition. For the purposes of this investigation, only hearts with a well-formed septum separating two ventricular sinuses were classed as corrected transposition. We did not, therefore, study any examples of single ventricle with inverted outlet chamber. Five of the cases formed the basis of a preliminary report, in which the distribution of conducting tissues in the anomaly was shown to differ from that reported in previous investigations. The six new cases confirmed this distribution. Thus, in all cases, the connecting atrioventricular node was anteriorly situated in the right atrium at the lateral junction of pulmonary and mitral valves. An anteriorly situated bundle descended into the morphologically left ventricle (right-sided) and encircled the anterolateral quadrant of the pulmonary outflow tract before descending on the anterior septum and bifurcating. The bundle branches were inverted. This distribution was observed in specimens with intact septa (three cases) and in specimens with ventricular septal defects (eight cases). In the latter cases the conducting tissues were related to the anterior quadrants of the defects. One case was of particular interest since the posterior node in the position of the normal atrioventricular node also made contact with the ventricles via a posterior bundle. In all other specimens this node was hypoplastic and did not have ventricular connections. It is considered that this finding provides a link with previous descriptions of posterior conducting tissue in congenitally corrected transposition. The findings are discussed with relation to the development of complete heart block in this anomaly.

Heart block in alcoholic cardiomyopathy

It is not unusual for cardiomyopathies to present with conduction abnormalities. However, reports of the occurrence of complete heart block in alcoholic cardiomyopathy are infrequent. Brigden and Robinson 1 reported 50 cases of alcoholic cardiomyopathy; 19 had some form of conduction disease. Eight patients had left bundle-branch block (LBBB), four had right bundle-branch block (RBBB), and seven had a prolonged RP interval, and one patient showed complete heart block. Tobin et al 2 reviewed 30 cases of alcoholic cardiomyopathy. One patient had a prolonged PR interval, one had LBBB, and two patients were noted to have RBBB. Evans 3 noted a bundle-branch block pattern in two of 20 patients having alcoholic cardiomyopathy. It appears that the development of complete heart block in alcoholic cardiomyopathy is unusual. We report, herein, a patient who developed cardiomyopathy secondary to excessive beer consumption that was then complicated by complete heart block. Bundle of His

Heart Block in Alcoholic Cardiomyopathy

It is not unusual for cardiomyopathies to present with conduction abnormalities. However, reports of the occurrence of complete heart block in alcoholic cardiomyopathy are infrequent. Brigden and Robinson 1 reported 50 cases of alcoholic cardiomyopathy; 19 had some form of conduction disease. Eight patients had left bundle-branch block (LBBB), four had right bundle-branch block (RBBB), and seven had a prolonged RP interval, and one patient showed complete heart block. Tobin et al 2 reviewed 30 cases of alcoholic cardiomyopathy. One patient had a prolonged PR interval, one had LBBB, and two patients were noted to have RBBB. Evans 3 noted a bundle-branch block pattern in two of 20 patients having alcoholic cardiomyopathy. It appears that the development of complete heart block in alcoholic cardiomyopathy is unusual. We report, herein, a patient who developed cardiomyopathy secondary to excessive beer consumption that was then complicated by complete heart block. Bundle of His

Left-posterior hemiblock. Clinical and vectorcardiographic study of twenty cases

Twenty patients with left posterior hemiblock (LPH), in whom one or more Frank vectorcardiograms had been obtained, were studied. In 13 of them this conduction defect was present in the isolated form, while in the remaining 7 subjects it was associated with complete right bundle-branch block (RBBB). The age group with isolated LPH was distinctly younger (mean 36 years) than that with combined LPH and RBBB (mean 67 years). Clinical evidence of coronary heart disease was rather common among this series with a higher incidence among those with LPH associated with RBBB. The possibility of the LPH being of congenital nature was entertained in 2 subjects with clinically diagnosed congenital aortic stenosis. In our patients, both with the isolated as well as the combined form of LPH, the prognosis regarding the eventual development of complete heart block (one out of twenty) was far better than that usually found in the literature. Most of the vectorcardiographic features in this series were quite similar to those reported by others. One important exception was that in a considerable number of patients with isolated LPH and in all of those with combined LPH and RBBB, the orientation of the maximum QRS frontal plane vector was inferior and to the left. In the present patients with LPH associated with RBBB there was a notorious anterior displacement of the QRS forces in the horizontal plane; this may be ascribed to the RBBB.

Electrocardiographic clues in diagnosing syncope.

Intermittent or transient episodes of cerebral dysfunction or syncope may result from complete heart block, which often goes unrecognized for years. Electrocardiographic patterns of conduction disturbances in one or both bundle branches are important clues to subsequent development of complete heart block.

The natural history of atrioventricular conduction defects in acute myocardial infarction

Of 446 patients admitted to the Coronary Care Unit, 54 (11.5 per cent) developed A-V conduction disturbance with a mortality rate of 33 per cent. Twenty-nine had complete heart block with a mortality rate of 45 per cent. There were three times as many patients with inferior infarction than anterior infarction and their mortality rate was only one third that of the latter. Approximately one third of those patients who developed first degree heart block progressed to complete heart block, and about one third of those who developed second degree heart block developed complete heart block. In those with first degree heart block, the site of infarction and time of onset was of no value in predicting those patients who might progress to complete heart block. It is suggested that the prophylactic insertion of an endocardial pacing catheter prior to the development of complete heart block is of little value in patients with inferior infarcts, but may be of value in those with anterior infarcts who develop first degree block.

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.

THERAPY OF COMPLETE HEART BLOCK COMPLICATING RECENT MYOCARDIAL INFARCTION.

ONE OF THE therapeutically reversible acute complications of recent myocardial infarction is the development of complete heart block. When the heart rate falls below 25 to 30 beats per minute, syncopal or convulsive seizures develop accompanied by the clinical picture of shock. This emergency requires immediate therapy not only for survival, but to prevent cerebral, cardiac, and renal complications resulting from repeated episodes of inadequate circulation. In the above situation we have employed a procedure similar to that described by Dr. C. W. Lillehei 1 for therapy of heart block complicating surgical repair of ventricular septal defects. The procedure consists of inserting a No. 18 spinal needle into the right ventricular cavity by puncturing the chest wall just medial to the point of maximal impulse and directing the needle superiorly and medially toward the second right costochondral junction. Then a No. 26 stainless steel wire is passed through the needle