Aubrey Leatham

Electrocardiographic changes subsequent to artificial ventricular depolarization.

Massive T wave inversion and ST depression occur in the unpaced electrocardiogram subsequent to ventricular pacing, and persist for a varying length of time depending on the duration of pacing. That artificial depolarization of the ventricle causes changes in repolarization which persist after stopping pacing is of considerable theoretical and practical importance, and we describe the findings in 31 patients both with and without disease of the conduction tissue.

Septicemia in patients with an endocardial pacemaker

The records of 1,235 consecutive patients treated with long-term pacing by the endocardial route between 1964 and 1977 were analyzed to determine the incidence, mechanism, course and treatment of septicemia. Septicemia developed in 12 patients (1 percent), and Staphylococcus aureus was isolated from the blood culture in 10. All patients were treated with the usual prolonged course of bactericidal drugs. Treatment was successful in only two of the seven patients whose endocardial pacing system was left in place; in three of the seven the septicemia recurred, necessitating removal of the endocardial system, and two of these patients died. In the remaining four patients the endocardial wire was promptly withdrawn, with use of a thoracotomy when necessary, and an epicardial system inserted; all of these patients survived. This is the treatment of choice.

Aetiology of chronic heart block. A clinico-pathological correlation in 65 cases.

The cause of chronic heart block is often obscure on clinical grounds alone. Consequently there is considerable difficulty in deciding the prognosis of a patient with complete heart block even with successful artificial pacing. Coronary artery disease has been generally accepted in the past as the predominant cause of heart block, and Penton, Miller, and Levine (1956) estimated an incidence of 43 per *cent, Wright et al. (1956) one of 69 per cent, and Friedberg, Donoso, and Stein (1964) one of 48 per cent. These estimates were based on clinical and electrocardiographic evidence. Other studies suggested that areas of fibrosis involving the conducting system, either alone or in association with scattered areas offibrosis in the myocardium, were responsible for heart block (Lenegre and Moreau, 1963; Lev, 1964; Zoob and Smith, 1963). In one of our earlier patients, the only cardiac abnormality was fibrotic lesions confined to the conducting tissue, a surprising finding as severe coronary disease had been suspected, and this made us realize the importance of developing techniques for long-term artificial pacing (Portal et al., 1962). With the continuing improvement of these techniques, the prognosis of a patient will become more dependent on the cause of the heart block. In an effort to improve the clinical diagnosis of the underlying cause of heart block, a retrospective survey was carried out in 65 consecutive patients with chronic heart block who had come to necropsy during the past 3 years.

The aetiology and course of isolated severe aortic regurgitation: a clinical, pathological, and echocardiographic study.

Seventy two consecutive patients with severe isolated aortic regurgitation were evaluated by preoperative echocardiographic and angiographic assessment of the aortic root. Biopsy specimens of the aortic wall were taken at operation. Two major groups of patients were found: those with cusp derangement but normal aortic roots and those with normal cusps but dilated aortic roots. Of the 42 cases of abnormal cusps, 20 were rheumatic, 15 were infective, and six were bicuspid. One patient had a tear in an otherwise normal cusp. Of the 30 cases of abnormal roots but normal cusps, six had inflammatory changes (syphilis, Reiters disease, giant cell aortitis) and 24 had root dilatation caused by non-inflammatory destruction of elastic laminae. Echocardiographic measurement of the aorta at the level of the top of the commissures predicted the findings at pathology. In 37 of 39 patients with cusp disease the measurement was less than 37 mm. In 27 of 33 patients with root disease the measurement was greater than or equal to 37 mm. This difference was statistically significant. There was no difference in the sizes of the prosthesis used in each group, suggesting that it was the diameter of the junction of the aorta with the sinuses rather than the junction of the sinuses with the ventricle that was important in aortic regurgitation. Clinical progression in patients with non-inflammatory aortic root disease is slower than in patients with infective disease but faster than in those with rheumatic cusp disease.

Long-term prognosis after acute anterior infarction with atrioventricular block.

The purpose of this study was to evaluate the need for permanent pacing in patients who have survived the effects of anterior myocardial infarction with complete heart block and have returned to sinus rhythm but who are left with impairment of intraventricular conduction. We have reviewed 52 patients with complete heart block complicating recent anterior myocardial infarction. Temporary pacing was instituted in all patients. There were 25 hospital survivors who were followed for an average of 49 months. Long-term pacing was established in 4 patients. Of the 21 patients in sinus rhythm, 14 had partial bilateral bundle-branch block with either right bundle-branch block and left anterior hemiblock or right bundle-branch block and left posterior hemiblock; at the end of the follow-up period, 10 of these 14 were alive and well. Furthermore, permanent pacing failed to prevent sudden death in 2 patients. At the present time, therefore, we conclude that long-term pacing is not justified in patients, otherwise asymptomatic, with partial bilateral bundle-branch block persisting after transient complete heart block in anterior myocardial infarction.

THE MANAGEMENT OF HEART BLOCK

In 1952, Zoll described a technique for artificial pacing of the heart. The method employed electrodes placed on the chest wall and electrical impulses of 2 msec. duration at 25-150 volts. Although this indirect technique proved successful in resuscitating and temporarily maintaining life in patients with Stokes-Adams attacks due to asystole, the high voltage required produced skin burns and painful contractions of the muscles of the thorax. Other methods were developed for the direct stimulation of the myocardium with low voltages, and permanent pacing of the heart with small pacemakers is now routinely performed (Bellet et al., 1960; Chardack, Gage, and Greatbatch, 1961; Elmqvist and Senning, 1960; Davies, 1962; Kahn et al., 1960; Landegren, 1962; Lillehei et al., 1960; Stephenson et al., 1959; Weirich et al., 1958; Zoll et al., 1961). Reports on the success of long-term pacing by many different systems have now appeared (Furman et al., 1961; Levitsky et al., 1962; Siddons, 1963). While artificial pacemaking is life saving and permits a return to a normal way of life in most cases, numerous problems have arisen in the maintenance of this artificial system. It is for this reason that we propose to describe our experiences in the management of heart block over the past four years at St. Georges Hospital, of which some have been previously reported by Portal et al. (1962) and Siddons (1963).

Mild mitral regurgitation and the mitral prolapse fiasco

The diagnosis, prognosis, and management of severe mitral regurgitation is comparatively well understood, and its exact cause is usually clear. Not surprisingly, the diagnosis of slight mitral reflux, its cause, prognosis, and management creates more difficulty and confusion, though some of this appears to result from some ill-considered statements and conclusions among the vast recent literature on the subject. Indeed, physicians may be puzzled by reading of chest pain,. dangerous dysrhythmias, and sudden death as serious considerations in what otherwise appears to be a trivial lesion, and even more puzzled by learning of the, great frequency of mitral valve prolapse on the echocardiogram varying from 4 to 21% of the population.‘. * These views are not in accord with our experience and continuing interest in this problem which extends over more than 25 years since we wrote on the subject in 1953.” Indeed, we hold the opinion that isolated disease of the mitral valve causing mild or moderate reflux seldom causes symptoms other than those of iatrogenic anxiety, and that the prognosis for this lesion is good, excepting the small risk of infective endocarditis and the very small one of progressive regurgitation usually as a result of chordal rupture. These divergent opinions result in uncertainties about the problem which appear to have arisen because there has been an “explosion of information,“” brought about by advances in the tools of biological research, and presented

T-WAVE CHANGES AFTER ARTIFICIAL PACING

Abstract Massive T-wave inversion and ST depression occurred in unpaced electrocardiograms of 31 patients after ventricular pacing, whether endocardial or epicardial, and were related to the power of the artificial electric stimulus and not to the presence of the electrode alone. They continued as long as pacing was continued but were always reversible. They should not be mistaken for evidence of myocardial injury or underlying coronary disease.

THE RISK OF PACING AFTER INFARCTION, AND CURRENT RECOMMENDATIONS

Abstract Experience of artificial pacing in 82 patients with acute myocardial infarction complicated by heart-block suggests that early electrode insertion, use of demand pacemakers with low power, awareness of the possibility of inappropriate stimulation due to low intracardiac potential, and liberal use of ventricular suppressant drugs appears to have reduced the mortality of this serious condition. The advantages of pacing, under the condition described, have outweighed the risks.

HEART-BLOCK FOLLOWING ACUTE MYOCARDIAL INFARCTION: Treatment with Demand and Fixed-rate Pacemakers

Abstract The mortality was 45·5% in 55 patients treated with artificial pacing for atrio-ventricular conduction disturbance complicating acute myocardial infarction. The mortality in 18 patients who had fixed-rate pacemakers was 56%, compared with 38% in 37 patients with demand pacemakers—a difference that was not statistically significant. Demand pacing did not remove the risk of ventricular fibrillation, and fast pacing rates and suppressant drugs are still needed when ectopic competition occurs. The most important factor in the high mortality was myocardial failure, which caused 21 of the 25 deaths. Anterior infarction and syncopal attacks also carried a high mortality, and prevention of syncope by early electrode insertion appears to be beneficial.