Andrew G. Wallace

Hemodynamic consequences of atrial fibrillation at constant ventricular rates

Abstract Dogs which were areflexic and had induced heart block were studied and the consequences of atrial fibrillation at a constant, regular ventricular rate were examined. Alterations incurred by this arrhythmia could thus be related to the absence of effective atrial function per se . The observed hemodynamic consequences of atrial fibrillation were (1) an increase of mean left atrial pressure and an increase of mean left atrial pressure relative to left ventricular end-diastolic pressure; and (2) a decrease of aortic pressure and aortic flow. Evidence is presented which supports the view that the absence of effective atrial activity during atrial fibrillation results in early mitral regurgitation. Criteria for atrial fibrillation were also established by using two bipolar recording electrodes attached to the left atrium. These were (1) lack of uniform polarity, (2) lack of a phase relationship of the depolarization complex recorded at these two points, and (3) irregular rate of depolarization at each recording site.

Ventricular aneurysm with ventricular tachycardia: Report of a case with epicardial mapping and successful resection

A case of ventricular aneurysm with refractory ventricular tachycardia is presented. Epicardial mapping was used to localize the site of earliest epicardial activity to the margin of the aneurysm, and subsequent resection of this area abolished the rhythm disturbance.

Duration of hospitalization in "uncomplicated completed acute myocardial infarction". An Ad Hoc Committee review.

The clinical and laboratory findings diagnostic of acute myocardial infarction include at least two of the following: (1) a history of pain consistent with myocardial ischemia, (2) electorcardiographic findings consistent with infarction, and (3) a rise in the serum level of specific cardiac enzymes. By the 4th or 5th day of illness, specific criteria can be applied to assign certain patients to a subset with uncomplicated completed acute myocardial infarction. These criteria include the absence of evidence of (1) continuing cardiac ischemia, (2) left ventricular failure, (3) shock, (4) important cardiac arrhythmias, (5) conduction disturbances, and (6) other serious illnesses in patients with an established acute myocardial infarction. In terms of prognosis and management, patients in this subset should be regarded as substantively different from patients in other subsets. They should respond favorably to short periods of immobilization and hospitalization than those generally used. They may remain at bed rest (modified in regard to sitting and the use of a commode) for 4 days. Subsequently, mobilization with a program of progressive activity over the ensuing 5 to 10 days should reduce the duration of hospitalization to less than the current average of 17.5 to 20.8 days for patients with acute myocardial infarction. Nine to 14 days should suffice in most instances. Current and future trials may indicate that still earlier mobilization and shorter hospitalization periods can be applied to certain patient groups, but the evidence on this point is incomplete. For the individual patient, many factors will determine the optimal duration of bed rest and hospital stay. The patients physician must consider the therapeutic benefits that may attend earlier mobilization and shorter hospitalization while weighing potential disadvantages. When the responsible physician does not regularly care for the patient, consultation with an experienced cardiologist is desirable. Patients whose condition is classified as uncomplicated may manifest deterioration during their illness and require assignment to a subset with a different prognosis and requiring different forms of treatment. For patients with uncomplicated acute myocardial infarction, as well as those in other subsets, absolute rules for therapy are unwise and application of broader principles by the alert physician is more likely to be beneficial.

Correlation Between Catheter Electrophysiological Studies and Findings on Mapping of Ventricular Excitation in the W.P.W. Syndrome

The electrophysiological assessment (281,293) of a patient with Wolff-Parkinson-White syndrome is a multifaceted study which attempts to: 1. confirm the presence of preexcitation; 2. identify the nature of the associated tachyarrhythmia; 3. confirm the participation of the accessory pathway in the tachyarrhythmia; 4. presumptively localize the site of the accessory pathway; 5. characterize the functional behavior of the accessory pathway; and 6. examine the effect of drugs or pacemaker therapy. The advent of surgical techniques (751) to interrupt accessory pathways (AP) as a treatment modality for the Wolff-Parkinson-White syndrome has made more apparent than ever the need to preoperatively localize the site(s) of the AP(s) and to implicate the participation of the latter in observed tachyarrhythmias. With such information one can then select optimal candidates for surgical intervention (lateral APs vs. septal APs) (292), identify the presence of multiple APS (81,148,419,511) or APs with unidirectional block (598, 821,960) and select the appropriate operative approach (thoracotomy vs. sternotomy). Importantly, electrophysiological studies of the type to be discussed can be carried out safely and systematically preoperatively, while the corresponding intra-operative investigations utilizing epicardial mapping are often hampered by limitations of time, poor patient tolerance of tachyarrhythmias while under general anesthesia as well as a number of technical problems which can arise.

Adverse effects of sympatholytic agents in patients with hypertension and sinus node dysfunction

Abstract Over a period of 15 months, symptomatic sinus bradycardia developed in eight hypertensive patients treated with various sympatholytic agents: α-methyldopa (0.5 to 1.5 g/day) in three patients; propranolol (80 to 120 mg/day) in two; clonidine (0.4 mg/day) in two; and guanethidine (25 mg/day) in one. On admission, in addition to sinus bradycardia (38 ± 5 beats/min) (mean ± standard deviation), neurologic symptoms or hypotension, or both, were present in all. After cessation of drug therapy, heart rate increased to a mean rate of 60 ± 7 beats/min and symptoms disappeared. During a mean follow-up time of 15 ± 3 months, six patients were managed successfully by appropriate manipulation of their medical regimen, and two required permanent ventricular pacing. Electrophysiologic studies were performed in four patients, three of whom were challenged with intravenously administered propranolol (0.1 mg/kg body weight). Abnormal responses to rapid atrial pacing occurred in all four patients. Increases in mean spontaneous cycle length of 28, 33 and 2.5 per cent and maximal sinus node recovery time of 412, 48 and 44 per cent occurred after propranolol administration. Severe bradyarrhythmias may be precipitated by sympatholytic agents, particularly in patients suspected of having sinus node disease. These bradyarrhythmias can usually be managed successfully by modification of their pharmacologic regimen.

Duration of hospitalization in 'uncomplicated completed acute myocardial infarction'. An ad hoc committee review

The clinical and laboratory findings diagnostic of acute myocardial infarction include at least two of the following: (1) a history of pain consistent with myocardial ischemia, (2) electorcardiographic findings consistent with infarction, and (3) a rise in the serum level of specific cardiac enzymes. By the 4th or 5th day of illness, specific criteria can be applied to assign certain patients to a subset with uncomplicated completed acute myocardial infarction. These criteria include the absence of evidence of (1) continuing cardiac ischemia, (2) left ventricular failure, (3) shock, (4) important cardiac arrhythmias, (5) conduction disturbances, and (6) other serious illnesses in patients with an established acute myocardial infarction. In terms of prognosis and management, patients in this subset should be regarded as substantively different from patients in other subsets. They should respond favorably to short periods of immobilization and hospitalization than those generally used. They may remain at bed rest (modified in regard to sitting and the use of a commode) for 4 days. Subsequently, mobilization with a program of progressive activity over the ensuing 5 to 10 days should reduce the duration of hospitalization to less than the current average of 17.5 to 20.8 days for patients with acute myocardial infarction. Nine to 14 days should suffice in most instances. Current and future trials may indicate that still earlier mobilization and shorter hospitalization periods can be applied to certain patient groups, but the evidence on this point is incomplete. For the individual patient, many factors will determine the optimal duration of bed rest and hospital stay. The patients physician must consider the therapeutic benefits that may attend earlier mobilization and shorter hospitalization while weighing potential disadvantages. When the responsible physician does not regularly care for the patient, consultation with an experienced cardiologist is desirable. Patients whose condition is classified as uncomplicated may manifest deterioration during their illness and require assignment to a subset with a different prognosis and requiring different forms of treatment. For patients with uncomplicated acute myocardial infarction, as well as those in other subsets, absolute rules for therapy are unwise and application of broader principles by the alert physician is more likely to be beneficial.

Supraventricular tachycardia dependent upon accessory pathways in the absence of ventricular preexcitation

Abstract Paroxysmal supraventricular tachycardia is a common disorder of cardiac rhythm, generally thought to be due to reentry within the atrioventrlcular (A-V) node. The possibility that this disorder may be a manifestation of the Wolff-Parkinson-White syndrome should always be considered, but this etiology is usually rejected if the electrocardiogram in sinus rhythm falls to demonstrate a delta wave (i.e., ventricular preexcitatlon). Several recent reports have demonstrated that an accessory A-V pathway may conduct impulses only in the retrograde or ventriculo-atrial direction. Hence, reentrant tachycardia based on a mechanism identical to that observed in patients with classic Wolff-Parkinson-White syndrome may occur, and the electrocardiogram in sinus rhythm fail to show a delta wave. This report describes 11 patients who presented with paroxysmal supraventricular tachycardia without QRS changes in sinus rhythm that suggested the Wolff-Parkinson-White syndrome. Electrophysiologic studies demonstrated that an accessory pathway participated in the mechanism of the tachycardia. Eight of these 11 patients were successfully treated by surgical interruption of either the accessory pathway or the bundle of His. Accessory pathways are not rare among patients with paroxysmal supraventricular tachycardia; and it follows that this variant of the Wolff-ParkinsonWhite syndrome is more common than would be suspected if the Wolff-Parkinson-White syndrome is considered only when delta waves are observed on the electrocardiogram.

Direct and Indirect Techniques in the Evaluation of Sinus Node Function

Interest in the electrophysiology of the human sinus node began at the turn of this century when techniques became available that provided the clinician with recordings of atrial activity initially as jugular venous pulse tracings (513) and later as electrocardiograms (235). These two techniques enabled clinical investigators to document the presence of atrial premature depolarizations (514), evaluate the effect of premature depolarizations on sinus rhythm (915,916) and document the presence of long atrial pauses which were interpreted as being due to sinoatrial block (258,356,468,488,515,917). Disturbance of sinus node function was initially recognized in the form of sinoatrial block that occurred in a patient who had influenza (515). Later patients with sinus bradycardia (138,442) and sinus pauses or sinus arrest (75,468,623,684) were described. The characteristics of four patients with alternating bradycardic and tachycardic rhythms were described in 1954 (757). In addition, as experience was gained in the use of DC countershock for interruption of atrial fibrillation, it was recognized that normal resumption of sinus rhythm failed to occur in some patients (507). These different electrocardiographic descriptors were recognized as being due to a disturbance of sinus node function and were designated as the ECG criteria that defined the ‘sick sinus syndrome’ (263).

Ventricular Excitation in the Wolff-Parkinson-White Syndrome

In January of 1967 Professor Durrer and his colleagues from Amsterdam published the first report which described epicardial excitation of the ventricles in a patient with the Wolff-Parkinson-White syndrome (220). Eleven months later Howard Burchell and his colleagues from the Mayo Foundation presented a similar report. (99) In both of these early studies anomalous excitation of the right ventricle was noted with epicardial activation beginning in the region of the atrio-ventricular groove. The reports demonstrated the feasibility of localizing the site of an accessory bypass at surgery; and when coupled with the report by Durrer, Schoo, Schuilenburg and Wellens, (221) implicating the accessory pathway in reentrant tachycardia, led our group at Duke (132) to undertake studies which will be reported in part in this communication. In this chapter we will attempt to present our present view of ventricular excitation in the Wolff-Parkinson-White syndrome. Professor Wellens also asked that we include comments concerning the relation between the morphology of the QRS complex and activation data obtained at the time of surgery.

Programmed Atrial Stimulation and Rapid Atrial Pacing in Patients with Sinus Pauses and Sinoatrial Exit Block

Although Eyster and Evans (1915) and Levine (1916) described second-degree sinoatrial block in ECG recordings many years ago they realized that other possible sinoatrial conduction disturbances eluded analysis, primarily because electrical activity in the sinus node cannot be directly recorded in vivo. In 1973, Strauss et al. proposed that the pre- mature atrial stimulation technique could be used to derive the sinoatrial conduction time. In the application of this technique a programmable stimulator is used to elicit variably coupled atrial premature depolarizations during spontaneous sinus rhythm. The last undisturbed spontaneous sinus cycle (A1A1), premature cycle (A1A2) and return cycle (A2A3) are analyzed and the normalized return cycles (A2 A3/A1 A1) are plotted as a function of the normalized premature cycles (A1A2/A1A1) (Figure 1). Late atrial premature cycles are followed by compensatory return cycles. Atrial premature depolarizations elicited earlier in atrial diastole are followed by less than compensatory return cycles. The duration of the less than compensatory A2A3 cycle is determined by the retro- grade conduction time from the atrium to the sinus node (A2SAN2), the sinus node return cycle (SAN2SAN3) and the antegrade sinoatrial conduction time (SAN3A3). The estimation of the sinoatrial conduction time is based on the assumption that the sinus node return cycle (SAN2SAN3) equals the spontaneous sinus node cycle (SAN1SAN1) or the corresponding spontaneous atrial cycle (A1A1) (Figure 1). Hence, the difference between the atrial return cycle (A2A3) and the spontaneous atrial cycle (A1A1) should equal the retrograde conduction time (A2SAN2) for A2 and the antegrade conduction time (SAN3A3) for the subsequent sinus node depolarization (SAN3). The difference between A2A3 and A1A1 computed for atrial premature depolarizations falling in the latest third of the reset zone (zone II) is used to derive a mean value for the estimated antegrade and retrograde sinoatrial conduction time (SACTA+R) (Strauss et al., 1976). It is also assumed that the sum of the A2SAN2 + SAN3A3 equals a value that is twice the normal antegrade sinoatrial conduction time (SAN1 A1). For this reason many investigators have divided SACTA+R by 2 to obtain a value that approximates the antegrade sinoatrial conduction (Dhingra et al., 1975; Breithardt et al., 1976; Jordan et al., 1977). Since antegrade and retrograde conduction times may not be equal, (Bonke et al., 1969; Klein et al., 1973; Miller and Strauss, 1974) we have chosen to express our sinoatrial conduction times as the total value, i.e. SACTA+R.