George E. Burch

The syndrome of papillary muscle dysfunction

Abstract The function of the papillary muscles to restrain the mitral valves is obvious. However, the dynamic nature of this function is not always appreciated. Failure of one or both papillary muscles to shorten during the ejection phase of ventricular systole, fibrosis, and atrophy of a papillary muscle or centrifugal migration of the papillary muscles due to left ventricular dilatation result in mitral incompetence. Depending upon the etiology of the papillary muscle dysfunction, apical systolic murmurs of varying characteristics may be heard. In general, a noncontracting papillary muscle in a normal-sized heart is associated with a murmur which is late in onset and crescendo-decrescendo in quality, whereas in the dilated heart the murmur is early, beginning with the first heart sound, and may be decrescendo, plateau, or crescendo-decrescendo in quality. Obviously, the murmurs of papillary muscle dysfunction may vary considerably depending upon the nature of the dysfunction and time course of activation of the muscle and other portions of the ventricular musculature. Associated electrocardiographic abnormalities may also occur. Mitral insufficiency due to acquired or congenital valvular disease has been exhaustively studied. On the other hand, mitral insufficiency secondary to disease of the papillary muscles has been almost completely neglected. Nevertheless, since our description of the papillary muscle syndrome in 1963, 1 more than 20 papers dealing directly or indirectly with this syndrome have appeared. In the present review we have extended the original description of the papillary muscle syndrome to include a number of diseases which either clinically or at necropsy have been implicated in the production of papillary muscle dysfunction in the hope that attention will be focused on those diseases, in addition to circulatory insufficiency, which may result in papillary muscle dysfunction.

Electrocardiographic alterations associated with electrically “silent” areas of myocardium

Abstract The purpose of this paper was to describe some instances in which there may be loss of electromotive force (emf) from myocardial tissue without biologic death of the tissue. Myocardial tissue which is electrically inactive although viable is considered to be electrically silent. Electrically silent myocardial tissue may, under the proper circumstances, regain electrical activity. The development of areas of electrical silence within the myocardium may be associated with electrocardiographic alterations, particularly pathologic Q waves. Such Q waves disappear after the area of electrical silence recovers. It is important to recognize the fact that loss of cardiac emf is not synonymous with tissue death. Judgment concerning the extent of a myocardial infarction or the significance of pathologic Q waves (or other changes in the QRS complex) in patients with tachycardia, angina pectoris, or electrolyte disturbances should take into consideration the possibility of the presence of electrically silent areas. Furthermore, awareness of the electrocardiographic alterations associated with electrically silent areas of myocardium provides an understanding of some difficult electrocardiographic problems and makes it unnecessary to invoke alterations in rotation, position, or sequence of depolarization to explain electrocardiographic findings which do not correlate with the autopsy data.

Chaotic atrial mechanism

Abstract A distinctive, sustained atrial arrhythmia, characterized by chaotic and random atrial activity with at least three different types of “P” waves in a single electrocardiographic lead and variability of the P-P, R-R, and P-R intervals, has been described in 31 patients. This disturbance has been named chaotic atrial mechanism (CAM). In the majority of patients, the cardiac (atrial and ventricular) rate with this rhythm disturbance ranged from 100 to 150 beats per minute, but in rare instances it was as low as 56 or as fast as 200 beats per minute. On physical examination, it was usually indistinguishable from atrial fibrillation. The average age of the patients was 68.5 years. Such a striking correlation with pulmonary disease (83.9 per cent) and with diabetes mellitus (74.2 per cent) occurred that a syndrome was almost suggested. Probable important factors in the pathogenesis of the arrhythmia are diffuse atrial disease (ischemia, fibrosis, distension, stress) and damage to the sinus node with disorderly competition for pacemaker control by other foci of atrial pacemaker tissue. In support of this, premature atrial beats were noted, either before the onset of the arrhythmia or after its termination, in 61.3 per cent of the patients studied. In the majority of patients the arrhythmia lasted less than two weeks. The shortest apparent sustained duration was several seconds and the longest six years. The best therapeutic approach appeared to be that directed toward any underlying pathologic condition, especially pulmonary disease, diabetes mellitus, congestive heart failure, and infection. Antiarrhythmic drugs did not prove effective at safe dosage levels in the instances in which they were tried. Direct current cardioversion has not been attempted. Response to digitalis was variable and unpredictable, and intoxication frequently occurred when high dosages were used in an attempt to control cardiac rate. The potentially grave prognosis in patients with this rhythm disturbance is underscored by the fact that 16 of the 31 patients (52 per cent) died during the hospital stay in which the arrhythmia occurred and that 9 of these died within 45 days of its onset. Twelve of those who died apparently had the arrhythmia at the time of death.

The necropsy incidence of gross scars or acute infarction of the papillary muscles of the left ventricle

Abstract Mechanical dysfunction of one or both papillary muscles of the left ventricle is probably a frequent cause of apical systolic murmurs. The present study was undertaken to determine the frequency of gross scarring or fresh infarction of the papillary muscles of the left ventricle. In a series of 420 consecutive necropsies, gross scars were found in one or both papillary muscles in 21.4 per cent of hearts, whereas acute infarction of one or both papillary muscles was found in 3.8 per cent of hearts. Although the clinical significance of these findings is unknown, it is suggested that papillary muscle dysfunction may be an important cause of apical systolic murmurs, especially in older patients.

A study at autopsy of the relation of absence of the Q wave in leads I, aVL, V5, and V6 to septal fibrosis.

Abstract In patients with an absolute absence of Q waves in Leads I, aV L , V 5 , and V 6 there is an 80 per cent possibility that septal fibrosis is present. If left ventricular hypertrophy is present and there are diminutive Q waves in these leads, septal fibrosis may be present; however, it is not possible to be certain of this. Twenty per cent of the patients without septal Q waves did not have septal fibrosis at autopsy. Most of the patients studied who had an absence of Q waves in Leads I, aV L , V 5 , and V 6 and septal fibrosis at necropsy, also had left ventricular hypertrophy and a prolonged period of angina pectoris.

The electrocardiogram in infarction of the anterolateral papillary muscle

Abstract An electrocardiographic syndrome has been described which allows fairly reliable prediction of the presence of infarction of the left ventricular anterolateral papillary muscle. The changes in the electrocardiogram generally fall into three major groups. One consists of moderate to marked depression of junction J in the middle and left precordial leads associated with a concavity-upward deformity of the ST-T interval. Another consists of changes in the same leads with, however, slight depression of junction J and a convexity-upward deformity of the ST-T interval and terminal inversion of the T wave. The third consists of changes in these leads with, however, an extremely marked depression of junction J, associated usually with slight initial convexity-upward deformity of the ST-T interval. The presence of apparent T-U segment depression or U-wave inversion was detectable in the majority of electrocardiograms in all three groups.

Methods for studying the influence of higher central nervous centers on the peripheral circulation of intact man

Abstract Although they are of clinical importance, relatively few studies have been conducted on the influence of orienting and conditional reflexes on the cardiovascular system. In addition, there are virtually no studies on the influence of such reflexes on the peripheral circulation of man. One of the difficulties involved in the study of vascular responses to orienting and conditional reflexes has been the lack of techniques which are quantitative and sensitive and which can be applied without disturbing the intact man. This report described two techniques used in our laboratory to study the peripheral circulation which are ideally suited for use with Pavlovian methodology.

An electrocardiographic and spatial vectorcardiographic pattern associated with diffuse myocardial damage and ventricular aneurysm.

Abstract Aspects of clinical, pathologic, electrocardiographic, and spatial vectorcardiographic findings in 24 patients with diffuse myocardial damage, infarction, and ventricular aneurysm have been described. A distinctive QRS pattern (0.10 to 0.16 second) in Leads I, V 5 , or V 6 characterized by a brief early upward deflection followed by a shallow downward deflection and, finally, a prolonged prominent R′ was found in 13 patients. Persistent elevation of the S-T segment was noted in 5 of the remaining patients. The same QRS pattern was found in 4 other patients with myocardial infarction and diffuse scarring but without ventricular aneurysm.

Vectorcardiographic defelections obtained with various reference systems in cadavers

Abstract A study of artificially applied dipoles in the heart of fresh cadavers clearly showed that some systems of electrode placement employed for spatial vectorcardiography are far from perfect.

Applications of digital biopsy to peripheral vascular investigations in man, with special consideration to dermal chromaffin cells

Previous studies have demonstrated that elevation of arterial pCO2 is associated with an increase in the amount of pressure required to inflate the lungs. These studies do not clearly indicate whether this increase in resistance is due to a change in non-elastic or elastic resistance of the lung. In the current study, dogs were anesthetized with chloralose, and a tracheostomy and a midline sternotomy were performed. Respiration was maintained with a Starling pump. Flow, volume, and airway pressures were recorded. The dogs were respired on varying concentrations of carbon dioxide and on air. Resistance was calculated at the same flow rate and lung volume for each of the experimental conditions. In ten dogs it was demonstrated that non-elastic resistance increased in a linear fashion as the level of arterial pCO2 was raised over the range of 25 to 80 mm. Hg. Elastic resistance was unchanged. Atropine given intravenously prevented the increase in airway resistance associated with hypercapnia. The level of non-elastic resistance for any given pCOz did not change over a fifteen-minute period. The clinical implications of this observation are many, and further studies are in progress to determine whether or not similar changes occur with more prolonged periods of hypercapnia.