Showing papers in "American Journal of Cardiology in 1965"
TL;DR: It was found that there appeared to be no such thing as “true” persistent truncus arteriosus in the timehonored sense of persistence of an undivided conotruncal channel, and a revised and simplified classification oftruncus is proposed.
Abstract: Based upon a series of 57 necropsy cases and upon the literature, it was found that there are two basic types of common aorticopulmonary (A-P) trunk: those with a ventricular septal defect, and those without. The latter is exceedingly rare and did not occur in this series. Truncus with a ventricular septal defect was found to consist of the following: (1) absence of the distal portion of the pulmonary infundibulum (very similar to tetralogy of Fallot with pulmonary atresia); (2) partial or complete absence of the pulmonary valve; (3) partial or complete absence of the aorticopulmonary septum; and (4) arterial arches 4 and 6 varied inversely in their development (e.g., well developed aortic arch with absent ductus arteriosus, or interrupted aortic arch with a large patent ductus arteriosus). Thus, there appeared to be no such thing as “true” persistent truncus arteriosus in the timehonored sense of persistence of an undivided conotruncal channel. While it is correct that the truncus is undivided (the aorticopulmonary septum being partially or totally absent), at the level of the conus the anomaly is not a failure of septation but absence of the entire distal portion of the pulmonary infundibulum (septum and free wall). Hence, at the level of the conus, common trunk is not a large infundibular septal defect but an extreme tetralogy of Fallot. At the distal conus, nothing has persisted. When the aortic arch was present, there was a high incidence of right aortic arch (27%) similar to tetralogy. The truncal valve basically was the aortic valve, explaining why it usually was tricuspid (67%). When some pulmonary leaflet tissue persisted, made possible by absence of the aorticopulmonary septum at the semilunar valve level, the truncal valve then was quadricuspid (24%). Failure of leaflet separation either in a basically tricuspid or quadricuspid valve occasionally resulted in a bicuspid truncal valve (7%). Truncus is not a form of transposition of the great arteries. Mitral-aortic fibrous continuity was present in all cases. The ventricular septal defect is not primarily “membranous.” It is due to absence of the distal pulmonary infundibulum. The coexistence of single ventricle and common aorticopulmonary trunk has been considerably overestimated. This combination did not occur in this series and is extremely rare (?non-existent). A revised and simplified classification of truncus is proposed.
491 citations
TL;DR: It is suggested that, since in infancy spontaneous closure or reduction in size of the ventricular septal defect is so common, most infants should be treated conservatively in the hope that spontaneous improvement will occur.
Abstract: Sixty-two infants with ventricular septal defects were first catheterized under 1 year of age and followed up for one to five years; 40 were recatheterized. Thirty-six infants were born in the Bronx Municipal Hospital Center or Lincoln Hospital (local group). These patients were unselected, in that the decision to catheterize them was based only on the clinical diagnosis of a ventricular septal defect and not on an assessment of its size or the presence of symptoms. As far as we know, these infants include most if not all of the children born with ventricular septal defects in these hospitals during the period of study. With this assumption, the incidence of ventricular septal defects per 1,000 live births was 0.94 for full term infants, 4.51 for premature infants, and 1.35 for the whole group. Twenty-six other infants were referred from other hospitals or doctors (referred group), and, compared to the local group, they had larger defects, were more often in congestive heart failure and were more often catheterized after 6 months of age. In the whole series, 31 of 62 had congestive heart failure. This began before 6 months of age in all and occurred much earlier in premature than in full term infants. In the local group, spontaneous functional closure of the ventricular septal defect took place in 13 of 36 (36%); this was proved by recatheterization in 10 and autopsy in 1. Marked decrease in size of the defect took place in another 10 (28%). In the referred group (26 cases) there were 2 (8%) spontaneous closures and 7 (27%) reductions in defect size. For the whole series, 52 per cent of the patients had defects which were known to have closed or become smaller; 32 per cent were doing well clinically (most were not recatheterized so that some of these defects might have become smaller); and only 16 per cent of the infants were seriously affected by their lesions. Complete closure occurred between 7 and 12 months of age, most often when the defect was small, but it could occur with large defects. Decrease in defect size, however, occurred as frequently with large as with small defects, and was found in many children with congestive heart failure and pulmonary arterial hypertension. The 10 infants with large ventricular septal defects who did not do well included 4 who had pulmonary arterial banding for severe, uncontrolled congestive heart failure (2 died); 1 premature baby who died at 6 weeks of age with severe congestive heart failure; and 5 with a very high pulmonary vascular resistance. One of these 5 had a high pulmonary vascular resistance when 1 month old, and this did not change significantly at 5 and 13 months of age. The other 4, however, had low pulmonary vascular resistance when first catheterized at 3, 6, 6 and 11 months of age, respectively, and significant rises of resistance to pathologic levels when recatheterized at 9, 15, 26 and 40 months of age, respectively. This suggests that a rise in pulmonary vascular resistance in infancy is not rare when the ventricular septal defect is big and that, even in these children, the pulmonary vascular resistance does not usually persist at the high level present at birth but first falls post natally to normal levels before rising. These 5 infants all had large left to right shunts, high left atrial pressures and marked pulmonary arterial hypertension. In 3 out of the 4 whose pulmonary vascular resistances rose after the first catheterization, there were no distinctive clinical indications of this rise which was detected only at recatheterization. The other child had increasing right ventricular hypertrophy on the electrocardiogram. From these findings we suggest that, since in infancy spontaneous closure or reduction in size of the ventricular septal defect is so common, most infants should be treated conservatively in the hope that spontaneous improvement will occur. If the defect is very big and the child is in severe congestive heart failure which cannot be well controlled, then surgical closure of the defect or banding of the pulmonary artery should be done. If, however, the defect is big but congestive heart failure can be controlled medically, then the infant should be followed up with the hope that spontaneous improvement will occur. Whether clinical improvement occurs or not, the infant should be recatheterized six to nine months after the initial catheterization to determine if a rise in pulmonary vascular resistance has occurred; if it has then surgery should be advised.
261 citations
TL;DR: Data indicate that the pressor reaction to the cold stimulus is not altered in hypertension, and major cardiodynamic changes during this stimulus include increased peripheral arterial resistance, increased cardiac output due to increased heart rate, and increased pulmonary artery pressures.
Abstract: Circulatory dynamics during the cold pressor test were studied in 10 normotensive and 8 hypertensive patients. Measurements were made before and during 5 minutes of immersion of the hand in ice water. The initial 60 seconds of the test represented vascular reactivity to the cold stimulus, and the hemodynamics at 5 minutes of hand immersion represented the degree of circulatory adaptation to this stimulus. Most patients responded to the cold pressor test with statistically significant increases in blood pressure. However, only 50 per cent of hypertensive patients demonstrated vascular hyperreactivity, i.e., a rise in blood pressure of 20/20 mm. Hg or more. In addition, the pressor responses were quantitatively similar in the hypertensive and normotensive groups. These data indicate that the pressor reaction to the cold stimulus is not altered in hypertension. The cold pressor test represents a widespread stimulation (neurogenic) of multiple components of the cardiovascular system, the quantitative and qualitative aspects of which are not predictable on a clinical basis and are similar in hypertensive and normotensive individuals. Major cardiodynamic changes during this stimulus, in addition to the pressor response, include increased peripheral arterial resistance, increased cardiac output due to increased heart rate, and increased pulmonary artery pressures. Cold adaptation, an almost universal occurrence, generally involves a gradual diminution in the pressor response, and the circulatory mechanisms responsible for it, to continued (cold) stimulation. The usefulness of this phenomenon in the study of the cardiovascular system in normal and hypertensive patients is negligible.
161 citations
TL;DR: Inability to maintain an adequate blood pressure in the face of a diminished cardiac output was directly associated with the onset of presyncopal symptoms, and physiologic changes induced by lower body negative pressure are apparently secondary to redistribution of blood volume with pooling in the pelvis and lower extremities, thus diminishing cardiac venous return.
Abstract: Application of negative pressures ranging between −25 and −80 mm. Hg to the lower half of the supine body produces cardiovascular changes similar to venesection and upright tilting. The heart rate increases between 13 and 67 per cent; central venous pressure decreases by 3 to 6 mm. Hg; cardiac index falls by 20 to 42 per cent; and stroke volume decreases by 28 to 64 per cent. In spite of these changes, systolic and pulse pressures are often well maintained. Calculated peripheral resistance increased significantly between 14 and 34 per cent, during lower body negative pressure; however, due to great individual variability, no significant difference was observed among the various negative pressures. Syncope very similar to that observed secondary to other vasodepressor stimuli is noted with increasing frequency as the amount of negative pressure is increased, i.e., 100 per cent at −80 mm. Hg, 70 per cent at −60, 58 per cent at −40, and none at −25. The cardiac output falls within three minutes atter the onset of negative pressure. The magnitude of the fall does not correlate with the subsequent development of presyncopal symptoms and does not significantly change with further exposure to negative pressure. Inability to maintain an adequate blood pressure in the face of a diminished cardiac output was directly associated with the onset of presyncopal symptoms. The physiologic changes induced by lower body negative pressure are apparently secondary to redistribution of blood volume with pooling in the pelvis and lower extremities, thus diminishing cardiac venous return. Compensatory mechanisms mediated neurogenically maintain adequate circulation to vital organs. The possible origins and controls of these mechanisms are discussed.
160 citations
TL;DR: The importance of atrial systole for maintenance of cardiac output is clearly demonstrated by these data.
Abstract: Cardiac output studies were performed in 6 patients with complete heart block during four kinds of ventricular rhythm. These include ventricular or His-bundle pacing at the control rate, right ventricular outflow tract catheter electrode pacing, and both synchronous and atrial synchronous pacing by means of a Cordis Synchrocor unit. The latter two rhythms are defined as those with P wave, ventricular stimulus and QRS complex sequences, and atrial stimulus, P wave, ventricular stimulus and QRS complex sequences, respectively. Thirty-four paired observations were made during equal atrial and ventricular pacing rates in these patients. The importance of atrial systole for maintenance of cardiac output is clearly demonstrated by these data.
157 citations
TL;DR: Comparisons of pressure curve data in patients with complete heart block and patients with sinus rhythm and atrial fibrillation show the physiologic importance of maintaining the normal temporal sequence of atrioventricular activity, as well as the observation that left ventricular end-diastolic pressures are higher during sinu rhythm than during a series of ventricular premature beats.
Abstract: The contributions of atrial systole to ventricular filling are emphasized by analyses of pressure curve data in (1) patients with complete heart block studied by right and left heart catheterization, (2) patients with sinus rhythm and atrial fibrillation and (3) sinus rhythm and ventricular premature beats. The level of systolic and diastolic right and left heart pressures varies with the temporal relation between the P and QRS complexes in patients with complete heart block. Peak pressures are recorded when there is a normal temporal relation between the P and QRS complexes. The rate of rise of the systemic arterial pressure curve is also at a maximum when the normal P-QRS relation is maintained. Comparison of left ventricular and systemic arterial pressures during sinus rhythm and ventricular premature beats demonstrates higher systolic peak pressures during sinus rhythm with normal atrioventricular conduction; of equal importance is the observation that left ventricular end-diastolic pressures are higher during sinus rhythm than during a series of ventricular premature beats. One subject was studied during both atrial fibrillation and normal sinus rhythm in the course of left heart catheterization. Left ventricular. systolic and end-diastolic pressures were higher during normal sinus rhythm than during atrial fibrillation. The development of mitral regurgitation during ectopic ventricular beats is also illustrated. These data demonstrate the physiologic importance of maintaining the normal temporal sequence of atrioventricular activity.
150 citations
147 citations
TL;DR: It appears that in the so-called myocardial infarct or the sudden “coronary” heart death in the human being, most of the cases develop independently of an acute occlusion and that it is incorrect to apply the term “myocardial Infarct” to the lesions.
Abstract: The incidence of acute occlusion was investigated in 208 hospitalized patients dying from acute or recent coagulative necrosis of the myocardium, in 116 cases of sudden, unexpected “coronary” heart death, and in 125 cases of sudden but not unexpected “coronary” heart death. The approximate ages of both the vascular and myocardial lesions and the prior sclerotic reduction of the lumen of the acute or recently occluded vessels were studied and correlated with the corresponding enlargement of the collateral arterial circulation. From the high incidence of acute or recent coagulation necrosis and/or sudden heart death without acute occlusion (53, 53, and 54% in the three groups studied), the low incidence of a “coeval” relation between the acute or recent occlusion and the stage of the myocardial damage (23, 22, and 19%, respectively), the high incidence of sclerotic reduction of the lumen in excess of 65 per cent in the acutely or recently occluded vessels (82, 91, and 96%, respectively), and the marked enlargement of the collateral circulation found in this study, it appears that in the so-called myocardial infarct or the sudden “coronary” heart death in the human being, most of the cases develop independently of an acute occlusion and that it is incorrect to apply the term “myocardial infarct” to the lesions. It is also our belief that the acute or recent thrombosis occurring in most of the instances should not be considered as the cause of the acute or recent myocardial coagulative necrosis or sudden death or both, but rather as the result of particular hemodynamic conditions existing in and around the involved vessel.
125 citations
TL;DR: There is a fine balance between heart rate and A-V conduction, and when the heart rate is increased by neurohumoral stimuli, there is a corresponding enhancement of A- V conduction.
Abstract: Atrioventricular conduction was studied in 14 patients. A bipolar electrode catheter was placed in the right atrium, and the heart rate was controlled by atrial pacing. Increases in the sinus heart rate were associated with decreases in atrioventricular conduction time. When the heart rate was increased by atrial pacing, there were progressive increases in atrioventricular conduction time. Exercise, isoproterenol and atropine shortened atrioventricular conduction time. In those cases where atrioventricular conduction block occurred during atrial pacing, there was a 1:1 atrioventricular response during exercise at the same paced heart rate. Stimuli which increase the rate of discharge of the sinus pacemaker also enhance atrioventricular conduction. It is concluded that there is a fine balance between heart rate and A-V conduction. When the heart rate is increased by neurohumoral stimuli, there is a corresponding enhancement of A-V conduction. When the heart rate is increased by artificial stimulation of the atria and neurohumoral effects are not altered, there is a progressive increase in conduction time and eventual blockage of conduction at the A-V nodal region.
124 citations
TL;DR: Experimental studies of the effects of lidocame and procainamide on the mongrel dog heart and peripheral vasculature have been performed in intact animals and in those with completely separated cardiopulmonary and systemic circulations, and lidocaine was found to be a myocardial depressant at all dosage levels.
Abstract: Experimental studies of the effects of lidocame and procainamide on the mongrel dog heart and peripheral vasculature have been performed in intact animals and in those with completely separated cardiopulmonary and systemic circulations. When these drugs were administered to intact dogs, initial depression of myocardial contractile force and arterial blood pressure was seen after administration of both lidocaine and procainamide, but at low to moderate dosage levels myocardial contractile force increased above control levels with procainamide by the end of a recovery period. In divided circulation experiments, both drugs, when administered into the systemic circuit, caused a marked vasodilation and a simultaneous transient drop in myocardial contractile force. When administered centrally, lidocaine was found to be a myocardial depressant at all dosage levels; procainamide was found to be a positive inotropic agent in this preparation at low to moderate dosage levels and was depressant at higher drug levels.
114 citations
TL;DR: Heart rate and cardiac output fell significantly and there was little change in mean arterial pressure but an increase in calculated peripheral resistance during oxygen inhalation at 3.04 atmospheres, indicating that the decrease in cardiac output was rate-dependent.
Abstract: Ten normal subjects were studied while they breathed air and 100% oxygen at 1 and 3.04 atmospheres. Oxygen inhalation at 3.04 atmospheres was associated with a significant increase in arterial and venous pO 2 and O 2 content. Hemoglobin in the venous circulation was completely saturated in 8 of 10 subjects. Oxygen inhalation at 3.04 atmospheres produced a small but significant increase in venous pCO 2 , presumably due to the loss of the buffering effect of reduced hemoglobin. Heart rate and cardiac output fell significantly with little change in stroke volume during oxygen inhalation at 3.04 atmospheres, indicating that the decrease in cardiac output was rate-dependent. There was little change in mean arterial pressure but an increase in calculated peripheral resistance during oxygen inhalation at 3.04 atmospheres. Two subjects who demonstrated signs of acute oxygen intoxication did not differ significantly from the group as a whole either in terms of blood gas values or patterns of hemodynamic response.
TL;DR: It would appear, therefore, that frequent bouts of acute alcoholism might result in permanent alterations of metabolic pathways or alterations in mitochondrial membrane permeability, the direction and magnitude of which await further detailed investigation.
Abstract: Hemodynamic and metabolic data of chronic alcoholic patients have been presented. The hemodynamic findings show distinct differences among the cardiomyopathic and cirrhotic patients and patients without liver or clinical heart disease. The balances of the redox potential were positive in all groups except the combined cirrhotic and cardiomyopathic patient. All groups released enzymes, and possible mechanisms for this have been discussed. This occurred even in those patients without clinical evidence of heart or liver disease. The consistently negative myocardial balances of isocitric dehydrogenase and malic dehydrogenase would appear to indicate that intramitochondrial enzymes are affected by chronic alcoholism even in patients without clinical, hemodynamic or other biochemical evidence of heart disease. In patients with clinical alcholic cardiomyopathy, evidence has been presented which indicates hemodynamic as well as myocardial cytoplasmic and intramitochrondrial metabolic alterations. It would appear, therefore, that frequent bouts of acute alcoholism might result in permanent alterations of metabolic pathways or alterations in mitochondrial membrane permeability, the direction and magnitude of which await further detailed investigation.
TL;DR: The ability of many to live active, productive lives and to withstand stress, surgery, both cardiac and non-cardiac, and pregnancy was impressive.
Abstract: Events in the natural course of 310 adult patients with proved significant congenital cardiac anomalies have been reviewed to determine incidence, longevity, complications and cause of death. Atrial septal defect and patent ductus arteriosus were the most frequently encountered lesions and comprised over one third of the entire series. Ventricular septal defect and pulmonic stenosis made up almost a quarter of the group. Twenty-two instances of the Eisenmenger syndrome secondary to a variety of shunting lesions are included. Bacterial endocarditis, sudden death and cardiac decompensation were the greatest threats to these patients. Symptoms were minimal until the appearance of heart failure, which was the most common cause of death, especially with older patients. Sudden death occurred most often in patients with ventricular septal defect. Although the clinical features are usually characteristic of a congenital malformation, young adults with acyanotic congenital heart disease are often misdiagnosed as rheumatic; and in older patients, presenting manifestations are frequently attributed to arteriosclerotic heart disease. At times an associated acquired cardiovascular disorder may alter the basic syndrome. Three quarters of the patients survive and continue under observation. The ability of many to live active, productive lives and to withstand stress, surgery, both cardiac and non-cardiac, and pregnancy was impressive. Further observation of the patient with congenital heart disease but without surgical intervention is essential for accurate evaluation of the long term efficacy of cardiac surgery.
TL;DR: It is concluded that atrial systole significantly improves cardiac function in man under the conditions of the authors' study.
Abstract: 1. 1. The contribution of atrial systole to cardiovascular dynamics was described in 21 patients with complete heart block at a fixed and at a variable ventricular rate. 2. 2. It was demonstrated that a properly timed atrial systole significantly improves cardiac function in patients with complete heart block. The optimal P-R interval was found to occur between 1 and 300 msec. For this range there were 13, 14, 6, 12, 14 and 33 per cent increases in ejection time, mechanical systole, isometric contraction time, systemic pressure, peak derivative of brachial artery pressure and tensiontime index, respectively, as compared with figures obtained when atrial systole occurred during ventricular systole. 3. 3. It was also found that the contribution of atrial systole to cardiac function occurs in all ranges of ventricular rates studied (20 to 125 beats/min.). However, the maximal beneficial effect of atrial systole was found to occur for the ventricular rate in the range of 51 to 80 beats/min. 4. 4. Very short or very long P-R intervals resulted in minor changes in the measured parameters, and the figures obtained closely approach the ones determined when atrial systole occurred during ventricular systole. 5. 5. It is, therefore, concluded that atrial systole significantly improves cardiac function in man under the conditions of our study.
TL;DR: A significant diurnal abbreviation in the duration of the phases of left ventricular systole was observed, lending evidence for a decrease in both the pre-ejection and ejection phases of the cardiac cycle.
Abstract: In the present investigation we studied the effect of deslanoside on the duration of the phases of left ventricular systole as derived indirectly from simultaneous tracings of the electrocardiogram, the heart sounds and the external carotid arterial tracing. The phases of systole measured included the interval between the beginning of electrical activity and the second heart sound (Q-S 2 ), the interval between the first and second heart sound S 1 -S 2 and the interval between beginning ejection and the trough of the incisura of the carotid pulse tracing (LVET). All data were expressed relative to the regression relationships between heart rate and each of the measured intervals. Deslanoside, administered intravenously (1.6 mg.), induced a decrease in the duration of each of the measured phases of left ventricular systole. The abbreviation in Q-S 2 and S 1 -S 2 exceeded that in LVET, lending evidence for a decrease in both the pre-ejection and ejection phases of the cardiac cycle. Studies on the temporal course of this action of deslanoside demonstrated the presence of an effect at 10 minutes, with progression to a maximum at one to two hours, after which the abbreviation in systole remained relatively constant for eight hours. Studies over the ensuing five days revealed a serial dissipation of the drug effect. The mean response in the duration of each of the phases of systole during the first eight hours following administration of deslanoside proved to be dose-dependent. A significant diurnal abbreviation in the duration of the phases of left ventricular systole was observed. This diurnal effect must be considered in all studies involving serial measurements of the duration of the phases of the cardiac cycle. The determination of the duration of the phases of left ventricular systole offers a useful means for assaying digitalis effects on the human ventricle.
TL;DR: Although some of the features suggest a state of hypersensitivity, recognition of the distinctive pattern found in 2 cases may allow the clinician to differentiate cholesterol embolism from polyarteritis nodosa and a new gradation of the histologic changes into four stages of evolution is suggested.
Abstract: The clinical picture and necropsy data of 2 cases of cholesterol embolism, clinically masquerading as polyarteritis nodosa, are described. In 1 case, the correct diagnosis was made during life by biopsy of the skin. The clinical entity of cholesterol embolism is defined as the rupture of intimal atheromas of the aorta causing impaction of cholesterol crystals in small arteries of many organs and a characteristic picture of sudden obliterative arteritis primarily throughout the lower half of the body. Some of the specific clinical features are (1) the abrupt onset of scattered intense pains in the legs and feet with subcutaneous and muscular nodules or gangrene despite, in some cases, paradoxically normal peripheral arterial pulses; (2) abdominal pain with nausea and vomiting suggesting pancreatitis and/or gastrointestinal or splenic infarction; (3) arterial hypertension thought to be secondary to impairment of renal function; (4) livedo reticularis or cyanosis of the legs and lower trunk within a few days after the onset of pain and hypertension; (5) less commonly, neurologic symptoms and possible funduscopic demonstration of retinal emboli; (6) laboratory evidence of neutrophilic leukocytosis, transient eosinophilia, markedly increased sedimentation rate, hematuria, albuminuria, azotemia and melena; and (7) a biopsy showing cholesterol crystal emboli. Although some of the features suggest a state of hypersensitivity, recognition of the distinctive pattern found in our 2 cases may allow the clinician to differentiate cholesterol embolism from polyarteritis nodosa. Final diagnosis rests upon the biopsy showing the characteristic histologic changes. A new gradation of the histologic changes into four stages of evolution is suggested.
TL;DR: In an acute coronary care area, early complications can be quickly detected and appropriate therapy instituted and the salvageable rate of unexpected cardiac arrest is far greater than when these emergency situations develop on the general hospital floors.
Abstract: One hundred and twenty-six cases of acute myocardial infarction have been treated in the Hartford Coronary Care Area at Bethany Hospital, Kansas City, Kansas, with an over all mortality rate of 15.9 per cent. In 16 patients unexpected cardiac arrest developed and 9 of these patients were discharged from the hospital alive and well. Electronic monitoring with a combined automatic external pacemaker is of great value, especially in the acute coronary patient who has varying degrees of A-V block. A high incidence of ventricular standstill was noted in this type of patient. Five days appears to be the optimal monitoring time since 95 per cent of all expected deaths and unexpected arrests occurred within this period. In an acute coronary care area, early complications can be quickly detected and appropriate therapy instituted. The salvageable rate of unexpected cardiac arrest is far greater than when these emergency situations develop on the general hospital floors.
TL;DR: Simultaneous recordings of respirations and instantaneous cardiac frequency by means of a cardiotachometer permit visualization of the sinus arrhythmia due to respiration, suggested to yield useful information regarding the integrity of the regulatory centers of cardiac activity.
Abstract: Simultaneous recordings of respirations and instantaneous cardiac frequency by means of a cardiotachometer permit visualization of the sinus arrhythmia due to respiration. Observations made on tracings obtained from 102 patients with a variety of neurologic disorders indicate that the typical respiration-heart rate response may be disturbed by lesions affecting the cardioregulatory mechanisms. Decerebration results in prominent periodic waves of acceleration of the heart rate followed by rebound deceleration. These waves coincide with each deep breath or outburst of periodic breathing. A fixed cardiac frequency is indicative of a complete disconnection between the cardiac pacemaker and the regulatory centers of cardiac activity. Cervical spinal cord transections may cause preponderant bradycardia. It is suggested that simultaneous recordings of the pneumogram and the cardiotachogram may yield useful information regarding the integrity of the regulatory centers of cardiac activity.
TL;DR: In this article, various pharmacologic agents were administered in 10 cases of muscular subaortic stenosis at the time of left heart catheterization in an attempt to determine the various factors affecting the severity of the outflow tract obstruction.
Abstract: Various pharmacologic agents were administered in 10 cases of muscular subaortic stenosis at the time of left heart catheterization in an attempt to determine the various factors affecting the severity of the outflow tract obstruction. Amyl nitrite-induced vasodilatation increased the degree of stenosis in 5 cases, whereas systemic vasoconstriction induced by angiotensin II, norepinephrine and methoxamine significantly decreased the degree of stenosis. These agents were believed to have affected the degree of stenosis principally by virtue of the changes they caused in the systolic “distending pressure” in the left ventricular outflow tract. This pressure, being equal to the aortic systolic pressure, would be decreased by vasodilatation, and increased by vasoconstriction. A decrease in the systolic “distending pressure” in the outflow tract would allow closer apposition of the walls of this tract in systole and result in increased severity of the muscular stenosis. A vasoconstriction-induced increase in this pressure would tend to distend the walls of the outflow tract in systole and decrease the severity of the muscular stenosis. By altering aortic diastolic pressure and, hence, the time of onset of ventricular ejection, these effects of vasodilatation and vasoconstriction on the degree of stenosis would be accentuated. By interrelating the outflow tract “distending pressure” (P) with the linear tension (T) initially developed by the deep constrictor muscles and the over-all ventricular volume (V), variations in severity of muscular subaortic stenosis were explicable. Any influence acting to increase T or decrease P or V would increase the severity of the stenosis (decrease orifice size); any influence acting to decrease T or increase P or V would decrease the severity of the stenosis (increase orifice size). By considering the orifice size of the left ventricular outflow tract in muscular subaortic stenosis to be governed in the above manner, the effect of arterial vasodilatation and vasoconstriction as well as the effect of acetylstrophanthidin, isoproterenol and most other reported influences on the degree of muscular subaortic stenosis could be explained.
TL;DR: These two cases are exceptional since in most of the other reported cases, patients have been cyanotic, and mechanisms which may possibly determine the direction of blood flow in a persistent left superior vena cava terminating in the left atrium are discussed.
Abstract: A 36 year old noncyanotic white man with coarctation of the aorta was found to have a left superior vena cava terminating in the left atrium on catheterization. A right to left shunt was demonstrated by dye-dilution studies; but, except for a mild decrease in the amount of dissolved oxygen in the plasma, there was no peripheral arterial oxygen unsaturation. Only one other case with this combination of anomalies has been reported, and this patient was found to have a shunt from the left to the right atrium via the two venae cavae and the connecting left innominate vein. These two cases are exceptional since in most of the other reported cases (listed in Table I) patients have been cyanotic. Mechanisms which may possibly determine the direction of blood flow in a persistent left superior vena cava terminating in the left atrium are discussed.
TL;DR: It is concluded that a late systolic murmur continuing to or through aortic valve closure probably always is caused by mitral insufficiency of mild to moderate degree, which in turn probably results from papillary muscle dysfunction, damage or slackening of the chordae tendineae, or both.
Abstract: Three cases are presented of patients who had systolic murmurs confined to mid- and late systole. Evidence of functional impairment of the heart was either minimal or lacking. Two of the three patients had mid-systolic clicks which initiated their murmurs. Two patients had electrocardiographic signs suggestive of papillary muscle damage. All 3 patients underwent cardiac catheterization studies, and a mild-to-moderate degree of mitral insufficiency was observed at cineangiocardiography. We conclude from these cases, and from 4 similar cases reported recently by others, that a late systolic murmur continuing to or through aortic valve closure probably always is caused by mitral insufficiency of mild to moderate degree, which in turn probably results from papillary muscle dysfunction, damage or slackening of the chordae tendineae, or both.
TL;DR: The heart adjusted to the increased diastolic load acutely by dilatation and chronically by hypertrophy and when the heart block was present for over four months heart failure ensued.
Abstract: The effects of acute and chronic complete heart block on the mechanical function of the heart were studied. Surgically produced heart block resulted in profound bradycardia. There was an immediate decrease in minute cardiac output, increase in stroke volume, decrease in aortic (and pulmonary artery) diastolic pressure, but no change in aortic systolic pressure. Enddiastolic volume increased due to increased filling time. The heart adjusted to the increased diastolic load acutely by dilatation and chronically by hypertrophy. When the heart block was present for over four months heart failure ensued. Each atrial contraction was associated with a forward and backward movement of blood (atrium to ventricle and back to atrium) and closing and opening of the A-V valve. There was no over-all contribution to ventricular volume as the result of each atrial contraction. The atrial contraction immediately preceding ventricular contraction did contribute to the magnitude of the ventricular response by increasing initial ventricular tension and fiber length. This contribution was greatest with an optimal P-Q interval found to be 0.085 to 0.125 sec.
TL;DR: The lethal potential of migrating orthopedic metallic fixation devices is evident and frequent postoperative radiographic examinations should be made if migration of the device occurs.
Abstract: A case of migration of a Kirschner wire from the right clavicle into the right pulmonary artery is presented. The lethal potential of migrating orthopedic metallic fixation devices is evident. Frequent postoperative radiographic examinations should be made. If migration of the device occurs, early removal seems indicated.
TL;DR: Whether or not one can accurately diagnose the various anatomic types of single ventricle by clinical and laboratory methods is sought.
Abstract: The present report seeks to determine whether or not one can accurately diagnose the various anatomic types of single ventricle by clinical and laboratory methods. The history, physical examination, chest roentgenograms and electrocardiogram usually were diagnostically nonspecific. Despite its lack of specificity, the electrocardiogram in single left ventricle with an infundibular outlet chamber usually could be understood in terms of the type of bulboventricular loop which was present. Cardiac catheterization often provided the first clue to the presence of a single ventricle: a large left to right shunt at the ventricular level, despite systemic pressure in the “right” ventricle; and an extraordinarily wide range of oxygen content from different sites in the ventricle, and even from the same site. Selective ventricular angiocardiography is the diagnostic method of choice. Two groups can be distinguished: (1) single ventricle with an outlet chamber, and (2) single ventricle without an outlet chamber. Those with an outlet chamber have absence of the right ventricular sinus (inflow tract). This results in a single left ventricle with an infundibular outlet chamber, the relatively frequent type of single ventricle (79% of this series).
TL;DR: The severity of the atherosclerotic process in terms of its stenosing effect on the vascular vessels increased materially as the electrocardiographic tracing deteriorated from normal to a pattern indicative of a past transmural myocardial infarction.
Abstract: Selective coronary arteriography is a satisfactory technic in the study of the distribution and severity of atherosclerosis in patients with coronary heart disease. This investigation analyzes the placement and gradation of pathology in patients with angina pectoris whose resting electrocardiograms varied from normal patterns to tracings indicative of past transmural myocardial infarctions. Atherosclerosis was visualized as a diffuse process involving two or three main arteries even in those individuals who had the earliest clinical form of coronary heart disease, namely, angina pectoris and a normal resting electrocardiogram. The severity of the atherosclerotic process in terms of its stenosing effect on the vascular vessels increased materially as the electrocardiographic tracing deteriorated from normal to a pattern indicative of a past transmural myocardial infarction. Channels of anastomosis did not develop when atherosclerosis was diffuse but not occlusive. Particular attention is drawn to patients with angina pectoris and normal resting electrocardiograms who had in the past RS-T or T wave abnormalities or both. The occlusive disease in these patients was considerable and hardly compatible with the term “mild coronary.”
TL;DR: It is concluded that the determination of serum creatine phosphokinase is of value in the diagnosis of acute myocardial infarction because of its increased specificity.
Abstract: Serum creatine phosphokinase activity was determined in 22 normal subjects and 146 patients with a variety of diseases. Serum CPK levels regularly rose early in the course of an acute myocardial infarction. Enzyme elevations were also encountered in the presence of skeletal muscle and brain damage. In contrast, patients with diseases of the liver and lung consistently had normal levels of serum CPK. Normal levels were always found in patients with congestive heart failure, rapid supraventricular arrhythmias, and acute coronary insufficiency without evidence of infarction. We conclude that the determination of serum creatine phosphokinase is of value in the diagnosis of acute myocardial infarction because of its increased specificity.
TL;DR: In a 2 year and 10 month old girl with external features of Marfan's syndrome, mitral insufficiency represented the major cardiovascular manifestation and appears to have resulted from elongation of the chordae tendineae of the mitral valve which, histologically, were composed of delicate connective tissue without mucoid cysts.
Abstract: In a 2 year and 10 month old girl with external features of Marfan's syndrome, mitral insufficiency represented the major cardiovascular manifestation. This appears to have resulted from elongation of the chordae tendineae of the mitral valve which, histologically, were composed of delicate connective tissue without mucoid cysts. Additional cardiovascular findings included mucoid cysts in the leaflets of the mitral valve and in the media of the aorta and pulmonary trunk. Dilatation of the aortic sinuses, without aortic valvular insufficiency, was yet another finding.
TL;DR: In this paper, the authors showed that digitoxin alone had no effect on the ventricular weight of the rats in group B. Although the rats had ventricular weights significantly greater than control, the administration of digitoxin resulted in significantly lesser degrees of myocardial hypertrophy and decreased the incidence of fatal congestive heart failure.
Abstract: Two hundred male Sprague-Dawley rats were divided into four groups of 50 animals each. Group A served as controls; group B received 0.1 mg. of digitoxin/100 gm. body weight daily for six days of each week; group C underwent subdiaphragmatic suprarenal aortic constriction but did not receive digitoxin; and group D received doses of digitoxin similar to those given to group B, beginning five to seven days prior to aortic constriction. After suitable corrections for differences in body weight among the different groups, it became clear that digitoxin alone had no effect on the ventricular weight of the rats in group B. Although the rats in both groups C and D had ventricular weights significantly greater than control, the administration of digitoxin resulted in the development of significantly lesser degrees of myocardial hypertrophy and decreased the incidence of fatal congestive heart failure. While the development of hypertrophy represents a fundamental adaptive mechanism to a chronic pressure load placed on the ventricle, the usefulness of this adaptive mechanism may well be limited. By reducing the development of myocardial hypertrophy, digitoxin permits the ventricle to sustain an excessive hemodynamic burden with less encroachment on this fundamental reserve mechanism, thus favorably influencing cardiac function.
TL;DR: The data indicate that the direct inotropic effect of the glycoside on the normal heart may be obscured in the intact animal by a reflex withdrawal of cardiac sympathetic tone, and support the position that there is no fundamental difference in glycosides action on thenormal versus the failing heart.
Abstract: In experiments designed to clarify the effects of glycoside on the normal heart, acetyl strophanthidin was found to increase myocardial contractility, as reflected by the relation of stroke work to left ventricular end-diastolic pressure in dogs deprived of autonomie control of cardiac performance by ganglionic blockade and chronic cardiac denervation. Reflexly intact animals showed no consistent change in left ventricular end-diastolic pressure at constant arterial pressure, cardiac output and heart rate. All animals receiving the glycoside demonstrated a significant increase in maximal rate of rise of left ventricular pressure. Peripheral vascular resistance following the glycoside increased only in animals whose peripheral autonomie reflexes were abolished by ganglionic blockade. These data indicate that the direct inotropic effect of the glycoside on the normal heart may be obscured in the intact animal by a reflex withdrawal of cardiac sympathetic tone. The data support the position that there is no fundamental difference in glycoside action on the normal versus the failing heart.