Showing papers in "American Journal of Cardiology in 1970"

The congenitally bicuspid aortic valve. A study of 85 autopsy cases.

Abstract: Clinical and necropsy observations are described in 85 autopsy cases in which the subjects had congenially bicuspid aortic valves. Sixty-one subjects had aortic stenosis with or without aortic regurgitation; 11, pure aortic regurgitation; and 13, unexpectedly, had a congenitally bicuspid aortic valve that apparently had functioned normally. The average age at death in patients with stenotic valves was 49 years, and in those with pure regurgitation, 31 years. Aortic valvular calcific deposits occurred in 59 of 61 patients with stenosis but was minimal or absent in the patients with pure regurgitation or normally functioning valves. Infective endocarditis appeared responsible for incompetency in 8 of 11 patients with pure regurgitation. Five of 61 patients with stenosis had had infective endocarditis, but infection occurred on a previously heavily calcified valve in only 1 patient. Sixty-nine of the 72 patients with functionally abnormal valves were observed in a study of 400 autopsy cases; all subjects were over age 14 years, with severe valvular cardiac disease. The 13 functionally normal valves were found during study of 1,440 necropsy cases in which the subjects were free of other valvular or septal defects. The bicuspid aortic valve is the most frequent congenital malformation of the heart or great vessels. It occurs in over 50 percent of patients with anatomically isolated aortic stenosis and in about 25 percent of patients with clinically pure aortic regurgitation. It is not certain why 1 congenitally bicuspid valve becomes severely scarred, calcified and stenotic, another only mildly scarred and incompetent, another the site of infection, and why another remains free of these complications during life.

Congenital anomalies of the coronary arteries

Abstract: The coronary arteries, like other organ arterial patterns in the body, are subject to congenital variations of both minor and major consequence. This paper presents a review of these variations based upon a series of 224 cases. There are three basic categories. First, minor anomalies in which there is a variation of the origin of the vessels from the aorta and the distal circulation is normal. Second, major anomalies in which there is an abnormal communication (arteriovenous) between an artery and a cardiac chamber or an abnormal origin of a major coronary artery from the pulmonary artery. Third, secondary anomalies in which the coronary arterial variation probably represents a circulatory response to the primary intracardiac pathologic defect. Each category is discussed in detail with reference to the specific anomalies and illustrated with examples from our study.

The hemodynamics of cardiac tamponade and constrictive pericarditis.

Abstract: This review of the hemodynamic alterations that accompany cardiac tamponade and constrictive pericarditis describes studies carried out in man and in experimental animals. Both constrictive pericarditis and cardiac tamponade increase pulmonary and systemic venous pressure and decrease cardiac output and stroke volume. In cardiac tamponade, the superior and inferior vena caval pressure record shows a single nadir, the x descent; this pressure event is accompanied by an increase in velocity of blood flow and, by inference, in quantity of blood flow. The y descent is absent from the vena caval and right atrial pressure curves, and no early diastolic dip appears in the right ventricular pressure tracing. During inspiration, blood flow velocity and, by inference, forward flow increase in the superior and inferior venae cavae and in the pulmonary artery. Pulsus paradoxus is almost invariably present. The major factors causing pulsus paradoxus are related to inspiratory augmentation of systemic venous return. The ensuing expansion of right-sided heart volume increases intrapericardial pressure, but does not increase systemic arterial pressure and flow until the subsequent expiration. In constrictive pericarditis a peak of blood flow velocity accompanies the x descent of superior vena caval pressure. A second flow velocity peak accompanies the y descent. Respiration fails to alter superior vena caval pressure or blood flow velocity, but during inspiration the velocity of pulmonary arterial blood flow increases. Pulsus paradoxus occurs much less often than in cardiac tamponade, and its mechanism is not well understood. Atrial fibrillation is common, and myocardial contractility is impaired.

Developmental landmarks in cardiac morphogenesis: Comparative chronology☆

Abstract: Data concerning the chronology of anatomic changes in the developing heart in a group of seven frequently studied species are presented in tabular form. Different modes of expression of levels of embryonic maturation for these species are correlated and listed. Examples of the possible significance of temporal sequences and of quantitative alterations accompanying the progression of developmental landmarks in cardiac morphogenesis are discussed.

The shape and movements of the human left ventricle during systole: A study by cineangiography and by cineradiography of epicardial markers☆

Abstract: The shape of the left ventricular cavity and the movements of the mitral valve, aorta and coronary arteries were studied in cineangiograms obtained from normal subjects and patients with coronary arterial disease, mitral stenosis or atrial septal defect. Movements of the left ventricular epicardial surface were studied by postoperative cineradiography of radiopaque markers previously attached during closed mitral valvotomy. The pre-ejection and ejection phases of systole were identified from the simultaneously recorded phonocardiogram, apex cardiogram, indirect carotid pulse pressure tracing and electrocardiogram. The left ventricular epicardial surface contracted in an approximately symmetrical fashion with slight rotational movements about the long axis most marked at the beginning and end of systole, but contraction of the left ventricular cavity appeared less symmetrical because of the systolic increase in wall thickness, approximation of trabeculae and movements of the mitral valve. During pre-ejection, the left ventricular cavity narrowed anteroposteriorly, the descent of the base began and a slight anticlockwise rotation of the epicardial surface was accompanied by a slight thrust of the apex toward the chest wall. During ejection, narrowing of the left ventricular cavity and the descent of the base continued, and a slight clockwise rotation and retraction of the apex occurred in late systole. The symmetry of left ventricular contraction may be due to the similarity of contractility and afterload of individual myocardial fibers, and the slight rotational movements may be a result of sequential activation of the left ventricular myocardium from endocardial to epicardial surface.

Cardiac conduction system: fetal and postnatal development.

Abstract: Development of the cardiac conduction system is considered from the standpoint of its fetal, neonatal and adult anatomy, histology and pathology. The perspectives provided by these multiple approaches indicate that postnatal developmental changes in the conduction system are extensive and important. The sinus node originates in the sinus venosus but subsequently a dense collagen framework develops, directly attached to a disproportionately large and consistently located central artery. Partitioning of the sinus node by collagen is important relative not only to the nature of its cellular development but also to its pacemaking function. A functional relation between pulse and impulse in the sinus node and a balancing postnatal maturation of its autonomic innervation are two of the important stabilizing influences in the optimal development of the adult sinus node as a pacemaker. The interatrial and internodal pathways develop precisely in the region of the primitive sinus venosus and provide the efficient means for selective conduction within the atria. The postnatal closure of the foramen ovale establishes the final form of the atrial septal route of these pathways, and malformation of the septum or the venous valves will lead to altered atrial conduction routes. Evidence is cited to support the concept that the atrioventricular (A-V) node and His bundle originate as separate structures that join together very early in fetal development. Histologic differences between the internal structure of the sinus node and A-V node are discussed, particularly as they relate to the pacemaking function of the nodes. Postnatal molding and shaping of His bundle is associated with cell death, just as morphogenesis usually is, but because of the small size and critical importance of the His bundle, this postnatal developmental change is fraught with potentially dangerous functional consequences.

Significance of calcification of the coronary arteries.

Abstract: The frequency of and association between calcification and occlusive disease of the coronary arteries were determined by roentgenographic and pathologic study of 200 human hearts obtained at autopsy of persons more than 30 years old. Calcification was present in 69 percent of the hearts, most frequently in the left anterior descending branch in men, and it occurred more frequently than significant narrowing, regardless of age, sex or presence of cardiac disease. The greater the degree of calcification, the more likely was the presence of significant narrowing. Absence of calcification indicated persons least likely to have significant narrowing. The presence of myocardial infarction associated with coronary artery calcification but without complete occlusion suggests that the advanced sclerosis of these vessels made them relatively insufficient to meet the needs of the myocardium.

Histogenesis of the embryonic myocardium

Abstract: The ultrastructure of the developing chick ventricular myocardium was examined between Hamburger-Hamilton stage 12 − (15 somites; about 45 hours incubation) and the time of hatching (about 21 days incubation). The myocardium is an epithelial tissue initially containing only developing myocytes. No epicardium is present and no mesenchymal cells such as fibroblasts are seen. By the third day of development, portions of the ventricular endocardium invade the myocardium. After this event and the development of the epicardium from an extramyocardial source, mesenchymal cells are seen within the myocardium. These cells, the first nonmuscular components seen within the myocardium, are probably fibroblasts derived from the endocardium or the epicardium. The myocardium is honeycombed with large anastomosing channels. The extracellular matrix within these spaces is electron-lucent until the nonmyocardial mesenchymal cells appear. A flocculent component then develops. Early cardiac myocytes contain few fibrils and large amounts of cytoplasm. The fibrils are not regularly oriented within the young cells. As development proceeds, more fibrils are formed; the cytoplasm decreases and the fibrils become aligned in the mature orderly pattern. Possible mechanisms to explain these phenomena are discussed.

Quantification of the contractile state of the intact human heart. Maximal velocity of contractile element shortening determined by the instantaneous relation between the rate of pressure rise and pressure in the left ventricle during isovolumic systole.

Abstract: A new and easily applicable means based on force-velocity principles within the framework of muscle mechanics is presented for quantification of ventricular contractility, independent of loading, in conscious patients. In the intact heart during isovolumic contraction, alterations in ventricular geometry are small, and thus contractile element velocity (VCE) can be assumed to equal series elastic elongation. It was therefore considered in this study that VCE during isovolumic portion of ejecting beats could be determined entirely from isovolumic pressure (IP) and its rate of rise ( dP dt ) without requiring knowledge of tension; this provided the rational basis for accurate calculation of instantaneous isovolumic VCE in the spherical or ellipsoidal ventricle as ( dP dt )/( K × IP ) , where K is series elastic constant of 32 per muscle length (ML) at body temperature. Further, it was recognized that VCE at the ordinate is identical when derived from pressure-velocity or tension-velocity curves, and since the left ventricular pressure-velocity relation can be defined precisely, construction of the isovolumic IP to VCE curve and extrapolation to zero load allowed determination of maximal VCE (vmax), the independent numerical measure of contractility. High fidelity left ventricular pressures and corresponding dP dt were continuously recorded in 23 studies in 8 conscious patients without valvular regurgitation or ventricular segmental disease. Increasing contractility by leg exercise raised VMAX from 1.19 to 1.58 ML/sec and by isoproterenol to 2.03 ML/sec (P dP dt during isovolumic systole affords a new, practical, sensitive and valid means of quantifying left ventricular contractility Without influence of preload and afterload from beat to beat in individual patients. In addition, since VMAX is expressed in terms of muscle units and is free of variables of left ventricular loading and wall thickness, this method permits specific comparison of inotropic state among different patients.

Clinically Significant Cardiac Amyloidosis. Clinicopathologic Findings in 15 Patients

Abstract: Clinical and necropsy findings in 15 patients with cardiac dysfunction secondary to cardiac amyloidosis are described. The most reliable anatomic indicator of clinically significant cardiac amyloidosis was a firm, rubbery noncompliant myocardium on gross examination. Twelve of 15 patients had congestive cardiac failure that was not alleviated by digitalis therapy, and 8 patients had documented arrhythmias while receiving this drug. Amyloidosis appears to be a cause of congestive cardiac failure in which digitalis is contraindicated. Electrocardiograms in 14 patients showed low voltage of the QRS complex in 13, axis deviation in 10, conduction disturbances in 9, patterns similar to old myocardial infarction in 9 and arrhythmias in 6 patients. In 6 patients the intramural coronary arteries were narrowed by amyloid without significant coronary atherosclerosis: 3 of the 6 had angina pectoris, and 1 of the 3 a recent myocardial infarct. The diagnosis of clinically significant cardiac amyloidosis should be questioned in the absence of congestive cardiac failure and low voltage in the electrocardiogram.

Shock after acute myocardial infarction: A clinical and hemodynamic profile

Abstract: Clinical features, predisposing factors, precipitating events, laboratory and hemodynamic observations, pathologic findings, prognostic indicators and the results of therapy are surveyed for 73 patients in whom shock developed after acute myocardial infarction. The incidence of shock was 15 percent, and the mortality 86 percent. It was not possible to differentiate patients with shock from those with acute infarction alone on the basis of age, anamnestic data, delay before hospitalization or anatomic location of infarction. No precipitating cause for shock other than acute infarction itself was consistently present. Hypovolemia, anemia, arrhythmia and drugs could not be incriminated as important factors in the genesis of shock. Extensive myocardial damage, coronary atherosclerosis and left ventricular hypertrophy were found at postmortem examination in most patients who died, but similar findings were noted in a group of patients in the coronary care unit who died without evidence of shock during the period of the study. Delay in onset of shock in many cases suggested progression of cardiac damage after the initial clinical event. Hemodynamic studies in 19 patients showed that cardiac index was less than half of the normal index, stroke volume index about a third of normal, and peripheral resistance generally increased. We conclude that patients who have the highest risk can be identified from various clinical and hemodynamic observations. It is appropriate to consider such patients for unconventional therapy.

Tetralogy of Fallot : Underdevelopment of the Pulmonary Infundibulum and Its Sequelae

Abstract: It is proposed that the tetralogy of Fallot basically is a “monology”, just 1 anomaly, namely, underdevelopment of the subpulmonary infundibulum and its sequelae. The parietal band (crista supraventricularis) and the adjacent infundibular free wall together form an abnormally small cone (conus) of muscle beneath the pulmonary artery, whereas the septal band is normally formed. The hypothesis that the essence of tetralogy is an abnormally small subpulmonary conus is illustrated by angiocardiographic and anatomic findings in typical tetralogy compared with the normal. This unifying concept, which needs experimental embryologic assessment, facilitates angiocardiographic diagnosis of “masked” tetralogy in which the presence of this anomaly may be obscured by associated malformations. To demonstrate this, a rare case is presented, the fourth known patient with coexisting tetralogy and cor triatriatum. This 20 year old man also had a patent ductus arteriosus and a right pulmonary sequestration. The resulting systemic level of pulmonary hypertension “masked” the coexistence of tetralogy, which angiocardiography made evident. Despite the absence of a pulmonary outflow tract gradient due to the association of severe pulmonary hypertension, autopsy confirmed that this patient displayed the angiocardiographic hallmark of tetralogy: an abnormally small subpulmonary infundibulum.

Pre-excitation Revisited

Abstract: Epicardial excitation mapping and the introduction of electrical stimulation of the heart have brought new techniques to the study of pre-excitation. The concept of three anomalous atrioventricular connections (Kent bundle, James bundle and Mahaim fibers) seems at present to be the most attractive means of explaining different electrocardiographic patterns found in this syndrome. The possible pathways and the mode of initiation of the frequently found tachycardias in such cases are outlined. An evaluation of our current knowledge on the pre-excitation syndrome confronts us with the many gaps in our knowledge of electrophysiology of the human heart.

Localization of A-V conduction defects in man by recording of the his bundle electrogram

Abstract: His bundle electrograms were recorded in 20 patients. Conduction times from atrium to His bundle (A-H time) and His bundle to ventricle (H-V time) were measured and the sites of delay or block were localized to the proximal or distal A-V junction. On progressively increasing the atrial rate by atrial pacing, the A-H time lengthened, while the H-V time remained constant. Premature atrial beats usually resulted in prolongation of the A-H time only. In some instances, premature atrial beats also resulted in prolongation of the H-V time and aberrant ventricular conduction (change in configuration of the QRS complex). In patients with first degree heart block during sinus rhythm the A-H time was prolonged and the H-V time was either normal or prolonged. In higher degrees of heart block, the block was localized either in the proximal or distal A-V junction.

The normal pericardium

Abstract: Under normal conditions the pericardium, with its fluid, lubricates the moving surfaces of the heart, holds the heart in a fixed geometric position and isolates the heart from other structures in the thorax, thus preventing adhesions and spread of infection. It also serves the following functions: (1) prevents dilatation of the heart chambers and insures that the level of transmural cardiac pressures will be low, never exceeding a few mm Hg; (2) prevents hypertrophy of the heart under conditions of strenuous exercise; (3) limits right ventricular stroke work under conditions of increased left ventricular outflow resistance; (4) prevents ventriculo-atrial regurgitation under conditions of increased ventricular end-diastolic pressures; (5) in association with the lungs and tissue surrounding the pericardium it facilitates the filling of the atria by the development of negative pericardial pressure during ventricular systole; (6) responds to nerve stimulation and reflexly affects blood pressure and heart rate; and (7) in association with the pleural fluid constitutes a hydrostatic system that automatically applies compensating hydrostatic pressures on the outside of the heart when gravitational or inertial forces acting on the heart are altered (during acceleration, for example). This automatic hydrostatic compensation insures that end-diastolic transmural pressure is the same at all hydrostatic levels of the ventricle; as a result the stretch of the muscle fibers is uniform, and the Frank-Starling mechanism operates equally at all hydrostatic levels within the ventricles.

The evolution of the stress concept: Stress and cardiovascular disease

Abstract: The fact that the adrenal cortex responds with increased secretion upon exposure to any type of stressor directed attention to its possible participation in the pathogenesis of diseases other than those caused by a simple deficiency or excess of corticoid production (Addison's disease, Cushing's disease, adrenocortical tumors). It became evident that the pathogenicity of corticoids depends largely upon conditioning factors which can modify their effects and thereby cause them to induce cardiovascular disease. Thus, an excess of mineralocorticoids can produce hypertension and hypokalemia, with or without hydrops, depending upon controllable conditioning factors. Both these reactions can be suppressed by antimineralocorticoids such as spironolactone. Combined pretreatment with gluco- and mineralocorticoids elicits a special predisposition for the development of cardiac necroses during stress or after excessive lipid ingestion. The induction of these necroses is enhanced by sodium (as is that of mineralocorticoid hypertension) and inhibited by potassium, magnesium or potassium-sparing agents such as amiloride, triamterene or spironolactone. Unlike the common myocardial infarcts, as described in textbooks, those elicited in animals after pretreatment with corticoids and sodium salts are unaccompanied by vascular occlusion. Hence, the inability to find an acute coronary occlusion in a patient who died with manifestations of acute cardiac infarction must not be necessarily ascribed to an oversight on the part of the pathologist. It remains to be seen to what extent the prophylactic measures effective in our experimental disease models will also be useful in clinical medicine.

Echocardiographic diagnosis of pericardial effusion.

Abstract: Echocardiography, because of its ability to detect intracardiac structures in a noninvasive manner, has been increasing in importance as a cardiologic diagnostic tool. The ultrasonic diagnosis of pericardial effusion has stimulated much of the interest in echocardiography in this country. With this technique pericardial fluid is recorded as a relatively echo-free space between the posterior left ventricular epicardium and the posterior pericardium. Anterior fluid is seen as a similar echo-free space between the anterior right ventricular wall and the anterior chest wall. Although the examination is fairly simple and frequently can be performed in a few minutes, the examiner must be aware of technical details, especially with respect to direction of the transducer and control settings on the echograph. In addition, it may be difficult to obtain satisfactory echocardiographic recordings in some patients, such as those with marked pulmonary emphysema. However, these few limitations are overshadowed by the many advantages of a harmless, sensitive, bedside examination for pericardial fluid. Thus, in many institutions echocardiography is becoming the examination of choice for the detection or exclusion of pericardial effusion.

True isovolumic contraction time. Its correlation with two external indexes of ventricular performance.

Abstract: The relation of true isovolumic contraction time with two external indexes of ventricular performance was studied in intact anesthetized dogs utilizing end-catheter micromanometers in the left ventricle and central aorta. The external indexes studied were (1) the pre-ejection period, the interval from the Q wave of the electrocardiogram to the aortic component of the second sound minus left ventricular ejection time; and (2) external isovolumic contraction time, the interval from the first heart sound to the aortic component of the second sound minus left ventricular ejection time. The isovolumic contraction time was shortened from the resting value by administration of isoproterenol and lengthened by vagal stimulation and administration of methoxamine. Excellent linear correlations were found between absolute values of true isovolumic contraction time and the two indexes during all interventions. When changes from control true isovolumic contraction time were plotted against similar changes in the pre-ejection period and external isovolumic contraction time, better linear correlations were found. In addition, the inverse relation between true isovolumic contraction time and the first derivative of left ventricular pressure (dp/dt) in the intact animal was reflected by the pre-ejection period and external isovolumic contraction time. The two external indexes were therefore shown to reflect reliably changes in true isovolumic contraction time. When changes in diastolic blood pressure are considered, and with only small alterations occurring in left ventricular end-diastolic pressure, they give useful information about changes in ventricular performance including an estimation of changes in left ventricular dp/dt. They relate directly to contractility only when diastolic pressure remains constant.

Ultrastructure of intercellular junctions in adult and developing cardiac muscle.

Abstract: The ultrastructure of the intercalated disc indicates that it is composed of three types of junctional specializations: the macula adherens (or desmosome), fascia adherens and nexus. Maculae and fasciae adherentes form the area of strong adhesion between adjacent cells. Their substructure is quite similar in some species. However, the thin actin filaments invariably insert into the fascia adherens, a feature particularly evident early in cardiogenesis when few myofibrils are present. The nexus is a region where the membranes of adjacent cells are physiologically and anatomically in contact, probably providing for electrical coupling of adjacent cells. The membranes at the nexus have a characteristic substructure consisting of hexagonally packed subunits that connect the two cell membranes. Nexuses are easily demonstrated in the 9 week human fetal heart. Frequently nexuses are adjacent to fasciae adherentes during cardiogenesis. Since examination of frozen, unfixed sarcolemma reveals that both the membranes of nexuses and fasciae adherentes are specialized membranes, it is postulated that the organization of the membranes themselves may produce the localization of these intercellular junctions within the intercalated disc.

Endocarditis in the drug addict

Abstract: The English literature is reviewed for reports of endocarditis in the drug addict, and 16 additional patients are described. Our series reveals a high incidence of Streptococcus viridans infections. In reviewing the previously recorded cases, we conclude that heroin addicts are not more likely to have endocarditis on the right side of the heart, but if this lesion does develop, the organism most likely responsible is the Staphylococcus. The mortality for this disease is high, and vigorous diagnostic and therapeutic measures are required.

Mitral regurgitation in muscular subaortic stenosis

Abstract: Mitral regurgitation was assessed in 34 patients with muscular subaortic stenosis by indicator-dilution studies. All patients with obstruction to left ventricular outflow at rest had evidence of mitral regurgitation. Infusion of angiotensin resulted in amelioration or abolition of both outflow tract obstruction and mitral regurgitation in 11 of 15 patients. In 4 patients abolition by angiotensin of the outflow tract obstruction produced no change in the degree of mitral regurgitation. One of these patients was demonstrated to have an abnormality of the mitral valve. Abolition of the outflow tract obstruction by ventriculomyotomy either abolished the mitral regurgitation or reduced it to a trivial degree if there was no additional abnormality of the mitral valve. Pharmacologic intensification of the obstruction by administration of isoproterenol or amyl nitrite increased the degree of mitral regurgitation in 15 of 18 studies. These pharmacodynamic studies provided evidence that, in the majority of patients with muscular subaortic stenosis and a normal mitral valve mechanism, the degree of mitral regurgitation varied directly with the severity of the outflow tract obstruction and was secondary to the obstruction.

The effect of lidocaine on atrioventricular and intraventricular conduction in man.

Abstract: Atrioventricular and intraventricular conduction were studied in 10 patients with arrhythmias before and after rapid administration of lidocaine (1 to 2 mg/kg by direct intravenous injection). Standard electrocardiographic lead II and catheter recordings of His bundle electrograms (H) were obtained. Recordings were made at varied heart rates, utilizing atrial pacing. P wave to H (P-H) interval was used as a measure of atrioventricular conduction. H to onset of the Q wave (H-Q), and H to the terminal deflection of the QRS complex (H-S) were used as measures of intraventricular conduction. After administration of lidocaine, P-H intervals were essentially unchanged in 4 patients, slightly decreased in 4 and slightly increased in 2 patients. H-Q intervals remained constant in all patients and at all rates both before and after lidocaine. H-S intervals were unchanged in 6 patients and increased in 4 patients by 8 to 18 msec (4 to 18 percent of total H-S interval). Thus, lidocaine in therapeutic doses had a minimal effect on atrioventricular and intraventricular conduction. This is in contrast to quinidine and procainamide, which may prolong atrioventricular and intraventricular conduction.

Effects of angiographic contrast media on cardiac function

Abstract: Alterations in cardiovascular dynamics after intravenous administration of angiographic media suggested that these effects might be due to the high sodium concentration of these agents. Experiments were performed on dog heart-lung preparations and intact dogs. Stroke volume, ventricular, atrial and arterial pressures, and serum osmolarity were measured. Responses were recorded to (1) conventional angiographic agents containing 2,000 to 2,500 milliosmols/ liter, (2) angiographic agents containing the same base but no sodium, (3) hypertonic glucose solutions and (4) hypertonic sodium solutions of equivalent osmolar concentrations. After injection of hyperosmolar sodium chloride or sodium-containing angiographic agents into the aortic root or left ventricle, left ventricular end-diastolic, left atrial and pulmonary arterial pressures increased and myocardial contractile force decreased for 10 to 15 minutes. Injection of hypertonic glucose solutions or angiographic agents containing no sodium produced no significant cardiovascular changes. Total serum osmolarity was similar after administration of each agent. These studies demonstrate that administration of hypertonic sodium solutions produces significant transient alterations in cardiovascular function and that it is one mechanism for changes observed with sodium-containing angiographic agents.

Comparative ultrastructure of cardiac cell membrane specializations. A review.

Abstract: Among animal hearts, there are many differences in the anatomic features of various myocardial cells, the occurrence of junctional complexes joining adjacent cells, the geometry of apposition of cells forming bundles of fibers, and the form and extent of specializations of intracellular membrane systems. The working fibers of chicken and frog hearts, which have no transverse tubules, are considerably smaller in diameter than those of their mammalian counterparts, which do have such tubules. Purkinje fibers in the hearts of small mammals differ in structure and appositional geometry from those of the larger mammals, and again from those of the chicken. All Purkinje fibers lack transverse tubules. Focal specializations of the sarcoplasmic reticulum, the junctional sarcoplasmic reticulum, are prominent in chicken and mammalian, but not in frog cardiac muscle. Gap junctions are frequent in mammalian hearts, but seem to be rare, small or absent altogether in both frog and chicken hearts.

Recurrent coarctation of the aorta after successful repair in infancy.

Abstract: Twenty unselected infants who survived repair of coarctation of the aorta were restudied an average of 6.2 years postoperatively. Eight patients (40 percent) showed no significant difference in blood pressures between the arms and legs and had normal pressures in their arms. These patients have been followed up for an average of 5.1 years postoperatively. Another 8 patients (40 percent) had moderate blood pressure differences between the upper and lower limbs. These patients have been followed up for an average of 6.6 years postoperatively. Further follow-up of this group will be required to determine how many will need reoperation. Four patients (20 percent), although asymptomatic, had recurrent severe coarctation of the aorta that will require reoperation. These patients have been followed up for an average of 6.9 years postoperatively. The mechanism of the recurrent coarctation is not clear, but there is evidence that the coarctation is incompletely relieved in some and that it develops with growth in others. All infants surviving repair of coarctation of the aorta must be closely followed up for possible recurrent coarctation until they reach adult size.

The biochemical techniques for detecting and establishing the presence of a pheochromocytoma. A review of ten years' experience.

Abstract: Pheochromocytoma, fatal if undetected, is a rare cause of hypertension, paroxysmal symptoms and a hypermetabolic state. The clinical signs and symptoms associated with this tumor rarely result in its detection. Advances in knowledge of catecholamine metabolism have markedly improved the diagnostic reliability for tumors of the neural crest. Large numbers of patients must be screened and the diagnosis ultimately proved by biochemical assays for the catecholamines and their catabolites, vanillylmandelic acid, total metanephrines, 3-methoxy-4-hydroxyphenylethyleneglycol and homovanillic acid. Many assay procedures are nonspecific, and therefore do not reliably differentiate the rare patient with pheochromocytoma from patients with more common maladies. We reviewed laboratory screening procedures in 92 subjects with proved pheochromocytoma and 9,500 control subjects. Excretion of the total metanephrines, although uniformly increased in the presence of a pheochromocytoma, was occasionally increased in its absence. Vanillylmandelic acid excretion, rarely increased in the absence of a neural crest tumor, was within normal limits in about 3 percent of patients with pheochromocytomas. Nonspecific techniques for colorimetric assay of vanillylmandelic acid, now widely used, had little diagnostic value in over 30 percent of cases of pheochromocytoma. Familiarity with the various biochemical procedures for assay of the catecholamines and their catabolites is essential in establishing a diagnosis of sufficient reliability to warrant surgical exploration.

Comparison between metabolic changes in local venous and coronary sinus blood after acute experimental coronary arterial occlusion

Abstract: A technique for the study of local metabolic changes in coronary venous blood draining from a small area of ischemic myocardium is described. Overt left ventricular failure, ventricular arrhythmias and possible secondary effects on local metabolic changes were avoided. Metabolic changes in local coronary venous blood and in coronary sinus blood were compared. Gross changes detected by local coronary venous sampling were not observed in coronary sinus blood samples. The possible relevance of this observation to clinical studies was noted. The small ischemic lesion usually involved less than 10 percent of the heart volume and was characterized by acute S-T segment elevation in the epicardial electrocardiogram and by positive changes in values for local coronary venous blood lactate, pyruvate, lactate/ pyruvate ratio, glucose, potassium and phosphate. Free fatty acids and beta hydroxybutyrate and acetoacetate levels were also studied. The technique and its results are compared with other methods of study of the metabolism of ischemic heart tissue.

Depression of cardiac function by streptomycin and other antimicrobial agents

Abstract: Signs of toxicity of the eighth cranial nerve in a patient receiving streptomycin who also had persistent hypotension after cardiac surgery led to investigation of the effects of streptomycin and other antibiotic agents on cardiac function. In 18 open chest dogs, there was a dose-dependent depression of cardiovascular function as a result of the intravenous administration of streptomycin in doses of 2.5, 10 and 40 mg/kg. Similar depressions were demonstrated after administration of tetracycline, kanamycin, vancomycin, erythromycin and colymycin. In 4 intact dogs given streptomycin, 2 g intramuscularly, cardiac output decreased 26 percent and mean arterial pressure decreased 22 percent 1 hour after administration. The average level of streptomycin in the blood at 1 hour was 35 μg/ml, within the usual therapeutic range for patients. In the isolated perfused cat heart, streptomycin, tetracycline, kanamycin, vancomycin and chloramphenicol caused a profound decrease in contractile force. These data should not be extrapolated directly to clinical situations since most of the experiments did not parallel precisely the usual form of antibiotic administration. In the presence of infection, antibiotic drugs are among the most effective agents available. However, the physician must be aware of the potential for cardiac depression, especially in patients with an already compromised cardiac status or with impaired renal function.

Alteration of mechanical performance of the ventricle by intraaortic balloon counterpulsation.

Abstract: Intraaortic balloon counterpulsation has been shown to reduce the immediate mortality due to acute myocardial infarction in dogs. Previous studies have emphasized the importance of the absolute or relative increases in coronary blood flow that result from augmentation of diastolic aortic pressure. This study was designed to clarify the role of the decreased systolic pressure characteristic of counterpulsation in increasing the cardiac output. Eleven dogs were studied without intervention except for counterpulsation. A decrease in peak left ventricular pressure from 138 ± 7 to 116 ± 6 mm Hg ( P Hg . As a result of the decreased impedance to ejection, peak aortic flow, stroke volume and cardiac output increased by 15 percent. In 6 dogs studied after acute myocardial infarction secondary to ligation of the left anterior descending coronary artery, there were parallel but less marked changes in the hemodynamic measurements. The external performance of the ventricle when evaluated in terms of peak flow, stroke volume and output was an inverse function of the impedance to ejection. Since effective assistance to the failing heart must result in increased external performance, the importance of adequate reduction of systolic impedance must not be underestimated.

The radiographic appearance of the tracheobronchial tree as an indicator of visceral situs.

Abstract: To arrive at an accurate anatomic diagnosis in patients with complex cardiovascular malformations or abnormal position of the heart, the situs of the viscera, or more specifically, that of the atria, must be known. Since the situs of the atria always corresponds to that of the tracheobronchial tree, the latter is a very reliable indicator of visceral (atrial) situs. A chest roentgenogram taken in the anteroposterior or posteroanterior projection will show the anatomy of the air-filled trachea and main bronchi, thus indicating whether there is situs solitus, situs inversus or “situs ambiguus”. The latter term is introduced to indicate that in many patients with asplenia or polysplenia syndrome, the visceral situs cannot be determined because of symmetrical development of normally asymmetrical organs.