Showing papers in "American Journal of Cardiology in 1969"

Bedside technics for the evaluation of ventricular function in man

Abstract: Characteristic changes in the systolic intervals of the left ventricle have been demonstrated among patients with arteriosclerotic, hypertensive and primary myocardial disease. These consist of a prolongation of the pre-ejection period and an abbreviation in the ejection time, while total electromechanical systole remains unaltered. The changes in the pre-ejection period and the left ventricular ejection time correlate well with the level of cardiac output and stroke volume. The ratio of the pre-ejection period to the left ventricular ejection time (PEP/LVET) lends a convenient expression of these changes in the systolic intervals. The ease with which these measures can be obtained, using a noninvasive technic, suggests their use in the bedside evaluation of cardiac performance in man.

The efficacy of anticoagulant therapy in preventing embolism related to D.C. electrical conversion of atrial fibrillation

Abstract: Among 437 patients in whom electrical conversion of atrial arrhythmia was attempted 228 were on long-term anticoagulant therapy and 209 were not given anticoagulants. Thirteen (3 per cent) had an embolic episode, 2 of the 186 patients in the anticoagulant group and 11 of the 162 patients in the comparative group whose arrhythmias were converted. This difference is statistically significant at the 5 per cent level (p = 0.012). Three of 11 patients with a history of embolic episodes, whose arrhythmia was converted without anticoagulants, had a new episode after conversion, compared to none of the 55 patients with previous episodes who were receiving anticoagulant therapy. We attach importance to the significant difference in embolic episodes between the two groups even if the patients were not allocated at random, perhaps even greater importance, because the difference in composition of the two groups produced a bias against the anticoagulant group. For example, patients with a history of previous embolic episodes and those with rheumatic valvular disease were considerably over-represented in this group. In both of these categories an increased risk of embolism is present. Our results lead to the conclusion that prophylactic anticoagulant therapy is clearly indicated before and after attempts to convert atrial fibrillation in patients with a history of previous embolic episodes. In our opinion such prophylaxis should preferably be given in connection with attempts at conversion in all cases.

The frequency of asymptomatic disturbances of cardiac rhythm and conduction in middle-aged men.

Abstract: A study of a random sample of 301 actively employed American men, of median age 55 years, employing cardiac recordings obtained during six-hour periods of ordinary activity indicates that asymptomatic periods of dysrhythmia and conduction disturbances occurred in 92.6 per cent of these men at some time during the recording period. Supraventricular premature contractions and other supraventricular dysrhythmias were found in 76.0 per cent of the recordings. These were not associated with present evidence of coronary heart disease or with subsequent death from coronary heart disease, except when supraventricular dysrhythmias were associated with other dysrhythmias or conduction defects. Ventricular premature contractions and complex ventricular dysrhythmias were found in 62.2 per cent of the recordings. These were significantly associated with the presence of coronary heart disease at the time of the examination. They were also associated with an enhanced risk of subsequent death from coronary heart disease. Defects of cardiac conduction, constant or transient, were found in 6.7 per cent of the men. These, too, were associated with an enhanced risk of subsequent death from coronary heart disease.

Implications of left ventricular asynergy

Abstract: Ventricular asynergy, local disturbances in ventricular wall motion which disrupt the normal coordinated pattern of left ventricular contraction, is described in a group of patients. There are four distinct types of asynergy: (1) akinesis, or local absence of wall motion; (2) dyskinesis, or local expansile or paradoxical wall motion; (3) asyneresis, or geometric distortion or inequality of wall motion; and (4) asynchrony, or a disturbed temporal sequence of contraction. These local abnormalities are closely related to anatomic, electrocardiographic and biochemical zones of ischemia in coronary heart disease and are also seen in cardiomyopathy and with ectopic excitation and activation of the left ventricle. Although often associated with clinical and more frequently, laboratory evidence of cardiac failure, asynergy sometimes occurs in the absence of cardiac enlargement. Such morphologic abnormalities provide a functional basis for the hemodynamic disturbances seen in coronary heart disease and so poorly explained at postmortem examination. Thus, ventricular asynergy represents a dynamic abnormality appreciated only in life as a derangement of the integrated function of the left ventricle and represents an important cause of cardiac failure.

Orthotopic cardiac prosthesis for two-staged cardiac replacement

Abstract: Clinical experience with cardiac transplantation has evidenced the feasibility of cardiac replacement in man but has made apparent the need for a mechanical device that will provide circulation and sustain life in emergency conditions while a suitable allograft is obtained. The cardiac prosthesis used in a 47 year old man consisted of two reciprocating pumps constructed entirely of synthetic materials and activated pneumatically in the orthotopic position by a control console connected by tubes passed through the patient's chest wall. The device supported the patient's circulation for 64 hours while a donor for cardiac transplantation was obtained. Death of the recipient from Pseudomonas pneumonia occurred 32 hours after the allografting. The first successful prolonged use of a total mechanical substitute for the human heart is recorded.

Estimation of right and left ventricular size by ultrasound: A study of the echoes from the interventricular septum

Abstract: A technic utilizing pulsed reflected ultrasound has been developed for estimating the size of both the right and left ventricles. The key to this technic is the recording of echoes from the interventricular septum. These echoes have been recognized previously but never have been described in any detail. With the septal echoes it is possible to obtain a right ventricular dimension between the echo originating from the anterior epicardial surface of the right ventricle to the right side of the interventricular septum. A left ventricular internal dimension is also obtainable between the left side of the septum and the echoes stemming from the endocardial surface of the posterior left ventricular wall. These ultrasound measurements were obtained during end-diastole in 26 normal subjects, 23 patients with atrial septal defects and large left to right shunts proved by cardiac catheterization and 12 patients with angiographically proved marked aortic or mitral regurgitation and dilated left ventricle. In the normal group the mean right ventricular dimension was 1.5 ± 0.4 cm. (range 0.5 to 2.1). The mean left ventricular dimension was 4.5 ± 0.5 cm. (range 3.5 to 5.3). The patients with the atrial septal defects had an increased mean right ventricular dimension of 3.7 ± 1.1 cm. (range 2.2 to 6.3), which differed significantly from the normal ( p p Besides facilitating measurements of the right and left ventricles, recognition of the interventricular septal echoes represents an important contribution to echocardiography because these echoes can be a source of confusion when examining for pericardial effusion or mitral stenosis. In addition, the location and motion of the interventricular septum introduces a new area of investigative and diagnostic possibilities for this increasingly popular technic.

The coronary collateral circulation in living man

Abstract: The coronary arteriograms of 100 patients studied in our laboratory were reviewed and searched for the presence or absence of coronary collaterals. Fiftythree had either normal coronary arteriograms or less than 50 per cent lumen reduction. We found no collaterals in this group. The remaining 47 patients had more than 50 per cent lumen reduction of one or more of the main trunks or major branches. There was collateral circulation in 37 cases. Five had normal electrocardiograms. In 13, the existence of collaterals was inferred by visualization of an artery distal to a complete occlusion or from its opacification after injection of contrast agent into the heterolateral artery. In the remaining 24, continuity could be traced from the feeding artery through the collateral vessel into the recipient vessel. We describe several patterns of anastomotic pathways. The presence of coronary collaterals is a reliable indication of severe coronary artery disease and may account for a normal resting electrocardiogram even in patients with major arterial occlusion.

Early phase of myocardial ischemic injury and infarction.

Abstract: The acute effects of ischemia on myocardial tissue are reviewed in this paper with emphasis on how the events observed in experimental myocardial ischemic injury in dogs relate to the sequential changes occurring in the myocardium of man during the first few hours after the onset of acute infarction. The general effects of ischemia on myocardium include those which are secondary to a diminished local supply of substances such as oxygen and metabolites as well as changes resulting from the impaired diffusion of substances such as lactic acid and electrolytes from the poorly perfused ischemic tissue to the general circulation. Cell death (irreversible injury) first develops after 20 minutes of ischemia in areas of maximum injury in the dog heart and infarcts are not fully developed for 60 to 120 minutes after occlusion. Prior to the development of cell death, the severely ischemic cells are reversibly injured and show a variety of alterations from normal. These changes include depletion of supplies of glycogen and high energy phosphate, increased content of lactic acid and hydrogen, relaxation of myofibrils and failure of contraction. Cells which have just died show the same changes as well as mitochondrial, electrolyte, and nuclear defects. Which, if any, of the preceding changes causes the development of irreversibility in ischemic injury remains to be established. Some data is presented in support of the hypothesis that mitochondrial defects may be critical in the genesis of the irreversible state.

Factors contributing to delay in responding to the signs and symptoms of acute myocardial infarction.

Abstract: The delay time between the onset of symptoms and arrival at a medical facility for examination was studied in 100 randomly selected patients who had been admitted to a coronary care unit with a diagnosis of suspected or proved acute myocardial infarction. 1. 1. The delay time did not differ significantly between private and ward patients. In general, the patient with coronary symptoms was apt to respond sooner than later. These patients who delayed 5 or 6 hours could easily have delayed 48 hours or longer. The half-time for reaching medical aid was 3.9 hours. 2. 2. There was no significant relation between delay and age, sex, history of previous myocardial infarctions, socioeconomic scores and presenting symptoms. 3. 3. The time of delay tended to diminish as the subjective severity of the symptoms mounted. However, there was no relation between the severity of the disease, as measured by the Peel score, and the time of delay. 4. 4. There was a significant relation between the source of the symptom and delay. Thus, patients who recognized their heart as causing the symptom sought help sooner than those who displaced the cause to other organ systems. Patients who interpreted the symptom solely in terms of excluding the heart as causal delayed the longest. 5. 5. The role of a second person in initiating the decision to seek help was significant. For the largest, number of patients, a family member made the decision. Spouses appeared to be less successful in reducing delay than friends or associates. The most influential person in reducing delay in our series was an unrelated friend or stranger who was not associated with the patient's work. 6. 6. Physicians caused or contributed to patient delay in 12 per cent of our cases. They rationalized the delay along the same lines as the patient. Other organ systems were blamed or the pain was minimized by calling it angina. Since referral to the hospital was a simple matter, no adequate reason can be given for the procrastination of these doctors. 7. 7. The defense of denial is commonly used by the patient with coronary disease to control anxiety. The finding that no significant relation could be established between denial and delay in our data is explained. Denial was found to be significantly related to symptom displacement and the influence of another person on delay. Those patients who denied minimally recognized the heart as the source of trouble and did not require outside help to seek the advice of a physician. Patients whose denial was major displaced the source of trouble from the heart to other organ systems and tended to put off consulting a physician until someone else urged them to do so.

Mechanisms of ventricular arrhythmias associated with myocardial infarction.

Abstract: Ventricular ectopic beats may be generated during acute myocardial infarction as the result of enhanced automaticity in the His-Purkinje system, focal reexcitation due to the flow of current between myocardial fibers which are repolarized at disparate times, or reentry of the impulse induced by local impairment of excitability and conductivity in the ventricular tissues. The ectopic beats occur more frequently when the basic ventricular rate is slow, and the danger of fatal episodes of ventricular fibrillation is also increased at slow ventricular rates. Fibrillation is more likely to be induced by early ectopic beats in the ventricle during myocardial infarction, because the development of sustained ectopic activity and turbulent impulse propagation is facilitated by increased inhomogeneity of the ventricular tissues with respect to excitability and conductivity. The aggressive prevention and treatment of ventricular ectopic beats and bradyarrhythmia was emphasized as one of the most effective means of preventing life-threatening ventricular fibrillation and lowering mortality rates from acute myocardial infarction. The mechanisms of action of various drugs and the efficacy of increased ventricular rates in suppressing ectopic activity were discussed. It was concluded that the artificial pacing of the heart at relatively rapid rates is a valuable adjunct to the measures used in the management of ventricular arrhythmias associated with acute myocardial infarction.

Lipid and carbohydrate abnormalities in patients with angiographically documented coronary artery disease

Abstract: An increased incidence of both abnormal lipoprotein patterns and abnormal reactions to glucose tolerance tests was found in 134 patients with documented coronary artery disease Fifty-four per cent had an abnormal lipoprotein pattern and 67 per cent an abnormal response to an intravenous glucose tolerance test Of subjects under age 50, 96 per cent had one or both of the metabolic abnormalities and 80 per cent had an abnormal lipoprotein pattern The lipoprotein abnormalities were almost equally divided between type II (29 per cent) and type IV (25 per cent) patterns The presence of a carbohydrate abnormality did not alter the age of appearance of coronary artery disease, but both the type II and type IV lipoprotein abnormalities decreased the mean age of appearance by approximately seven years The morphologic features of the atherosclerosis as revealed by coronary angiography did not appear to differ among the different metabolic groups The importance of determining specific metabolic abnormalities is stressed as (1) an aid in predicting risk from coronary artery disease, (2) an aid in making diagnoses in patients with chest pain and (3) a guide to rational therapy in patients with coronary artery disease

Left ventricular volume and mass and their significance in heart disease

Abstract: Methods are now available for determining left ventricular chamber dimensions, volume, volume curves, wall thickness and mass. These observations, when taken together with left ventricular pressure, can be used to characterize the left ventricle as a pump and determine end-diastolic volume, stroke volume, ejection fraction, rates of ejection and filling, mass, work and work components and power. Methods for deriving these values and their significance in the evaluation of the functional state of the left ventricle in patients with heart disease are discussed.

Cystic Medial Necrosis of the Ascending Aorta in Relation to Age and Hypertension

Abstract: The presence of cystic medial necrosis in the human ascending thoracic aorta was determined by histologic examination in a series of 250 necropsies. Cases of Marfan's syndrome, idiopathic dilatation of the aorta and dissecting aneurysm were not included. The severity of lesions of cystic medial necrosis were graded on the basis of 1 to 4 according to the amount of basophilic ground substance and fragmentation of elastic tissue. In most positive cases the lesion was of minimal (grade 1 or 2) severity. The incidence of cystic medial necrosis increased progressively from 10 percent in the first two decades of age to 60 and 64 percent in the seventh and eighth decades, respectively. Using the Fisher probability test, this difference is highly significant (P < 0.01). Among hypertensive subjects, the incidence of cystic medial necrosis was consistently higher than in normotensive subjects of comparable ages. Using the chi square test by decades and “all together”, this difference could easily be due to chance alone (P = 0.36 → 0.94).

Ventricular vulnerability during acute coronary occlusion

Abstract: Ventricular fibrillation thresholds were determined by delivering gated trains of pulses to the ventricle, spanning the vulnerable period. The coupling interval of premature beats decreased and the number of subsequent repetitive responses increased with an increase in the intensity of gated stimuli. Although fibrillation thresholds were determined before and during coronary occlusion at an identical site unaffected by ischemia, they were consistently lower in the ventricle with an ischemic area. The decrease in fibrillation threshold resulted because the ventricle with an ischemic area could be fibrillated by premature beats with longer coupling intervals and fewer subsequent repetitive responses. It was concluded that reentrant activity and resulting fibrillation are more likely to be induced in the ventricle with an ischemic area because of the increased irregularity in the propagation of premature impulses. This irregularity is a result of a marked depression of excitability and conduction velocity in the ischemic area. The results emphasize the greater chance that premature ventricular beats will induce fibrillation in patients with myocardial infarction.

The paradox of myocardial ischemia and necrosis in young women with normal coronary anteriograms. Relation to abnormal hemoglobin-oxygen dissociation.

Abstract: A double-blind study was carried out on 15 premenopausal women under 40 years of age who showed objective evidence of myocardial ischemia or necrosis as demonstrated by electrocardiogram or enzyme studies, or both. In each, selective coronary arteriography was normal. Three women later died with single or multiple subendocardial infarcts. None had disease of the large or small coronary arteries. None had a predisposing cause of premature coronary artery disease, except that 8 smoked cigarettes and 4 were obese. Abnormal hemoglobin-oxygen dissociation was found in 14 of the 15 women with myocardial ischemia or necrosis. Among 3 who discontinued cigarette smoking, the anomalous dissociation returned to normal within one month of cessation of cigarettes. In the other 5 it remained anomalous. Fifteen age-matched control women were also studied by double-blind technic. Abnormal dissociation was found in the 1 control subject who smoked (more than 12 cigarettes daily for more than 15 years). Selective coronary arteriograms were not performed among women in the control group. The strong correlation between the empiric observation of abnormal hemoglobin-oxygen dissociation and the presence of myocardial ischemia and necrosis with normal coronary arteriograms suggests that there may be a relation. This may be true in view of the high oxygen demands of the myocardium (especially the subendocardium). It is possible that inefficient or slow release of oxygen by hemoglobin could contribute to myocardial ischemia or necrosis. Alternatively, the hemoglobin-oxygen affinity changes may be secondary “stress phenomena.” Electrocardiographic abnormalities occurring at rest during forced hyperventilation appear to aid in predicting the laboratory abnormality. Propranolol is often effective in treating this condition.

Clinical and pathologic features of postinfarction cardiac rupture.

Abstract: In a 15 year period 106 instances of myocardial rupture after myocardial infarction were observed at autopsy, an incidence of 8.6 per cent of fatal acute myocardial infarcts. This complication occurred most frequently in the seventh and eighth decades and was slightly more common in women. Clinically, rupture occurred most frequently during the first week after infarction. Historical evidence of previous coronary artery disease was uncommon. Hypertension had been present in 70 percent of the patients, but it persisted after the infarct in less than a third. Pathogenetic factors were sought in the clinical aspects of the patients. No definite role could be ascribed to anticoagulant or sympathomimetic drugs or digitalis. Physical activity after infarction may be a predisposing factor in some instances. Sudden death without antecedent change in symptoms most often occurred. Cardiac tamponade or vascular collapse was documented in a few instances prior to death. In most instances no physical findings, laboratory tests, or electrocardiographic features that indicated cardiac rupture could be ascertained. Based on histologie data, 90 per cent of the ruptures occurred during the first two weeks after infarction, at an average time of five days; 22 per cent were in the first 24 hours, and 69 per cent were in the first week. All of the infarcts were transmural and involved large areas of the left ventricle. Ruptures presented as distinct tears (79 per cent) or large areas of hemorrhagic dissection (9 per cent), or both (12 per cent). The most common site of rupture was through the anterior wall of the left ventricle; commonly, ruptures were near the septum or near the base of papillary muscle. The areas of rupture were more common in the basal two thirds of the ventricle than in the apical portion. The ruptures varied greatly in size. Most were situated within the area of infarction rather than at the junction between the infarcted and the normal myocardium. Unusual accumulations of polymorphonuclear leukocytes were not found in most specimens. Most hearts had severe coronary artery disease, but myocardial scarring was present in only a fourth. Cardiac hypertrophy was usually present. The amount of hemopericardium varied widely and was the apparent mechanism responsible for death in some patients. Mural hemorrhage, hypertension, degree of polymorphonuclear infiltration, degree of myocardial fibrosis and location of the infarct may all be of pathogenetic significance in post-infarction rupture in different situations, but these considerations did not have universal applicability. The only common morphologic features among the infarcts that ruptured were their large size and transmural extent. The major pathogenetic considerations probably are loss of tensile strength of the infarcted segment, increased tension in this area, and, in some cases, divergent vector forces.

Ventricular fibrillation in the Wolff-Parkinson-White syndrome∗

Abstract: In a 27 year old white woman with a 5 to 10 year history of bouts of palpitations, documented ventricular fibrillation developed and was treated effectively with electrical defibrillation. Multiple subsequent electrocardiograms revealed the presence of the Wolff-Parkinson-White syndrome. The patient was studied extensively, and no evidence of organic heart disease was obtained. This report suggests that the Wolff-Parkinson-White anomaly is more than just an innocuous electrocardiographic finding and may be a potentially fatal condition.

Autoimmunity to the heart in cardiac disease: Current concepts of the relation of autoimmunity to rheumatic fever, postcardiotomy and postinfarction syndromes and cardiomyopathies

Abstract: Current information on the role of immune mechanisms in rheumatic fever, postcardiotomy and postinfarction syndromes, cardiomyopathies and other cardiac disorders is reviewed The possible role of autoimmunity is emphasized in view of the evidence that serum autoantibodies to diverse constituents of heart tissue frequently may be detected in these cardiac disorders In rheumatic fever, experimental and clinical data indicate that autoimmunity to heart tissue may be induced in response to a constituent of group A streptococci, antigenically cross-reactive with heart tissue Populations of autoantibodies with divergent specificities are present in the sera of patients with rheumatic disease Certain of these autoantibodies exhibit correlation with the severity of disease and with the presence of carditis The differentiation of those autoantibodies reactive with streptococcal crossreactive antigen seems essential for further understanding of the possible role of autoimmunity in pathogenesis Evidence for such a role is provided by immunopathologic findings of bound gamma globulin and complement in postmortem rheumatic hearts and in biopsy specimens of atrial appendage Circulating autoantibodies to heart tissue occur frequently after cardiotomy and myocardial infarction and are commonly associated with postcardiotomy and postmyocardial infarction syndromes They may reappear during symptomatic recurrent episodes but are not present in quiescent intervals between attacks Further efforts should be directed to definition of the specific antigens stimulating such autoantibodies, to the biologic and physicochemical properties of the autoantibodies related to clinical symptoms, as well as to immunopathologic observations in these syndromes In recurrent acute benign pericarditis and in primary cardiomyopathies, viral infection, complicated by hypersensitivity or autoimmunity, or both, has been proposed as a pathogenetic mechanism Autoimmune bodies have been described in varying frequency in these conditions, and their possible role in pathogenesis should be investigated further, using combined immunologie, virologie and immunopathologic approaches in the early phases of disease Abnormal immune mechanisms are strongly suspect in the pathogenesis of the cardiac involvement of rheumatoid arthritis, systemic lupus and polyarteritis, but progress must await further understanding of the cause of the primary lesions in these conditions In tropical endomyocardial fibrosis, an abnormal autoimmunologic diathesis, presumptively related to malarial infection, has been implicated Animal models of autoimmune myocarditis have been explored The available data suggest that experimental cardiac lesions of a focal nature may be produced in a variety of animal species Their relevance as a model for human cardiac disease is under current study

Delay in hospitalization during the acute coronary period

Abstract: Sixty-four patients with definite or probable acute myocardial infarction admitted to a coronary care unit were interviewed with regard to the time intervals and time delays during the pre-hospital period of their acute illness. The average time interval between the onset of symptoms and the patient's arrival in the hospital emergency department was 306 min., and this time was fractionated in a decision time of 200 min., 77 min. of unaccounted for time and 29 min. of transportation time. The decision time was longer in those patients who arrived by car rather than by ambulance, increased progressively with age and was twice as long for women as for men. It was three times longer when the symptom occurred on a weekend as opposed to a weekday, and it was generally longer when the symptom occurred during daylight hours than when it occurred at night. The significance of this prolonged pre-hospital delay during the acute phase of a potentially fatal illness is discussed.

The heart in Fabry's disease. A histochemical and electron microscopic study.

Abstract: Histochemical and electron microscopic studies of the heart of a patient with Fabry's disease (angiokeratoma corporis diffusum universale) revealed the presence of extensive glycolipid deposits in the cardiac muscle fibers, vascular smooth muscle, endothelium and connective tissue cells of the mitral valve. These deposits formed lamellae arranged either concentrically or in parallel stacks; the lamellae were often enclosed by limiting membranes and showed a periodic spacing of 40 to 45 A. The cardiovascular manifestations of Fabry's disease, which consist of cardiac hypertrophy and dilatation, congestive heart failure, anginal chest pain, myocardial infarction and hypertensive heart disease, are reviewed in detail. The association of this disorder with valvular heart disease is discussed.

The contractile state of the heart as expressed by force-velocity relations.

Abstract: A PROBLEM OF increasing concern and interest to the cardiologist in the evaluation and care of the patient with known or suspected heart disease is an assessment of the contractility of the myocardium. Unless cardiac function is markedly reduced, impairment of myocardial performance may not be evident in terms of hemodynamic dysfunction. Conversely, in the presence of abnormal hemodynamic loads such as occur with valvular disease, abnormal shunts, or hypertension, the secondary effects of congestive heart failure and circulatory insufficiency may ensue; it then becomes difficult or even impossible to assess the primary and intrinsic defect in the performance of the ventricular muscle. For example, congestive heart failure may ensue in the presence of severe valvular abnormalities despite an ostensibly normal myocardium. Various methods and approaches to the problem which have been extended from the animal laboratory to the evaluation of the human heart have been based on the characteristics of the ventricle as a pump. Unfortunately, most, if not all, of these methods are limited by the associated effects of abnormal loading. Further, it is now increasingly clear that a definition of the contractility of the myocardium per se requires the consideration of the heart as a muscle, as well as a pump.

Pre-hospital coronary care. The mobile coronary care unit.

Abstract: The majority of deaths from myocardial infarction occur soon after the onset of symptoms and before the victims reach hospital coronary care units. The mobile scheme described allows intensive care to commence in the patient's own home or at the site of infarction and thus reduces considerably the interval between the onset of symptoms and the initiation of intensive care. The prevention of fatal dysrhythmias by early pre-hospital care should have a significant effect on the early high mortality rates. Since the correction of ventricular fibrillation outside the hospital is a practical proposition, a further impact on the early high mortality will result when mobile units are supported by first aid training programs in methods of resuscitation.

Surgical correction of aneurysm of the sinus of Valsalva: A Report of forty-five consecutive patients including eight with total replacement of the aortic valve

Abstract: Pathologic, diagnostic and therapeutic aspects of 45 patients with an aneurysm of the sinus of Valsalva are discussed. The surgical procedure must be individualized for a patient according to the pathologic situations when fibrotic or prolapsing aortic cusps are encountered. Three choices are available in the surgical correction of this lesion: simple circumferential Teflon patch, circumferential sandwiched Ivalon-Teflon patch and, finally, prosthetic replacement of the aortic valve after a patch. The presence of fibrotic prolapsing aortic cusps will dictate the choice of valve replacement, while the prolapse alone may be corrected by means of sandwiched patch technic.

Syncope and sudden death in aortic stenosis

Abstract: A correlated study was made of the clinical manifestations and the electrocardiograms of 9 adult patients with aortic stenosis before, during and after the development of syncopal seizures. In 12 other patients with aortic stenosis, the mode of sudden death was registered by the “cardiac arrest” team of the hospital. All syncopal seizures were associated with a sudden drop in blood pressure, pallor, absent pulses and heart sounds and the disappearance of the aortic murmurs with loss of consciousness. If the attacks lasted from 20 to 40 seconds, the electrocardiograms revealed a regular sinus rhythm with changes in the form and height of the QRS complexes and the S-T segments. If the attacks were longer than 40 seconds, then either standstill of the whole heart, ventricular standstill, or ventricular flutter or fibrillation were the cardiac mechanisms responsible for the syncopal attacks. These longer seizures were accompanied by twitching of the body with convulsions and incontinence of feces and urine. Long periods of apnea alternated with Cheyne-Stokes respirations, and cyanosis supervened until the return of sinus rhythm. In addition, the electrocardiograms showed changes similar to those obtained experimentally and clinically during coronary artery obstruction and diminished coronary arterial blood flow. Sudden death in such patients was found to be due to ventricular standstill, ventricular flutter or ventricular fibrillation, or a combination of these. Syncope and sudden death in patients with aortic stenosis is an expression of diminished coronary arterial blood flow as a result of acute left ventricular failure and diminished cardiac output in a diseased heart.

Persistent fifth arterial arch in man: Congenital Double-Lumen aortic arch☆

Abstract: To our knowledge, this is the first reported case of persistence of the left fifth arterial arch in man. The persistent fifth arch forms a sizable subway beneath the fourth (aortic) arch, forming a congenital double-lumen aortic arch. The double lumen extends from the level of the innominate artery proximally to the level of the left subclavian artery and ductus arteriosus distally.

Biochemical aspects of early myocardial ischemia.

Abstract: The biochemical disturbances resulting from inadequate coronary blood flow are briefly reviewed. Results of experiments in which the onset of myocardial ischemia was examined by use of a continuous sampling technic are presented. At the point of maximal coronary arteriolar dilatation, a rise in coronary sinus lactate and potassium levels occurred simultaneously, accompanied by a rise in left atrial pressure. The rates of potassium loss and lactate production from ischemic tissue were directly related; the ratio was approximately 1:2 on a molar basis. The total amount of potassium lost by the left ventricle after 7 minutes of ischemia was estimated to be 1.0 per cent of its normal content, and 5.4 per cent after 17 minutes of ischemia. Restoration of coronary flow resulted in potassium uptake, indicating that potassium lost from an ischemic area is replaced quickly in the presence of adequate coronary flow. Electrocardiographic correlation showed that depression of the junction between the QRS complex and the S-T segment appeared simultaneously with the rise in coronary sinus potassium and lactate levels. The junction became progressively more depressed as metabolic evidence of ischemia increased. The flat “ischemic” S-T segment depression was a later feature, appearing only after ischemia had been well established for several minutes. The early electrocardiographic changes seen in these experiments are not currently accepted as evidence of ischemia in clinical practice. A reexamination of electrocardiographic criteria for ischemia in man, with metabolic correlation, seems warranted.

Sudden death in arteriosclerotic heart disease: The case for preventive medicine☆

Abstract: Arteriosclerotic heart disease is the leading cause of death among adults in the United States. The distribution of deaths due to arteriosclerotic heart disease in relation to demographic factors, time, space and medical care has been studied in several different ways. Data from cross-sectional and prospective studies disclose that the incidence of sudden death due to arteriosclerotic heart disease is higher in male than in female subjects and increases with age. Approximately 25 to 30 per cent of patients with incident cases of myocardial infarction die suddenly, and for a cohort of myocardial patients with myocardial infarction there are as many deaths within the first 24 hours as during the next 5 years. A variety of studies in the United States and England have shown that in about 70 per cent of all deaths due to arteriosclerotic heart disease the individuals died outside of a hospital or were dead on arrival. Relatively few of the deaths occur after 24 hours of hospitalization. Survivors of a myocardial infarction have a very high risk of dying suddenly. This risk also may exist for patients with angina pectoris. A retrospective study of sudden death in Baltimore has shown that 60 per cent of all deaths due to arteriosclerotic heart disease were sudden and that 61.4 per cent of all sudden deaths were due to arteriosclerotic heart disease. Sudden death due to arteriosclerotic heart disease was the single most important type of death in subjects aged 40 to 64 years, accounting for 20 per cent of the nontraumatic deaths. Approximately one half of the individuals with arteriosclerotic heart disease dying suddenly had a history of heart disease, and 23 per cent had seen a physician within a week before death. Finally, of the 585 white men who died of arteriosclerotic heart disease, only 52 (8.4 per cent) had died within two hours, had no history of heart disease and had not seen a physician within one month before death. A review of these studies, therefore, shows that either a program of primary prevention of myocardial infarction and sudden death or methods of early diagnosis and treatment outside of the hospital and in a coronary care facility will be necessary to reduce the death rates from arteriosclerotic heart disease in the community.

Circulatory dynamics during high altitude pulmonary edema

Abstract: Cardiac catheterization studies have been carried out in 2 young male subjects who experienced acute pulmonary edema after a brief sojourn at sea level, when they returned to their native town located at 14,200 feet above sea level. The investigation was performed at this altitude during the acute episode and was repeated after complete recovery. Further studies were made in 1 subject after prolonged residence at sea level. Severe hypoxemia, a marked degree of pulmonary hypertension and increased pulmonary vascular resistance were found during the acute pulmonary edema. These findings were associated with low cardiac output and pulmonary wedge pressure. The degree of pulmonary hypertension was significantly reduced after inhalation of 100 per cent oxygen. Following recovery, physiologic observations were similar to those seen in healthy residents well acclimatized to high altitudes. The data obtained suggest the presence of arteriolar constriction at the precapillary level due to severe hypoxia. Several factors may explain the severe hypoxemia observed in patients with high altitude pulmonary edema. Exercise and sleeping may decrease significantly the arterial oxygen saturation at high altitudes. Pulmonary edema occurred during exercise in our first case, and during sleep in the second. However, special susceptibility appears to be present in humans who develop pulmonary edema after rapid exposure to high altitudes. The role of a sudden rise of pulmonary artery pressure in producing pulmonary edema without elevation of pulmonary wedge pressure is not clear.

Angina pectoris in patients with normal and abnormal coronary arteriograms

Abstract: Ten patients with typical angina pectoris and normal coronary arteriograms were evaluated. Hemodynamic measurements and clinical features were analyzed and compared to those in a similar group of patients with angina secondary to demonstrable coronary artery disease. Both hemodynamic and clinical abnormalities were observed in those patients with angina and normal coronary arteries. However, with the exception that exercise elicited angina and electrocardiographic changes more consistently in the group with coronary artery disease, there were no significant differences between the two groups.