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Background: Aneurysm of the fossa ovalis is an out pouching, space-occupying, interatrial septal structure. The anatomic morphology and characteristics of this aneurysm are of interest for pathologists and cardiologists alike. Methods: We identified 33 specimens of adult hearts with a large size aneurysm of the fossa ovalis (length equal to or more than 10 mm from the plane of the atrial septum) in a registry of cardiovascular disease. Anatomic–morphologic features of these aneurysms were examined by macroscopic and histopathologic studies. Results: Nineteen aneurysms were from females (57%) and 14 were from males (43%). Most aneurysms had a dome shape with maximal length of the aneurysmal excursion into an atrium varying from 10 to 35 mm (mean 16±5 mm) and width varying from 16 to 40 mm (mean 24±6 mm). Twenty-four aneurysms (73%) protruded into the right atrium while only nine (27%) penetrated into the left atrium. In 24 patients the interatrial ostium II was patent, and in 22 (91%) of them, abnormal increased intracardiac pressure was deemed responsible for the formation of the aneurysm. Among nine patients in whom the foramen ovale was closed, eight (89%) had an aneurysm protruding into the right atrium, and only one aneurysm penetrated into the left atrium. In six patients, the aneurysm further stretched an already patent foramen ovale resulting in creation of an atrial septal defect so that bidirectional shunting could occur, and in three cases, the aneurysm narrowed the inferior vena caval orifice. In three hearts, the aneurysm wall had endocardial fibrosis, and in three other specimens, a focal mural thrombus was present on the aneurysmal surface. Most common associated cardiac conditions in this series included atherosclerotic coronary artery disease (51%), aortic valvular disease (21%) and mitral valve disease (24%). Conclusions: Aneurysm of the fossa ovalis is a space-occupying, redundant structure, most commonly with a dome shape. In a majority of cases, the formation of this aneurysm relates to the effect of extrinsic mechanisms, which create abnormally elevated intracardiac pressures. The aneurysm protruded into the right atrium in 73% of cases. Endocardial fibrosis and a focal mural thrombus were present in several cases on the aneurysmal wall. Bidirectional shunt via stretched patent foramen ovale and distal embolization can contribute to complications related to the aneurysm.

Sudden, unexpected cardiac death in the age group 1 to 21 years usually is due to myocarditis, hypertrophic cardiomyopathy, aortic valvar stenosis, and coronary arterial abnormalities. The hearts of 70 patients

Our goal was to identify the most appropriate material for right ventricle-pulmonary artery conduits in growing animals. We used 100 lambs that were 3 to 4 weeks old (mean weight 11.7 kg). Follow-up was up to 24 months. Group I received plain tubular conduits: (1) Dacron knitted fabric, (2) collagen-coated knitted fabric, (3) Milliknit and Microknit material, (4) woven Dacron fabric, (5) three-dimensional Dacron fabric (crossweave 500 and 800), or (6) polytetrafluoroethylene. Group II received either a (1) woven Dacron fabric conduit with a built-in tissue valve or (2) polytetrafluoroethylene graft with a built-in St. Jude Medical valve. We did angiograms and catheterizations every 3 to 6 months and killed the lambs at 6, 12, 18, or 24 months. Tubular Dacron fabric woven or knitted grafts, regardless of matrix, pore size, thickness, or coating, caused formation of a thick acellular pseudointima buildup, which led to progressive obstruction starting as early as 3 months. Polytetrafluoroethylene grafts in groups I and II showed the formation of thin inner and outer capsules (0.5 mm) and none developed obstruction despite wall calcification. Conduits of woven Dacron fabric with a built-in tissue valve degenerated rapidly, leading to calcification thrombosis and obstruction within 3 months; no lamb survived 12 months. Polytetrafluoroethylene conduits with a St. Jude Medical valve in lambs receiving anticoagulants remained free of obstruction and continued to function well. It appears that synthetic conduits of polytetrafluoroethylene perform well in either of the situations here tested and may be the best choice at present. (J THORAC CARDIOVASC SURG 1995;110:427-35)

Anomalous origin of the right subclavian artery (ARSA) from the aorta distal to the normally positioned left subclavian artery is a relatively frequent congenital anomaly in subjects with left aortic arch. The purpose of this study was to determine the relative frequency of associated cardiovascular anomalies in individuals with this anomaly. From the records of approximately 11,000 pathologic specimens in the Registry of Cardiovascular Disease of United Hospital (St. Paul, MN, USA), we found 128 (1.2%) with ARSA. Of the 128 ARSA, 117 (2.9%) occurred among 4102 instances of congenital heart disease. The 117 cases with congenital heart disease and ARSA were conotruncal anomalies in 38%, septal defects in 28%, obstructive anomalies of the left side of the heart in 21%, right heart anomalies in 5%, and miscellaneous conditions in the other 8%. Down syndrome existed in 14 (12%) of the 117 specimens with ARSA and some congenital cardiac anomaly; nine of the latter had an atrioventricular canal (AVC) malformation.

Interruption of the aortic arch and hypoplastic left heart syndrome in the same patient is exceptional. In the combined collections of the Registry of Cardiovascular Disease (St. Paul, Minnesota, U.S.A.) and the Registry of Congenital Heart Defects of the Rijksuniversiteit Gent (Gent, Belgium) three specimens were found with this unusual combination. These cases are herein described and compared with four similar cases previously reported in the literature.

Interruption of the aortic arch (IAA) is an important congenital cardiac malformation occurring in 1.4% of cases with a congenital cardiac malformation. Only two reports have described IAA in siblings, each with type B and an anomalous right subclavian artery. We report the occurrence of IAA type B with an anomalous right subclavian artery in two siblings and their half-sibling, each of whom had additional conotruncal cardiac malformations. Recent evidence suggests that conotruncal cardiac malformations, including IAA type B, are related to abnormalities of neural crest cell migration. Thus, the family reported herein may manifest a syndrome related to alterations in mesenchymal tissue/neural crest cell migration.

Objective. The goal of this study was to determine the patterns of the pulmonary circulation in patients with pulmonary atresia and asplenia.Background. The asplenic cardiac syndromes characteristically have complex cardiac anomalies including pulmonary stenosis or atresia. Definition of the pulmonary artery circulation and pulmonary venous connections is needed for consideration of surgical procedures.Methods. In 35 patients, the sources of pulmonary blood flow, anatomic features of pulmonary arteries and pulmonary venous connections were determined from angiograms or autopsy specimens.Results. The pulmonary artery was absent or hypoptestic in 91% of patients; most had a ductes arteriosus. The right and left pulmonary arteries were confluent in 90% and usually of normal size (right 71%, left 63%). Total anomalous pulmonary venous connections were present in 38%.Conclusions. The anatomic features of the pulmonary arteries in pulmonary atresia associated with the asplenic cardiac syndrome are usually favorable for palliative surgical procedures. Total anomalous pulmonary venous connection may exist as a complicating factor.

Objective. —To determine the clinical significance of silent and symptomatic myocardial ischemia detected by noninvasive testing in stable postcoronary patients. Design. —Cohort study with a mean 23-month follow-up. Setting. —Ambulatory outpatients after recent hospitalization for an acute coronary event. Patients. —Nine hundred thirty-six patients (76% male; mean age, 58 years) who were clinically stable 1 to 6 months after hospitalization for acute myocardial infarction or unstable angina. Interventions. —Noninvasive testing involved rest, ambulatory, and exercise electrocardiograms and stress thallium-201 scintigraphy. Main Outcome Measures. —Cox regression analysis was used to evaluate the risk (hazard ratio) of first recurrent primary events (cardiac death, nonfatal infarction, or unstable angina) or restricted events (cardiac death or nonfatal infarction) associated with ischemic noninvasive test results. Results. —ST segment depression on the rest electrocardiogram was the only noninvasive test variable that identified a significantly increased risk (P=.05) for first recurrent primary events (hazard ratio; 95% confidence limits): rest electrocardiogram ST depression (1.5; 1.00,2.25); ambulatory electrocardiogram ST depression (0.86; 0.49,1.51); exercise electrocardiogram ST depression (1.13; 0.82,1.56); and stress thallium-201 reversible defects (1.3; 0.96,1.74). Test results were similar for first recurrent restricted events, and in patients with and without angina. Significantly increased risk (P Conclusion. —Detection of silent or symptomatic myocardial ischemia by noninvasive testing in stable patients 1 to 6 months after an acute coronary event is not useful in identifying patients at increased risk for subsequent coronary events. (JAMA. 1993;269:2379-2385)

A correlative study in 50 cases of healed myocardial infarction compared the 12 lead electrocardiogram with pathologic observations. The electrocardiogram was interpreted according to established Minnesota codes with some modifications. The following conclusions were reached: (1) The electrocardiogram underestimates the extent of myocardial infarction. (2) When a healed myocardial infarct at a specific location is recognized with electrocardiographic criteria, it is likely that there are unrecognized infarcts involving other areas of the left ventricle. (3) Infarctions involving the lateral and inferobasal areas are frequently unrecognized. (4) The electrocardiogram is more likely to miss myocardial infarcts in patients with multiple, than in those with single, electrocardiographically diagnosed infarcts. (5) Apical myocardial infarction does not appear to have specific electrocardiographic findings, other than those related to general infarct localization by electrocardiogram, particularly in patients with anteroseptal or anterolateral infarction. (6) Abnormal Q waves, generally thought to indicate transmural myocardial infarction, are frequently found in subendocardial infarction. (7) The simplified electrocardiographic classification of myocardial infarct site (anteroseptal, inferior, anterolateral) used in this study is preferable to more detailed classifications previously suggested by others.

Three cases of persistent ostium primum coexisting with atresia of an atrioventricular valve (tricuspid atresia in one case and mitral atresia in two cases) are described. The presence of a persistent ostium primum in association with an atretic atrioventricular valve allows easy escape of blood from the atrium with an atretic valve. To our knowledge, this association of anomalies has not been previously reportd.

Coronary atherosclerotic lesions are more often located eccentrically (70%) than concentrically (30%). In this study, the configuration of eccentric coronary artery atherosclerotic lesions was assessed by means of computerized planimetry in 100 specimens of eccentric arterial lesions. Special attention was given to the relation between the disease-free wall and the severity of obstruction. The mean disease-free wall arc length measured between 17 and 23% of the total vessel circumference in eccentric coronary artery lesions that obstructed 50 to 90% of the cross-sectional area. This ratio persisted irrespective of the location of the lesion within the vessel and was not significantly different with vessels of different sizes. The presence of disease-free arcs of coronary artery wall as observed in this pathologic study may relate to three factors in clinical coronary artery disease: 1) The published observations of spasm in segments of arteries harboring structural obstructive lesions may be explained by the frequent presence of uninvolved arcs of coronary artery walls. 2) Multiple views during coronary arteriography are necessary to accurately reflect the degree of obstruction. 3) The results of percutaneous transluminal coronary angioplasty may be influenced by both the disease-free arc and the atheromatous obstruction.

An aneurysm of the fossa ovalis was identified at autopsy in 17 infants. In each case the aneurysm of the fossa ovalis was considered to have resulted from excessive elevation of pressure in that atrium contralateral to the side into which the aneurysm bulged. The aneurysms were divided into two types: intrinsic (three cases) and extrinsic (14 cases). The intrinsic types of aneurysms of the fossa ovalis were considered to have started in fetal life and were consequences of abnormally narrow states of interatrial ostium II. Each intrinsic aneurysm bulged toward the left. Among the extrinsic types of aneurysm of the fossa ovalis, each was considered to have resulted from the hemodynamic consequences of a congenital anomaly in one side of the heart or other. Six aneurysms of extrinsic type bulged toward the left and eight toward the right. Aneurysm of the fossa ovalis should be included in the differential diagnosis of space-occupying conditions within the atria.

Pathologic investigation of 50 children, adolescents, and young adults who died suddenly and unexpectedly revealed that the most frequently encountered cardiovascular diseases were mitral valve prolapse (12 cases), myocarditis (12 cases), hypertrophic cardiomyopathy (six cases), and anomalous origin of a coronary artery from the aorta (two cases). Five subjects had no evidence of cardiac abnormalities. A striking family history of sudden death was encountered among eight subjects, of whom three had mitral valve prolapse and three had normal hearts. Assessing the circumstances surrounding sudden death, it was found that at the time of collapse, 32 subjects were engaged in regular activity, eight subjects were engaged in active athletics, and ten were found dead in bed. A relationship of the terminal event to emotional stress was reported in three subjects.

A prospective study to determine prognostic factors for risk stratification in 867 patients surviving the coronary care unit phase of acute myocardial infarction (AMI) is reported. During a 48-month follow-up, 144 patients (17%) died. The deaths were examined for the chronology, cause, mechanism, location and presence of myocardial ischemia in the terminal event. A classification previously proposed by Hinkle and Thaler was used to define the mechanism of cardiac death and the presence of ischemia. There were 113 deaths due to coronary atherosclerotic coronary artery disease, including 5 due to complications of coronary artery bypass graft surgery. Of the remaining 108 of these deaths, 74% were classified as due to an arrhythmic mechanism and 26% as myocardial failure. Of the deaths due to an arrhythmia or to myocardial failure, 56 (52%) occurred out of hospital. The ratio of arrhythmic: myocardial failure deaths was not different for the patients who died within 3 months after the index AMI compared with later deaths. Sudden death (less than or equal to 1 hour of new symptoms) was strongly associated with arrhythmic death but 32 (54%) of patients who died greater than 1 hour after the onset of symptoms were also classified as having an arrhythmic cause of death. Previously described risk factors, including an ejection fraction less than 0.40 and greater than or equal to 10 ventricular premature complexes/hour, were independent predictors of mortality but did not differentially predict the mechanism of cardiac death. Evidence of myocardial ischemia before the terminal event was found in about 50 (60%) patients whose deaths were witnessed and who died from an arrhythmia or myocardial failure.

Clinical and pathologic observations were made in four infants who died with asymmetric septal hypertrophy in the first five months of life. One of these infants was stillborn and the other three were aged 1½ months, 4½ months, and 5 months at the time of their deaths. The three live-born infants demonstrated severe congestive heart failure and cardiac enlargement. The clinical features present in these three infants during life suggested a variety of other congenital cardiac malformations, including congenital mitral regurgitation, pulmonary stenosis, and endocardial fibroelastosis. In each of the four infants the ventricular septum was markedly hypertrophied and was thicker than the postero-basal left ventricular wall; septal to postero-basal free wall thickness ratios ranged from 1.8 to 2.6. Moreover, the septum of each infant contained a disordered arrangement of hypertrophied cardiac muscle cells. In three of the infants the myocardial cellular abnormalities were less marked in the left ventricular free walls than in the ventricular septum. In the fourth infant disorganized cardiac muscle cells were distributed widely in both the ventricular septum and left ventricular free wall; the clinical findings suggested the absence of left ventricular outflow obstruction in this infant. Asymmetric septal hypertrophy was documented in one first degree relative of each infant. It is concluded that asymmetric septal hypertrophy is a genetically transmitted disease that may present clinically in infancy and lead to infant death. Furthermore, the characteristic pathologic feature of asymmetric septal hypertrophy in adults, a disproportionately thickened ventricular septum containing numerous hypertrophied and disorganized cardiac muscle cells, can be present at birth.

Four patients with atherosclerotic disease were found to have a recanalized coronary arterial thrombus on angiography. The functional significance of this finding varied. In 2 cases, flow (judged by collaterals) was insignificant in spite of the recanalization. In the other 2, collateral supply had been shown to be absent during the initial stage of thrombosis. In one case, recanalization was confirmed pathologically.

In five patients with aortic dissection, signs and/or symptoms of pericarditis were part of the early manifestations of the aortic disease. Signs of inflammatory pericarditis were noted clinically in four patients and were found at autopsy in one. In the three nonoperated patients who died of aortic rupture leading to fatal hemopericardium, symptoms of pericarditis preceded fatal rupture of the aorta by four to five days. A fourth patient died after surgical repair of aortic dissection 35 days after the onset of pericarditis. In the fifth patient, manifestations of chronic constrictive pericardial disease occurred over a period of seven months after which old aortic dissection was first identified. In each case, the internal tear of classic aortic dissection was located in the ascending aorta. Microscopic evidence of cystic medial necrosis of the aorta was present in each case. In each of two cases, there was a congenital bicuspid aortic valve. The phenomenon observed represents acute aortic dissection in which slow penetration of blood into the pericardial space caused inflammatory pericarditis. The interval between the onset of pericarditis and rupture of the aorta may allow sufficient time for appropriate diagnosis and potentially lifesaving treatment of the aortic disease.

Interruption of the aortic arch may occur with aorticopulmonary septal defect (APSD) as part of a developmental complex. The anatomic details of 46 cases of interruption of the aortic arch with APSD revealed the following characteristics: (1) type A interruption of the aortic arch occurred nearly six times more commonly than type B interruption; (2) the APSD was variable in size and position, conforming to the types previously described; (3) the ventricular septum was usually intact, but a ventricular septal defect was present in six cases and occurred more frequently with type B interruption of the aortic arch; (4) subaortic stenosis was not present in any of the 16 cases in which adequate details were available to make a judgment. The association of APSD with interruption of the aortic arch in infancy is not uncommon. Evaluation of infants with APSD should thus include evaluation of the aortic arch. The occurrence of interruption of the aortic arch with an intact ventricular septum is distinctly unusual. In such cases an APSD should be suspected and sought.

Fifty-seven cases of single (common) ventricle with transposition of the great vessels are reviewed. The diagnosis had been confirmed by necropsy in 25 and by angiocardiography in 32 cases. Single (common) ventricle is defined as that condition in which both atrioventricular valves separately enter a single ventricular cavity. According to this definition, cases presenting with common atrioventricular valve, atresia of one atrioventricular valve, or straddling valves have been excluded. Two structural types of common ventricle are identified: the left ventricular type and the primitive type of single ventricle. The former showed anatomic features similar to a left ventricle, whereas in the latter, features characteristic of a left ventricle were not present. The latter was considered a more primitive condition than the former. A classification based upon the type of single ventricle and its outflow tract and upon the relationship of the great vessels is presented. Of the 25 cases of single ventricle with transposition studied pathologically, 21 were of the left ventricular type and four of the primitive type. Of the four cases with double conus three were among the four examples of primitive ventricle. Among the 21 cases with a single conus, the type of transposition was about equally divided between the d -type (ten cases) and the l -type (11 cases). Pulmonary stenosis or atresia was observed in seven of the 21 cases with a single conus and in one of the four cases with double conus. In the clinical cases, only angiocardiography could establish the diagnosis and delineate the different types of great vessel-ventricular relationships.

The clinical, hemodynamic, and pathologic findings in two newborn infants with persistent truncus arteriosus and stenosis of the truncal valve are described. In one case the anatomic features of the basic condition were classic, with a dysplastic semilunar valve which was mainly stenotic and also incompetent, while in the other the truncus arteriosus arose exclusively from the right ventricle and was almost exclusively stenotic. A ventricular septal defect was the only outlet for the left ventricle. In this case, mitral stenosis was also present and associated with a left-to-right shunt at the atrial level.

In three cases, two in children and one in a young adult, ventricular outflow obstruction was caused by a valvelike flap of accessory endocardial tissue. The angiocardiographic feature was that of a narrow radiolucent, crescent-shaped or linear filling defect corresponding to the site of obstruction. Resection of the accessory tissue was performed in each case at the time of correction of associated conditions. In one case (a woman 20 years of age) the obstructing membrane was in the outflow tract of the right ventricle, and a ventricular septal defect was associated. In each of the other two cases the outflow tract of the left ventricle was the site of obstruction. In one (a 14-month-old boy), an ostium primum type of atrial septal defect and cleft mitral valve were associated; in the remaining case (a 7-year-old boy) complete transposition and ventricular septal defect were also present. In the latter case a Mustard procedure was performed and was followed by death. Successful results were obtained in the first two patients.

Restrictive cardiomyopathy characterized by evidence of left ventricular inflow obstruction was studied in four cases--one child and three adults. In three of the cases, including the child, there was pathologic evidence of hypertrophic cardiomyopathy with asymmetric septal hypertrophy. In the fourth case, no cardiac disease was identified as the anatomic basis for the inflow restriction. This latter case broadens the concept of restrictive cardiomyopathies.

Specimens of heart from 30 subjects with persistent truncus arteriosus were studied for the nature and sites of coronary arterial origin. These factors were related to the sinuses of the truncus valve. Bicuspid truncal valve was observed in six cases (20%) and tricuspid in 21 cases (70%). Single coronary artery was observed in four cases (three with tricuspid and one with quadricuspid truncal valves). In three other cases the coronary arteries arose separately but near one another. There was a strong tendency for the left coronary artery to arise from a more posterior level than it does normally from the aorta. It was common for the posterior descending artery to arise from the left circumflex artery. This arrangement was noted in eight of 25 cases (32%) with single posterior descending coronary artery. In five other cases, two posterior descending arteries were present, one arising from the left circumflex and the other from the right coronary artery.

The previously unreported occurrence of a true vascular ring in association with interruption of the aortic arch resulting from bilateral persistence of the ductus arteriosi is described. Division of both ductus is necessary to minimize the potential for tracheobronchial compression. This should be accomplished either during definitive (one-stage) repair of the interrupted aortic arch and associated anomalies or at the initial procedure of a staged repair.

Twenty pathologic specimens of heart, each with a cleft in the anterior leaflet of the mitral valve not associated with septal defects of persistent common atrioventricular canal (isolated cleft of the mitral valve), were studied. In 9 cases, there were either no associated anomalies or ones not of functional significance. In each of the other 11 cases there were other significant associated cardiac anomalies, including ventricular septal defect and d-transposition of the great arteries. Functional consequences of the mitral anomaly were mitral insufficiency, subaortic stenosis, or both. Mitral insufficiency was related principally to the width of the cleft. Subaortic stenosis, when present, was due to the position of insertion of accessory chordae in the ventricular septum in a position under the commissure, between the left and right aortic cusps or under the right aortic cusp.

The necropsy specimens of 33 examples of double-outlet right ventricle were studied. In 31 of the 33 cases, a ventricular septal defect (VSD) was present, and in two the ventricular septum was intact. Two of the VSDs appeared small and obstructive, while the remainder were of the large variety. Among the 31 cases the VSD was located in one of four locations: below the aortic valve (15 cases), below the pulmonary valve (nine cases), below both valves (four cases), and remote from either semilunar valve (three cases). Associated cardiovascular anomalies were present in 28 of the 33 cases and were usually obstructive to blood flow. Pulmonary stenosis or subpulmonary stenosis, or both, were confined to patients with the subaortic location of VSD and were seen in six of 15 such cases. Obstruction to systemic flow, either subaortic or within the aortic arch, was observed in 19 cases. There was a strong tendency for obstruction to systemic flow to be associated with a subpulmonary VSD. Various anomalies, usually of the mitral apparatus, causing obstruction to pulmonary venous flow were common but without a trend for association with a particular location of the VSD.

A model was developed which allows the dilatation of iliac cadaver arteries under normal blood pressure conditions (mean pressure 100 mmHg). Segments of the iliac artery were put under pressure and dilated with balloons under similar conditions as in clinical practice. Purposely oversized balloons were used because most of the arteries did not contain severely stenotic plaques and consequently the commercially available balloons had no effect because of their comparatively small diameter. In spite of the use of oversized balloons, the cadaver arteries could not be significant dilated. Rupture of the intima and media was almost invariably present. Leakage of distending fluid through the adventitia occurred commonly. The "therapeutic range" between minimal dilation and partial or total rupture in postmortem studies is small.

The nature and incidence of postoperative mural thrombosis of the septal and/or posterior walls of the left atrium were studied in autopsy specimens of hearts from patients in whom the mitral valve had been replaced by a prosthesis I day or longer before death. The cases were divided into length of postoperative period as follows: Group I, 1 to 60 days, 57 cases; Group II, 61 days or longer, 36 cases. In Group I mural thrombus of the septal and/or posterior walls of the left atrium was found in 35 of 57 patients (61%). Thrombi against the septal wall tended to be broad and flat. Thrombi involving the posterior wall tended to be multifocal. In Group II, lesions interpreted as old thrombi of the atrial septum were found in 23 of 36 subjects (64%). Grossly, the old lesions were represented by gray nodularity. Histologically such lesions were consistent with organized thrombi. Superimposed recent thrombosis occurred in some cases. Systemic embolism occurred in each group. In the cases in which left-sided thrombi were restricted to the septal and/or posterior walls of the left atrium, systemic embolism was observed in 10 of 23 cases in Group I (43%) and in two of seven cases in Group II (29%). Obstruction of the mitral prosthesis by bulky mural thrombosis originating at the septal wall of the left atrium was observed in one case. The study suggests that the process of postoperative mural thrombosis of the septal and posterior walls of the left atrium may result from trauma to these structures during the operative procedure.

The pathological anatomy of 109 specimens of aortic valvular atresia was reviewed for the purpose of identifying the cardiovascular anomalies associated with that condition. We found the most commonly associated anomaly to be coarctation of the aorta, which was present in 71 percent of our cases and judged to be hemodynamic significance in one-third of the involved cases. Other associated anomalies, in order of decreasing frequency, were mitral atresia, anomalous systemic and pulmonary venous connections, abnormalities of branching of the aortic arch, and ventricular septal defect. The study demonstrated that aortic atresia is associated with a significant incidence of other cardiovascular anomalies. Additional anomalies, when present, may complicate emerging attempts at surgical correction of this condition.

A rare form of common ventricle with normally related great vessels and normal tricuspid and mitral valves should be considered in the differential diagnosis of cardiac anomalies presenting with cyanosis. Fourteen cases of this type of common ventricle were studied; in seven the diagnosis was made at necropsy and in seven it was based on angiographic evidence. That the common ventricle was morphologically a left ventricle was determined in the seven necropsy cases, and angiocardiographic examination confirmed the finding in the others. Continuity of the aortic valve and the mitral valve was observed in all the necropsy cases and in five of the clinical cases. Cyanosis had been observed clinically in 13 of the 14 cases, and pulmonary stenosis was present in four necropsy and three clinical cases. Electrocardiograms showed left axis deviation in nine of the 13 cases studied. Vectorcardiographic findings, though variable and available in only seven cases, tended to show a narrow horizontal plane QRS vector loop in patients with restricted pulmonary blood flow and a wide loop in those with increased pulmonary flow. The clinical, laboratory, and pathologic findings are reported and the differential diagnosis and the profile of the condition are considered.

This study correlated the location and size of posterolateral myocardial infarcts (Mls) measured anatomically with that estimated by quantitative criteria derived from the standard 12-lead ECG. Twenty patients were studied who had autopsy-proved, single, posterolateral Mls and no confounding factors of ventricular hypertrophy or bundle branch block in their ECG. Left ventricular anatomic Ml size ranged from 1 to 46%. No patient had a ≥ 0.04-second Q wave in any electrocardiographic lead and only 55% had a 0.03-second Q wave. A 29-point, simplified QRS scoring system consisting of 37 weighted criteria was applied to the ECG. Points were scored by the ECG in 85% of the patients (range 1 to 8 points). Ml was indicated by a wide variety of QRS criteria; 19 of the 37 criteria from 8 different electrocardiographic leads were met. The correlation coefficient between MI size measured anatomically and that estimated by the QRS score was 0.72. Each point represented approximately 4% Ml of the left ventricular wall.

The related atrioventricular valves in 11 instances of polypoid atrial tumors were examined grossly and histologically. Nine of the tumors involved the left atrium and, of these, seven were myxomas. The two right atrial tumors were myxomas. Histologically evident lesions of the mitral valve were present in seven of the nine left atrial tumors. The most common change consisted of fibrous thickening of the endocardium in the angle between the left atrium and posterior mitral leaflet and fibrous thickening of the atrial surfaces of the leaflet. Less common changes were a fibrous thickening of the chordae and of the left ventricular mural endocardium in relation to chordae inserting into the posterior leaflet. The changes described were also evident at gross examination in two of the nine cases with left atrial tumors. In the two cases of right atrial myxoma, both showed fibrous thickening of the atrial surfaces of the tricuspid leaflets; one also exhibited fibrous thickening of the right ventricular endocardium beneath the septal leaflet of the tricuspid valve. The lesions described are considered responses to the effects of friction by the tumor upon the surfaces involved. It is significant that grossly evident lesions may evolve from this rubbing action.

A total of 31 specimens of hearts with congenital pulmonary valvar stenosis were studied. To define the anatomy of the normal pulmonary valve, 210 specimens of hearts considered to have a normal pulmonary valve were also reviewed. On the basis of gross morphology of the valve leaflets and annulus, the stenotic valves were subgrouped into domed, unicommissural, bicuspid, tricuspid, hypoplastic annulus, and dysplastic. The valve leaflets in all subgroups were thickened. The thickness varied in degree, but involved the entire length of the leaflet. Microscopically, the thickness in most cases was due to an increase in myxomatous tissue. In a few cases, the elastic and collagen components of the leaflet were increased. The valve annulus was abnormal in most cases. The abnormalities included replacement of the fibrous backbone of the annulus by myxomatous tissue and partial or complete absence of the annulus. The impact on valvar anatomy by direct surgical valvotomy (14 patients) and closed Brock valvotomy (two patients) was reviewed. Precise knowledge of pulmonary valve anatomy is an aid to successful balloon pulmonary valvuloplasty.

This report reviews the findings in a calcified lesion involving the ridge at the junction of the sinus and tubular portions of the ascending aorta. The histologic features resemble the alterations in calcified aortic valve and do not exhibit those of atherosclerosis. The 37 cataloged cases are among the more severe and dramatic instances of a lesion more common than the cataloged number would suggest. The involved ridge may be related to any of the sinuses, although that related to the right aortic sinus is most commonly affected. Major complications include coronary ostial stenosis or embolism in an epicardial coronary artery. Ostial stenosis results either from overhanging of an ostium by the aortic lesion or from invasion of the wall of the aorta at the site of the arterial takeoff.