True left ventricular aneurysm and healed myocardial infarction: Clinical and necropsy observations including quantification of degrees of coronary arterial narrowing

Clinical and necropsy observations are described in 28 patients (24 men) aged 31 to 85 years (mean 62) with healed myocardial infarction and a true left ventricular aneurysm. In contrast to findings in other subsets of necropsy patients with fatal coronary heart disease, chronic congestive heart failure was frequent (22 patients); angina pectoris was infrequent (4 patients) and, when present, never severe; recurrence of acute myocardial infarction (2 patients), sudden death (2 patients) and clinically evident systemic emboli (1 patient) were infrequent; survival for more than 5 years after healing of the acute infarction was infrequent (in 3 of 21 patients with clinically diagnosed acute myocardial infarcts); and survival for longer than 1 year after aneurysmectomy was lacking (0 of 7 patients). Additionally, 23 of the 28 patients had a large heart (greater than 400 g [mean 523], 26 had dilated nonaneurysmal portions of the left ventricle, and all but 1 had a large (greater than 30 percent of the left ventricular wall) myocardial infarct. In 25 of the 28 patients, two or more of the four major epicardial coronary arteries were greater than 75 percent narrowed in cross-sectional area by atherosclerotic plaques. In 992 segments (each 5 mm long) of a major coronary artery examined in 22 patients (45 segments/patient), narrowing was greater than 75 percent in 323 segments (33 percent) and ranged from 51 to 75 percent in 419 (42 percent), from 26 to 50 percent in 210 (21 percent) and from 0 to 25 percent in 40 (4 percent). Thus, the scarred, hypertrophied and aneurysmally dilated left ventricle infrequently produces chest pain or fatal arrhythmia despite diffuse, severe coronary narrowing.     

Complications of the intraaortic balloon counterpulsation device: Clinical and morphologic observations in 45 necropsy patients

Of 45 patients who died after insertion of an intraaortic balloon assist device and who were studied at necropsy, 16 (36 percent) were found to have one or more complications (total 20) related to use of the device. The 20 complications consisted of dissection of the aorta or its distal branches, or both (9), arterial perforation (3), arterial thrombi (3), arterial emboli (3), limb ischemia (1) and local wound infection (1). Of the nine cases of arterial dissection, none were diagnosed or suspected before necropsy. Of the entire 20 complications, only 4 (20 percent) were suspected before death. Although the operating team frequently encountered no difficulty at the time of insertion of the device, 12 of the 20 complications were a direct result of insertion of the intraaortic balloon assist device. In two patients in whom insertion of the balloon caused dissection of the aorta, hemodynamic improvement occurred for 2 and 3 days, respectively, even though the “intraaortic” balloon (as well as the catheter) was not located in the true lumen of the aorta. Thus, clinical evaluation of complications related to use of the intraaortic balloon assist device underestimates their frequency. Most complications are consequences of insertion of the device, not consequences of its being in place.     

Origin of the right coronary artery from the left sinus of Valsalva and its functional consequences: Analysis of 10 necropsy patients

Clinical and necropsy findings are described in 10 patients in whom the right coronary artery arose from the left coronary sinus and then passed to the right atrioventricular (A-V) sulcus by coursing between the aorta and the pulmonary trunk. In 7 of the 10 patients, the coronary anomaly never caused symptoms of cardiac dysfunction. In the other three, all of whom died suddenly, the coronary anomaly was the only significant abnormality found at necropsy: One patient had recurring ventricular tachycardia, one had typical angina pectoris and, in one, sudden death was the initial manifestation of cardiac dysfunction. Review of previous angiographic studies during life of 31 patients reported to have origin of the right coronary artery from the left sinus of Valsalva indicated that 9 had symptoms of cardiac dysfunction in the absence of intraluminal coronary narrowing or associated noncoronary cardiac disease. Thus, origin of the right coronary artery from the left sinus may produce cardiac dysfunction that can be fatal.     

The floating heart or the heart too fat to sink: Analysis of 55 necropsy patients

Certain clinical and morphologic findings are described in 55 patients whose hearts at necropsy contained so much fat that they floated in water. The patients were 47 to 89 years old (mean 67). Symptomatic coronary heart disease was present in 28 (51%) and valvular heart disease (mitral stenosis) in 3 (5%). The heart at necropsy was enlarged (>350 g for women and >400 g for men) in 45 patients (82%). The mean heart weight for the 31 women was 470 g and for the 24 men, 515 g. In addition to the severe increase in fat in the atrioventricular sulci and over both ventricles, the amount of fat in the atrial septum was increased in all patients. In 14 patients (25%), the thickness of the atrial septum cephaled to the fossa ovale was ≥2 cm. Excessive fat in this location is called “lipomatous hypertrophy of the atrial septum.” Of the 16 patients (29%) with fatal acute myocardial infarction, 7 (44%) had rupture of either the left ventricular free wall or ventricular septum. The high frequency of cardiac rupture in these patients supports the contention that rupture during acute myocardial infarction is more common in the fatty than in the non-fatty heart.     

Quantitative comparison of extent of coronary narrowing and size of healed myocardial infarct in 33 necropsy patients with clinically recognized and in 28 with clinically unrecognized (“silent”) previous acute myocardial infarction

Clinical and necropsy observations are described in 61 patients with a healed transmural myocardial infarction, 33 with and 28 without a clinical history of acute myocardial infarction. There were no significant differences between the 2 groups of patients in mean age, sex, or frequency of angina pectoris, chronic congestive heart failure, systemic hypertension, sudden coronary death, or fatal acute myocardial infarction. Compared with the patients with clinically recognized acute myocardial infarction, the patients with clinically unrecognized (silent) infarction had a significantly (p < 0.05) higher incidence of diabetes mellitus (43 versus 15%), death from noncardiac causes (39 versus 9%), posterior (inferior) wall infarcts (82 versus 55%), and smaller infarcts (mean size 7 versus 17% of left ventricular wall). The patients with and without clinically recognized infarction had similar numbers of the 4 major coronary arteries severely (76 to 100% in cross-sectional area) narrowed (mean 2.8 versus $\text{2.9}\text{4.0}$ per patient), insignificant differences in incidence of severe narrowing of the left main coronary artery (18 versus 29%), similar overall percents of 5 mm segments of the 4 major coronary arteries severely narrowed (43 versus 42%), and similar percents of severely narrowed 5 mm segments of the right (46 versus 55%), left anterior descending (39 versus 33%), and left circumflex (41 versus 41%) coronary arteries.     

Cardiac amyloidosis causing cardiac dysfunction: Analysis of 54 necropsy patients

Clinical and morphologic findings are described in 54 necropsy patients (32 men [59%]) aged 21 to 97 years (mean 64) with cardiac amyloid deposits extensive enough to cause fatal cardiac dysfunction. Chronic congestive heart failure (CHF) was present in 46 (85%). The duration of CHF, known in 39 patients, ranged from 1 to 108 months (mean 18) and lasted ≤ 12 months in 25 patients (64%). All 8 patients without CHF died suddenly and unexpectedly. Systemic arterial pressures were recorded in the last 3 months of life in 43 patients: the peak indirect systolic pressure was ≤ 130 mm Hg and the diastolic pressure < 90 mm Hg in all. Electrocardiograms, recorded in the last 6 months of life in 40 patients, were abnormal in each: low voltage in 35 (63%); “myocardial infarction pattern” in 33 (83%); abnormal QRS axis in 29 (73%); arrhythmias in 29 (73% ); first, second, or third degree heart block in 28 (45%); and complete bundle branch block in 7 (18%). In 30 patients, the QRS amplitude in all 12 leads was measured: in the 15 men it ranged from 60 to 197 mm (mean 99) (10 mm = 1 mV) and in the 15 women from 58 to 199 mm (mean 109). Diagnosis of amyloidosis was established by biopsy of noncardiac organs or tissues during life in only 18 (33%) patients. During life the condition simulated hypertrophic cardiomyopathy in 5 patients, constrictive pericardial disease in 3, and coronary heart disease (because of angina pectoris) in 4.At necropsy, the hearts ranged in weight from 300 to 900 g (mean 554), and all but 1 had a “rubbery,” noncompliant consistency. In addition to their presence in myocardial interstitium (53 patients) and in intramural coronary arteries (54 patients), amyloid deposits were present grossly in mural endocardium in all 54 patients and in valvular endocardium in 46 (85% ). The cardiac ventricles were not dilated in 43 patients (80%), but both atria were dilated in all 54 patients. Intracardiac thrombi were present in 14 patients (26% ). Cardiac amyloidosis must be considered in any elderly patient with chronic CHF unassociated with chest pain when blood pressure is normal and the electrocardiogram discloses low voltage and a pattern of “healed myocardial infarction.”     

Right ventricular infarction complicating left ventricular infarction secondary to coronary heart disease: Frequency, location, associated findings and significance from analysis of 236 necropsy patients with acute or healed myocardial infarction

Right ventricular infarction associated with left ventricular infarction was identified by gross examination at necropsy in 33 (14 percent) of 236 patients with transmural myocardial infarction. Right ventricular infarction occurred exclusively as a complication of posterior left ventricular infarction. Associated right ventricular infarction occurred in none of the 97 patients with isolated anterior wall infarction of the left ventricle, but in 33 (24 percent) of the 139 patients with posterior left ventricular infarction. Transmural infarction of the posterior ventricular septum was an additional prerequisite for right ventricular infarction. Of the 139 patients with infarction of the posterior left ventricular wall, 74 had no transmural infarction of the ventricular septum and none of these 74 had associated right ventricular infarction. In contrast, of the 65 patients with infarction of the posterior left ventricular wall and transmural infarction of the ventricular septum, 33 (50 percent) had associated right ventricular infarction.

Among the 33 patients with right ventricular infarction, the infarct was limited to the posterior right ventricular free wall in 27 (82 percent); in the other 6 patients (18 percent) it extended to involve the anterolateral right ventricular free wall. Among patients with a posterior left ventricular infarct, those with a right ventricular infarct had right ventricular dilatation nearly three times (P < 0.05) more frequently than the patients without a right ventricular infarct. Comparison of the same two groups disclosed no differences in the patients' age, sex, extent of coronary arterial luminal narrowing, right ventricular hypertrophy, right ventricular thrombi or duration of symptoms of myocardial ischemia.

Hemodynamic data in four patients with a right ventricular infarct disclosed previously reported characteristic hemodynamics of right ventricular infarction in only one patient. Recognition of right ventricular infarction is important because it implies specific therapy, namely, aggressive volume administration. Clinical evidence of posterior left ventricular infarction and right ventricular dilatation should arouse strong suspicion of associated right ventricular infarction.     

Sudden death in prinzmetal's angina with coronary spasm documented by angiography: Analysis of three necropsy patients

Clinical and necropsy findings are described in three patients who had angina pectoris at rest, S-T segment elevation on electrocardiography during chest pain, coronary arterial spasm on angiography and sudden death. Although significant “fixed” coronary narrowing (that is, narrowing due to atherosclerotic plaques) was appreciated by angiography in only one of the three patients, necropsy disclosed in all three patients severe fixed coronary narrowings involving particularly the artery in which spasm had been demonstrated during life. Additionally, examination of each 5-mm long segment of the coronary artery that had been spastic during life (two patients) disclosed several focally spastic segments at necropsy, indicating that spasm persisted after death. Although most previously described necropsy patients with Prinzmetal's angina had some fixed coronary narrowing, underlying fixed narrowing may be difficult to identify angiographically as demonstrated by the three patients in this study.     

Coronary artery disease in the hurler syndrome: Qualitative and quantitative analysis of the extent of coronary narrowing at necropsy in six children

The amount of cross-sectional area luminal narrowing in each 5 mm segment of each of the four major epicardial coronary arteries (right, left main, left anterior descending and left circumflex) is described at necropsy in six children (aged 3 to 16 years) with the Hurler syndrome. In five patients at least one of the four major coronary arteries was narrowed 76 to 100 percent, and in four of these five patients all four major arteries were narrowed to this extent. Of the 24 major coronary arteries in the six patients, 17 (71 percent) were narrowed 76 to 100 percent at some point. A total of 182 segments were examined from the 24 major coronary arteries, and the extent of narrowing was as follows: 96 to 100 percent, 14 (8 percent); 76 to 95 percent, 61 (34 percent); 51 to 75 percent, 59 (32 percent); 26 to 50 percent, 39 (21 percent) and 0 to 25 percent, 9 (5 percent). By applying a score of 1 to 4 to each 5 mm segment according to its category of narrowing (1 = 0 to 25 percent; 2 = 26 to 50 percent; 3 = 51 to 75 percent and 4 = 76 to 100 percent), the 182 segments had a total score of 570 and a mean score of 3.2, indicating that each segment was narrowed an average of about 67 percent in cross-sectional area. Thus, narrowing of the major epicardial coronary arteries at necropsy is usually diffuse and severe in the Hurler syndrome, which is the cause of the most severe coronary narrowing in childhood.     

Sudden coronary death: comparison of patients with to those without coronary thrombus at necropsy

Among 70 victims of sudden coronary death (SCD), certain clinical and morphologic findings in the 13 with a coronary thrombus are compared with the findings in 57 victims without a coronary thrombus. The 13 with a thrombus were younger than those without (mean age 43 vs 51 years, p less than 0.02); had a lower mean percent of cross-sectional area (XSA) narrowing by plaque at the site of maximal coronary stenosis (89% vs 95%, p less than 0.01); and had a higher mean percent of 5-mm segments of the 4 major epicardial coronary arteries minimally narrowed (0 to 25% in XSA) by plaque (27% vs 19%, p less than 0.001). No differences occurred in the 2 groups with regard to sex, previous angina pectoris or clinical acute myocardial infarction, healed myocardial infarction at necropsy, mean heart weight, number of major coronary arteries narrowed 76 to 100% in XSA by atherosclerotic plaque, or the mean percent of 5-mm segments of the 4 major epicardial coronary arteries narrowed 76 to 100% in XSA by atherosclerotic plaque. Thus, coronary thrombi are infrequent in victims of SCD, and when observed, their significance is uncertain because victims of SCD without coronary thrombi have similar amounts of severe coronary narrowing.     

Late (5 to 132 months) clinical and hemodynamic results after either tricuspid valve replacement or anuloplasty for ebstein's anomaly of the tricuspid valve

Late clinical and hemodynamic observations are described in 6 patients who had either tricuspid valve anuloplasty (TVA) (2 patients) or tricuspid valve replacement (TVR) (4 patients) 5 to 132 months earlier for Ebstein's anomaly of the tricuspid valve unassociated with right ventricular outflow obstruction. Of the 6 patients, 4 had improved postoperatively by 1 New York Heart Association functional class and 2 had improved by 2 functional classes. The cardiothoracic ratio decreased 5 to 12 months after either TVR or TVA in all 6 patients (from a mean of 0.72 to 0.62). Repeat cardiac catheterization 5 to 12 months after TVA or TVR disclosed that the right atrial mean pressure had increased from a median of 4.0 to 10.5 mm Hg (p = 0.05); the right ventricular peak systolic pressure had increased from 19.0 to 31.5 mm Hg (p = 0.02); the right ventricular end-diastolic pressure had increased from 5.0 to 9.0 mm Hg (p = 0.05); the systemic arterial peak systolic pressure had increased from 115 to 123 mm Hg (p = 0.03); and the cardiac index had increased (in all 4 patients in whom both pre- and postoperative values were available) from 1.7 to 2.9 liters/min/m² (p = 0.06). Thus, the tricuspid valve operations in our 6 patients with Ebstein's anomaly were associated with a decrease in symptoms of cardiac dysfunction, a decrease in cardiac size, an increase in cardiac index and an increase in right ventricular and right atrial pressures. The elevation of the right atrial pressures postoperatively may have resulted from increased right ventricular filling pressures, persistent tricuspid regurgitation or bioprosthetic stenosis.     

Amount of narrowing by atherosclerotic plaque in 44 nonbypassed and 52 bypassed major epicardial coronary arteries in 32 necropsy patients who died within 1 month of aortocoronary bypass grafting

In 32 necropsy patients who died within 30 days of an aortocoronary bypass operation performed for relief of angina pectoris, the lumens in 42 (95 percent) of 44 nonbypassed and in 52 (100 percent) or 52 bypassed arteries were narrowed 76 to 100 percent in cross-sectional area by atherosclerotic plaque. Of 616 five mm segments of the 44 nonbypassed arteries examined histologically, 292 (47 percent) were narrowed 76 to 100 percent in cross-sectional area by atherosclerotic plaque; of 728 segments examined in the 52 bypassed arteries, 375 (52 percent) were similarly narrowed. Thirty-two (73 percent) of the 44 nonbypassed coronary arteries (in 23 patients) had been judged to be narrowed 50 percent or less in diameter on preoperative coronary angiography, but at necropsy 31 (97 percent) of these arteries were narrowed 76 to 100 percent in cross-sectional area and the other artery was narrowed 51 to 75 percent. Thus, significant amounts of atherosclerotic plaque tend to be present at necropsy in all three major coronary systems of patients with angina pectoris who die early after an aortocoronary bypass operation.     

Amounts of coronary arterial narrowing by atherosclerotic plaques in clinically isolated,chronic, pure aortic regurgitation: Analysis of 37 necropsy patients older than 30 years

The degree of cross-sectional area (XSA) narrowing by atherosclerotic plaque in each of the 4 major epicardial coronary arteries (right, left main, left anterior descending and left circumflex) was determined at necropsy in 37 patients (30 men and 7 women) aged 34 to 77 years (mean 54) with severe, isolated, chronic, pure aortic regurgitation (AR). In 7 patients (19%), ≥ 1 major coronary artery was narrowed 76 to 100% in XSA at some point. Of the 148 major coronary arteries examined in the 37 patients, 12 arteries (8% ) were narrowed at some point 76 to 100% in XSA. Each of the 148 major coronary arteries were divided into 5-mm-long segments (average 53 per patient) and a histologic section from each segment was examined. Of the 1,977 segments, 1,087 were narrowed 0 to 25%, 669 (34%) 26 to 50%, 170 (9%) 51 to 75%, 48 (2%) 76 to 95% and 3 (0.001%) 96 to 100%. The average amount of XSA narrowing by atherosclerotic plaque per segment was about 28%. Of the 37 patients, 9 had had angina pectoris, 2 of whom had significant (> 75% XSA reduction) coronary narrowing; 2 other patients had had acute myocardial infarction clinically, 1 of whom had significant coronary narrowing at necropsy. Thus, in general, the amount of coronary narrowing in our 37 adults with severe, pure, isolated, chronic AR was relatively mild.     

Severe aortic regurgitation from systemic hypertension (without aortic dissection) requiring aortic valve replacement: Analysis of four patients

Clinical and morphologic observations are described in four patients who had severe aortic regurgitation from severe systemic hypertension un-associated with aortic dissection; each patient underwent aortic valve replacement. Although aortic regurgitation of minimal or mild degree is well recognized to occur in patients with systemic hypertension, severe degrees of aortic regurgitation are rare in such patients; aortic valve replacement in such patients has not previously been reported. Why these four patients had such severe aortic regurgitation was not determined. Although systemic hypertension is rarely a cause, it nevertheless must be added to the list of causes of severe pure aortic regurgitation.     

Status of the major epicardial coronary arteries 80 to 150 days after percutaneous transluminal coronary angioplasty. Analysis of 3 necropsy patients

Certain clinical and necropsy cardiac findings are described in 3 men who had percutaneous transluminal coronary angioplasty (PTCA) of the left anterior descending (LAD) coronary artery 80, 90, and 150 days before sudden death. Each patient had a decrease in the mean transstenotic coronary gradient (17, 38, and 43 mm Hg) and an angiographic increase in the LAD luminal diameter (55, 60, and 65%). At necropsy, the LAD coronary artery in the area of the PTCA in each patient was narrowed 76 to 95% in cross-sectional area by atherosclerotic plaques. No cracks in plaques or other lesions which may have resulted from the PTCA procedure were identified histologically in the LAD coronary artery of any patient.     

Sudden coronary death: relation of amount and distribution of coronary narrowing at necropsy to previous symptoms of myocardial ischemia, left ventricular scarring and heart weight

The amount and distribution of coronary arterial narrowing by atherosclerotic plaque at necropsy is described in 70 victims, aged 22 to 81 years (mean 50), of sudden coronary death. Of 3,484 five-millimeter segments examined (mean 50 per patient) from the 4 major (left main, left anterior descending, left circumflex and right) coronary arteries, 950 (27%) were narrowed 76 to 100% in cross-sectional area (XSA), 1,127 (32%), 51 to 75%; 689 (20%), 26 to 50%; and 718 (21%), 0 to 25%. More extensive severe narrowing occurred in the proximal than in the distal halves of the left anterior descending, left circumflex and right coronary arteries. Comparison between the 31 previously symptomatic victims (angina pectoris or a clinical acute myocardial infarction or both) with the 39 victims who had previously been asymptomatic disclosed a significantly higher mean percent of severely narrowed (76 to 100% XSA) 5-mm segments (30 vs 25%, p less than 0.005) and lower mean percent of minimally narrowed (0 to 25% XSA) segments in the symptomatic group (15 vs 25%, p less than 0.001). Comparison of the 31 patients who had a healed myocardial infarction at necropsy with the 39 patients who did not disclosed a higher mean percent of 5-mm segments narrowed 76 to 100% in XSA (33 vs 24%, p less than 0.001) and a lower mean percent of segments narrowed minimally in those with a left ventricular scar (13 vs 26%, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Sucking action of the left ventricle: Demonstration of a physiologic principle by a gunshot wound penetrating only the right side of the heart

This report describes a man who died after a gunshot wound that entered the right atrium and exited from the right ventricle without entering the cardiac septa or the left side of the heart. At necropsy, the left atrial appendage was found to be inverted and invaginated into the mitral orifice. The invagination of the left atrial appendage is viewed as anatomic evidence that a negative left ventricular pressure was created as the left ventricular volume rapidly decreased as a result of right-sided cardiac exsanguination. Previously reported experiments in animals demonstrating the sucking (negative pressure) action of the left ventricle during ventricular diastole are summarized. The prerequisite for creation of a negative pressure in the ventricles during diastole is an extreme diminution in left ventricular volume, in this case as a result of right-sided cardiac bleeding. Only a vacuum effect of the left ventricle during diastole can explain the inversion and invagination of the left atrial appendage in this patient.