Morphologic comparison of frequency and types of acute lesions in the major epicardial coronary arteries in unstable angina pectoris, sudden coronary death and acute myocardial infarction

The frequency and type of acute lesions in the four major (right, left main, left anterior descending, left circumflex) epicardial coronary arteries were examined at necropsy in 14 patients with unstable angina pectoris, 21 patients with sudden coronary death and 32 patients with a fatal first acute myocardial infarction. None of the 67 patients had a grossly visible left ventricular scar (healed myocardial infarct) and only the group with acute myocardial infarction had left ventricular myocardial necrosis. Although the frequency of intraluminal thrombus was similar in patients with unstable angina (29%) and sudden death (29%) and significantly lower than in those with acute infarction (69%) (p = 0.02), the thrombus in the patients with unstable angina and sudden death consisted almost entirely of platelets and was nonocclusive, whereas the thrombus in the group with acute infarction consisted almost entirely of fibrin and was occlusive. The frequency of plaque rupture was insignificantly different in the groups with unstable angina (36%) and sudden death (19%), and was significantly lower than in the group with acute infarction (75%) (p = 0.02). The frequency of plaque hemorrhage was insignificantly different in the groups with unstable angina (64%) and sudden death (38%) and was significantly lower than in the group with acute infarction (90%) (p = 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)     

Amounts of coronary arterial narrowing by atherosclerotic plaque at necropsy in patients with lower extremity amputation.

In 26 patients (mean age at death 68 +/- 9 years) who had undergone amputation (at mean age 63 +/- 12 years) of 1 or both lower extremities due to severe peripheral arterial atherosclerosis, the amounts of narrowing at necropsy in the 4 major (left main, left anterior descending, left circumflex, and right) epicardial coronary arteries were determined. During life, 15 of the 26 patients (58%) had symptoms of myocardial ischemia: angina pectoris alone in 1, acute myocardial infarction alone in 5, and angina and/or infarction plus congestive heart failure or sudden coronary death in 9. Twelve of the 26 patients (42%) died from consequences of myocardial ischemia: acute myocardial infarction in 5, sudden coronary death in 3, chronic congestive heart failure in 3, and shortly after coronary bypass surgery in 1. Grossly visible left ventricular necrosis or fibrosis, or both, was present in 21 patients (81%). Of the 26 patients, 24 (92%) had narrowing 76 to 100% in cross-sectional area of 1 or more major coronary arteries by atherosclerotic plaque. The mean number of coronary arteries per patient severely (> 75%) narrowed was 2.3 +/- 1.0/4.0. Of the 104 major coronary arteries in the 26 patients, 60 (58%) were narrowed > 75% in cross-sectional area by plaque. The 4 major coronary arteries in the 26 patients were divided into 5-mm segments and a histologic section, stained by the Movat method, was prepared from each segment.(ABSTRACT TRUNCATED AT 250 WORDS)     

Qualitative and quantitative comparison of amounts of narrowing by atherosclerotic plaques in the major epicardial coronary arteries at necropsy in sudden coronary death, transmural acute myocardial infarction, transmural healed myocardial infarction and unstable angina pectoris

The amounts of narrowing of the 4 major (left main, left anterior descending, left circumflex and right) epicardial coronary arteries by atherosclerotic plaques were compared in 4 subsets of coronary patients. Of the 129 patients studied at necropsy, an average of 2.7 of the 4 arteries was narrowed greater than 75% in cross-sectional area at some point (0.7/4 in controls), and the group with unstable angina pectoris (3.2/4) had more narrowing than did the groups with sudden coronary death (2.8/4), acute myocardial infarction (2.7/4) and healed myocardial infarction (2.3/4). Each of the 4 major epicardial coronary arteries was divided into 5-mm long segments and a histologic section was prepared and stained by the Movat method of each of the 6,461 segments in the 129 patients and in the 1,849 segments in the 40 control subjects. In the 129 patients, 35% of the 5-mm segments were narrowed 75 to 100% in cross-sectional area (3% in controls) and the group with unstable angina had the highest percent (48%) of segments severely narrowed compared to the groups with sudden coronary death (36%), acute myocardial infarction (34%) and healed myocardial infarction (31%). Thus, of the 4 subsets of patients with fatal coronary artery disease studied at necropsy, those with unstable angina pectoris had the most severe and extensive coronary atherosclerosis.     

Diffuse extent of coronary atherosclerosis in fatal coronary artery disease

In 4 subsets of patients with coronary artery disease, the amounts of narrowing of the 4 major epicardial coronary arteries were compared (left main, left anterior descending, left circumflex and right) by atherosclerotic plaques. Among 129 patients studied at necropsy, an average of 2.7 of the 4 arteries were narrowed greater than 75% in cross-sectional area at some point; in control subjects, narrowing was seen in an average of 0.7 arteries. Patients with unstable angina pectoris had a greater incidence of narrowing (3.2 arteries) than did patients with sudden coronary death (2.8), acute myocardial infarction (MI) (2.7) or healed MI (2.3). Each of the 4 major arteries was divided into segments 5 mm in length, and histologic sections were prepared and stained by the Movat method. A total of 6,461 segments were analyzed from the 129 patients and 1,849 from the 40 controls. In the 129 patients, 35% of the 5-mm segments were narrowed 75 to 100% in cross-sectional area (compared with 3% in control subjects). The group with unstable angina had the highest percentage (48%) of severely narrowed segments compared with the groups with sudden coronary death (36%), acute (34%) and healed MI (31%). Only 8% of the 6,461 segments were narrowed less than or equal to 25% in cross-sectional area, and virtually none of the 6,461 segments was normal; thus, 92% of the coronary segments were narrowed greater than 25% in cross-sectional area by atherosclerotic plaque alone. Among patients with fatal coronary artery disease studied at necropsy, therefore, the atherosclerotic process is severe and diffuse in the major epicardial coronary arteries.     

Degrees of coronary arterial narrowing at necropsy in men with large fusiform abdominal aortic aneurysm.

In 27 patients (mean age at death 72 +/- 9 years) with abdominal aortic aneurysm (AAA) > or = 5.0 cm in its widest transverse diameter, the amounts of narrowing at necropsy in the 4 major (left main, left anterior descending, left circumflex, and right) epicardial coronary arteries were determined. During life, 12 of the 27 patients (44%) had symptoms of myocardial ischemia: angina pectoris alone in 2, acute myocardial infarction alone in 3, angina pectoris and acute myocardial infarction in 5, and sudden coronary death in 2. Ten of the 27 patients (37%) died from consequences of myocardial ischemia. Six (22%) died from rupture of the AAA. Grossly visible left ventricular necrosis or fibrosis, or both, was present in 15 patients (56%). Of the 27 patients, 23 (85%) had narrowing 76 to 100% in cross-sectional area of 1 or more major coronary arteries by atherosclerotic plaque. The mean number of coronary arteries per patient severely (> 75%) narrowed was 2.0 +/- 1.3/4.0. Of the 108 major coronary arteries in the 27 patients, 55 (51%) were narrowed > 75% in cross-sectional area by plaque. The 4 major coronary arteries in the 27 patients were divided into 5-mm segments and a histologic section, stained by the Movat method, was prepared from each segment. The mean percentages of the resulting 1,475 five-mm segments narrowed in cross-sectional area 0 to 25%, 26 to 50%, 51 to 75%, 76 to 95% and 96 to 100% were 17, 37, 28, 15 and 3%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Treatment of stable angina.

Severe atherosclerotic narrowing of one or more coronary arteries is responsible for myocardial ischemia and angina pectoris in most patients with stable angina pectoris. The coronary arteries of patients with stable angina also contain many nonobstructive plaques, which are prone to fissures or rupture resulting in presentation of acute coronary syndromes (unstable angina, myocardial infarction, sudden ischemic death). In addition to symptomatic relief of symptoms and an increase in angina-free walking time with antianginal drugs or revascularization procedures, the recent emphasis of treatment has been to reduce adverse clinical outcomes (coronary death and myocardial infarction). The role of smoking cessation, aspirin, treatment of elevated lipids, and treatment of high blood pressure in all patients and of beta-blockers and angiotensin-converting enzyme inhibitors in patients with diminished systolic left ventricular systolic function in reducing adverse outcomes has been well established. What is unknown, however, is whether any anti-anginal drugs (beta-blockers, long-acting nitrates, calcium channel blockers) effect adverse outcomes in patients with stable angina pectoris. Recent trials evaluated the usefulness of suppression of ambulatory ischemia in patients with stable angina pectoris, but it remains to be established whether suppression of ambulatory myocardial ischemia with antianginal agents or revascularization therapy is superior to pharmacologic therapy targeting symptom relief. Patients who have refractory angina despite optimal medical treatment and are not candidates for revascularization procedures may be candidates for newer techniques of transmyocardial revascularization, enhanced external counterpulsation, spinal cord stimulation, or sympathectomy. The usefulness of these techniques, however, needs to be confirmed in large randomized clinical trials.     

Mode of death, frequency of healed and acute myocardial infarction, number of major epicardial coronary arteries severely narrowed by atherosclerotic plaque, and heart weight in fatal atherosclerotic coronary artery disease: analysis of 889 patients studied at necropsy

Mode of death, frequency of a healed or an acute myocardial infarct, or both, number of major epicardial coronary arteries severely narrowed by atherosclerotic plaque, and heart weight were studied at necropsy in 889 patients 30 years of age or older with fatal atherosclerotic coronary artery disease. No patient had had a coronary bypass operation or coronary angioplasty. The 889 patients were classified into four major groups and each major group was classified into two subgroups: 1) acute myocardial infarct without (306 patients) or with (119 patients) a healed myocardial infarct; 2) sudden out of hospital death without (121 patients) or with (118 patients) a healed myocardial infarct; 3) chronic congestive heart failure with a healed myocardial infarct without (137 patients) or with (33 patients) a left ventricular aneurysm; and 4) sudden in-hospital death without (20 patients) or with (35 patients) unstable angina pectoris. The mean age of the 687 men (77%) was 60 +/- 11 years, and of the 202 women (23%), 68 +/- 13 years (p = 0.0001). Although men included 77% of all patients, they made up approximately 90% of the out of hospital (nonangina) sudden death group. The frequency of systemic hypertension and angina pectoris was similar in each of the four major groups. The frequency of diabetes mellitus was least in the sudden out of hospital death group and similar in the other three major groups. The mean heart weight and the percent of patients with a heart of increased weight were highest in the chronic congestive heart failure group; values were lower and similar in the other three major groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sudden coronary death

Many reports have described the amounts of atherosclerotic plaque in victims of sudden coronary death, defining the number of coronary arteries narrowed at some point greater than 75% in cross-sectional area (XSA). In order to quantitate more precisely the amount and distribution of plaque, 70 victims of sudden coronary death aged 22-81 years (mean 50) were studied. The four major epicardial coronary arteries (left main, left anterior descending, left circumflex, and right) from each of 70 victims were cut into 5-mm segments (average 50 per patient) and a histologic section prepared from each segment. The amount of luminal narrowing by plaque was categorized into five groups (0-25%, 26-50%, 51-75%, 76-95%, 96-100%). Of 3,484 five-mm segments, 950 (27%) were narrowed 76-100% in XSA. Comparison of 31 previously symptomatic victims (angina pectoris and/or myocardial infarction) to 39 victims who had been asymptomatic disclosed a higher mean percent of severely narrowed segments (30% vs. 25%, p = less than 0.005) and a lower mean percent of minimally narrowed segments in the symptomatic group. Comparison of the 31 patients with a healed myocardial infarction at necropsy with 39 patients with no left ventricular scar disclosed a higher mean percent of segments severely narrowed (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)     

Morphologic findings in sudden coronary death: a comparison of those with and those without previous symptoms of myocardial ischemia

In this article, the amount and distribution of coronary arterial narrowing by atherosclerotic plaque at necropsy are described in 70 victims of sudden coronary death. Of 3484 5-mm segments examined from the four major coronary arteries, 950 (27 per cent) were narrowed 76 to 100 per cent in cross-sectional area by atherosclerotic plaque; 1127 (32 per cent) were narrowed 51 to 75 per cent; 689 (20 per cent) were narrowed 26 to 50 per cent; and 718 (21 per cent) were narrowed 0 to 25 per cent. More extensive severe narrowing occurred in the proximal halves compared with the distal halves of the left anterior descending and left circumflex coronary arteries. Comparison between the 31 previously symptomatic victims (either angina pectoris and/or a clinical acute myocardial infarction) and the 39 victims who had previously been asymptomatic disclosed a significantly higher mean percentage of severely narrowed 5-mm segments and a lower mean percentage of minimally narrowed segments in the symptomatic group.     

The coronary arteries and left ventricle in clinically isolated angina pectoris: a necropsy analysis.

Certain clinical and morphologic observations are described in 27 patients with severe isolated angina pectoris of either the stable (five patients) or the unstable form (22 patients). Twenty-four patients died during or shortly after cardiac operations designed to relieve angina pectoris and three died during cardiac catheterization. During life none had had clinical evidence of acute myocardial infarction or congestive cardiac failure. At necropsy, each had diffuse, extensive coronary atherosclerosis with severe luminal narrowing: the lumens of at least two, an average of three, of the four major epicardial coronary arteries were narrowed greater than 75% in cross-sectional area by old atherosclerotic plaques. Despite the severe coronary narrowing, there was little myocardial damage. Left ventricular scarring (excluding papillary muscle) was observed grossly in only 14 (52%) of the 27 patients and in each it involved only a small portion of myocardial wall. The left ventricular cavity was of normal size in all except two patients. The hearts were of normal weight in 15 (56%) patients, and the average increase above the upper range of normal for the other 12 hearts was 19%. Thus, clinically isolated, severe angina pectoris is associated with severe, diffuse luminal narrowing but relatively little myocardial damage.     

Intracoronary temperature in patients with coronary artery disease

OBJECTIVES: Measurements of changes in plaque temperature may predict plaque rupture. The present study investigated variations in temperature within the atherosclerotic coronary artery using a pressure guide wire with thermal sensor (dual sensor guide wire). METHODS AND RESULTS: Seventy-seven patients (78 lesions), who had no significant lesion at the orifice of the culprit coronary artery, were studied. The patients had acute myocardial infarction (22 patients), unstable angina pectoris (20 patients), and stable angina pectoris (35 patients). The thermal sensor was calibrated at the orifice of the coronary artery, and then inserted into the culprit coronary artery. deltaT was defined as the difference between the intracoronary temperature at the position of the pressure gradient and at the orifice. deltaT was higher in patients with acute myocardial infarction and unstable angina pectoris than in patients with stable angina pectoris (0.09 +/- 0.07 and 0.07 +/- 0.07 vs 0.03 +/- 0.04 degrees C, p < 0.001, p = 0.02, respectively). There was no significant difference in deltaT between patients with acute myocardial infarction and unstable angina pectoris (p = 0.48). Patients with acute myocardial infarction and unstable angina pectoris showed a significant relationship between deltaT and C-reactive protein (r = 0.59, p = 0.0004). CONCLUSIONS: The variations in intracoronary temperature of the culprit coronary arteries in patients with acute coronary syndrome were higher than those in patients with stable angina pectoris. These variations may be related to inflammation of vulnerable plaque.     

Morphologic features of unstable atherothrombotic plaques underlying acute coronary syndromes

Unstable angina appears to be a good clinical marker for rapidly progressing coronary artery disease. Pathologically, an unstable atherothrombotic coronary lesion, represented by a raised atherosclerotic plaque with ruptured surface causing variable degree of hemorrhage into the plaque and luminal thrombosis (rapid plaque progression), usually is present in patients at autopsy after a period of unstable angina. The thrombus at the rupture site may be mural and limited (just sealing the rupture) or occlusive, depending on the degree of preexisting atherosclerotic stenosis. An occlusive thrombus is seldom seen over ruptured plaques causing less than 75% stenosis (histologic cross-sectional area reduction), but it is found with increasing frequency when severity of stenosis increases beyond 75%. Most occlusive thrombi have a layered structure with thrombus material of differing age indicating an episodic growth by repeated mural deposits, and microemboli/microinfarcts are frequently found in the myocardium downstream to coronary thrombi, indicating intermittent thrombus fragmentation with peripheral embolization. Such a "dynamic thrombosis" (with or without a concomitant focal vasospastic phenomenon) at the site of an unstable (ruptured) atherosclerotic lesion obviously may lead to the other thrombus-related acute coronary events: myocardial infarction or sudden death. Accordingly, progression of unstable angina to myocardial infarction or sudden death should, in principle, be preventable by the correct timing of current available therapies aimed to prevent or eliminate (1) the chronic atherosclerotic obstruction, (2) the acute plaque disruption, (3) luminal thrombosis, and (4) vasospasm.     

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.     

Sudden cardiac death: a diversity of causes with focus on atherosclerotic coronary artery disease

There are many causes of sudden cardiac death, and the younger the patient the more diverse the cause. Among persons dying suddenly in the Western World atherosclerotic coronary artery disease is the most common. This group might best be called atherosclerotic sudden coronary death. This article summarizes a previously published necropsy study by Warnes and Roberts of 70 victims aged 22 to 81 years (mean 50) of sudden coronary death. Of 3,484 five-mm coronary 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 by plaque; 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 compared with the distal halves to the left anterior descending, left circumflex and right coronary arteries. Comparison between the 31 previously symptomatic victims (either angina pectoris and/or a clinical acute myocardial infarction) to the 39 victims who had previously been asymptomatic disclosed a significantly higher mean percent of severely (76 to 100% in cross-sectional area) narrowed 5-mm segments (30 vs 25% [p less than 0.0051]) and a lower mean percent of minimally (0 to 25%) narrowed segments in the symptomatic group (15 vs 25%, p less than 0.001). Thus, the major coronary arteries at necropsy in victims of sudden coronary death are diffusely involved by atherosclerotic plaque and in nearly one-third of the lengths of the major arteries the lumens are narrowed greater than 75% in cross-sectional area by plaque.(ABSTRACT TRUNCATED AT 250 WORDS)     

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)     

Severe atherosclerotic coronary artery disease, healed myocardial infarction and chronic congestive heart failure: analysis of 81 patients studied at necropsy

Observations are described in 81 necropsy patients (aged 29 to 91 years [mean 62]; 77 [95%] men) with severe congestive heart failure (CHF) more than 3 months in duration, left ventricular (LV) transmural scar and greater than 75% cross-sectional area narrowing by atherosclerotic plaque of 1 or more of the 4 major epicardial coronary arteries. The duration of symptoms from initial onset of acute myocardial infarction (59 patients) or CHF (18 patients) or angina pectoris (2 patients) to death ranged from 0.5 to 18 years (mean 7.1) (2 unknown). Angina pectoris occurred at some time, however, in 31 patients (38%). Cause of death was CHF in 48 patients (59%), sudden (arrhythmia) in 16 (20%), acute myocardial infarction in 11 (14%), and emboli in 6 (7%). The heart weight ranged from 410 to 800 g (mean 585). Left or right ventricular thrombi or both occurred in 37 patients (46%), only 4 (10%) of whom had systemic emboli; of the 44 patients without intracardiac thrombi, none had any form of emboli. The severity of coronary narrowing was variable. In 24 patients (30%) only 1 artery was narrowed greater than 75% in cross-sectional area; in 22 patients (27%), 2 arteries were so narrowed; in 32 patients (39%), 3 arteries; and in 3 patients (4%), 4 arteries. The size of the LV scar also varied. Of the 81 patients, 58 (72%) had large scars (involving greater than 40% of the LV wall); 10 (12%) had moderate-sized scars (6 to 40% of the LV wall); and 13 (16%) had small scars (less than or equal to 5% of the LV wall).(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Rupture of a left ventricular papillary muscle during acute myocardial infarction: analysis of 22 necropsy patients

Certain clinical and cardiac morphologic findings are described in 22 patients, aged 45 to 80 years (mean 64) (15 men [68%]), in whom rupture of a papillary muscle occurred during acute myocardial infarction. In most, the acute infarction associated with papillary muscle rupture was a first coronary event (only 18% had a myocardial scar consistent with prior infarction and 29% had angina pectoris). The posteromedial papillary muscle, presumably because of its more tenuous blood supply, ruptured almost three times more frequently than the anterolateral one (73 and 27%, respectively). Quantitative examination of the amounts of narrowing by atherosclerotic plaque in each of the four major epicardial coronary arteries (right, left main, left anterior descending and left circumflex) disclosed less narrowing in the patients with rupture than in the patients with fatal acute myocardial infarction unassociated with rupture. Of the 519 five mm sections of coronary artery examined (11 patients), only 68 sections (13%) were narrowed greater than 75% in cross-sectional area compared with 34% of 1,403 sections from 27 patients with fatal myocardial infarction without rupture.     

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.     

Angina pectoris, myocardial infarction and sudden cardiac death with normal coronary arteries: a clinicopathologic study of 9 patients with progressive systemic sclerosis

The syndrome of angina pectoris or acute myocardial infarction without obstructive coronary artery disease has been the subject of much interest. We studied nine autopsied patients with progressive systemic sclerosis and evidence of ischemic heart disease but morphologically normal coronary arteries. Three patients had angina pectoris and three others chest pains of unknown etiology, six had ventricular arrhythmias, four had clinically suspected acute myocardial infarction, and eight had sudden cardiac death. At autopsy extensive focal myocardial necrosis was present in seven patients and myocardial scarring in all nine, but all patients had widely patent intramural and extramural coronary arteries. The finding of contraction band myocardial necrosis in seven of the eight patients who experienced sudden death suggests that the myocardial damage was a consequence of reperfusion of focally nonperfused myocardium, and thus due to a myocardial Raynaud's phenomenon. Patients with PSS may provide a model of spasm of intramyocardial vessels causing angina pectoris or myocardial infarction with morphologically normal coronary arteries.