Jay M. Kalan

Comparison of coronary and myocardial morphologic findings in patients with and without thrombolytic therapy during fatal first acute myocardial infarction

The hearts of 61 patients (39 men aged 64 +/- 11 years) who died from 5 hours to 42 days (median 3 days) after a fatal first acute myocardial infarction without having undergone percutaneous transluminal coronary angioplasty or coronary bypass surgery were studied to compare clinical and cardiac morphologic features of patients receiving thrombolytic therapy with tissue-plasminogen activator (t-PA) to those not receiving thrombolytic therapy. Comparison of findings in the 23 patients who received t-PA intravenously 3 +/- 1 hours after onset of symptoms, with the 38 patients who did not, showed similar baseline characteristics with respect to: age, gender, history of hypertension; location of the infarct; heart weight; severity and numbers of coronary arteries narrowed; and frequencies of plaque rupture, plaque hemorrhage and coronary thrombi. Among the patients receiving t-PA, however, there was a greater frequency of platelet-rich (fibrin-poor) thrombi in the infarct-related coronary arteries (6 of 11 vs 4 of 25 thrombi; p = 0.02), more nonocclusive than occlusive thrombi (6 of 11 vs 4 of 25 thrombi; p = 0.02), and a lower frequency of myocardial rupture (left ventricular free wall or ventricular septum) (5 of 23 [22%] vs 18 of 38 [46%]; p = 0.045).

Cardiac morphologic findings in patients with acute myocardial infarction treated with recombinant tissue plasminogen activator

The hearts of 52 patients (aged 61 +/- 11 years, 34 men) who participated in the Thrombolysis in Myocardial Infarction (TIMI) Study and died from 5 hours to 260 days (median 2.7 days) after onset of chest pain were studied. One heart became available at cardiac transplantation. Of the 52 patients, 38 received recombinant tissue plasminogen activator (rt-PA) not followed by percutaneous transluminal coronary angioplasty (PTCA) or coronary artery bypass grafting (CABG). Eight had PTCA, and 6 had CABG. The infarcts were hemorrhagic by gross inspection (with histologic confirmation) in 23 patients, nonhemorrhagic in 20, not visible grossly in 2 and, in 7, there was no myocardial necrosis by either gross or histologic examination.(ABSTRACT TRUNCATED AT 250 WORDS)

The heart in fatal unstable angina pectoris

Compared to patients with sudden coronary death and acute myocardial infarction, relatively little morphologic data has been reported in patients with unstable angina pectoris. This article reviews necropsy data collected from one laboratory on unstable angina pectoris. From these data, several observations are appropriate: (1) Patients with unstable angina as a group have more coronary narrowing by atherosclerotic plaque than do patients with sudden coronary death or acute or healed myocardial infarction. (2) Patients with unstable angina have a much higher frequency of severe narrowing of the left main coronary artery than do patients in other coronary subsets. (3) The coronary atherosclerotic plaques in unstable angina consist primarily of fibrous tissue, and they are more similar to those found in patients with sudden coronary death than in patients with acute myocardial infarction. (4) The frequency of acute coronary lesions (thrombi, plaque rupture, and plaque hemorrhage) is similar to that observed in patients with sudden coronary death and significantly less than that observed in acute myocardial infarction. (5) The frequency of multiluminal channels throughout the major coronary arteries is significantly higher in unstable angina compared to sudden coronary death or acute myocardial infarction. (6) The major epicardial arteries and the heart are smaller in patients with unstable angina than in patients with sudden coronary death or acute myocardial infarction. (7) The left ventricular cavity is usually of normal size in patients with unstable angina and therefore left ventricular function is usually normal.

Significance of cardiac weight in patients having coronary artery bypass grafting for angina pectoris

Cardiac weight at necropsy in 211 patients who had coronary artery bypass grafting (CABG) for angina pectoris, and its relation to early (less than 60 days) and late (greater than 60 days) death after CABG was sought. The 121 patients dying early had a lower mean heart weight than did the 90 patients dying late (444 +/- 94 vs 498 +/- 107 g; p less than 0.001). The mean heart weight of the 85 men dying early was less than that of the 75 men dying late (472 vs 506 g; p less than 0.05), and the mean heart weight of the 36 women dying early was less than that of the 15 women dying late (377 vs 459 g; p less than 0.005). Most patients with hearts of normal weight were in the early death group: of the 17 women with hearts of normal weight (less than or equal to 350 g), 16 (94%) died early (p less than 0.01), and of the 34 men with hearts of normal weight (less than or equal to 400 g), 21 (62%) died early (difference not significant). Conversely, most patients in the late death group had hearts of increased weight: of the 15 women dying late, 14 (93%) had hearts of increased weight, and of the 75 men dying late, 62 (83%) had hearts of increased weight.(ABSTRACT TRUNCATED AT 250 WORDS)

Development of severe stenosis in a previously purely regurgitant, congenitally bicuspid aortic valve

Abstract Acongenitally bicuspid aortic valve may function normally, it may be stenotic with or without associated regurgitation or it may be purely regurgitant (no associated stenosis). 1,2 Such a valve may function normally for many years and then it may become stenotic (as calcific deposits build up) or it may become purely regurgitant (because of superimposed infective endocarditis or because of reasons unclear). Once a bicuspid valve develops some degree of stenosis, its course thereafter is one of gradually worsening stenosis; once a bicuspid valve develops some degree of pure regurgitation (without associated stenosis), its course thereafter is one of gradually worsening regurgitation. Recently, we encountered a man who 8 years earlier had evidence of severe pure aortic regurgitation (no element of stenosis) and thereafter he went on to develop severe aortic valve stenosis with virtual loss of the regurgitation. To our knowledge, conversion from pure aortic regurgitation to severe aortic stenosis has not been reported. This report records such an occurrence.

Effects of tissue plasminogen activator therapy on the frequency of acute right ventricular myocardial infarction associated with acute left ventricular infarction

To assess the effects of reperfusion therapy on acute right ventricular myocardial infarction, we studied at necropsy the hearts from 51 patients who died after receiving intravenous recombinant tissue plasminogen activator for acute left ventricular myocardial infarction as part of the Thrombolysis in Myocardial Infarction (TIMI) study. Right ventricular infarction occurred in none of 29 patients with infarction of the anterior wall of the left ventricle and in 8 of 22 patients (36%) with infarction of the posterior (inferior) wall of the left ventricle. Of the 22 patients with posterior wall infarction, the 8 patients with right ventricular infarction were compared to the 14 patients without right ventricular infarction. The patients with right ventricular infarction had a longer mean interval from tissue plasminogen activator infusion to peak creatine phosphokinase level (19 vs. 11 h, P < 0.03), a lower frequency of hemorrhagic necrosis (2 of 8 vs. 10 of 14, P < 0.04) and higher frequency of luminal thrombus in the infarct-related coronary artery (6 of 8 vs. 3 of 14, P = 0.054). Each of these findings is associated with the absence of coronary reperfusion. Thus, successful reperfusion following acute left ventricular myocardial infarction appears to be associated with a decreased frequency of concomitant right ventricular myocardial infarction.

Rupture of the ventricular septum or left ventricular free wall from acute myocardial infarction early after coronary artery bypass grafting

Abstract Rupture of the ventricular septum or of the left ventricular free wall from acute myocardial infarction (AMI) after coronary artery bypass grafting (CABG) is rare. Such was the case, however, in the 2 patients to be described below.

Juvenile diabetes mellitus with 50-year survival

Abstract Although extracts of pancreatic islet cells were found to lower blood sugar levels of mammals in 1922,1,2 it was several years before insulin became readily available for patients with diabetes mellitus (DM). A protamine zinc insulin preparation was introduced in 19343 and an improved preparation (neutral protamine Hagadorn [NPH]) became available in 1936.4 We recently studied at necropsy 2 patients who were found to have DM in 1935 and 1937. They had received insulin subcutaneously for 53 and 50 years, respectively. Because of the rarity of such long survival with onset of DM in childhood, a recording of certain morphologic findings in them appeared appropriate.