To clarify the pathophysiologic role of intramyocardial small artery (IMSA) diseases in hypertrophied hearts, narrowings of the IMSA were quantitatively evaluated in 39 autopsied hearts, 10 from patients with typical hypertrophic cardiomyopathy (HCM), four from patients with HCM showing features mimicking dilated cardiomyopathy (DCM-like HCM), 10 from patients with hypertension, and 15 from normal adults. The relations of narrowings of the IMSA to myocytic hypertrophy, myocardial fiber disarray, and fibrosis were also examined. The external caliber and the ratio of the luminal area to the total vascular area (percent luminal area, %lumen) were calculated by an image analyzer in 85 to 203 IMSAs from each patient. The external calibers of the IMSAs were similar among groups of hearts with HCM, hypertensive hearts, and normal hearts but were greater in those with DCM-like HCM. The mean %lumen of the IMSAs was similarly reduced in the hearts with HCM (29 + 5% in the ventricular septum and 31 5% in the left ventricular free wall) and in hypertensive hearts (30 + 8% and 31 + 7%) compared with that in normal hearts (40 5% and 38 + 5%) and was the lowest in the ventricular septum of hearts with DCM-like HCM (17 3%). The mean %lumen of the IMSA was inversely cortelated with heart weight (r = -.59), the mean size of myocytes (r = -.66 in the ventricular septum, r = -.63 in the free wall), and percent fibrotic area in the septum (r = -.68). The mean %lumen values of the IMSAs in the tissues with and without disarray in the hearts with HCM were similar. Thus IMSA disease is of pathophysiologic importance in patients with HCM, DCM-like HCM in particular, or with hypertension. Circulation 75, No. 6, 1130No. 6, -1139No. 6, , 1987 CHEST PAIN is a common symptom of patients with hypertrophic cardiomyopathy (HCM)`2 or systemic hypertension3 despite angiographically normal epicardial coronary arteries. Moreover, these patients often demonstrate abnormal findings on myocardial thallium-201 imaging6 or abnormal lactate metabolism during pacing.7 Pathologically, these hearts show a greater amount of fibrosis distributed predominantly in the subendocardium than in the subepicardium,' and myocardial infarction is sometimes evident.9 Although
SUMMARYThe distribution offibrosis was studied quantitatively in the entire left ventricular wall of a transverse slice of the heart from 10 necropsy cases of hypertrophic cardiomyopathy, 10 cases of hypertensive heart disease, and 20 normal adults. The percentage area (mean (SD)) of fibrosis in the left ventricular wall in hypertrophic cardiomyopathy (10-5 (4-3)%) was significantly greater than that in hypertensive heart disease (2-6 (1-5)%) or in normal hearts (1L1 (0-5)%). In hypertrophic cardiomyopathy the percentage area of fibrosis was greater (13 1 (4-8)%) in the ventricular septum than in the left ventricular free wall (7 7 (4-2)%) whereas in hypertensive heart disease and normal hearts values in these two areas were similar. The percentage area of fibrosis in the left ventricular free wall (where myocardial fibre disarray was not extensive even in hypertrophic cardiomyopathy) was greater in hypertrophic cardiomyopathy than in hypertensive heart disease. The percentage area of fibrosis correlated with heart weight in hypertensive heart disease, but not in hypertrophic cardiomyopathy. These results suggest that widespread fibrosis in hypertrophic cardiomyopathy cannot be explained by cardiac hypertrophy alone, and that disarray and other factors are also important in pathogenesis. The increase in the percentage area of fibrosis from the outer to the inner third of the left ventricular free wall in hypertrophic cardiomyopathy and in hypertension probably reflected transmural gradients of wall stress and myocardial fibre diameter.Although fibrosis is not specific to hypertrophic cardiomyopathy, its quantification and analysis of its regional distribution provide information that is useful in investigating the pathophysiology of the disorder. Patients and methodsForty hearts from necropsy cases were studied-10 with hypertrophic cardiomyopathy, 10 with concentric hypertrophy secondary to hypertension, and 20 normal adult hearts.
on behalf of the J-RHYTHM Registry Investigators* Background--To clarify the influence of hypertension and blood pressure (BP) control on thromboembolism and major hemorrhage in patients with nonvalvular atrial fibrillation, a post hoc analysis of the J-RHYTHM Registry was performed.
To assess the importance of contraction band necrosis (CBN) in reperfusion, CBN, coagulation necrosis (CN), and infarct size, expressed as CBN + CN, were quantitatively analyzed in 25 porcine hearts without collateral circulation. The left anterior descending coronary artery was ligated for 20, 30, 60, and 120 min and then reperfused for 8 hr (groups 1 to 4, respectively). Five hearts were not reperfused (group 5). The areas of CBN and CN were traced at a magnification of X 100 under an inverted microscope and quantified with use of an image analyzer. There was no change in hemodynamics with either occlusion or reperfusion. Regional myocardial blood flow, measured by the generated hydrogen gas clearance method. decreased to almost zero after occlusion but recovered during reperfusion. Percent of risk area infarcted in groups 1 to 4 was 0 ± 0%, 1 1 + 7%, 80 ± 9%, and 96 ± 2%, respectively, and the percent of risk area infarcted in group 4 was the same as that in hearts subjected to permanent occlusion (95 ± 3%). The percent area of CBN was 100 ± 0% in group 2 68 ± 1 1% in group 3, 2 ± 1% in group 4, and 2 ± 2% in group 5. In group 3, the inner third of the ischemic left ventricular wall showed CN and the middle and outer third CBN. These findings show that in pig hearts without collateral circulation, the transmural infarct, two-thirds of which is occupied by CBN, is evident even when reperfusion is achieved after 1 hr occlusion. Therefore, protection against CBN might reduce infarct size after reperfusion.
percutaneous coronary intervention (PCI). However, trials referenced in the ARC-HBR criteria were conducted outside Japan and several Japanese-specific factors associated with HBR were not included. 1 Patient characteristics that are not included in the ARC-HBR criteria, such as low T he Academic Research Consortium criteria for high bleeding risk (ARC-HBR) were proposed from literature review and by consensus of experts from the USA, Asia, and Europe to standardize the definition of high bleeding risk (HBR). 1 In the ARC-HBR initiative, HBR was arbitrarily defined as Bleeding Academic Research Consortium (BARC) type 3 or 5 bleeding ≥4% at 1 year or a risk of an intracranial hemorrhage ≥1% at 1 year after Editorial p ????
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