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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reperfusion that is too late to salvage ischemic myocardium reduces early infarct expansion, and captopril therapy favorably alters long-term left ventricular remodeling. To study whether the beneficial effects of these two therapies are additive, we examined the effects of captopril therapy after late reperfusion on left ventricular remodeling after acute myocardial infarction. Female Sprague-Dawley rats (n = 67) were randomly assigned to one of four groups: group 1, sham surgery and no treatment; group 2, left coronary artery ligation and no treatment (myocardial infarction [r MI]); group 3, left coronary artery ligation, reperfusion 2 hours later, and no treatment (late reperfusion [LR]); and group 4, left coronary artery ligation, reperfusion 2 hours later, and captopril treatment (LR-Cap). Captopril therapy (2 gm/L of drinking water) was begun in the LR-Cap group in the immediate post-operative period and continued for 20 days. Twenty-one days postoperatively, hemodynamic measurements were made before and after volume loading. The rats were killed, their hearts were removed, and passive pressure-volume curves were obtained. The hearts were then fixed at a constant pressure for morphometric analysis. Compared with the MI group, the LR group had a lower expansion index and a higher thinning ratio. There were no differences in hemodynamics, left ventricular volumes, or other morphometric indexes between the two groups. Compared with the MI and LR groups, the LR-Cap group had lower peak left ventricular end-diastolic pressure, lower left ventricular volume, lower left and right ventricular weights, and a leftward shift of pressure-volume curves.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of captopril therapy after late reperfusion on left ventricular remodeling after experimental myocardial infarction. 815 12

The effects of metoprolol on early infarct expansion after acute myocardial infarction were studied in rats (n = 54) that underwent either left coronary artery ligation (MI) or sham operation. Immediately after surgery, the rats received either metoprolol (M) by mouth, which had been dissolved in drinking water, for 72 hours supplemented with three intraperitoneal doses over the first 24 hours or no treatment (H2O). Three days after the initial surgery, hemodynamic measurements were made before and after volume loading. The rats were killed, the hearts were removed, and passive pressure-volume curves were obtained. The hearts were then fixed at a constant pressure and analyzed morphometrically. Infarct size was nonsignificantly lower in the metoprolol-treated group compared with the untreated group (38% +/- 5% MI-M vs 48% +/- 3% MI-H2O, p = 0.10) Compared with infarcted untreated rats, infarcted metoprolol-treated rats had a lower heart rate (322 +/- 13 beats/min MI-M vs 452 +/- 19 beats/min MI-H2O, p < 0.001), lower left ventricular systolic pressure (63 +/- 4 mm Hg MI-M vs 90 +/- 6 mm Hg MI-H2O, p = 0.004), and lower +dp/dt (1340 +/- 169 mm Hg/sec MI-M vs 2872 +/- 273 mm Hg/sec MI-H2O, p < 0.001), but left ventricular end-diastolic pressure and cardiac index did not differ between the two groups. Left ventricular weight corrected for body weight was higher in infarcted rats treated with metoprolol compared with infarcted untreated rats (2.76 +/- 0.07 gm/kg MI-M vs 2.41 +/- 0.09 gm/kg MI-H2O, p < 0.05). The initial slope of the pressure-volume relationship Ki, an index of operative volume stiffness, was lower in infarcted rats treated with metoprolol compared with infarcted untreated rats (p = 0.03). There were, however, no significant differences in the expansion index, thinning ratio, or left ventricular volume between the two infarcted groups. Thus metoprolol therapy begun in the immediate postinfarction period promotes an increase in left ventricular weight and reduces operative volume stiffness but has no significant effect on indexes of early infarct expansion.
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PMID:Effects of metoprolol on early infarct expansion after acute myocardial infarction. 815 13

The hypothesis that nitrates might effectively limit left ventricular remodeling and improve function after acute myocardial infarction has been tested in experimental and clinical models, with special attention to the pathophysiologic evolution of remodeling. In 1 clinical study, before the thrombolytic era, the effects of low-dose intravenous nitroglycerin infusion for the first 48 hours during acute myocardial infarction was evaluated in a prospective, randomized, single-blinded, placebo-controlled study of 310 patients (154 nitroglycerin; 156 placebo). Nitroglycerin proved to be safe and produced several benefits compared with placebo: (1) smaller infarct size; (2) less left ventricular dysfunction; (3) less infarct expansion and thinning; (4) better functional status; (5) fewer in-hospital complications such as left ventricular failure, left ventricular thrombus, cardiogenic shock, and infarct extension; and (6) fewer deaths up to 1 year. Two subsequent clinical studies in the thrombolytic era, with low-dose intravenous nitroglycerin infusion during infarction over the first 48 hours followed by buccal nitrate (eccentric dose regimen) or placebo during healing over 6 weeks postinfarction, indicated that prolonged nitrate therapy effectively limited left ventricular remodeling and improved function further compared with placebo.
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PMID:Effects of nitrate therapy on ventricular remodeling and function. 827 53

An historical background of the use of nitrates in the setting of acute myocardial infarction gives way to the successive steps this therapy gave in the last 15 years. The pioneer investigations of John Flaherty proving the usefulness of nitroglycerin in reducing infarct size followed by the works by Bussman and Jugdutt notably on the limitation of infarct size but also on the prevention of infarct expansion and ventricular wall thinning are reviewed. The adjunctive role of nitrates in thrombolytic therapy is appraised and its absolute and relative contraindications are pointed out. Finally and based on the statistical works by Yusuf, the real impact of nitrate therapy in mortality of acute myocardial infarction is emphasised.
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PMID:[Treatment of the acute phase of myocardial infarction with nitrates]. 849 17

Rupture of the left-ventricular free wall may not always result in immediate irreversible hemodynamic collapse. We report a series of five patients (4 male, 1 female; age 59-79 years) successfully operated for postinfarction free-wall rupture with good long-term results. Two patients presented with syncopy and acute tamponade three days after an acute myocardial infarction. In two patients with atypical chest pain and congestive heart failure, a large pericardial effusion and an extreme localized thinning of a myocardial scar region was seen several weeks after an uncomplicated myocardial infarct. In one patient a pseudoaneurysm was detected, which developed asymptomatically within three weeks after a posterior myocardial infarct. In all cases myocardial rupture was suspected after an echocardiographic examination. At surgery a hemopericardium and a localized rupture site were found. The surgical procedure included closure of the defect by direct suture or patch, CABG in 3 cases, and mitral valve replacement in one patient. The postoperative course was uneventful, only one patient needed IABP for 24 hours. Three patients returned to NYHA functional class I, one patient to class II, and one patient to class III. The latter patient died of heart failure 17 months postoperatively, and the other patients are still alive 4,18,24, and 26 months postoperatively. Thus clinical representation of left-ventricular free-wall rupture after myocardial infarction can be highly variable. But close cooperation between experienced echocardiographers and surgeons may allow successful corrections with good long term-results.
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PMID:Clinical presentation of rupture of the left-ventricular free wall after myocardial infarction: report of five cases with successful surgical repair. 878 31

Rupture of plaque is an important factor in the initiation of acute myocardial infarction. Plaque rupture is related to stress distribution in atheroma, but morphological alteration in coronary atheroma plaque in vivo is little understood. Atheroma plaque was observed during the cardiac cycle using 3.5 or 2.8 F, 30 MHz intracoronary ultrasound (ICUS) in seven patients with coronary artery disease. Coronary ostial pressure (P) measurements were simultaneously performed. Seven of the eccentric stenotic sites were analyzed. Intima-medial thickness (Th) and regional radius of curvature (R) at the middle and lateral portions of the atheroma were measured. Delta Th and % delta Th were calculated from change in thickness from end-diastole to peak systole. These parameters of the middle portion were compared with those of the lateral portion. The lateral % delta Th was 20.1 +/- 13.6% (delta Th 0.13 +/- 0.08 mm; 0.69 to 0.56 mm), and was significantly greater than the middle % delta Th [5.8 +/- 6.6% (delta Th 0.06 +/- 0.08 mm; 1.24 to 1.18 mm), p < 0.05]. Regional radius of curvature did not significantly differ. Wall stress calculated as P x R/Th was greater at the lateral portion (peak systole 3.7 x 10(5) dynes/cm2, end-diastole 1.9 x 10(5) dynes/cm2) than at the middle portion (peak systole 1.4 x 10(5) dynes/cm2, end-diastole 0.9 x 10(5) dynes/cm2). The change in stress from end-diastole to peak systole at the lateral portion was significantly greater (1.8 x 10(5) dynes/cm2) than that at the middle portion (0.5 x 10(5) dynes/cm2). The change in stress during the cardiac cycle, caused by the increase in intracoronary pressure, was greater at the lateral than at the middle of the plaque. This imbalanced distribution of stress may result in greater thinning of plaque at the lateral portion. Therefore, the distortion of plaque may be a mechanism for atheroma rupture at the lateral portion.
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PMID:[Cyclic alteration in atheroma plaque morphology observed by intracoronary ultrasound: initiation mechanism of acute myocardial infarction]. 886 81

Reperfusion alone during acute myocardial infarction (AMI) preserves left ventricular (LV) topography but causes 'stunning', with delayed or no recovery of function. To determine whether adjunctive intravenous nitroglycerin (NTG) accelerates functional recovery, we prospectively measured function and topography by repeated two-dimensional echocardiography between 1 day and 6 months in 5 groups of patients (n = 73) with a first AMI: placebo (group 1), NTG alone (group 2), NTG combined with successful reperfusion after 4 h (group 3) or failed reperfusion (group 4), and successful reperfusion alone (group 5). Asynergy decreased promptly (p < 0.001) and ejection fraction improved (p < 0.001) between day 1 and 6 months in groups 2 and 3 compared to baseline and groups 1, 4 and 5. Infarct expansion and thinning found in group 1 were prevented in groups 2, 3, 4 and 5. Diastolic volume increased in the anterior subgroup 1 but not 2, 3, 4 and 5. This is the first demonstration that reperfusion combined with adjunctive NTG produces earlier, greater and persistent recovery of LV function in addition to attenuation of remodeling in patients after AMI.
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PMID:Prompt improvement of left ventricular function and preservation of topography with combined reperfusion and intravenous nitroglycerin in acute myocardial infarction. 909 19

Cardiac remodeling following myocardial infarction denotes changes of left ventricular shape, chamber size and wall thickness. It involves both the infarcted and the noninfarcted segments. This process begins at the time of acute myocardial infarction, progresses by stages, and can lead to congestive heart failure. The major determinants of lest ventricular remodeling are infarct size and transmural, adequacy of the healing process, mechanical deformation forces, and progressive ventricular dilation. Infarct expansion is a relatively frequent, early occurring alteration of the ventricular shape. It denotes thinning and lengthening of the infarct segment. The progressive ventricular remodeling can be halted by reactive hypertrophy of the viable myocytes, on condition that it is appropriate. The left ventricular increase results from myocytes hypertrophy, partly their hyperplasia, and increase of fibrosis. Major ways of action in order to limit the cardiac remodeling after myocardial infarction are: reperfusion of the infarct-related vessel by thrombolysis, nitrate therapy, and angiotensin-converting enzyme inhibitors administration. Maximum benefit is when therapy is begun very early.
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PMID:[Remodeling of the left ventricle after myocardial infarction]. 915 27

Coronary artery diseases may categorized into asymptomatic disease, angina pectoris, myocardial infarction, chronic heart failure, and sudden coronary death. Unstable angina, acute myocardial infarction, and sudden cardiac death are known as the acute coronary syndromes. Coronary atheroma is unstable in the patients with acute coronary syndromes. Stable plaques will be unstable when dynamic alterations occur. The alterations are plaque rupture, plaque hemorrhage, coronary thrombosis and vasospasm. They act each other. We analysed the histopathology of coronary arteries who died of acute myocardial infarction in 85 cases. It showed that the risk factors of plaque rupture are clusters of form cells, eccentric plaque with soft lipid rich core, and thinning of fibrous cap in atheroma. Most of these cases ruptured at edge of the atheroma.
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PMID:[Pathogenesis of acute coronary syndromes]. 978 Jul 33

In order to forecast the clinical course of acute myocardial infarction (MI), the time course of the functional changes of the left ventricular myocardium that result in remodeling was evaluated with two-dimensional echocardiography (2DE). The study group comprised 45 patients with anterior MI treated with successful percutaneous transluminal coronary angioplasty. 2DE studies were performed on days 1, 3, 7 and 14; months 1 and 3 and 1 year after MI, and the following parameters were recorded: (1) infarcted wall thickness, (2) traced length of the endocardium and of the epicardium on end-diastolic apical long axis images, and (3) wall motion score (total of asynergy scores of 16 segments of left ventricle (LV); normal: 0, hypokinesis: 1, akinesis: 2, dyskinesis: 3). According to the peak creatine kinase (CK) level, patients were classified into L group (CK > or =8000 U/L, n=16), M group (8000> CK > or =4000, n=13) and S group (CK <4000, n=16). The following results were obtained. (1) There was progressive thinning of the infarcted myocardium up to 1 month after (1 day: 9.3+/-1.7, 14 days: 6.3+/-1.7 vs 1 month: 5.9+/-1.8 mm, p<0.05; vs 1 year: 5.9+/-1.9 mm, NS). (2) Dilatation of the LV cavity occurred shortly after MI and continued up to 14 days (endocardium at 14 days: 176.8+/-13.6 vs 1 day: 164.1+/-11.4 mm, p<0.01; vs 1 year: 176.3+/-12.7 mm, NS). (3) The wall motion score improved rapidly by 14 days, and continued to improve gradually to 1 year (1 day: 12.2+/-3.4, 14 days: 6.8+/-4.0, 1 year: 4.6+/-3.1). (4) The expansion ratio (endocardial length at 14 days/1 day) was significantly greater in the L group than in the S group (p<0.05). Comparing the groups, the LV cavity of the L group remained dilated up to 14 days, whereas that of the S and M groups was dilated up to 7 days (L group 14 days: 179.3+/-11.9 vs 1 day: 156.9+/-9.2mm, p<0.01; vs 1 year: 180.0+/-14.1 mm, NS) (S group 7 days: 171.7+/-13.6 vs 1 day: 161.5+/-7.2 mm, p<0.01; vs 1 year: 172.7+/-14.4 mm, NS) (M group 7 days: 170.5+/-10.5 vs 1 day: 157.7+/-14.5 mm, p<0.05; vs 1 year: 177.08+/-9.6 mm, NS). Serial 2DE on days 1 and 14 after MI were useful for evaluating the course of LV remodeling and to forecast cardiac function in the chronic phase of MI. Determining the length of hospital stay on the basis of infarction size is justified.
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PMID:Time course of left ventricular remodeling after myocardial infarction: a two-dimensional echocardiographic study. 1087 32


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