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PubMed1991

Effects of milrinone on left ventricular remodeling after acute myocardial infarction.

BACKGROUND: Left ventricular remodeling after an acute myocardial infarction may result in progressive left ventricular dilation that may be associated with increased mortality. We studied the effects of the phosphodiesterase inhibitor milrinone on left ventricular remodeling after acute myocardial infarction. METHODS AND RESULTS: Rats (n = 90) were randomized to undergo either left coronary artery ligation or sham operation. Three weeks after surgery, rats received either no treatment or milrinone, which was continued until 2 days before the rats were killed. Ninety 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 fixed at a constant pressure and analyzed morphometrically. Compared with untreated infarcted rats, milrinone-treated infarcted rats had a lower left ventricular end-diastolic pressure (1.7 +/- 0.4 versus 4.3 +/- 1.4 mm Hg, p less than 0.05), a lower left ventricular volume (1.25 +/- 0.20 versus 2.37 +/- 0.30 ml/kg, p less than 0.001) and a lower left ventricular wall stress index (1.3 +/- 0.2 versus 1.7 +/- 0.1, p less than 0.05). Left ventricular chamber stiffness was higher in milrinone-treated infarcted rats than in untreated infarcted rats. Milrinone had no cardiac effect on uninfarcted animals. CONCLUSION: Chronic milrinone therapy after acute myocardial infarction improves cardiac hemodynamic indexes and attenuates progressive left ventricular dilation.

Animals↗
PubMed1999

Early predictors of left ventricular remodeling after acute myocardial infarction.

Ventricular remodeling after acute myocardial infarction is characterized by alteration in left ventricular (LV) size, shape, and wall thickness and involves both the infarcted and the noninfarcted regions of the ventricle. These structural changes are the result of several distinct pathologic processes that contribute to progressive LV dilation: rearrangement of wall structure, myocyte hypertrophy, and increasing muscle mass without an increase in wall thickness (eccentric hypertrophy). The pathogenesis of LV remodeling is multifactorial. Multiple factors may in fact contribute at different stages from the time of coronary occlusion until the development of ventricular dilation: These include the magnitude of the loss of contractile elements, the abrupt alteration in systolic and diastolic loading conditions, the activation of circulating neurohormones and local autocrine trophic factors, and the patency of the infarct-related artery. Although remodeling occurring early after infarction may be an appropriate compensatory response to preserve ventricular function, recent observations have suggested that this long process has a deleterious effect on LV function and prognosis. Thus attempts to inhibit these structural changes have been the focus of recent experimental and clinical studies. This review focuses on interactive factors that influence postinfarction LV remodeling, emphasizing the role of some new emerging determinants such as the extent of surviving myocardium within the infarcted and noninfarcted zones.

Autocrine Communication↗
PubMed1999

Left ventricular remodelling: common process in patients with different primary myocardial disorders.

Currently the problem of left ventricular remodelling in the early and late stages after myocardial infarction are under intense study. Studies of the role of remodelling of the left ventricle in patients with long-term arterial hypertension have been recently initiated. The purpose of this investigation was to study whether left ventricular remodelling is common for different primary myocardial disorders. The study population consisted of 212 patients with primary myocardial lesions (121 with dilated cardiomyopathy, 45 with chronic myocarditis and 46 with prolonged damage of the myocardium with alcohol; 196 male and 16 female, mean age 42.6+/-11.3 years) and 32 age matched normal subjects (24 male and eight female). Cardiac catheterization for ventriculography and coronary angiography was performed in all subjects for detection of left ventricular haemodynamics, including chamber volume and shape at end-systole and end-diastole. Worsening of heart failure was associated with a progressive enlargement of the left ventricle, with increases in end-systolic left ventricular wall stress, that lead to increases in left ventricular muscle mass, alteration of left ventricular geometry from a more ellipsoid to a more spherical shape and a progressive decrease of relative wall thickness index that reflects inadequate enlargement of the ventricular chamber in comparison with the increase in muscle mass. This process of left ventricular remodelling was common to all the primary myocardial disorders studied. Thus, regardless of the different etiological nature, most primary myocardial disorders show a similar left ventricular remodelling process suggesting common mechanisms for the development of chronic heart failure.

Adult↗
PubMed2004

Progressive left ventricular remodeling in patients with hypertrophic cardiomyopathy and severe left ventricular hypertrophy.

OBJECTIVES: The aim of this study was to determine the natural history of patients with hypertrophic cardiomyopathy (HCM) and severe left ventricular hypertrophy (LVH) (i.e., maximal left ventricular wall thickness [MLVWT] >/=30 mm) and whether changes in cardiac morphology influence the course of the disease. BACKGROUND: Severe LVH is common in young and rare among elderly patients with HCM. This has been explained by a high incidence of sudden death. We hypothesized that this age-related difference might be explained by left ventricular wall thinning. METHODS: A total of 106 (age 33 +/- 15 years; 71 males) consecutive patients with severe LVH underwent history taking, examination, electrocardiography, echocardiography, cardiopulmonary exercise testing, and Holter analysis. Survival data were collected at subsequent clinic visits or by communication with patients and their general practioners. In order to assess morphologic and functional changes, 71 (67.0%) patients (mean age 31 +/- 15 years; 47 males) followed at our institution underwent serial (>/=1 year) assessment. RESULTS: Of the 106 patients, the majority (78 [71.6%]) were <40 years of age. During follow-up (92 +/- 50 months [range 1 to 169]), 18 (17.0%) patients died or underwent heart transplantation (13 sudden cardiac deaths, 2 heart failure deaths, 1 heart transplantation, 1 stroke, 1 postoperative death). Five-year survival from sudden death was 90.1% (95% confidence interval [CI] 84.0% to 96.3%), and that from heart failure death or transplantation was 97.7% (95% CI 94.5 to 100). In patients serially evaluated over 85 +/- 51 months, there was an overall reduction in MLVWT of 0.6 mm/year (95% CI 0.31 to 0.81, p = 0.00004). Wall thinning >/=5 mm was observed in 41 patients (57.7%; age 35 +/- 13 years; 28 males). On multivariate analysis, the follow-up duration only predicted wall thinning (0.6 mm/year, 95% CI 0.38 to 0.85, p < 0.00001). CONCLUSIONS: Left ventricular remodeling is common in patients with severe LVH and contributes to the low prevalence of severe LVH seen in middle age and beyond.

Adult↗
PubMed1993

Long-term oral nitrate therapy prevents chronic ventricular remodeling in the dog.

OBJECTIVES: The purpose of this experiment was to assess the long-term effects of oral nitrate therapy on ventricular remodeling in a canine model of discrete myocardial damage. BACKGROUND: A progressive increase in left ventricular mass and volume has been documented after experimental and clinical myocardial infarction. This ventricular remodeling has been associated with the development of congestive heart failure. Nitrate therapy, especially when combined with hydralazine, is effective in the management of clinical heart failure. Moreover, nitrates inhibit infarct expansion, one of the earliest manifestations of ventricular remodeling. Whether nitrates can attenuate chronic left ventricular remodeling is unknown. METHODS: Dogs with discrete myocardial necrosis produced 24 h earlier by transmyocardial direct current shock were randomized to receive isosorbide mononitrate, 30 mg twice daily (n = 10), or no treatment (n = 4); the latter group was augmented by 13 control dogs from a prior study in which an identical protocol was used. Ventricular structure was assessed with nuclear magnetic resonance imaging at baseline and at 1 and 16 weeks after myocardial damage. RESULTS: Left ventricular mass increased at 1 week in the control group (mean +/- SD 68.1 +/- 10.7 g to 80.1 +/- 12.1 g, p = 0.0001) but not in the nitrate-treated group (70.2 +/- 7.7 g to 69.6 +/- 7.3 g, p = NS). No change in left ventricular volume was observed in either group during the 1st week after myocardial damage. After 16 weeks of follow-up left ventricular mass had increased by 12.7 +/- 7.1 g (p = 0.001) in the control group and had decreased by 1.2 +/- 7.7 g in the nitrate group. Left ventricular volume was increased at 16 weeks by 14.2 +/- 10.3 ml in the control group but was decreased by 3.7 +/- 7.5 ml in the nitrate group. Isosorbide mononitrate produced transient hemodynamic effects with a return of most measured variables toward baseline within 2 h after administration of the drug. At 1 week there was no intergroup difference in rest hemodynamic variables assessed 12 h after drug administration. At 16 weeks, pulmonary capillary wedge pressure (15 +/- 4 vs. 8 +/- 3 mm Hg, p = 0.0001), pulmonary artery pressure (24 +/- 5 vs. 16 +/- 3 mm Hg, p = 0.0001) and right atrial pressure (10 +/- 3 vs. 6 +/- 3 mm Hg, p = 0.008) were all higher in the control group. CONCLUSIONS: Long-term oral nitrate therapy attenuates the early and late manifestations of ventricular remodeling after myocardial damage in the dog. Hemodynamic observations suggest the possibility that drug-induced preload or afterload reduction does not completely explain this effect.

Administration, Oral↗
PubMed2002

Do diuretics and aldosterone receptor antagonists improve ventricular remodeling?

There is no evidence that loop diuretics improve ventricular remodeling in patients with heart failure. Aldosterone receptor antagonists, which have an effect on natriuresis and diuresis, especially in conjunction with an angiotensin converting enzyme-inhibitor, have been shown to improve ventricular remodeling in patients with left ventricular systolic dysfunction. The mechanisms for this beneficial effect and a reduction in death due to progressive heart failure seen in the randomized aldosterone evaluation study (RALES) is likely related to the effect of aldosterone receptor antagonism on myocardial collagen formation and ventricular hypertrophy. Further proof of this hypothesis should be forthcoming from the results of the Eplerenone Heart Failure Efficacy and Survival Study (EPHESUS) early in 2003 in which the aldosterone receptor antagonist eplerenone is being evaluated in patients with systolic left ventricular dysfunction post myocardial infarction.

Diuretics↗
PubMed2006

Elevated levels of brain natriuretic peptide as a predictor of impaired coronary endothelial function in patients with left ventricular remodeling.

BACKGROUND: Plasma levels of brain natriuretic peptide (BNP) correlate with left ventricular remodeling, but the relationship between BNP induction and coronary function remains unclear. OBJECTIVES: The present study assessed BNP production in response to left ventricular enlargement and investigated the relationship between BNP production and coronary vasodilating function in patients with left ventricular remodeling. METHODS: Patients (n = 63) with normal or mildly diseased coronary arteries underwent Doppler flow study of the left anterior descending coronary artery. Vascular reactivity was examined using intracoronary acetylcholine, papaverine and nitroglycerin using a Doppler guidewire. RESULTS: Left ventricular end-diastolic dimension was positively correlated with BNP (r = 0.45, p < 0.001) in all patients. BNP was significantly and inversely correlated with percentage change in coronary artery diameter induced by acetylcholine (r = -0.56, p < 0.001) but not by nitroglycerin (r = -0.20, p = 0.28) in patients with left ventricular end-diastolic dimension > or = 55 mm (n = 32). By contrast, BNP was not significantly correlated with percentage change in coronary artery diameter induced by either acetylcholine or nitroglycerin in patients with left ventricular end-diastolic dimension < 55 mm (n = 31). Further, BNP was not correlated with the percentage change in coronary blood flow induced by acetylcholine or by papaverine in patients with or without left ventricular remodeling. CONCLUSIONS: The elevation in plasma BNP levels that occurs in association with left ventricular enlargement is a predictor of impaired endothelium-dependent vasodilation in conductance coronary arteries.

Adult↗
PubMed1994

Angiotensin-converting enzyme inhibition and beta-adrenoceptor blockade regress established ventricular remodeling in a canine model of discrete myocardial damage.

OBJECTIVES: This study was designed to assess the effect of angiotensin-converting enzyme inhibition and beta-adrenoreceptor blockade on established ventricular remodeling. BACKGROUND: Angiotensin-converting enzyme inhibitor therapy attenuates the development of ventricular remodeling when given shortly after myocardial infarction. However, regression of established ventricular remodeling after infarction has received little attention. METHODS: The relative effects of angiotensin-converting enzyme inhibitor therapy and beta-adrenoceptor blockade on established ventricular remodeling were assessed in a canine model characterized by increased left ventricular mass and chamber dilation as a result of localized myocardial necrosis produced by transmyocardial direct current shock. Dogs were randomly assigned to 3 months of therapy with captopril (25 mg twice daily, n = 7) or metoprolol (100 mg twice daily, n = 7) or to a control group with no intervention (n = 6), 11 +/- 4 (mean +/- SD) months after acute myocardial damage. RESULTS: Compared with the control group, dogs in both the captopril and metoprolol groups had reduced left ventricular mass as measured by magnetic resonance imaging (-8.1 +/- 3.8 vs. 1.7 +/- 2.8 g, p = 0.003 and -9.6 +/- 5.6 vs. 1.7 +/- 2.8 g, p = 0.001), respectively. Captopril and metoprolol also produced a reduction in left ventricular end-diastolic volume (-7.6 +/- 6.0 and -6.0 +/- 5.8 ml, respectively) compared with the control value (-1.6 +/- 3.8 ml) (p = 0.14 [NS]). Both agents reduced mean arterial pressure but had disparate effects on pulmonary wedge pressure and right atrial pressure. There was no significant correlation between change in ventricular mass or volume and change in any measured hemodynamic or neurohormonal variable. CONCLUSIONS: These data suggest that pharmacologic intervention with angiotensin-converting enzyme inhibition or beta-adrenoceptor blockade can result in regression of established ventricular remodeling. The mechanism of this response will require further study, but these data did not support a close association between regression of remodeling and hemodynamic unloading of the ventricle or systemic neuroendocrine factors.

Animals↗
PubMed2005

Effect of coronary artery bypass graft in patients with unstable angina on left ventricular remodelling in medium-term follow-up.

INTRODUCTION: Left ventricular remodelling is a process of change in size, shape, wall thickness and heart function, initiated by a noxious stimulus such as ischaemia. Methods of pharmacological and surgical inhibition or reversal of remodelling are being sought. AIM: To assess the influence of coronary artery bypass grafting on echocardiographic measures of left ventricular size and shape in medium-term follow-up. METHODS: In a group of 30 patients three echocardiographic examinations were performed: before CABG operation, 3 months after and 20 months after the operation. Left ventricular area and volumes as well as indices of sphericity, thinning and expansion were calculated. RESULTS: After the operation, left ventricular areas measured in short axis and in apical four-chamber view increased among patients with a history of myocardial infarction. Improvement in the sphericity index occurred after the operation in patients with a history of myocardial infarction in whom the ejection fraction before the operation was less than 50%. CONCLUSIONS: The left ventricular remodelling process progresses after coronary artery bypass grafting in patients with a history of myocardial infarction. Inhibition of remodelling may be expected in patients without myocardial infarction, with preserved left ventricular systolic function.

Aged↗
PubMed2003

Relation between heart rate, heart rhythm, and reverse left ventricular remodelling in response to carvedilol in patients with chronic heart failure: a single centre, observational study.

OBJECTIVE: To determine whether the process of reverse left ventricular remodelling in response to carvedilol is dependent on baseline heart rate (BHR), heart rhythm, or heart rate reduction (HRR) in response to carvedilol. DESIGN: Retrospective analysis of serial echocardiograms in 257 patients with chronic systolic heart failure at baseline and at 12-18 months after starting carvedilol. Reverse left ventricular remodelling was determined by changes in left ventricular end diastolic dimension (LVEDD), end systolic dimension (LVESD), and fractional shortening (LVFS). SETTING: Heart failure clinic within a university teaching hospital. MAIN OUTCOME MEASURES: Changes in LVEDD, LVESD, and LVFS. RESULTS: LVEDD and LVESD decreased by 2.6 (0.4) mm and 4.9 (0.5) mm, respectively (mean (SEM)), and LVFS increased by 4.3 (0.5)% (all p < 0.0001 v baseline). Simple regression revealed no significant relation between BHR or HRR and the changes in LVEDD, LVESD, or LVFS. Stratification of patients into high and low BHR groups (above and below the mean) or according to the baseline heart rhythm (sinus rhythm v atrial fibrillation) showed no differences between groups in the extent of reverse left ventricular remodelling. Improvements in left ventricular function and dimensions were associated with significant improvements in New York Heart Association functional class. CONCLUSIONS: The benefits of carvedilol in terms of reverse left ventricular remodelling and symptomatic improvement in patients with chronic heart failure are independent of BHR, heart rhythm, and the HRR that occurs in response to carvedilol.

Adrenergic beta-Antagonists↗
PubMed1999

Circulating levels of carboxyterminal propeptide of type I procollagen and left ventricular remodeling after myocardial infarction.

Alteration in myocardial collagen metabolism is an important factor in the progression of ventricular remodeling after myocardial infarction (MI). This study examined sequential changes in circulating levels of carboxyterminal propeptide of type I procollagen (PICP) as a collagen synthesis marker in order to assess the value of PICP for predicting the progression of left ventricular remodeling after MI. The study group comprised 20 patients with first MI undergoing reperfusion therapy. Peripheral blood samples were obtained on admission and serially up to 4 weeks after admission. Circulating levels of PICP and B-type natriuretic peptide (BNP), a tentative biochemical marker for the severity of MI, were measured by direct radioimmunoassay. Left ventricular end-diastolic volume index (EDVI) in acute and chronic phases were determined by left ventriculography, and changes (Delta) in EDVI were used as an index of left ventricular remodeling. Plasma PICP levels in the non-dilation group (< median DeltaEDVI) showed no significant change. However, in the dilation group (> median DeltaEDVI) PICP started to increase significantly 3 days after admission, peaking on day 14 (from 74 +/- 6 to 104 +/- 19 ng/ml, p < 0.05). DeltaEDVI was significantly correlated with plasma PICP at 2 and 3 weeks, and with plasma BNP at 1, 2 and 3 weeks. Plasma PICP 2 weeks after MI was the only independent predictor of DeltaEDVI (p < 0.001). These results suggest that an increase in plasma PICP levels 2 weeks after admission is a useful biochemical predictor of the progression of ventricular remodeling after MI.

Aged↗
PubMed2005

Enalapril suppresses ventricular remodeling more effectively than losartan in patients with acute myocardial infarction.

BACKGROUND: Ventricular remodeling after acute myocardial infarction (AMI) is associated with increased morbidity and mortality. ELITE II study showed that losartan, an angiotensin receptor blocker, shows a survival benefit to the same degree as captopril, an angiotensin-converting enzyme inhibitor, does in patients with heart failure. However, recent OPTIMAAL study showed that clinical outcomes after losartan are not superior to those after captopril in patients with AMI. We examined the effect of losartan on ventricular remodeling after AMI comparatively with that of enalapril. METHODS: We enrolled 203 consecutive patients with AMI (mean age 62 +/- 11 years). All patients underwent primary percutaneous coronary intervention and were randomly assigned to losartan (25-50 mg, n = 101) or enalapril (2.5-10 mg, n = 102) treatment. Biplane left ventriculography was performed just after primary percutaneous transluminal coronary angioplasty (acute phase) and 6 months after the onset of AMI. RESULTS: Any of the maximal creatine kinase level, left ventricular end-diastolic volume index, end-systolic volume index, and ejection fraction measured at acute phase was not different between losartan and enalapril groups. However, changes in left ventricular end-diastolic index (18 +/- 25 vs 8 +/- 24 mL/m2) and left ventricular end-systolic volume index (10 +/- 20 vs 2 +/- 18 mL/m2) from acute phase to 6 months were significantly greater in losartan than in enalapril group. Change in left ventricular ejection fraction (0.2% +/- 10.3% vs 3.4% +/- 11.6%) from acute phase to 6 months was significantly smaller in losartan than in enalapril group. The plasma level of brain natriuretic peptide at 6 months was significantly higher in losartan than in enalapril group (all P < .05). CONCLUSION: These indicate that enalapril suppresses ventricular remodeling after AMI more effectively than losartan.

Angioplasty, Balloon, Coronary↗
PubMed2005

Left ventricular remodeling after primary coronary angioplasty in patients treated with abciximab or intracoronary adenosine.

BACKGROUND: Primary angioplasty is the best treatment of acute myocardial infarction but fails to achieve adequate myocardial reperfusion in 25% to 30% of patients, despite TIMI grade 3 flow. Drug treatment aimed at reducing the no-reflow phenomenon may improve myocardial salvage, thus preventing left ventricular remodeling. Our aim was to evaluate the impact of abciximab and adenosine on immediate angiographic results and on 6-month left ventricular remodeling. METHODS: Ninety consecutive patients undergoing primary angioplasty with coronary stenting were randomized in a sequential alternating fashion to standard abciximab treatment (ABCX) group, intracoronary adenosine distal to the occlusion (ADO) group, or neither (CTRL) group. All patients underwent a clinical and echocardiographic follow-up at 1 and 6 months. The primary end point was the prevalence of 6-month left ventricular remodeling. RESULTS: Baseline clinical, echocardiographic, and angiographic characteristics were similar. Mean final corrected TIMI frame count was 17 +/- 9, 16 +/- 12, and 23 +/- 11 frames in ABCX, ADO, and CTRL patients, respectively (P = .002). Angiographic no-reflow was observed in 7%, 13%, and 17% of ABCX, ADO, and CTRL patients, respectively (P > .20). At 6 months, left ventricular remodeling occurred in 7%, 30%, and 30% of ABCX, ADO, and CTRL patients, respectively (P = .045), with a percent increase in end-diastolic volume of 5% +/- 13%, 15% +/- 15%, and 12% +/- 18% (P = .04). CONCLUSIONS: During primary angioplasty, abciximab enhances myocardial reperfusion, translating into a reduced incidence of 6-month left ventricular remodeling. In contrast, adenosine administration improves angiographic results but does not prevent left ventricular remodeling.

Abciximab↗
PubMed2007

Reverse right ventricular remodeling after pulmonary endarterectomy in patients with chronic thromboembolic pulmonary hypertension: utility of magnetic resonance imaging to demonstrate restoration of the right ventricle.

OBJECTIVES: Pulmonary arterial hypertension causes right ventricular remodeling; that is, right ventricular dilatation, hypertrophy, and leftward ventricular septal bowing. We studied the effect of pulmonary endarterectomy on the restoration of right ventricular remodeling in patients with chronic thromboembolic pulmonary hypertension by magnetic resonance imaging. METHODS: In 17 patients with chronic thromboembolic pulmonary hypertension, before and at least 4 months after pulmonary endarterectomy, and in 12 healthy controls, right ventricular and left ventricular end-diastolic and end-systolic volumes (milliliters) and mass (grams per meter squared) and leftward ventricular septal bowing (1 divided by the radius of curvature in centimeters) were determined by magnetic resonance imaging. RESULTS: Before pulmonary endarterectomy, right ventricular volumes, left ventricular end-diastolic volume, right ventricular mass, and leftward ventricular septal bowing differed significantly between patients with chronic thromboembolic pulmonary hypertension and healthy control subjects. After pulmonary endarterectomy, pulmonary hemodynamics improved, and right and left ventricular volumes and leftward ventricular septal bowing normalized; right ventricular mass decreased significantly (46 +/- 14 to 31 +/- 9 g x m(-2), P< .0005), but did not completely normalize. The change in total pulmonary resistance correlated with the change in right ventricular ejection fraction (r = 0.50, P < .05), right ventricular mass (r = 0.63, P < .01), and leftward ventricular septal bowing (r = 0.50, P < .05). CONCLUSIONS: Right ventricular remodeling was observed in patients with chronic thromboembolic pulmonary hypertension and restored almost completely after a hemodynamically successful pulmonary endarterectomy. Magnetic resonance imaging is a valuable tool to evaluate cardiac remodeling and function in patients with chronic thromboembolic pulmonary hypertension, both before and after pulmonary endarterectomy.

Adult↗
PubMed2005

Angiotensin II AT1 receptor density on blood platelets predicts early left ventricular remodelling in non-reperfused acute myocardial infarction in humans.

BACKGROUND: Renin-angiotensin-system activity, a principal factor determining ventricular remodelling after myocardial infarction (MI), is dependent on local angiotensin II concentration and angiotensin AT1 receptor (AT1R) density. The latter is regulated by systemic factors acting independently from angiotensin II concentration. OBJECTIVE: To test the hypothesis that AT1R density at the onset of MI determines post-MI ventricular remodelling. METHODS: In 48 patients with first acute MI who did not undergo reperfusion therapy, angiotensin AT1R density on blood platelets (reflecting cardiovascular AT1R density) was assessed 13+/-5 h after the onset of MI, using radioligand binding assay. Left ventricular end-systolic (LVESVI) and end-diastolic volume indices (LVEDVI) and ejection fraction (EF) were assessed by two-dimensional echocardiography as measures of ventricular remodelling. RESULTS: Predischarge LVESVI and LVEDVI positively and EF negatively correlated with AT1R density. Patients with AT1R density below median had significantly lower LVESVI (33.2+/-2.4 mL/m2), LVEDVI (70.0+/-2.8 mL/m2) and higher EF (52.8+/-2.3%) than patients with AT1R density above median (LVESVI = 44.9+/-2.6, LVEDVI = 81.3+/-3.9 mL/m2 and EF = 44.9+/-2.6%, all p<0.01). In multivariate analysis, only AT1R density and infarct size were independent predictors of early post-MI ventricular dilation. CONCLUSIONS: High density of AT1R at the onset of MI is a predictor of early left ventricular remodelling.

Aged↗
PubMed2005

[Influence of fluvastatin on left ventricular remodeling after myocardial infarction in rats].

OBJECTIVE: To investigate the effect of long-term administration of fluvastatin on improvement of ventricular remodeling of rats after myocardial infarction and its mechanism. METHODS: Sprague-Dawley rats were subjected to ligation in anterior descending branch of coronary artery and treated with fluvastatin (20 mg.kg(-1) d(-1)) or distilled water for 8 weeks. Doppler echocardiography, hemodynamic study and cardiac histomorphometry were used to estimate the ventricular remodeling and cardiac function. Laser scanning confocal microscope was used to definite the distribution of superoxide anion (O(2)(*-)) and nitrogen monoxide. RT-PCR and immunohistochemistry were used to detect the expression of NOS2 and p22phox in mRNA and protein level. The level of lipid peroxidation, glutathione peroxidase, nitrogen monoxide and total cholesterol were detected too. RESULTS: Administration of fluvastatin ameliorated left ventricular remodeling without affecting the infarct size [(40 +/- 6 vs 42 +/-5)%, P>0.05]. The level of left ventricular end-diastolic pressure [(18.24 +/-6.58 vs 10.74 +/-4.71) mmHg, P<0.05], right ventricular ameliorated relative weight [(0.92 +/-0.19 vs 0.71 +/-0.13) g/kg, P<0.05], the thickness of left ventricular posterior wall [(3.04 +/-0.28 vs 2.60 +/-0.36) mm, P<0.05] decreased after fluvastatin treatment. The left ventricular ejection fraction was not influenced, the relative lung weight and the left atrium diameter reduced [(5.79 +/-2.92 vs 3.69 +/-0.68) g/kg, (0.55 +/-0.12 vs 0.45 +/-0.04) mm, P<0.05]; the expressions of LPO in the plasma and myocardium [(8.64 +/-0.59 vs 7.71 +/-0.66) U/dl, P<0.05; (3.12 +/-0.38 vs 1.93 +/-0.40) ng/microg.pro, P<0.01] were reduced, and the overexpressed NO was inhibited [(436.87 +/-47.22 vs 313.78 +/-34.35) mg/dl, P<0.01], but the expression of GPx increased [(66.13 +/-8.31 vs 79.78 +/-2.38) mg/dl, P<0.01]. The expression of O(2)(*-) and the activity of NADPH oxidase subunit p22phox increased; NOS2 and its products NO were over-expressed too. CONCLUSION: Ventricular remodeling and hemodynamics are improved profoundly in MI rats treated with fluvastatin. The effect of antioxidative stress of fluvastatin might be involved in the mechanism.

Animals↗
PubMed2005

[Effects of pravastatin, fosinopril and their combination on myocardium TNF-alpha expression and ventricular remodeling after myocardial infarction in rats].

OBJECTIVE: To investigate the effects of pravastatin, fosinopril and their combination on ventricular remodeling, cardiac function, tumor necrosis factor-alpha (TNF-alpha) mRNA expression, and matrix metalloproteinases (MMPs) activities after myocardial infarction (MI) in rats. METHODS: Acute myocardial infarction (AMI) was established by ligation of the anterior descending coronary artery in male Sprague-Dawly (SD) rats. Twenty-four hours after the procedure, the 48 surviving rats were grouped randomly as AMI control, fosinopril (10 mg.kg(-1).d(-1)), pravastatin (20 mg.kg(-1).d(-1)) and a combined use of the 2 drugs. Sham-operated group (n = 8) was taken randomly as non-infarction control. Six weeks after treatment with the drugs by gastric gavage, heart function and left ventricular remodeling were assessed. Left ventricular weight (LVW)/body weight (BW) ratio was determined. The relative expression of myocardium TNF-alpha mRNA was assessed by reverse transcription-polymerase chain reaction. Left ventricular myocardium MMPs activities were assessed by Zymography. RESULTS: There were no significant differences among the four AMI groups in infarction size (P > 0.05). In comparison with the AMI group, left ventricular end-diastolic pressure, left ventricular end-diastolic diameter, LVW/BW all decreased significantly (P < 0.05 - 0.01); while dp/dtmax, dp/dtmin, fractional shortening (FS) and ejection fraction (EF) increased significantly in all three drug-treated groups (P < 0.05 - 0.01); increments of FS, LVEF and dp/dtmax were more evident in the combination group than either the fosinopril or pravastatin group (P < 0.05). The levels of TNF-alpha mRNA in AMI rats treated with fosinopril, pravastatin and their combination reduced 29%, 26% and 33%, respectively (P < 0.01); MMP-2 activity reduced 25%, 30% and 35%, respectively (P < 0.01); MMP-9 activity reduced 20%, 18% and 24%, respectively (P < 0.01). There were no significant differences in other variables among the 3 treatment groups (P > 0.05). CONCLUSION: Pravastatin, fosinopril and their combination showed favorable effects on left ventricular remodeling after AMI in rats and demonstrated improved cardiac function. The combined treatment group yielded better results in the context of improving left ventricular systolic function. These effects could be relevant to the attenuation of increased MMP-2 and MMP-9 activities and left ventricular expression of TNF-alpha.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2006

Early, intracoronary growth hormone administration attenuates ventricular remodeling in a porcine model of myocardial infarction.

OBJECTIVE: Ventricular remodeling is a common corollary of myocardial infarction. We hypothesized that this process may be attenuated by growth hormone, administered as a single high-dose, selectively in the infarct zone, early postmyocardial infarction. DESIGN: In 35 pigs (29+/-4 kg), myocardial infarction was generated by inflation of an over-the-wire angioplasty balloon in the circumflex artery for 60 min and 5 further pigs were sham-operated. Ten minutes after reperfusion, the pigs were randomized (2:1) to either growth hormone (1 IU/kg) (n=23) or normal saline (n=12), delivered via the balloon catheter. All survivors were treated with captopril and were sacrificed 4 weeks after myocardial infarction. RESULTS: Compared to controls, growth hormone-treated animals displayed lower heart weight (4.1+/-0.5 g/kg body weight, versus 3.4+/-0.4 g/kg, respectively, p=0.003) and dimensions (left ventricular short axis diameter 46+/-7 mm versus 37+/-6 mm, p=0.01; right ventricular short axis diameter 38+/-7 mm versus 30+/-5 mm p=0.001). Growth hormone increased wall thickness in the infarct (6.0+/-1.8 in controls versus 9.9+/-3.7 in treated animals, p=0.004) and non-infarct zones (10.6+/-1.8 in controls versus 15.5+/-3.8 in treated animals, p=0.0006) and produced higher (p<0.05) microvascular density in both zones. CONCLUSION: Intracoronary administration of growth hormone attenuates left and right ventricular remodeling by inducing hypertrophy and by enhancing angiogenesis.

Animals↗