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Ventricular Remodeling (ventricular + remodeling)

Distribution by Scientific Domains
Medical Sciences85%
Life Sciences14%

Kinds of Ventricular Remodeling

  • leave ventricular remodeling
    		•

    Selected Abstracts

    The Effect of Erythropoietin on Exercise Capacity, Left Ventricular Remodeling, Pressure-Volume Relationships, and Quality of Life in Older Patients With Anemia and Heart Failure With Preserved Ejection Fraction

    CONGESTIVE HEART FAILURE, Issue 3 2010
    Rose S. Cohen MD
    A prospective, open-label, 3-month study was conducted to evaluate the feasibility and short-term clinical effect of subcutaneous erythropoietin injections in patients with anemia and heart failure with preserved ejection fraction (ejection fraction, 55%±2%). Using a dose-adjusted algorithm to effect a rate of rise in hemoglobin not to exceed 0.4 g/dL,/wk, hemoglobin (10.8±0.3 to 12.2±0.3 g/dL) and red blood cell volume (1187±55 to 1333±38 mL) increased with an average weekly dose of 3926 units. Functional measures increased from baseline (6-minute walk test [289±24 to 331±22 m], exercise time [432±62 to 571±51 s], and peak oxygen consumption [8.2±0.7 to 9.4±0.9 mL/kg/min], all P<.05). End-diastolic volume declined significantly (8% volumetric decrease, 108±3 to 100±3 mL, P =.03), but there were no significant changes in left ventricular mass or estimated left ventricular end-diastolic pressure. Pressure-volume analysis demonstrated a reduction in ventricular capacitance at an end-diastolic pressure of 30 mm Hg without significant changes in contractile state. Congest Heart Fail. 2010;16:96,103. © 2009 Wiley Periodicals, Inc. [source]

    Feasibility of Biventricular Pacing in Patients With Recent Myocardial Infarction: Impact on Ventricular Remodeling

    CONGESTIVE HEART FAILURE, Issue 1 2007
    Eugene S. Chung MD
    To test the hypothesis that biventricular pacing after a myocardial infarction with reduced ejection fraction can attenuate left ventricular (LV) remodeling, the authors studied 18 patients (myocardial infarction within 30,45 days, ejection fraction ,30%, narrow QRS) randomized to biventricular therapy (biventricular therapy + defibrillator) (biventricular group) or implantable cardioverter-defibrillator alone (control group). At 1, 6, and 12 months, there were no differences in functional or clinical parameters (New York Heart Association, quality of life, 6-minute walk). Twelve-month LV volume remained stable in the biventricular group, but increased in the control group (median LV end-diastolic volume increase, 6.5 mL in biventricular vs 35 mL in control; P=.03; median LV end-diastolic volume decrease, 5.5 mL in biventricular vs 30.5-mL increase in control; P=.11). Biventricular therapy also prevented an increase in sphericity index at 12 months (median, ,2% in biventricular vs 37% in control; P=.06). Delivery of biventricular therapy early after myocardial infarction appears safe and feasible and may attenuate subsequent LV dilation. [source]

    Right Ventricular Adaptations Along with Left Ventricular Remodeling in Older Athletes

    ECHOCARDIOGRAPHY, Issue 3 2009
    Oner Ozdogan M.D.
    Background: Afterload changes and anatomic interaction between the ventricles cause right ventricle (RV) adaptation along with left ventricle (LV) remodeling. This study was designed to evaluate RV adaptations along with LV remodeling and to determine the effect of aging on both ventricles in a population of older athletes. Methods: Echocardiographic characteristics of 48 endurance trained older athletes were examined by tissue Doppler imaging (TDI) and integrated backscatter (IBS). Results: Mean LV mass index was calculated as 107.8±17.0 g/m2. Twenty-two athletes were > 55 years old. Age was found to be a risk factor for diastolic dysfunction regarding lateral TDI velocities (Em < Am) (r = 0.385, P < 0.001). RV long-axis (LAX) diameters were associated with LA volumes and LV masses (r = 0.380, P < 0.01 and r = 0.307, P < 0.05). RV LAX diameters were correlated with RV TDI E-wave (r =,0.285, P < 0.05), RV LAX average, and peak IBS values (r = 0.36, P < 0.05 and r = 0.348, P < 0.05). Conclusions: TDI and IBS are applicable methods to evaluate the relationship between the two ventricles in athletes' heart. Increased RV LAX IBS values indicate increased LV mass and LA volume as a result of RV changes along with LV remodeling. Our data suggest that RV TDI E-wave and average RV IBS values reflect cardiac adaptations of both RV and LV in older athletes. [source]

    An Echocardiographic Analysis of the Long-Term Effects of Carvedilol on Left Ventricular Remodeling, Systolic Performance, and Ventricular Filling Patterns in Dilated Cardiomyopathy

    ECHOCARDIOGRAPHY, Issue 7 2005
    Peter S. Rahko M.D.
    Background: The long-term clinical benefit of beta blockade is well recognized, but data quantifying long-term effects of beta blockade on remodeling of the left ventricle (LV) is limited. Methods: This consecutive series evaluates the long-term response of the LV to the addition of carvedilol to conventional therapy for dilated cardiomyopathy. There were 33 patients who had a LV ejection fraction <45%, LV enlargement and symptomatic heart failure. Quantitative Doppler echocardiography was performed at baseline 6, 12, 24, and 36 months after initiation of carvedilol to evaluate LV ejection fraction, LV volume, wall stress, mass, regional function, and diastolic performance. Results: Compared to baseline there was a significant and sustained reduction in end-systolic volume and end-systolic wall stress with a corresponding improvement in LV ejection fraction. The LV mass did not decline but relative wall thickness increased toward normal. An analysis of regional wall motion responses showed an improvement in all areas, particularly the apical, septal, and lateral walls that was significantly more frequent in patients with a nonischemic etiology. Filling patterns of the LV remained abnormal throughout the study but changed with therapy suggesting a decline in filling pressures. These changes were sustained for 3 years. Conclusion: (1) The addition of carvedilol to conventional therapy for a dilated cardiomyopathy significantly improves LV ejection fraction and reduces LV end-systolic volume and wall stress for at least 3 years, (2) the response to 6 months of treatment predicts the long-term response, (3) the typical response is partial improvement of the LV, complete return to normal size, and function is uncommon, and (4) abnormalities of LV filling persist in virtually all patients throughout the course of treatment. [source]

    Sex-Specific Impact of Aldosterone Receptor Antagonism on Ventricular Remodeling and Gene Expression after Myocardial Infarction

    CLINICAL AND TRANSLATIONAL SCIENCE, Issue 2 2009
    Ph.D., Rosemeire M. Kanashiro-Takeuchi D.V.M.
    Abstract Aldosterone receptor antagonism reduces mortality and improves post-myocardial infarction (Ml) remodeling. Because aldosterone and estrogen signaling pathways interact, we hypothesized that aldosterone blockade is sex-specific. Therefore, we investigated the mpact of eplerenone on left ventricular (LV) remodeling and gene expression of male infarcted rats versus female infarcted rats. Ml and Sham animals were randomized to receive eplerenone (100 mg/kg/day) or placebo 3 days post-surgery for 4 weeks and assessed by echocardiography. In the Ml placebo group, left ventricular end-diastolic dimension (LVEDD) increased from 7.3 ± 0.4 mm to 10.2 ± 1.0 mm (p < 0.05) and ejection fraction (EF) decreased from 82.3 + 4% to 45.5 + 11% (p < 0.05) in both sexes (p= NS between groups). Eplerenone attenuated LVEDD enlargement more effectively in females (8.8 ± 0.2 mm, p < 0.05 vs. placebo) than in males (9.7 ± 0.2 mm, p= NS vs. placebo) and improved EF in females (56.7 ± 3%, p < 0.05 vs. placebo) but not in males (50.6 + 3%, p= NS vs. placebo). Transcriptomic analysis using Rat_230,2.0 microarrays (Affymetrix) revealed that in females 19% of downregu-lated genes and 44% of upregulated genes post-MI were restored to normal by eplerenone. In contrast, eplerenone only restored 4% of overexpressed genes in males. Together, these data suggest that aldosterone blockade reduces Ml-induced cardiac remodeling and phenotypic alterations of gene expression preferentially in females than in males. The use of transcriptomic signatures to detect greater benefit of eplerenone in females has potential implications for personalized medicine. [source]

    Carvedilol Produces Sustained Long-Term Benefits: Follow-Up at 12 Years

    CONGESTIVE HEART FAILURE, Issue 1 2009
    John F. MacGregor MD
    The authors measured long-term outcomes of patients who initiated carvedilol between 1990 and 1992 to test the hypothesis that carvedilol produces sustained benefits in heart failure patients. The study population consisted of 57 patients who completed a carvedilol placebo-controlled phase II trial. Patients were given open-label carvedilol and were titrated to the maximum dose. Patients were assessed by serial multigated acquisition, echocardiography, and symptom scores. Survival was assessed for all patients and censored as of January 1, 2004. Survival for ischemic vs nonischemic patients was compared using the log-rank test and further compared using Cox regression, controlling for covariates. Etiology of heart failure was ischemic in 15 patients and nonischemic in 42 patients. Median follow-up was 12.9 years. Resting left ventricular ejection fraction (LVEF) and heart failure symptom scores improved at 4 months of treatment and were sustained at 24 months. Left ventricular internal diameter in systole (LVIDS) and left ventricular internal diameter in diastole decreased significantly at 4 and 8 months, respectively, and LVIDS continued to improve at 24 months. Overall mortality was 43% in nonischemic patients and 73% in ischemic patients. In a multivariate analysis, ischemic etiology and baseline LVEF were significant predictors of mortality. Carvedilol produces sustained improvements in left ventricular remodeling and symptoms. Long-term survival is good, particularly in nonischemic patients. [source]

    The Effects of Antihypertensive Treatment on the Doppler-Derived Myocardial Performance Index in Patients with Hypertensive Left Ventricular Hypertrophy: Results from the Swedish Irbesartan in Left Ventricular Hypertrophy Investigation Versus Atenolol (SILVHIA)

    ECHOCARDIOGRAPHY, Issue 7 2009
    Stefan Liljedahl M.D.
    Objectives: To investigate the effects of antihypertensive treatment on the Doppler-derived myocardial performance index (MPI) in patients with hypertensive left ventricular hypertrophy. Methods: The MPI was measured at baseline and after 48 weeks of antihypertensive treatment in 93 participants of the SILVHIA trial, where individuals with primary hypertension and left ventricular hypertrophy were randomized to double blind treatment with either irbesartan or atenolol. Results: Antihypertensive treatment lowered MPI (mean difference ,0.03 ± 0.01, P = 0.04). Changes in MPI by treatment were associated with changes in left ventricular ejection fraction (,-coefficient ,0.35 P = 0.005), stroke volume/pulse pressure (reflecting arterial compliance, ,-coefficient ,0.39 P < 0.001) and peripheral vascular resistance (,-coefficient 0.28 P < 0.04). Furthermore, there was a borderline significant association between changes in MPI and changes in E-wave deceleration time (reflecting diastolic function, ,-coefficient 0.23, P = 0.06). No associations were found between changes in MPI and changes in blood pressure, E/A-ratio, left ventricular mass index, relative wall thickness or heart rate. A stepwise multivariable regression model confirmed the association between changes in MPI and changes in ejection fraction and stroke volume/pulse pressure (all P < 0.05), as well as the trend for E-wave deceleration time (P = 0.08), but not in the case of peripheral vascular resistance. Conclusion: The MPI exhibited a modest decrease after 48 weeks of antihypertensive treatment in patients with hypertensive left ventricular hypertrophy. Changes in MPI were associated with changes in left ventricular function and vascular compliance, rather than with changes in left ventricular remodeling or blood pressure. [source]

    Elongation Index as a New Index Determining the Severity of Left Ventricular Systolic Dysfunction and Mitral Regurgitation in Patients with Congestive Heart Failure

    ECHOCARDIOGRAPHY, Issue 7 2005
    Mehmet Yokusoglu M.D.
    The shape of the left ventricle is an important echocardiographic feature of left ventricular dysfunction. Progression of the mitral regurgitation and consequent left ventricular remodeling is unpredictable in heart failure. Elongation index is an index of left ventricular sphericity. The surface area of the elongated ventricle is larger than that of a spherical one. The objective of this study was to assess the relation between elongation index and the degree of mitral regurgitation along with noninvasive indices of left ventricular function. Thirty-two patients (21 male, 11 female, mean age: 57 ± 6 yrs) with congestive heart failure and mitral regurgitation were included. Patients were stratified into three groups according to vena contracta width as having mild (n = 11), moderate (n = 11) and severe mitral regurgitation (n = 10). The elongation index (EI) was considered as equal to {[(left ventricular internal area-measured) , (theoretical area of the sphere with measured left ventricular volume)]/(theoretical area of the sphere with measured left ventricular volume)}. Ejection fractions by the modified Simpson rule, dP/dt and sphericity index (SI) were also recorded. The relationship between (EI), ejection fraction, dP/dt and SI reached modest statistical significance (p < 0.05). When the EI and SI were compared, the correlation was also significant (p < 0.01). The areas under the receiver operator curve of EI and SI for discriminating dP/dt < 1000 mm Hg/s were 0.833 and 0.733, respectively. In conclusion, the elongation, which defines the shape of the left ventricle, might be related to the systolic function of the left ventricle and the degree of the mitral regurgitation. Further studies are needed to demonstrate its use in other clinical entities. [source]

    Effects of trimetazidine, a partial inhibitor of fatty acid oxidation, on ventricular function and survival after myocardial infarction and reperfusion in the rat

    FUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 4 2010
    Frederic Mouquet
    Abstract Trimetazidine (TMZ), a partial inhibitor of fatty acid oxidation, has been effective in treating chronic angina, but its effects on the development of post-myocardial infarction (MI) left ventricular remodeling are not defined. In this study, we tested whether chronic pre-MI administration of TMZ would be beneficial during and after acute MI. Two-hundred male Wistar rats were studied in four groups: sham + TMZ diet (n = 20), sham + control diet (n = 20), MI + TMZ diet (n = 80), and MI + control diet (n = 80) splitted into one short-term and one long-term experiments. Sham surgery consisted of a thoracotomy without coronary ligation. MI was induced by coronary occlusion followed by reperfusion. Left ventricle (LV) function and remodeling were assessed by serial echocardiography throughout a 24-week post-MI period. LV remodeling was also assessed by quantitative histological analysis of post-MI scar formation at 24 weeks post-MI. During the short-term experiment, 10/80 rats died after MI, with no difference between groups (MI + control = 7/40, MI + TMZ = 3/40, P = 0.3). In the long-term experiment, the deaths occurred irregularly over the 24 weeks with no difference between groups (MI + control = 16% mortality, MI + TMZ = 17%, P = 0.8). There was no difference between groups as regard to LV ejection fraction (MI + control = 36 ± 13%, MI + TMZ = 35 ± 13%, P = 0.6). In this experimental model, TMZ had no effects on the post-MI occurrence of LV dysfunction or remodeling. Further investigations are warranted to assess whether the partial inhibition of fatty acid oxidation may limit the ability of the heart to respond to acute severe stress. [source]

    Gene and Cell Therapy for Heart Disease

    IUBMB LIFE, Issue 2 2002
    Regina M. Graham
    Abstract Heart disease is the most common cause of morbidity and mortality in Western society and the incidence is projected to increase significantly over the next few decades as our population ages. Heart failure occurs when the heart is unable to pump blood at a rate to commensurate with tissue metabolic requirements and represents the end stage of a variety of pathological conditions. Causes of heart failure include ischemia, hypertension, coronary artery disease, and idiopathic dilated cardiomyopathy. Hypertension and ischemia both cause infarction with loss of function and a consequent contractile deficit that promotes ventricular remodeling. Remodeling results in dramatic alterations in the size, shape, and composition of the walls and chambers of the heart and can have both positive and negative effects on function. In 30-40% of patients with heart failure, left ventricular systolic function is relatively unaffected while diastolic dysfunction predominates. Recent progress in our understanding of the molecular and cellular bases of heart disease has provided new therapeutic targets and led to novel approaches including the delivery of proteins, genes, and cells to replace defective or deficient components and restore function to the diseased heart. This review focuses on three such strategies that are currently under development: (a) gene transfer to modulate contractility, (b) therapeutic angiogenesis for the treatment of ischemia, and (c) embryonic and adult stem cell transfer to replace damaged myocardium. [source]

    Pathophysiologic role of myocardial apoptosis in post-infarction left ventricular remodeling

    JOURNAL OF CELLULAR PHYSIOLOGY, Issue 2 2002
    Antonio Abbate
    Left ventricular (LV) remodeling and heart failure (HF) complicate acute myocardial infarction (AMI) even weeks to months after the initial insult. Apoptosis may represent an important pathophysiologic mechanism causing progressive myocardiocyte loss and LV dilatation even late after AMI. This review will discuss the role of apoptosis according to findings in animal experimental data and observational studies in humans in order to assess clinical relevance, determinants, and mechanisms of myocardial apoptosis and potential therapeutic implications. More complete definition of the impact of myocardiocyte loss on prognosis and of the mechanisms involved may lead to improved understanding of cardiac remodeling and possibly improved patients' care. Mitochondrial damage and bcl-2 to bax balance play a central role in ischemia-dependent apoptosis while angiotensin II and ,1 -adrenergic-stimulation may be major causes of receptor-mediated apoptosis. Benefits due to treatment with ACE-inhibitors and ,-blockers appear to be in part due to reduced myocardial apoptosis. Moreover, infarct-related artery patency late after AMI may be a major determinant of myocardial apoptosis and clinical benefits deriving from an open artery late post AMI (the "open artery hypothesis") may be, at least in part, due to reduced myocardiocyte loss. © 2002 Wiley-Liss, Inc. [source]

    Cardiac Allograft Remodeling After Heart Transplantation Is Associated with Increased Graft Vasculopathy and Mortality

    AMERICAN JOURNAL OF TRANSPLANTATION, Issue 1 2009
    E. Raichlin
    The aim of this study was to assess the patterns, predictors and outcomes of left ventricular remodeling after heart transplantation (HTX). Routine echocardiographic studies were performed and analyzed at 1 week, 1 year and 3,5 years after HTX in 134 recipients. At each study point the total cohort was divided into three subgroups based on determination of left ventricle mass and relative wall thickness: (1) NG,normal geometry (2) CR,concentric remodeling and (3) CH,concentric hypertrophy. Abnormal left ventricular geometry was found as early as 1 week after HTX in 85% of patients. Explosive mode of donor brain death was the most significant determinant of CH (OR 2.9, p = 0.01) at 1 week. CH at 1 week (OR 2.72, p = 0.01), increased body mass index (OR 1.1, p = 0.01) and cytomegalovirus viremia (OR , 4.06, p = 0.02) were predictors of CH at 1 year. CH of the cardiac allograft at 1 year was associated with increased mortality as compared to NG (RR 1.87, p = 0.03). CR (RR 1.73, p = 0.027) and CH (RR 2.04, p = 0.008) of the cardiac allograft at 1 year is associated with increased subsequent graft arteriosclerosis as compared to NG. [source]

    Glucagon-like Peptide-1 and Myocardial Protection: More than Glycemic Control

    CLINICAL CARDIOLOGY, Issue 5 2009
    Anjali V. Fields MD
    Pharmacologic intervention for the failing heart has traditionally targeted neurohormonal activation and ventricular remodeling associated with cardiac dysfunction. Despite the multitude of agents available for the treatment of heart failure, it remains a highly prevalent clinical syndrome with substantial morbidity and mortality, necessitating alternative strategies of targeted management. One such area of interest is the ability to modulate myocardial glucose uptake and its impact on cardioprotection. Glucose-insulin-potassium (GIK) infusions have been studied for decades, with conflicting results regarding benefit in acute myocardial infarction. Based on the same concepts, glucagon-like peptide-1-[7,36] amide (GLP-1) has recently been demonstrated to be a more effective alternative in left ventricular (LV) systolic dysfunction. This paper provides a review on the current evidence supporting the use of GLP-1 in both animal models and humans with ischemic and nonischemic cardiomyopathy. Copyright © 2009 Wiley Periodicals, Inc. [source]

    The Late Open Infarct-related Artery Hypothesis: Evidence-based Medicine or Not?

    CLINICAL CARDIOLOGY, Issue 11 2007
    Martin Brueck M.D.
    Abstract Randomized clinical trials have clearly shown that early reperfusion of coronary arteries is the established treatment of myocardial infarction preserving left ventricular function and reducing mortality. However, late patency of the infarct-related artery is an independent predictor of survival leading to the late open-artery hypothesis. This concept implies restoration of antegrade blood flow of the infarct-related artery in patients with myocardial infarction to improve survival by mechanisms less time-dependent or even time-independent. Possible explanations for this benefit include improved left ventricular function and electrical stability by perfusion of hibernating myocardium, accelerated infarct healing and limitation of ventricular remodeling. This review focuses on the evidence of late recanalization of occluded infarct-related arteries in patients with coronary artery disease. Copyright © 2007 Wiley Periodicals, Inc. [source]