Disease relevance of Ventricular Remodeling

• These results suggest that G-CSF promotes survival of cardiac myocytes and prevents left ventricular remodeling after myocardial infarction through the functional communication between cardiomyocytes and noncardiomyocytes [1].
• BACKGROUND: Endothelin A (ETA) receptor antagonists have been shown to improve ventricular remodeling and survival in rats when started 10 days after infarction [2].
• Nonetheless, favorable ventricular remodeling has been reported in asymptomatic patients, and long-term nifedipine use has delayed the need for operation in asymptomatic patients with chronic aortic regurgitation [3].
• Angiotensin II contributes to ventricular remodeling by promoting both cardiac hypertrophy and apoptosis; however, the mechanism underlying the latter phenomenon is poorly understood [4].
• Prevention of further left ventricular dysfunction can be accomplished by inhibiting neurohormonal processes and ventricular remodeling that occur in heart failure using ACE inhibitors, nitrates and hydralazine, or beta blockers [5].

High impact information on Ventricular Remodeling

• Ventricular remodeling: hype or hope [6]?
• Angiotensin-converting enzyme inhibition and ventricular remodeling after myocardial infarction [7].
• Targeted deletion of apoptosis signal-regulating kinase 1 attenuates left ventricular remodeling [8].
• We evaluated the role of kinins in postinfarction ventricular remodeling and their potential contribution to the antiremodeling effects of ACE inhibition and angiotensin II type 1 (AT1) receptor blockade [9].
• Cardiovascular death and left ventricular remodeling two years after myocardial infarction: baseline predictors and impact of long-term use of captopril: information from the Survival and Ventricular Enlargement (SAVE) trial [10].

Chemical compound and disease context of Ventricular Remodeling

• Effect of enalapril on ventricular remodeling and function during healing after anterior myocardial infarction in the dog [11].
• Effect of prolonged nitrate therapy on left ventricular remodeling after canine acute myocardial infarction [12].
• Relationship between transcardiac extraction of aldosterone and left ventricular remodeling in patients with first acute myocardial infarction: extracting aldosterone through the heart promotes ventricular remodeling after acute myocardial infarction [13].
• Impact of hydroxymethylglutaryl coenzyme a reductase inhibition on left ventricular remodeling after myocardial infarction: an experimental serial cardiac magnetic resonance imaging study [14].
• We sought to compare the effects of captopril plus isosorbide dinitrate versus monotherapy on infarct collagen content and left ventricular remodeling and function during healing after myocardial infarction [15].

Biological context of Ventricular Remodeling

• Conscious hemodynamic measurements and remodeling data obtained at 1 year in the surviving rats (n = 5 for captopril; n = 9 for losarton) revealed no differences in heart weight, left ventricular pressure, dP/dt, cardiac index, time constant of relaxation or any variable of left ventricular remodeling [16].
• OBJECTIVE: The purpose of this study was to examine the effect of amlodipine, a long-acting calcium antagonist, on the left ventricular remodeling, including systolic and diastolic dysfunction, the change of cardiac gene expression in the myocardial infarcted rats (MI) [17].
• We investigated whether clenbuterol improves left ventricular remodeling, myocardial apoptosis and has synergy with a beta(1) antagonist, metoprolol, in a model of ischemic HF [18].
• However, the effect of angiotensin on the signal transduction pathway of left ventricular remodeling after myocardial infarction is as yet unknown [19].
• In the longitudinal assessment, left ventricular remodeling was dependent on change of dosage of cyclosporine and interval changes of blood pressure levels [20].

Anatomical context of Ventricular Remodeling

• Intrinsic myocyte dysfunction and tyrosine kinase pathway activation underlie the impaired wall thickening of adjacent regions during postinfarct left ventricular remodeling [21].
• CONCLUSIONS--Pathogenetic changes of the residual myocardium associated with NIDDM may adversely influence the process of left ventricular remodeling after MI, especially in patients with increased left ventricular EDV [22].
• Peroxisome proliferator activated-receptor agonism and left ventricular remodeling in mice with chronic myocardial infarction [23].
• Recently, we showed that 1) increased mast cell density is associated with adverse ventricular remodeling and 2) chemically induced mast cell degranulation using compound 48/80 resulted in remarkable changes in matrix metalloproteinase (MMP) activity, cardiac collagen structure, and cardiac diastolic function in normal male rats [24].
• To characterize the effect of enalapril on immune alterations in the late phase of ventricular remodeling after myocardial infarction, rats underwent left coronary artery ligation followed by 6 weeks of either enalapril or placebo treatment [25].

Associations of Ventricular Remodeling with chemical compounds

• Relative effects of alpha 1-adrenoceptor blockade, converting enzyme inhibitor therapy, and angiotensin II subtype 1 receptor blockade on ventricular remodeling in the dog [26].
• Those changes were suggestive of partial reversal of left ventricular remodeling by enalapril administration [27].
• Progressive ventricular remodeling in response to diffuse isoproterenol-induced myocardial necrosis in rats [28].
• These changes demonstrate a beneficial effect of carvedilol on left ventricular remodeling in heart failure [29].
• Whether nitrates can attenuate chronic left ventricular remodeling is unknown [30].

Gene context of Ventricular Remodeling

• Interaction between AT1 and AT2 receptors during postinfarction left ventricular remodeling [31].
• Alteration in erythropoietin-induced cardioprotective signaling by postinfarct ventricular remodeling [32].
• Adipocytes and VAT are able to produce large amounts of monocyte chemoattractant protein 1 (MCP-1), a chemokine directly involved in ventricular remodeling [33].
• BACKGROUND: Matrix metalloproteinase (MMP) plays an important role in the development of ventricular remodeling in an animal model of acute myocardial infarction (AMI) [34].
• Thus, the serum HGF concentration on day 7 after AMI is mostly from noncardiac sources and predicts left ventricular remodeling [35].

Analytical, diagnostic and therapeutic context of Ventricular Remodeling

• Echocardiography demonstrated beneficial effects of CCR2 deficiency on left ventricular remodeling at 7 and 28 days after MI [36].
• This thesis has been supported and furthered by studies in animal models of heart failure that demonstrate the salutary, short-term effects of ET-1 receptor antagonists on hemodynamic function, as well as improved ventricular remodeling and survival with long-term administration [37].
• Because ANG-(1-7) is elevated after treatment with angiotensin-converting enzyme inhibitors or AT(1) receptor blockers, ANG-(1-7) may contribute to their beneficial effects on cardiac dysfunction and ventricular remodeling after myocardial infarction [38].
• 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 [39].
• CONCLUSIONS: In patients with ischemic cardiomyopathy not only the amount of dysfunctional but viable myocardium but also the extent of left ventricular remodeling determines the improvement in function following myocardial revascularization [40].

References