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LV End-diastolic Diameter (lv + end-diastolic_diameter)
Selected AbstractsBaseline Characteristics of Patients Randomized in the Resynchronization Reverses Remodeling in Systolic Left Ventricular Dysfunction (REVERSE) StudyCONGESTIVE HEART FAILURE, Issue 2 2008Cecilia Linde MD The Resynchronization Reverses Remodeling in Systolic Left Ventricular Dysfunction (REVERSE) study is a randomized controlled trial currently assessing the safety and efficacy of cardiac resynchronization therapy in patients with asymptomatic left ventricular (LV) dysfunction with previous symptoms of mild heart failure. This paper describes the baseline characteristics of randomized patients; 610 patients with New York Heart Association (NYHA) class II (82.3%) heart failure or asymptomatic (NYHA class I) LV dysfunction with previous symptoms (17.7%) were randomized in 73 centers. The mean age was 62.5±11.0 years, the mean LV ejection fraction was 26.7%±7.0%, and the mean LV end-diastolic diameter was 66.9±8.9 mm. A total of 97% of patients were taking angiotensin-converting enzyme inhibitors or angiotensin receptor blockers and 95.1% were taking ,-blockers, which were at the target dose in 35.1% of patients. Compared with previous randomized cardiac resynchronization therapy trials, REVERSE patients are on better pharmacologic treatment, are younger, and have a narrower QRS width despite similar LV dysfunction. [source] Prognostic significance of soluble interleukin-2 receptor levels in patients with dilated cardiomyopathyEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 6 2003C. J. Limas Abstract Background Activation of T lymphocytes is thought to mediate myocardial dysfunction in dilated cardiomyopathy (CMP), probably through cytotoxic cytokines, but its value as a prognostic factor has not been evaluated. Methods For 2 years we prospectively followed 76 patients (65 males, 11 females, age 49 ± 7 years) with CMP and New York Heart Association(NYHA) Class II,III heart failure; left ventricular (LV) function was assessed echocardiographically. Thirty-three patients (28 males, five females, age 52 ± 6 years) with ischaemic heart disease (IHD) and similar NYHA and LV function characteristics were used as controls. Serum sIL-2R levels, peripheral blood lymphocyte proliferation (basal, + concanavalin A) and HLA-DQB1 genotyping was carried out in all patients. Results The CMP patients had increased sIL-2R levels (1259 ± 130 pg mL,1) compared with the IHD patients (703 ± 80 pg mL,1, P < 0·01, only 3 > 800 pg mL,1). In the CMP patients, there was a significant (r = +0·45, P= 0·04) correlation between sIL-2R and the LV end-diastolic diameter but not with the LV ejection fraction or NYHA Class. During the 24-month follow up, 17 of the CMP patients had an adverse clinical course (death, need for cardiac transplantation, or worsening heart failure). Of these, 14 (75%) had elevated (, 800 pg mL,1) sIL-2R levels (Group I) compared with only five (6%) with a stable clinical course (Group II). Neither [3H] thymidine incorporation into the peripheral blood lymphocytes nor the excess of HLA-DQB1-30 histidine homozygotes in the Group I patients (38% vs. 17%, P < 0·05) could predict the clinical outcome. Conclusion Increased sIL-2R levels in CMP patients are an independent predictor of a more aggressive clinical course. [source] Left Ventricle and Left Atrium Remodeling after Mitral Valve Replacement in Case of Mixed Mitral Valve Disease of Rheumatic OriginJOURNAL OF CARDIAC SURGERY, Issue 4 2010n Ender Topal M.D. Methods: Thirty consecutive elective patients with MVR for mixed mitral disease of rheumatic origin formed the study group. Of these, 21 (70%) were women and the mean age was 37 years. Transthoracic echocardiography was performed prior to surgery, at three-month follow-up, and at three-year follow-up except for the latest nine patients. Results: The mean duration of follow-up was 3.6 ± 1.8 years. MVR surgery improved the functional class (mean New York Heart Association [NYHA] class) at three-year follow-up (p = 0.008). LV end-diastolic diameter and LA sizes decreased after MVR. Total chordal preservation causes better outcome, regarding to LV ejection fraction (LVEF) and NYHA functional class of patients. Preoperative high NYHA class, low LVEF, and high LV end-systolic diameter (LVESd) resulted with postoperative LV dysfunction (p were < 0.001, < 0.001, and 0.006, respectively). Conclusion: In patients with mixed mitral valve disease, MVR enhanced LV and LA remodeling resulting in better NYHA function. Preoperative NYHA, LVEF, and LVESd were significant predictors of postoperative LV function. (J Card Surg 2010;25:367-372) [source] Calcineurin Inhibition Ameliorates Structural, Contractile, and Electrophysiologic Consequences of Postinfarction RemodelingJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 9 2001LILI DENG M.S. Calcineurin Inhibition and Postinfarction Remodeling.Introduction: After myocardial infarction (MI), the heart undergoes an adaptive remodeling process characterized by hypertrophy of the noninfarcted myocardium. Calcineurin, a Ca2+, calmodulin-regulated phosphatase, has been shown to participate in hypertrophic signal transduction. Methods and Results: We investigated the effects of calcineurin inhibition by cyclosporin A on key structural, contractile, and electrophysiologic alterations of post-MI remodeling. Male Sprague-Dawley rats were divided into four groups: (1) sham-operated; (2) sham + cyclosporin A; (3) post-MI (left anterior descending coronary artery ligation); and (4) MI + cyclosporin A. Cyclosporin A (25 mg/kg/day) was initiated 2 days before surgery and continued for 30 days. Hypertrophy was evaluated by echocardiography and by changes in membrane capacitance of isolated myocytes from noninfarcted left ventricle (LV). The effects of cyclosporin A on hemodynamics and cardiac dimensions were investigated, and changes in diastolic function were correlated with changes in protein phosphatase 1 activity and the basal level of phosphorylated phospholamban. The effects of cyclosporin A on Kv4.2/Kv4.3 genes expression and transient outward K + current (Ito) density also were evaluated. One of 12 rats in the post-MI group and 2 of 12 rats in the post-MI + cyclosporin A group died within 48 hours after MI. There were no late deaths in either MI group. There was no evidence of heart failure (lung congestion and/or pleural effusion) in the two groups 4 weeks post-MI. Calcineurin phosphatase activity increased 1.9-fold in post-MI remodeled LV myocardium, and cyclosporin A administration resulted in an 86% decrease in activity. There were statistically significant decreases of LV end-diastolic pressure, LV end-diastolic diameter, and LV relative wall thickness in the post-MI + cyclosporin A group compared with the post-MI group. On the other hand, there was no significant difference in LV end-systolic diameter or peak rate of LV pressure increase between the two post-MI groups. Protein phosphatase 1 activity was elevated by 36% in the post-MI group compared with sham, and this correlated with a 79% decrease in basal level of p16, phospholamban. In the post-MI + cyclosporin A group, the increase in protein phosphatase 1 activity was much less (18% vs 36%; P < 0.05), and the decrease in basal level of p16-phospholamban was markedly ameliorated (20% vs 79%; P < 0.01). The decreases in mRNA levels of Kv4.2 and Kv4.3 and Ito density in the LV of the post-MI + cyclosporin A group were significantly less compared with the post-MI group. Conclusion: Our results show that calcineurin inhibition by cyclosporin A partially ameliorated post-MI remodeled hypertrophy, diastolic dysfunction, decrease in basal level of phosphorylated phospholamban, down-regulation of key K + genes expression, and decrease of K + current, with no adverse effects on systolic function or mortality in the first 4 weeks after MI. [source] Effects of combined inhibition of the Na+,H+ exchanger and angiotensin-converting enzyme in rats with congestive heart failure after myocardial infarctionBRITISH JOURNAL OF PHARMACOLOGY, Issue 5 2005Hartmut Ruetten We investigated the single vs the combined long-term inhibition of Na+,H+ exchanger-1 (NHE-1) and ACE in rats with congestive heart failure induced by myocardial infarction (MI). Rats with MI were randomized to receive either placebo, cariporide (3000 p.p.m. via chow), ramipril (1 mg kg,1 day,1via drinking water) or their combination for 18 weeks starting on day 3 after surgery. Cardiac morphology and function was assessed by echocardiography and by means of a 2.0 F conductance catheter to determine left ventricular (LV) pressure volume relationships. MI for 18 weeks resulted in an increase in LV end-diastolic diameter (LVDed) in the placebo-treated group when compared to sham (placebo: 1.1±0.04 cm; sham: 0.86±0.01; P<0.05). Combined inhibition of NHE-1 and ACE, but not the monotherapies, significantly reduced LVDed (1.02±0.02 cm). Preload recruitable stroke work (PRSW), dp/dtmax (parameter of systolic function) and end-diastolic pressure volume relationship (EDPVR, diastolic function) were significantly impaired in placebo-treated MI group (PRSW: 39±7 mmHg; dp/dtmax: 5185±363 mmHg s,1; EDPVR: 0.042±0.001 mmHg ,l,1; all P<0.05). Cariporide treatment significantly improved PRSW (64±7 mmHg), dp/dtmax (8077±525 mmHg s,1) and EDPVR (0.026±0.014 mmHg ,l,1), and reduced cardiac hypertrophy in rats with MI. Combined inhibition of NHE-1 and ACE had even a more pronounced effect on PRSW (72±5 mmHg) and EDPVR (0.026±0.014 mmHg ,l,1), as well as cardiac hypertrophy that, however, did not reach statistical significance compared to cariporide treatment alone. The NHE-1 inhibitor cariporide significantly improved LV remodeling and function in rats with congestive heart failure induced by MI. The effect of cariporide was comparable or tended to be stronger (e.g. systolic function) compared to ramipril. Combined treatment with cariporide and ramipril tended to be more effective on LV remodeling in rats with heart failure than the single treatments. Thus, inhibition of the NHE-1 may be a promising novel therapeutic approach for the treatment of congestive heart failure. British Journal of Pharmacology (2005) 146, 723,731. doi:10.1038/sj.bjp.0706381 [source] | ||||||||||