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End-systolic Diameter (end-systolic + diameter)
Selected AbstractsOutcomes and Prognostic Factors of Systolic as Compared With Diastolic Heart Failure in Urban AmericaCONGESTIVE HEART FAILURE, Issue 1 2005Peter A. McCullough MD We sought to describe a large heart failure (HF) population with respect to systolic and diastolic abnormalities in terms of demographics, echocardiographic parameters, and survival. Using data abstracted from the Resource Utilization Among Congestive Heart Failure (REACH) study, a targeted subpopulation of 3471 patients had electrocardiographic, echocardiographic, and clinical data taken from automated sources during the first year of diagnosis. Among the HF population, 1811 (52.2%) had diastolic HF. Prevalence of diastolic HF trended with age, from 46.4% in those less than 45 years to 58.7% in those 85 years or older (p=0.001 for trend). Patients with diastolic HF had a higher mean ejection fraction (55.7% vs. 28.0%), lower left ventricular end-systolic diameter (3.11 vs. 4.74 cm), and lower left atrium: aortic outlet ratio (1.28 vs. 1.38) (p=0.001 for each comparison). Annualized age, sex, and race-adjusted mortality were 11.2% and 13.0% for those with diastolic and systolic HF, respectively (p=0.001). In a large, racially mixed, urban HF population, those with diastolic HF predominate and enjoy better-adjusted survival than counterparts with systolic HF. [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] Predictors of Failure to Cure Atrial Fibrillation with the Mini-Maze OperationJOURNAL OF CARDIAC SURGERY, Issue 1 2004Zoltan A. Szalay M.D. A reduction in the number of right and left atrial incisions could decrease the operative time. The aim of this study was to assess the results of a mini-maze operation and to define predictors of its failure. Methods: Between 1995 and 2000, 72 patients (mean age 64 ± 9 years) undergoing cardiac surgery had a concomitant mini-maze operation for symptomatic chronic atrial fibrillation. Three and 12 months postoperatively, heart rhythm and left atrial transport functions were assessed by electrophysiology, echocardiography, and magnetic resonance imaging. Multivariate analysis was performed to identify predictors of failure of the mini-maze operation. Results: Operative mortality was 1.4% (1/72). Death during follow-up occurred in 5.6% of patients (4/71), in one due to chronic heart failure. After 1 year, 80% of patients (48/60) were either in sinus rhythm (n = 43; 72%) or had a pacemaker (n = 5; 8%) implanted due to sick sinus syndrome. Intermittent and chronic atrial fibrillation was found in 20% of patients (12/60). Preoperative duration of atrial fibrillation (p = 0.05), preoperative left atrial diameter (p = 0.001), preoperative right atrial diameter (p = 0.02), a reduced left ventricular ejection fraction (p = 0.03), an increased left ventricular end-diastolic diameter (p = 0.04), and the presence of mitral valve stenosis (p = 0.001) were found to be univariate predictors of failure of the mini-maze operation 1 year postoperatively. Multivariate analysis defined preoperative diagnosis of mitral valve stenosis (p = 0.005; OR 117.5), longer duration of preoperative atrial fibrillation (p = 0.01; OR 1.33), and increased preoperative left ventricular end-systolic diameter (p = 0.02; OR 1.2) as incremental independent risk factors for failure of the mini-maze operation to cure chronic atrial fibrillation. Conclusion: The mini-maze operation is a safe procedure with similar results to that of Cox's Maze-III operation. The less-invasive mini-maze operation could be applicable even to patients with severely reduced left ventricular function, in whom complex cardiac surgery has to be performed concomitantly as well as in those presenting severe comorbidities. (J Card Surg 2004;19:1-6) [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] Response to Cardiac Resynchronization Therapy in Patients with Heart Failure and Renal InsufficiencyPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 7 2010EVAN C. ADELSTEIN M.D. Background: Renal insufficiency (RI) adversely impacts prognosis in heart failure (HF) patients, partly because renal and cardiac dysfunction are intertwined, yet few cardiac resynchronization therapy (CRT) studies have examined patients with moderate-to-severe RI. Methods: We analyzed 787 CRT-defibrillator (CRT-D) recipients with a glomerular filtration rate (GFR) measured prior to implant. Patients were grouped by GFR (in mL/min/1.73 m2): ,60 (n = 376), 30,59 (n = 347), and <30 (n = 64). Overall survival, changes in left ventricular (LV) ejection fraction and LV end-systolic diameter, and GFR change at 3,6 months were compared among CRT-D groups and with a control cohort (n = 88), also stratified by GFR, in whom LV lead implant was unsuccessful and a standard defibrillator (SD) was placed. All patients met clinical criteria for CRT-D. Results: Among CRT-D recipients, overall survival improved incrementally with higher baseline GFR (for each 10 mL/min/1.73 m2 increase, corrected hazard ratio [HR] 1.21, 95% confidence interval [CI] 1.13,1.30, P < 0.0001). Survival among SD and CRT-D patients within GFR < 30 and GFR , 60 groups was similar, whereas CRT-D recipients with GFR 30,59 had significantly better survival compared to SD counterparts (HR 2.23, 95% CI 1.34,3.70; P = 0.002). This survival benefit was associated with improved renal and cardiac function. CRT recipients with GFR , 60 derived significant echocardiographic benefit but experienced a GFR decline, whereas those with GFR < 30 had no echocardiographic benefit but did improve GFR. Conclusions: CRT may provide the largest survival benefit in HF patients with moderate RI, perhaps by improving GFR and LV function. Severe baseline RI predicts poor survival and limited echocardiographic improvement despite a modest GFR increase, such that CRT may not benefit those with GFR < 30 mL/min/1.73 m2. CRT recipients with normal renal function derive echocardiographic benefit but no overall survival advantage. (PACE 2010; 850,859) [source] The Effect of Beta-Blocker (Carvedilol) Therapy on N-Terminal Pro-Brain Natriuretic Peptide Levels and Echocardiographic Findings in Patients with Congestive Heart FailureECHOCARDIOGRAPHY, Issue 2 2007Fuat Gundogdu M.D. Background: The favorable effects of beta-blockers on decreasing mortality in contemporary heart failure management have been demonstrated in recent years. N-terminal pro-brain natriuretic (NT-proBNP) peptide levels increase in patients with heart failure. The purpose of this study was to investigate the correlation between the NT-proBNP levels and echocardiographic findings for the patients who received carvedilol therapy in addition to standard therapy for congestive heart failure. Methods and Results: A total of 25 patients with symptomatic congestive heart failure and 25 healthy individuals were enrolled in the study. Before introducing beta-blocker into their therapy regimens, baseline transthoracic echocardiography recordings were made and venous blood samples were drawn for establishing NT-proBNP levels. The patients were administered with a minimum dose of carvedilol. Three months after reaching the maximum tolerable dose, blood samples were drawn from the patients once again for NT-proBNP measurements, and transthoracic echocardiography was performed. There was a significant drop in plasma NT-proBNP levels at the end of the study in comparison to the baseline values (baseline: 381.20±35.06 pg/mL, at the end of the third month: 254.44±28.64 pg/mL; P < 0.001). While left ventricular end-diastolic and end-systolic diameters were observed to have significantly decreased as a result of the therapy (P < 0.001), left ventricular ejection fraction (P<0.001) was established to have increased significantly. Conclusions: Carvedilol therapy resulted in a marked decrease in plasma NT-proBNP levels and increase left ventricular ejection fraction in patients with congestive heart failure. [source] Long-Term Survival in Patients Treated with Cardiac Resynchronization Therapy: A 3-Year Follow-Up Study from the InSync/InSync ICD Italian RegistryPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2006MAURIZIO GASPARINI Background: Studies reporting the long-term survival of patients treated with cardiac resynchronization therapy (CRT) outside the realm of randomized controlled trials are still lacking. The aim of this study was to quantify the survival of patients treated with CRT in clinical practice and to investigate the long-term effects of CRT on clinical status and echocardiographic parameters. Methods: The study population consisted of 317 consecutive patients with implanted CRT devices from eight Italian University/Teaching Hospitals. The patients were enrolled in a national observational registry and had a minimum follow-up of 2 years. A visit was performed in surviving patients and mortality data were obtained by hospital file review or direct telephone contact. Results: During the study period, 83 (26%) patients died. The rate of all-cause mortality was significantly higher in ischemic than nonischemic patients (14% vs 8%, P = 0.002). Multivariate analysis showed that ischemic etiology (HR 1.72, CI 1.06,2.79; P = 0.028) and New York Heart Association (NYHA) class IV (HR 2.87, CI 1.24,6.64; P = 0.014) were the strongest predictors of all-cause mortality. The effects of CRT persisted at long-term follow-up (for at least 2 years) in terms of NYHA class improvement, increase of left ventricular ejection fraction, decrease of QRS duration (all P = 0.0001), and reduction of left ventricular end-diastolic and end-systolic diameters (P = 0.024 and P = 0.011, respectively). Conclusions: During long-term (3 years) follow-up after CRT, total mortality rate was 10%/year. The outcome of ischemic patients was worse mainly due to a higher rate of death from progressive heart failure. Ischemic etiology along with NYHA class IV was identified as predictors of death. Benefits of CRT in terms of clinical function and echocardiographic parameters persisted at the time of long-term follow-up. [source] P-Wave Duration and Dispersion in Obese SubjectsANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 1 2008Feridun Kosar M.D. Background: Although previous studies have documented a variety of electrocardiogram (ECG) abnormalities in obesity, P-wave alterations, which represent an increased risk for atrial arrhythmia, have not been studied very well in these patients. The aim of the present study was to evaluate P-wave duration and P dispersion (Pd) in obese subjects, and to investigate the relationship between P-wave measurements, and the clinical and echocardiographic variables. Methods: The study population consisted of 52 obese and 30 normal weight control subjects. P-wave duration and P-wave dispersion were calculated on the 12-lead ECG. As echocardiographic variables, left atrial diameter (LAD), left ventricular end-diastolic, and end-systolic diameters (LVDD and LVSD), left ventricular ejection fraction (LVEF), interventricular septum thickness (IVST), left ventricular posterior wall thickness (LVPWT), and left ventricular mass (LVM) of the obese and the control subjects were measured by means of transthoracic echocardiography. Results: There were statistically significant differences between obese and controls as regards to Pmax (maximum P-wave duration) and Pd (P dispersion) (P < 0.001 and P < 0.001, respectively). Pmin (minimum P wave duration) was similar in both groups. Correlation analysis showed that Pd in the obese patients was related to any the clinical and echocardiographic parameters including BMI, LAD, LVDD, IVST, LVPWT, and LVM. Conclusion: Our data suggest that obesity affects P-wave dispersion and duration, and changes in P dispersion may be closely related to the clinical and the echocardiographic parameters such as BMI, LAD, IVST, LVPWT, and LVM. [source] | ||||||||||