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Relative Wall Thickness (relative + wall_thickness)
Selected AbstractsBaseline Echocardiographic Predictors of Dynamic Intraventricular Obstruction of the Left Ventricle during Dobutamine Stress EchocardiogramECHOCARDIOGRAPHY, Issue 10 2009Edmundo Jose Nassri Cāmara M.D., Ph.D. Background: Intraventricular obstruction (IVO) during dobutamine stress echocardiogram (DSE) may be associated with or reproduce symptoms. Predictors of IVO are not well established. Methods: 149 patients were studied at rest and during DSE. The normal range of the left ventricular outflow tract (LVOT) velocities was investigated in 68 healthy patients. Results: 19 patients (13%) developed IVO (peak LVOT velocity > 271 cm/sec). A significant linear correlation was observed between peak LVOT velocity during DSE and the following rest parameters: LV end-diastolic dimension (r =,0.20, P = 0.018), LV end-systolic dimension (r =, 0.27, P = 0.001), relative wall thickness (r = 0.23, P = 0.006), shortening fraction (r = 0.24, P = 0.004), LVOT diameter (r =, 0.20, P = 0.023) and LVOT velocity (r = 0.29, P < 0.0001). Only relative wall thickness (P = 0.012) and LVOT diameter (P = 0.027) were independent predictors of IVO. As a dichotomous variable, a relative wall thickness ,0.44 was the only independent predictor of IVO (OR 5.7, 95% CI 1.6,20, P = 0.006), with sensitivity, specificity, negative predictive value, and positive predictive value of 77%, 62%, 95%, and 21%, respectively, and global accuracy of 63% (area under the ROC curve = 0.7). IVO was significantly associated with general cardiovascular symptoms (P = 0.0006) and with chest pain (P = 0.008). Conclusions: Relative wall thickness and LVOT diameter were independent predictors of obstruction. As a dichotomous variable, a relative wall thickness , 0.44 was the only independent predictor of dynamic IVO. [source] Diagnostic utility of brain-natriuretic peptide for left ventricular diastolic dysfunction in asymptomatic type 2 diabetic patientsDIABETES OBESITY & METABOLISM, Issue 3 2007M. Shimabukuro Aim:, Left ventricular (LV) diastolic dysfunction has been reported to be prevalent in diabetic subjects, but this recognition could often be missed. We evaluated prevalence of LV diastolic dysfunction and diagnostic utility of brain-natriuretic peptide (BNP) in asymptomatic patients with type 2 diabetes mellitus. Research design and methods:, Plasma BNP levels and LV geometry and diastolic filling indices, including the ratio of peak early transmitral Doppler flow (E) over flow propagation velocity (Vp) measured by colour M-mode Doppler echocardiography, were analysed in 98 consecutive asymptomatic patients with type 2 diabetes mellitus and 51 age-matched controls. Results:, The LV mass index and relative wall thickness were higher in diabetic groups than controls without any differences in LV systolic function. The frequency of diastolic dysfunction defined as E/Vp , 1.5 were 31% in diabetic groups and 15% in controls (,2 = 4.364, p = 0.037). By receiver-operating characteristic (ROC) curve analysis, a BNP cutoff value of 19.2 pg/ml in controls had a 53.1% positive predictive value (53.1%) and a high negative predictive value (94.4%) for E/Vp , 1.5, whereas a BNP cutoff value of 18.1 pg/ml in diabetic groups had a 61.8% positive and 97.3% negative predictive values. Conclusions:, The frequency of E/Vp , 1.5 was higher in asymptomatic diabetic patients, suggesting that LV diastolic dysfunction was prevalent. The plasma concentration of BNP could be used to depict LV diastolic dysfunction in such population. [source] Baseline Echocardiographic Predictors of Dynamic Intraventricular Obstruction of the Left Ventricle during Dobutamine Stress EchocardiogramECHOCARDIOGRAPHY, Issue 10 2009Edmundo Jose Nassri Cāmara M.D., Ph.D. Background: Intraventricular obstruction (IVO) during dobutamine stress echocardiogram (DSE) may be associated with or reproduce symptoms. Predictors of IVO are not well established. Methods: 149 patients were studied at rest and during DSE. The normal range of the left ventricular outflow tract (LVOT) velocities was investigated in 68 healthy patients. Results: 19 patients (13%) developed IVO (peak LVOT velocity > 271 cm/sec). A significant linear correlation was observed between peak LVOT velocity during DSE and the following rest parameters: LV end-diastolic dimension (r =,0.20, P = 0.018), LV end-systolic dimension (r =, 0.27, P = 0.001), relative wall thickness (r = 0.23, P = 0.006), shortening fraction (r = 0.24, P = 0.004), LVOT diameter (r =, 0.20, P = 0.023) and LVOT velocity (r = 0.29, P < 0.0001). Only relative wall thickness (P = 0.012) and LVOT diameter (P = 0.027) were independent predictors of IVO. As a dichotomous variable, a relative wall thickness ,0.44 was the only independent predictor of IVO (OR 5.7, 95% CI 1.6,20, P = 0.006), with sensitivity, specificity, negative predictive value, and positive predictive value of 77%, 62%, 95%, and 21%, respectively, and global accuracy of 63% (area under the ROC curve = 0.7). IVO was significantly associated with general cardiovascular symptoms (P = 0.0006) and with chest pain (P = 0.008). Conclusions: Relative wall thickness and LVOT diameter were independent predictors of obstruction. As a dichotomous variable, a relative wall thickness , 0.44 was the only independent predictor of dynamic IVO. [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 2009Stefan 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] Quantitative Evaluation of Left Ventricle Performance from Two Dimensional Echo ImagesECHOCARDIOGRAPHY, Issue 2 2006J. Manivannan M.E. Objectives: We sought to quantify the left ventricle systolic dysfunction by a geometric index from two-dimensional (2D) echocardiography by implementing an automated fuzzy logic edge detection algorithm for the segmentation. Background: The coronary injuries have repercussions on the left ventricle producing changes on wall contractility, the shape of the cavity, and as a whole changes on the ventricular function. Methods: 2D echocardiogram and M-mode recordings were performed over the control group and those with the dysfunctions. From 2D recordings, individual frames were extracted for at least five cardiac cycles and then segmentation of left ventricle was done by automated fuzzy systems. In each frame, the volumes are measured and a geometric index, eccentricity ratio (ER), was derived. The endocardial fractional shortening (FS), midwall fractional shortening (mFS), and the relative wall thickness (RWT) were also measured in each case. Results: Depressed value of endocardial FS (20.39 ± 5.43 vs 34.28 ± 9.36, P = 0.0046), mFS (33 ± 8.3 vs 52.5 ± 11.7, P = 0.0047), and the RWT (0.337 ± 0.096 vs 0.525 ± 0.119, P = 0.0002) was observed with dysfunction. ER measured at end-diastole (2.86 ± 0.703 vs 4.14 ± 0.38) and end-systole (3.14 ± 0.79 vs 5.48 ± 0.74) was found to be decreased in the dysfunction group and more significant at the end-systole (P = 0.00017 vs 6.6E,06). Conclusion: This work concludes that the regional and global left ventricle systolic dysfunction can be assessed by the ER measured at end-diastole and end-systole from 2D echocardiogram and may contribute to the high rate of cardiovascular disorders. [source] An Echocardiographic Analysis of the Long-Term Effects of Carvedilol on Left Ventricular Remodeling, Systolic Performance, and Ventricular Filling Patterns in Dilated CardiomyopathyECHOCARDIOGRAPHY, Issue 7 2005Peter 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] Catheterization,Doppler Discrepancies in Nonsimultaneous Evaluations of Aortic StenosisECHOCARDIOGRAPHY, Issue 5 2005Payam Aghassi M.D. Prior validation studies have established that simultaneously measured catheter (cath) and Doppler mean pressure gradients (MPG) correlate closely in evaluation of aortic stenosis (AS). In clinical practice, however, cath and Doppler are rarely performed simultaneously; which may lead to discrepant results. Accordingly, our aim was to ascertain agreement between these methods and investigate factors associated with discrepant results. We reviewed findings in 100 consecutive evaluations for AS performed in 97 patients (mean age 72 ± 10 yr) in which cath and Doppler were performed within 6 weeks. We recorded MPG, aortic valve area (AVA), cardiac output, and ejection fraction (EF) by both methods. Aortic root diameter, left ventricular end-diastolic dimension (LVIDd) and posterior wall thickness (PWT) were measured by echocardiography and gender, heart rate, and heart rhythm were also recorded. An MPG discrepancy was defined as an intrapatient difference > 10 mmHg. Mean pressure gradients by cath and Doppler were 36 ± 22 mmHg and 37 ± 20 mmHg, respectively (P = 0.73). Linear regression showed good correlation (r = 0.82) between the techniques. An MPG discrepancy was found in 36 (36%) of 100 evaluations; in 19 (53%) of 36 evaluations MPG by Doppler was higher than cath, and in 17 (47%) of 36, it was lower. In 33 evaluations, EF differed by >10% between techniques. Linear regression analyses revealed that EF difference between studies was a significant predictor of MPG discrepancy (P = 0.004). Women had significantly higher MPG than men by both cath and Doppler (43 ± 25 mmHg versus 29 ± 15 mmHg [P = 0.001]; 42 ± 23 mmHg versus 32 ± 15 mmHg [P = 0.014], respectively). Women exhibited discrepant results in 23 (47%) of 49 evaluations versus 13 (25%) of 51 evaluations in men (P = 0.037). After adjustment for women's higher MPG, there was no statistically significant difference in MPG discrepancy between genders (P = 0.22). No significant interactions between MPG and aortic root diameter, relative wall thickness (RWT), heart rate, heart rhythm, cardiac output, and time interval between studies were found. In clinical practice, significant discrepancies in MPG were common when cath and Doppler are performed nonsimultaneously. No systematic bias was observed and Doppler results were as likely yield lower as higher MPGs than cath. EF difference was a significant predictor of discrepant MPG. Aortic root diameter, relative wall thickness, heart rate, heart rhythm, cardiac output, presence or severity of coronary artery disease, and time interval between studies were not predictors of discrepant results. [source] Fatty acid metabolism assessed by 125I-iodophenyl 9-methylpentadecanoic acid (9MPA) and expression of fatty acid utilization enzymes in volume-overloaded heartsEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 3 2004T. Miyamoto Abstract Background, The peroxisome proliferator-activated receptor (PPAR) , is a member of the nuclear receptor superfamily and regulates gene expression of fatty acid utilization enzymes. In cardiac hypertrophy and heart failure by pressure-overload, myocardial energy utilization reverts to the fetal pattern, and metabolic substrate switches from fatty acid to glucose. However, myocardial metabolism in volume-overloaded hearts has not been rigorously studied. The aim of the present study was to examine fatty acid metabolism and protein expressions of PPAR, and fatty acid oxidation enzymes in volume-overloaded rabbit hearts. Methods, Volume-overload was induced by carotid-jugular shunt formation. Sham-operated rabbits were used as control. Chronic volume-overload increased left ventricular weight and ventricular cavity size, and relative wall thickness was decreased, indicating eccentric cardiac hypertrophy. 125I-iodophenyl 9-methylpentadecanoic acid (9MPA) was intravenously administered, and animals were sacrificed at 5 min after injection. The 9MPA was rapidly metabolized to iodophenyl-3-methylnonanoic acid (3MNA) by ,-oxidation. Lipid extraction from the myocardium was performed by the Folch method, and radioactivity distribution of metabolites was assayed by thin-layer chromatography. The protein was extracted from the left ventricular myocardium, and levels of PPAR, and fatty acid oxidation enzymes were examined by Western blotting. Results, Myocardial distribution of 9MPA tended to be more heterogeneous in shunt than in sham rabbits (P = 0·06). In volume-overloaded hearts by shunt, the conversion from 9MPA to 3MNA by ,-oxidation was faster than the sham-control hearts (P < 0·05). However, protein levels of PPAR, and fatty acid utilization enzymes were unchanged in shunt rabbits compared with sham rabbits. Conclusions, These data suggest that myocardial fatty acid metabolism is enhanced in eccentric cardiac hypertrophy by volume-overload without changes in protein expressions of PPAR, and fatty acid utilization enzymes. Our data may provide a novel insight into the subcellular mechanisms for the pathological process of cardiac remodelling in response to mechanical stimuli. [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] Cardiac Allograft Remodeling After Heart Transplantation Is Associated with Increased Graft Vasculopathy and MortalityAMERICAN JOURNAL OF TRANSPLANTATION, Issue 1 2009E. 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] |