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LV Wall Thickness (lv + wall_thickness)
Selected AbstractsImpact of Body Mass Index on Markers of Left Ventricular Thickness and Mass Calculation: Results of a Pilot AnalysisECHOCARDIOGRAPHY, Issue 3 2005Ranjini Krishnan M.D. Specific correlations between body mass index (BMI) and left ventricular (LV) thickness have been conflicting. Accordingly, we investigated if a particular correlation exists between BMI and echocardiographic markers of ventricular function. Methods: A total of 122 patients, referred for routine transthoracic echocardiography, were included in this prospective pilot study using a 3:1 randomization approach. Patient demographics were obtained using a questionnaire. Results: Group I consisted of 80 obese (BMI was >30 kg/m2), Group II of 16 overweight (BMI between 26 and 29 kg/m2), and Group III of 26 normal BMI (BMI < 25 kg/m2) individuals. No difference was found in left ventricular wall thickness, LV end-systolic cavity dimension, fractional shortening (FS), or pulmonary artery systolic pressure (PASP) among the groups. However, mean LV end-diastolic cavity dimension was greater in Group I (5.0 ± 0.9 cm) than Group II (4.6 ± 0.8 cm) or Group III (4.4 ± 0.9 cm; P < 0.006). LV mass indexed to height2.7 was also significantly larger in Group I (61 ± 21) when compared to Group III (48 ± 19; P < 0.001). Finally, left atrial diameter (4.3 ± 0.7 cm) was also larger (3.8 ± 0.6 and 3.6 ± 0.7, respectively; P < 0.00001).Discussion: We found no correlation between BMI and LV wall thickness, FS, or PASP despite the high prevalence of diabetes and hypertension in obese individuals. However, obese individuals had an increased LV end-diastolic cavity dimension, LV mass/height2.7, and left atrial diameter. These findings could represent early markers in the sequence of cardiac events occurring with obesity. A larger prospective study is needed to further define the sequence of cardiac abnormalities occurring with increasing BMI. [source] Induction of Angiogenesis and Inhibition of Apoptosis by Hepatocyte Growth Factor Effectively Treats Postischemic Heart FailureJOURNAL OF CARDIAC SURGERY, Issue 1 2005Vasant Jayasankar M.D. Hepatocyte growth factor (HGF) is a potent angiogenic and anti-apoptotic protein whose receptor is upregulated following MI. This study was designed to investigate the ability of HGF to prevent heart failure in a rat model of experimental MI. Methods: The rats underwent direct intramyocardial injection with replication-deficient adenovirus encoding HGF (n = 7) or null virus as control (n = 7) 3 weeks following ligation of the left anterior descending coronary artery. Analysis of the following was performed 3 weeks after injection: cardiac function by pressure,volume conductance catheter measurements; LV wall thickness; angiogenesis by Von Willebrand's factor staining; and apoptosis by the TUNEL assay. The expression levels of HGF and the anti-apoptotic factor Bcl-2 were analyzed by Western blot. Results: Adeno-HGF-treated animals had greater preservation of maximum LV pressure (HGF 77 ± 3 vs. control 64 ± 5 mmHg, p < 0.05), maximum dP/dt (3024 ± 266 vs. 1907 ± 360 mmHg/sec, p < 0.05), maximum dV/dt (133 ± 20 vs. 84 ± 6 ,L/sec, p < 0.05), and LV border zone wall thickness (1.98 ± 0.06 vs. 1.53 ± 0.07 mm, p < 0.005). Angiogenesis was enhanced (151 ± 10.0 vs. 90 ± 4.5 endothelial cells/hpf, p < 0.005) and apoptosis was reduced (3.9 ± 0.3 vs. 8.2 ± 0.5%, p < 0.005). Increased expression of HGF and Bcl-2 protein was observed in the Adeno-HGF-treated group. Conclusions: Overexpression of HGF 3 weeks post-MI resulted in enhanced angiogenesis, reduced apoptosis, greater preservation of ventricular geometry, and preservation of cardiac contractile function. This technique may be useful to treat or prevent postinfarction heart failure. [source] Impact of QT Variables on Clinical Outcome of Genotyped Hypertrophic CardiomyopathyANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 1 2009Katsuharu Uchiyama M.D. Background: Although QT variables such as its interval and/or dispersion can be clinical markers of ventricular tachyarrhythmia, few data exist regarding the role of QT variables in genotyped hypertrophic cardiomyopathy (HCM). Therefore, we analyzed QT variables in genotyped subjects with or without left ventricular hypertrophy (LVH). Methods: QT variables were analyzed in 111 mutation and 43 non-mutation carriers who were divided into three groups: A, those without ECG abnormalities and echocardiographically determined LVH (wall thickness ,13 mm); B, those with ECG abnormalities but LVH; and C, those with ECG abnormalities and LVH. We also examined clinical outcome of enrolled patients. Results: Maximal LV wall thickness in group C (19.0 ± 4.3 mm, mean ±SD) was significantly greater than that in group A (9.2 ± 1.8) and group B (10.4 ± 1.8). Under these conditions, maximum QTc interval and QT dispersion were significantly longer in group C than those in group A (438 ± 38 ms vs 406 ± 30 and 64 ± 31 vs 44 ± 18, respectively; P < 0.05). QTc interval and QT dispersion in group B (436 ± 50 and 64 ± 22 ms) were also significantly greater than those in group A. During follow-up periods, four sudden cardiac deaths and one ventricular fibrillation were observed in group C, and two nonlethal ventricular tachyarrhythmias were observed in group B. Conclusions: Patients with HCM-related gene mutation accompanying any ECG abnormalities frequently exhibited impaired QT variables even without LVH. We suggest that careful observation should be considered for those genotyped subjects. [source] Adaptative or maladaptative hypertrophy, different spatial distribution of myocardial contractionCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 1 2010Francesco Cappelli Summary Background:, Left ventricular hypertrophy (LVH) may be an adaptative remodelling process induced by physical training, or result from pathological stimuli. We hypothesized that different LVH aetiology could lead to dissimilar spatial distribution left ventricular (LV) contraction, and compared different components of LV contraction using 2-dimensional (2-D) speckle tracking derived strain in subjects with adaptative hypertrophy (endurance athletes), maladaptative hypertrophy (hypertensive patients) and healthy controls. Method:, We enrolled 22 patients with essential hypertension, 50 endurance athletes and 24 healthy controls. All subjects underwent traditional echocardiography and 2-D strain evaluation of LV longitudinal, circumferential and radial function. LV basal and apical rotation and their net difference, defined as LV torsion, were evaluated. Results:, LV wall thicknesses, LV mass and left atrium diameter were comparable between hypertensive group and athletes. LV longitudinal strain was reduced only in hypertensive patients (P < 0·05). LV apex circumferential strain was higher in hypertensive patients than in other groups (P < 0·001), LV basal circumferential strain, although slightly increased, did not reach significant difference. Hypertensive patients showed significantly increased rotation and torsion (P < 0·001), while no differences were observed between athletes and control. Conclusion:, In patients with pathological LVH, LV longitudinal strain was reduced, while circumferential deformation and torsion were increased. No differences were observed in LV contractile function between subjects with adaptative LVH and controls. In pathological LVH, increasing torsion could be considered a compensatory mechanism to counterbalance contraction and relaxation abnormalities to maintain a normal LV output. [source] | ||||||||||