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LV Hypertrophy (lv + hypertrophy)
Selected AbstractsLeft ventricular diastolic dysfunction in patients with chronic renal failure: impact of diabetes mellitusDIABETIC MEDICINE, Issue 6 2005J. Miyazato Abstract Aims Left ventricular (LV) hypertrophy and LV diastolic dysfunction are cardiac changes commonly observed in patients with chronic renal failure (CRF) as well as hypertension. Although the impairment of LV diastolic function in patients with diabetes mellitus has been shown, little is known about the specific effect of diabetes on LV diastolic function in patients with CRF. The present study was designed to investigate the impact of diabetic nephropathy on LV diastolic dysfunction, independent of LV hypertrophy, in CRF patients. Methods In 67 patients with non-dialysis CRF as a result of chronic glomerulonephritis (n = 33) or diabetic nephropathy (n = 34), and 134 hypertensive patients with normal renal function, two-dimensional and Doppler echocardiographic examinations were performed, and LV dimension, mass, systolic function, and diastolic function were evaluated. Results LV mass was increased and LV diastolic dysfunction was advanced in subjects with CRF compared with hypertensive controls. In the comparison of echocardiographic parameters between the two groups of CRF patients, i.e. chronic glomerulonephritis and diabetic nephropathy groups, all indices of LV diastolic function were more deteriorated in the diabetic nephropathy group than in the chronic glomerulonephritis group, although LV structure including hypertrophy and systolic function did not differ between the groups. In a multiple regression analysis, the presence of diabetes (i.e. diabetic nephropathy group) was a significant predictor of LV diastolic dysfunction in CRF subjects, independent of other influencing factors such as age, blood pressure, renal function, anaemia and LV hypertrophy. Conclusion The present findings suggest that LV diastolic dysfunction, independent of LV hypertrophy, is specifically and markedly progressed in patients with CRF as a result of diabetic nephropathy. [source] Echocardiographic Left Ventricular Mass in a Multiethnic Southeast Asian Population: Proposed New Gender and Age-Specific NormsECHOCARDIOGRAPHY, Issue 8 2008M.R.C.P., Raymond Ching-Chiew Wong M.B.B.S. Background: Left ventricular mass (LVM) is an independent risk factor for cardiovascular outcome. We aimed to define normal reference values of LVM/body surface area (BSA) in a multiethnic Southeast Asian population across ages, and define demographic parameters that predict LVM/BSA. Methods: 198 subjects (44% men, mean age 40 ± 14 years, 82% Chinese, 13% Malay and 5% Indian) with no cardiovascular comorbidity and had normal echo images for age were included in the analysis. Echo LVM was calculated as: 1.04 ×[(left ventricular internal diameter at end-diastole {LVIDd}+ interventricular septal thickness at end-diastole {IVSd}+ left ventricular posterior wall thickness at end-diastole {LVPWd})3, LVIDd3× 0.8]+ 0.61, indexed by BSA (LVM/BSA)* and expressed as g/m2. Results: BSA and blood pressure (BP) were comparable between dichotomous age groups < or , 50 years within the same gender. Women aged , 50 years had larger IVSD, LVPWd, LVM and LVM/BSA compared to younger cohort. (p < 0.01 for all variables). The 95th percentile of LVM in men and women were 189 g and 148 g respectively; corresponding values for LVM/BSA were 106 and 96 g/m2. These values are consistently smaller than published values from the West. Age (r = 0.27, P < 0.001), gender (r =,0.30, P < 0.001), and systolic BP (r = 0.25, P = 0.003) were significant univariate predictors of LVM/BSA. Conclusion: We therefore propose a different cutoff value for the diagnosis of LV hypertrophy among Southeast Asians. [source] A Pilot Study of the Clinical Impact of Hand-Carried Cardiac Ultrasound in the Medical ClinicECHOCARDIOGRAPHY, Issue 6 2006Lori B. Croft M.D. Background: Small, hand-carried ultrasound devices have become widely available, making point-of-care echocardiograms (echos) accessible to all medical personnel as a means to augment and improve the increasingly inefficient physical examination. This study was designed to determine the clinical utility of hand-carried echo by medical residents in clinical decision making. Methods: Nine residents underwent brief, practical echo training to perform and interpret a limited hand-carried echo as an integral component of their office examination. The residents' hand-carried echo consisting of four basic views to define left ventricular (LV) function and wall thickness, valvular disease, and any pericardial effusions was compared to one performed by a level III echocardiographer. Results: Seventy-two consecutive medical clinic patients were enrolled with an average image acquisition time of 4.45 minutes. Residents obtained diagnostic images in 94% of the cases and interpreted them correctly 93% of the time. They correctly identified 92% of the major echo findings and 78% of the minor findings. Their diagnosis of LV dysfunction, valvular disease, and LV hypertrophy improved by 19%, 39%, and 14% with hand-carried echo compared to history and physical alone. Management decisions were reinforced in 76% and changed in 40% of patients with the use of hand-carried echo. Conclusion: This study demonstrates that it is possible to train medical residents to perform an effective and reasonably accurate hand-carried echo during their physical examination, which can impact clinical management. [source] Echocardiographic Left Ventricular Mass in African-AmericansECHOCARDIOGRAPHY, Issue 2 2003The Jackson Cohort of the Atherosclerosis Risk in Communities Study Characterization of target organ damage from hypertension is of particular interest in African-Americans, and evidence from electrocardiographic studies suggests that left ventricular hypertrophy is a frequent clinical finding of considerable prognostic importance. Echocardiographic studies may permit more precise characterization of the pathologic impact of hypertension on cardiac structure and function. The objective of this study is to characterize left ventricular (LV) structure including measures of wall thickness, septal thickness, internal dimension, and mass in a middle-aged sample of African-Americans using echocardiography. This study is a cohort (cross-sectional) study in which 2445 middle-aged African-American study participants from a population-based sample initially enrolled by the Atherosclerosis Risk in Communities, Jackson, Mississippi Examination Center in 1987,1989 underwent an M-mode echocardiograpic examination at their third or fourth clinic visit in 1993,1996. Measures of LV mass, even where indexed by size were conspicuously greater in men compared to women, and men exhibited a demonstrably steeper gradient of LV mass across the rather restricted age range of the study. However, when gender specific thresholds for LV hypertrophy were utilized, African-American men appear to have lower prevalence of LV hypertrophy than women. The lowest prevalence of LV hypertrophy was observed in African-American men who did not have hypertension (28.4%). The findings confirm previous suggestions from electrocardiographic investigations that cardiac hypertrophy is common, if not epidemic in middle-aged African-American men and women, whether or not they have hypertension. (ECHOCARDIOGRAPHY, Volume 20, February 2003) [source] Left ventricular hypertrophy in rats with biliary cirrhosisHEPATOLOGY, Issue 3 2003Javier Inserte Portal hypertension induces neuroendocrine activation and a hyperkinetic circulation state. This study investigated the consequences of portal hypertension on heart structure and function. Intrahepatic portal hypertension was induced in male Sprague-Dawley rats by chronic bile duct ligation (CBDL). Six weeks later, CBDL rats showed higher plasma angiotensin-II and endothelin-1 (P < .01), 56% reduction in peripheral resistance and 73% reduction in pulmonary resistance (P < .01), 87% increase in cardiac index and 30% increase in heart weight (P < .01), and increased myocardial nitric oxide (NO) synthesis. In CBDL rats, macroscopic analysis demonstrated a 30% (P < .01) increase in cross-sectional area of the left ventricular (LV) wall without changes in the LV cavity or in the right ventricle (RV). Histomorphometric analysis revealed increased cell width (12%, P < .01) of cardiomyocytes from the LV of CBDL rats, but no differences in myocardial collagen content. Myocytes isolated from the LV were wider (12%) and longer (8%) than right ventricular myocytes (P < .01) in CBDL rats but not in controls. CBDL rats showed an increased expression of ANF and CK-B genes (P < .01). Isolated perfused CBDL hearts showed pressure/end-diastolic pressure curves and response to isoproterenol identical to sham hearts, although generated wall tension was reduced because of the increased wall thickness. Coronary resistance was markedly reduced. This reduction was abolished by inhibition of NO synthesis with N -nitro-L-arginine. Expression of eNOS was increased in CBDL hearts. In conclusion, portal hypertension associated to biliary cirrhosis induces marked LV hypertrophy and increased myocardial NO synthesis without detectable fibrosis or functional impairment. This observation could be relevant to patients with cirrhosis. [source] Determinants of Incomplete Left Ventricular Mass Regression Following Aortic Valve Replacement for Aortic StenosisJOURNAL OF CARDIAC SURGERY, Issue 4 2005Naoji Hanayama M.D. In this prospective study, we identified the predictors of Abn-LVMI. Methods: Between 1990 and 2000, 529 patients undergoing AVR for AS had clinical and hemodynamic data collected prospectively. Preoperative and annual postoperative transthoracic echos were employed to assess left ventricular mass index (LVMI) and hemodynamics. Abn-LVMI was defined as the 75th percentile of the lowest postoperative LVMI (>128 mg/m2, n = 133). All other patients were included in the normal regression group (N-LVMI). Univariate and multivariable logistic regression analyses were used to determine the predictors of Abn-LVMI. Results: Preoperative hypertension, diabetes, coronary disease, valve size, mean postoperative gradients, effective orifice area, and patient-prosthesis mismatch (PPM, indexed EOA <0.60 cm2/m2) did not predict Abn-LVMI. By logistic regression the most important positive predictor of Abn-LVMI was the extent of preoperative LVMI, with an odds ratio of 37.5 (p < 0.0001). Survival (93.4 ± 1.8% vs 94.8 ± 2.3%, p = 0.90) and freedom from NYHA III,IV (75.0 ± 3.7% vs 76.6 ± 5.3%, p = 0.60) were similar for both groups at 7 years. Conclusions: Measures of valve hemodynamics were not important predictors of incomplete regression of hypertrophy. The extent of preoperative hypertrophy was the most important predictor, suggesting that earlier surgical intervention may reduce the extent of hypertrophy postoperatively. Furthermore, the significance of LV hypertrophy to long-term survival must be reassessed, in the absence of scientific evidence. [source] The effects of ACE inhibitor therapy on left ventricular myocardial mass and diastolic filling in previously untreated hypertensive patients: A Cine MRI studyJOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 1 2001U. Hoffmann MD Abstract Cardiac remodeling in case of hypertension induces hypertrophy of myocytes and elevated collagen content and, subsequently, impaired diastolic filling of the left ventricle. The purpose of this prospective study was to evaluate changes of left ventricular (LV) myocardial mass, as well as diastolic filling properties, in hypertensive patients treated with the ACE inhibitor fosinopril. Sixteen hypertensive patients with echocardiographically documented LV hypertrophy and diastolic dysfunction received fosinopril (10,20 mg daily). Measurements of LV myocardial mass and properties of diastolic filling (peak filling fraction (PFF); peak filling rate (PFR)) were performed prior to medication, as well as after 3 and 6 months of therapy using cine magnetic resonance imaging (MRI). Ten healthy subjects served as a control group. LV myocardial mass (g/m2) decreased continuously within 3,6 months of follow-up by 32% (148 ± 40 vs. 120 ± 26 vs. 101 ± 22 g/m2; P < 0.0001/0.005). The extent of regression correlated to the severity of LV hypertrophy at baseline (r = 0.77; P < 0.004). Early diastolic filling increased significantly within 6 months of therapy (PFF (%): 36 ± 6 vs. 61 ± 7, P < 0.0001; PFR (mL/second): 211 ± 48 vs. 282 ± 48, P < 0.001). Cine MRI can be used to assess the time course of pharmacological effects on cardiac remodeling in the course of hypertension. ACE inhibitor therapy results in a significant reduction of LV mass within 3 months and is accompanied by a normalization of diastolic filling that is completed after 6 months. J. Magn. Reson. Imaging 2001;14:16,22. © 2001 Wiley-Liss, Inc. [source] Independent association of rheumatoid arthritis with increased left ventricular mass but not with reduced ejection fractionARTHRITIS & RHEUMATISM, Issue 1 2009Rebecca L. Rudominer Objective Rheumatoid arthritis (RA) is a chronic inflammatory disease associated with premature atherosclerosis, vascular stiffening, and heart failure. This study was undertaken to investigate whether RA is associated with underlying structural and functional abnormalities of the left ventricle (LV). Methods Eighty-nine RA patients without clinical cardiovascular disease and 89 healthy matched controls underwent echocardiography, carotid ultrasonography, and radial tonometry to measure arterial stiffness. RA patients and controls were similar in body size, hypertension and diabetes status, and cholesterol level. Results LV diastolic diameter (4.92 cm versus 4.64 cm; P < 0.001), mass (136.9 gm versus 121.7 gm; P = 0.004 or 36.5 versus 32.9 gm/m2.7; P = 0.01), ejection fraction (71% versus 67%; P < 0.001), and prevalence of LV hypertrophy (18% versus 6.7%; P = 0.023) were all higher among RA patients versus controls. In multivariate analysis, presence of RA was an independent correlate of LV mass (P = 0.004). Furthermore, RA was independently associated with presence of LV hypertrophy (odds ratio 4.14 [95% confidence interval 1.24, 13.80], P = 0.021). Among RA patients, age at diagnosis and disease duration were independently related to LV mass. RA patients with LV hypertrophy were older and had higher systolic pressure, damage index scores, C-reactive protein levels, homocysteine levels, and arterial stiffness compared with those without LV hypertrophy. Conclusion The present results demonstrate that RA is associated with increased LV mass. Disease duration is independently related to increased LV mass, suggesting a pathophysiologic link between chronic inflammation and LV hypertrophy. In contrast, LV systolic function is preserved in RA patients, indicating that systolic dysfunction is not an intrinsic feature of RA. [source] Transforming growth factor ,1 genotype and change in left ventricular mass during antihypertensive treatment,results from the swedish irbesartan left ventricular hypertrophy investigation versus atenolol (Silvhia)CLINICAL CARDIOLOGY, Issue 3 2004Pär Hallberg M.D. Abstract Background: Angiotensin II, via the angiotensin II type 1 (AT1) receptor, may mediate myocardial fibrosis and myocyte hypertrophy seen in hypertensive left ventricular (LV) hypertrophy through production of transforming growth factor ,1(TGF-,1); AT1-receptor antagonists reverse these changes. The TGF-(,1 G + 915C polymorphism is associated with in-terindividual variation in TGF- ,1 production. No study has yet determined the impact of this polymorphism on the response to antihypertensive treatment. Hypothesis: We aimed to determine whether the TGF- ,1 G + 915C polymorphism was related to change in LV mass during antihypertensive treatment with either an AT1 -receptor antagonists or a beta1 -adrenoceptor blocker. The polymorphism was hypothesized to have an impact mainly on the irbesartan group. Methods: We determined the association between the TGF-,1 genotype and regression of LV mass in 90 patients with essential hypertension and echocardiographically diagnosed LV hypertrophy, randomized in a double-blind study to receive treatment for 48 weeks with either the AT1 -receptor antagonist irbesartan or the beta1 -adrenoceptor blocker atenolol. Results: Irbesartan-treated patients who were carriers of the C-allele, which is associated with low expression of TGF-,1, responded with a markedly greater decrease in LV mass index (LVMI) than subjects with the G/G genotype (adjusted mean change in LVMI ,44.7 g/m2 vs. ,22.2 g/m2, p = 0.007), independent of blood pressure reduction. No association between genotype and change in LVMI was observed in the atenolol group. Conclusions: The TGF- ,1 G + 915C polymorphism is related to the change in LVMI in response to antihypertensive treatment with the AT1 -receptor antagonist irbesartan. [source] | ||||||||||