Ratio Of Left Ventricular Wall Thickness Research Articles

Surgical as Opposed to Transcatheter Aortic Valve Replacement Improves Basal Interventricular Septal Hypertrophy

Basal interventricular septum (IVS) hypertrophy (BSH) with reduced basal IVS contraction and IVS-aorta angle is frequently associated with aortic stenosis (AS). BSH shape suggests compression by the longitudinally elongated ascending aorta, causing basal IVS thickening and contractile dysfunction, further suggesting the possibility of aortic wall shortening to improve the BSH. Surgical aortic valve replacement (SAVR), as opposed to transcatheter AVR (TAVR), includes aortic wall shortening by incision and stitching on the wall and may potentially improve BSH. We hypothesized that BSH configuration and its contraction improves after SAVR in patients with AS. Methods and Results: In 32 patients with SAVR and 36 with TAVR for AS, regional wall thickness and systolic contraction (longitudinal strain) of 18 left ventricular (LV) segments, and IVS-aorta angle were measured on echocardiography. After SAVR, basal IVS/average LV wall thickness ratio, basal IVS strain, and IVS-aorta angle significantly improved (1.11±0.24 to 1.06±0.17; -6.2±5.7 to -9.1±5.2%; 115±22 to 123±14°, P<0.001, respectively). Contractile improvement in basal IVS was correlated with pre-SAVR BSH (basal IVS/average LV wall thickness ratio or IVS-aorta angle: r=0.47 and 0.49, P<0.01, respectively). In contrast, BSH indices did not improve after TAVR. In patients with AS, SAVR as opposed to TAVR improves associated BSH and its functional impairment.

A 4-Tiered Classification of Left Ventricular Hypertrophy Based on Left Ventricular Geometry

Background— Left ventricular hypertrophy (LVH) is traditionally classified as concentric or eccentric, based on the ratio of LV wall thickness to chamber dimension. We propose a 4-tiered LVH classification based on LV concentricity 0.67 (mass/end-diastolic volume 0.67 ) and indexed LV end-diastolic volume (EDV). Methods and Results— Cardiac MRI was performed in 2803 subjects and LVH (n=895) was defined by increased LV mass/height 2.7 . Increased concentricity 0.67 and indexed EDV were defined at the 97.5th percentile of a healthy subpopulation. Four geometric patterns resulted: increased concentricity without increased EDV (“thick hypertrophy,” n=361); increased EDV without increased concentricity (“dilated hypertrophy,” n=53); increased concentricity with increased EDV (“both thick and dilated hypertrophy,” n=13); and neither increased concentricity nor increased EDV (“indeterminate hypertrophy,” n=468). Compared with subjects with isolated thick hypertrophy, those with both thick and dilated hypertrophy had a lower LV ejection fraction and higher NT-pro-BNP and BNP levels ( P ≤0.001 for all). Subjects with dilated hypertrophy had a lower LV ejection fraction and higher troponin T, NT-pro-BNP, and BNP levels versus those with indeterminate hypertrophy ( P &lt;0.001 for all). Subjects with indeterminate LVH versus those without LVH had increased LV mass (by definition) but also a higher LV ejection fraction and no increase in troponin or natriuretic peptide levels. Conclusions— Concentric or eccentric LVH can each be subclassified into 2 subgroups, yielding 4 distinct geometric patterns. Many subjects currently classified with eccentric LVH can be reclassified into an indeterminate subgroup that has better LV function and comparable levels of biomarkers reflecting cardiac stress as compared with those without LVH.

The Association of HIV Infection with Left Ventricular Mass/Hypertrophy

Left ventricular hypertrophy (LVH) is an independent predictor of major cardiovascular events. Cardiovascular risk is increased among human immunodeficiency virus (HIV)-infected patients. To assess LV mass/hypertrophy in HIV infection, 654 women enrolled in the Women's Interagency HIV Study underwent transthoracic echocardiography. There were 454 HIV-infected and 200 uninfected women, mean age 40.8 +/- 9.3 years. LV mass/height(2.7) was similar between the HIV-infected and the HIV-uninfected groups (41.4 +/- 11.1 vs. 39.9 +/- 10.3 g/h(2.7); p = 0.37). The prevalence of LVH was similar between the two groups (LVH by LV mass/height(2.7) criteria 15.0% vs. 13.0%, p = 0.29). Relative wall thickness (RWT), defined as the ratio of LV wall thickness to cavity diameter, was also similar between the HIV-infected and HIV-uninfected groups (0.36 +/- 0.05 vs. 0.37 +/- 0.06, p = 0.16). On multiple linear regression analysis adjusting for age, W/H ratio, triceps skinfold thickness, systolic/diastolic BP, diabetes, hypertension and dyslipidemia; HIV status (b = 2.08, p = 0.02, CI 0.27-3.88); weight (b per kg = 0.15, p < 0.01, CI 0.08-0.22); and smoking duration (b per one-year increase = 0.08, p = 0.03, CI 0.01-0.16) were independent correlates of LV mass/height(2.7) (Model R(2) = 0.20, p < 0.001). Weight (aOR = 1.04, CI 1.01-1.06) and smoking duration (aOR = 1.03, CI 1.01-1.06) were independent correlates of LVH. Being HIV negative, increased age, increased triceps skinfold thickness, and higher W/H ratio were independent correlates of higher RWT. Among HIV-infected women, higher LV mass was not associated with a history of AIDS-defining illness, nadir CD4(+) count <200 cells/microl, or with the duration of highly active antiretroviral therapy (HAART). Women taking NRTIs had higher LV mass. Higher RWT was associated with current CD4(+) count. In conclusion, HIV infection is associated with greater LV mass but not with a higher prevalence of LVH. Among HIV-infected women, RWT, but not LV mass, is associated with the degree of immunosuppression.

PPAR gamma agonist normalizes glomerular filtration rate, tissue levels of homocysteine, and attenuates endothelial-myocyte uncoupling in alloxan induced diabetic mice

Homocysteine (Hcy) is an independent cardiovascular risk factor; however, in diabetes, the role of tissue Hcy leading to cardiac dysfunction is unclear. To determine whether tissue Hcy caused endothelial-myocyte uncoupling and ventricular dysfunction in diabetes. Diabetes was created in C57BL/6J male mice by injecting 65 mg/kg alloxan. To reverse diabetic complications, ciglitazone (CZ) was administered in the drinking water. Plasma glucose, Hcy, left ventricular (LV) tissue levels of Hcy and nitric oxide (NO) were measured. Glomerular filtration rate (GFR) was measured by inulin-FITC. Endothelial-myocyte coupling was measured in cardiac rings. In vivo diastolic relaxation and LV diameters were measured by a Millar catheter in LV and by M-mode echocardiography, respectively. Plasma glucose, GFR and LV tissue Hcy were increased in diabetic mice and were normalized after CZ treatment; whereas, elevated plasma Hcy level remained unchanged with or without CZ treatment. NO levels in the LV were found inversely related to tissue Hcy levels. Attenuated endothelial-myocyte function in diabetic mice was ameliorated by CZ treatment. Cardiac relaxation, the ratio of LV wall thickness to LV diameter was decreased in diabetes, and normalized after CZ treatment. CZ normalized LV tissue levels of Hcy and ameliorated endothelial-myocyte coupling; therefore, specifically suggest the association of LV tissue Hcy levels with impair endothelial-myocyte function in diabetes.

Ventricular remodeling induced by retinoic acid supplementation in adult rats.

Retinoic acid (RA) plays a role in regulating cardiac geometry and function throughout life. The aim of this study was to analyze the cardiac effects of RA in adult rats. Wistar rats were randomly allocated to a control group (n = 18) receiving standard rat chow and a group treated with RA (n = 14) receiving standard rat chow supplemented with RA for 90 days. All animals were evaluated by echocardiography, isolated papillary muscle function, and morphological studies. Whereas the RA-treated group developed an increase in both left ventricular (LV) mass and LV end-diastolic diameter, the ratio of LV wall thickness to LV end-diastolic diameter remained unchanged when compared with the control group. In the isolated papillary muscle preparation, RA treatment decreased the time to peak developed tension and increased the maximum velocity of isometric relengthening, indicating that systolic and diastolic function was improved. Although RA treatment produced an increase in myocyte cross-sectional area, the myocardial collagen volume fraction was similar to controls. Thus our study demonstrates that small physiological doses of RA induce ventricular remodeling resembling compensated volume-overload hypertrophy in rats.

Changes in patterns of left ventricular hypertrophy after aortic valve replacement for aortic stenosis and regurgitation with St. Jude Medical cardiac valves.

In this study, we analyzed the extent and pattern of regression of left ventricular (LV) hypertrophy after aortic valve replacement in patients with aortic stenosis (AS) and compared the results with those of another group of patients with aortic regurgitation (AR). Seventy patients who underwent isolated aortic valve replacement were divided into 2 groups. Group 1 was comprised of 29 patients who underwent aortic valve replacement for aortic stenosis, and Group 2 of 41 patients who underwent aortic valve replacement for aortic regurgitation. A third group of 10 healthy subjects served as a healthy control group. Echocardiographic studies were done before the operation and 5 years postoperatively. At follow-up, a significant reduction in the left ventricular mass was found in both groups, but it remained significantly greater than in the healthy control group. The ratio of LV wall thickness to radius (th/r) in Group 1 decreased significantly, and at follow-up it was within the normal value. In Group 2, the th/r ratio increased, and at follow-up it was within the normal value. After aortic valve replacement, the wall thickness remained significantly greater than normal for patients with AS, and the chamber radius remained significantly greater than normal for patients with AR. For these reasons, LV hypertrophy still existed in both groups at postoperative follow-up. The actuarial survival rate was 85.3% at 16 years for Group 1 and 83.4% at 18 years for Group 2. There was no significant difference in the long-term survival rates between the 2 groups. Actuarial freedom from valve-related events was 91.9% at 16 years for Group 1 and 82% at 18 years for Group 2. There was no significant difference in the valve-related event free curves between groups. After 5 years of follow-up, th/r reached normal for both groups, indicating remodeling of the LV geometry after aortic valve replacement.

Influence of the α-Tropomyosin 180 mutation on in vivo left ventricular systolic and diastolic function

Familial hypertrophic cardiomyopathy (FHC) is a genotypically heterogenous disease produced by mutations in sarcomeric proteins. A missense mutation in the o~-tropomyosin gene at amino acid residue 180 (TMGIul80GIy) is a recently reported cause of FftC. Transgenic mice (TG) with mutant TM driven by the MHC promotor (4 lines, 10-40 copy number), die at 3-4 months of age, and at necropsy exhibit 3-fold cardiac enlargement, ventricular hypertrophy, and atrial fibrosis. In order to evaluate in vivo effects of TMGIuI80Gly on LV function and geometry, 2D-guided M-mode and color flow-guided Doppler were performed in 6 TG and 6 littermate controls (WT) aged 3 months. LV mass normalized to body weight (LV/BW) and the ratio of LV wall thickness to cavity (h/r) were significantly greater in TG than WT:

Alpha- and beta-adrenoceptor blockade fail to prevent high sodium diet-induced left ventricular hypertrophy.

High sodium diet (HS, 8% NaCl) induces left ventricular hypertrophy (LVH) in normotensive rats without an increase in pressure or volume load or in resting cardiac sympathetic activity. HS may affect LV adrenoceptors density or affinity or their postreceptor pathways, thereby causing LVH. We therefore assessed the effects of HS with and without blockade of alpha1- or beta-adrenoceptors by terazosin or nadolol, alone or in combination, on resting hemodynamics, LV and right ventricular (RV) weights, and LV dimensions of male WKY rats. HS increased LV weight by 14% to 17%, and the ratio of LV wall thickness to radius by 18% to 23%. Singly or in combination, the adrenoceptor antagonists did not prevent HS-induced LVH, but instead aggravated it. The increased ratio of LV wall thickness to radius and of LV to RV were attenuated by terazosin or nadolol alone. Neither the resting LV peak-systolic or end-diastolic pressures nor the right atrial pressure was changed by HS, either alone or in combination with the blockers. The failure of chronic alpha1- or beta-blockade to prevent HS-induced LVH suggests that adrenoceptor activation is not important in evoking the LVH. However, the blockers shifted the LVH from a concentric to an eccentric form, suggesting an involvement of additional trophic factors during adrenoceptor blockade.

Correlates of the estimated arterial compliance in the population of Tecumseh, Michigan.

An estimate of arterial compliance--the stroke volume/pulse pressure ratio (SV/PP)--was studied in 801 participants in the Tecumseh Blood Pressure Study, a population-based ongoing cardiovascular, epidemiological investigation. The subjects were normal young adults (mean age 30 +/- 5.6 years) and 373 were females. Cardiac anatomy and function were studied by echo-Doppler methods, blood pressure being measured at the same time by the indirect method. The distribution of the SV/PP ratio was skewed toward higher values in larger subjects. After statistical adjustments for body surface area, this estimate of arterial compliance was found to be higher in females (2.00 +/- 0.62) than in males (1.90 +/- 0.58) (p < 0.05). When subjects were divided into tertiles, the group with the lowest estimated arterial compliance was normotensive but had higher systolic pressure, lower diastolic pressure, a similar mean arterial pressure, higher heart rate and higher left ventricular wall thickness ratio compared to subjects with higher arterial compliance. Indices of systolic ejection decreased and diastolic function was altered in the low compliance subjects. In addition, low compliance subjects also had higher fasting insulin levels. These findings suggest that the low arterial compliance in an otherwise normal population has negative cardiovascular correlates. The early association of decreased arterial compliance with anatomic, functional and biochemical aberrations suggests that estimates of arterial compliance might prove useful for prediction of cardiovascular complications.

Reliable estimation of peak left ventricular systolic pressure by M-mode echographic-determined end-diastolic relative wall thickness: Identification of severe valvular aortic stenosis in adult patients

In compensated hearts, left ventricular systolic pressure (LVSP) can be estimated from the ratio of LV wall thickness to chamber radius (RWT). To determine the clinical value of such estimates, we examined echocardiographic RWT in an unscreened series of 81 individuals with aortic valve disease, hypertension, or normal hearts. Despite the presence, in many subjects, of symptoms of congestive heart failure, reduced ejection fraction, or coronary disease, end-diastolic RWT (RWT D) correlated well with peak LVSP ( r = 0.77); 45 of 55 patients with LVSP ≥ 140 mm Hg had RWT D ≥ 0.45, while 26 of 26 with LVSP < 140 mm Hg had lower values ( p < 0.005). RWT D was ≥ 0.50 in 30 of 34 patients with LVSP ≥ 180 mm Hg and in 6 of 21 with LVSP 140 to 180 mm Hg. RWT D correctly estimated LVSP range in 26 of 27 severe aortic stenosis (AS) patients and, combined with echocardiographic aortic valve calcification, correctly recognized the presence or absence of severe AS in 99% of the series. The RWT D for any given LVSP was higher in patients on antihypertensive treatment and lower in patients with severe aortic regurgitation. In contrast to series based on patients with normal LV function, end-systolic RWT correlated poorly with LVSP.