Correlates of left ventricular mass in a population sample aged 36 to 37 years. Focus on lifestyle and salt intake.

Kupari, Markku; Koskinen, Pekka; Virolainen, Juha

doi:10.1161/01.cir.89.3.1041

Cited by 114 publications

(81 citation statements)

References 46 publications

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“…Moreover, several studies reported a good correlation between stroke volume and LVM. [61][62][63][64][65] The data of this study do not permit separation of the direct contribution of leptin deficiency from mechanical effects of obesity on the LVM. As leptin/fat mass ratio correlated with the FFM, the influence of each of these variables cannot be isolated.…”

Section: Discussionmentioning

confidence: 68%

Myocardial collagen turnover in normotensive obese patients: relation to insulin resistance

et al. 2005

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OBJECTIVES:The present study was undertaken to assess the differential impact of insulin resistance, leptin and body composition on myocardial mass and serum markers of cardiac fibrosis in obese subjects, within a small range of elevated BMI (30-40 kg/m 2 ), without pulmonary disease, cardiovascular disease, hypertension, cardiac hypertrophy or other cardiovascular disease. BACKGROUND: Obesity is an independent predictor of left ventricular mass (LVM) and is associated with disturbances in cardiac structure. The extent of the interstitial fibrosis in obese patients is not known, especially in the absence of cardiac hypertrophy. METHODS AND RESULTS:We included 160 obese subjects. The LVM was obtained using the Devereux formula. Body composition was estimated from a total body scan. Insulin sensitivity was assessed by homeostasis model assessment (HOMA), and cardiac collagen turnover by measurement of procollagen type III aminopeptide (PIIINP). PIIINP was correlated to the E/A ratio (r ¼ 0.24; P ¼ 0.012), a marker of ventricular function. PIIINP was independently correlated with glucose concentration (r ¼ 0.27; P ¼ 0.004), indexes of insulin resistance (HOMA (r ¼ 0.27; P ¼ 0.003), insulin (r ¼ 0.24; P ¼ 0.008)), and parameters associated with the insulin-resistance syndrome (HDL-cholesterol r ¼ À0.27; P ¼ 0.004) and fat trunk/fat leg ratio (r ¼ 0.24; P ¼ 0.053)). The variable most correlated with PIIINP was HDL-cholesterol, followed by HOMA (r 2 ¼ 0.13). When HOMA was substituted for blood glucose concentration and insulinemia (Model 2), HDL-cholesterol was strongly related to lower PIIINP levels, followed by higher glucose concentration (r 2 ¼ 0.21). Regression analyses showed that LVM had the strongest independent positive correlation with fat-free mass (FFM) (r ¼ 0.39; P ¼ 0.0002), followed by systolic blood pressure (r ¼ 0.19; P ¼ 0.034). Neither adipose mass nor height independently added information to multivariate models. The ratio leptin/fat mass was correlated with LVM (r ¼ À0.27; P ¼ 0.004), but not independently of the FFM. Markers for fibrosis were not significantly correlated with LVM. As a result, FFM was the most predictive factor of LVM in obese subjects. CONCLUSION: We found that serum levels of markers of cardiac collagen synthesis were significantly associated with insulin resistance in normotensive, nondiabetic obese subjects, and not related to the LVM. As a result, PIIINP could be a very early marker of ventricular dysfunction in these patients. Furthermore, we suggest that, for better detection of left ventricle hypertrophy in obese subjects, LVM should be indexed to FFM rather than to body surface area, or height.

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Section: Discussionmentioning

confidence: 68%

Myocardial collagen turnover in normotensive obese patients: relation to insulin resistance

et al. 2005

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“…In patients with hypertension, a close relation between high sodium intake and the presence of LVH has been shown in several crosssectional studies (12)(13)(14)(15).…”

Section: Discussionmentioning

confidence: 85%

Effects of Renin-Angiotensin System Blockade and Dietary Salt Intake on Left Ventricular Hypertrophy in Dahl Salt-Sensitive Rats.

et al. 1998

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We studied the effects of chronic blockade of the renin-angiotensin system on hypertension and cardiac left ventricular hypertrophy (LVH) in Dahl salt-sensitive (DS) rats given a high-salt or low-salt diet. [Experiment 1] Twelve-week-old male DS rats were fed an 8% NaCI diet and received the angiotensin II receptor (AT1) antagonist, candesartan (3 mg/kg/d), the angiotensin converting enzyme inhibitor enalapril (30 mg/kg/d), or vehicle for 6 wk after 3 wk of 8 % salt-loading. Neither candesartan nor enalapril with concomitant high salt-loading attenuated the blood pressure (BP) elevation. LVH was also not attenuated significantly by these treatments. [Experiment 2] After 8 wk of 8 % salt-loading, the rats were given a 0.3% NaCI diet and concurrently received candesartan, enalapril, or vehicle for 5 wk. Switching from the high-salt to low-salt diet significantly decreased BP and left ventricular mass in the vehicle-treated animals. Both candesartan and enalapril normalized BP during salt-depletion; the blockade of the reninangiotensin system produced an additive reduction in LVH. These findings suggest that sodium intake and hemodynamic load, but not the renin-angiotensin system, may be major determinants of the development of LVH in DS rats. Numerous studies have demonstrated that angiotensin II (Ang II) plays a key role in the development and maintenance of hypertensive cardiac hypertrophy in experimental animals and humans. Blockade of Ang II receptors inhibits intracellular signaling of stretch-mediated hypertrophy of cultured cardiomyocytes, suggesting that pure mechanical stimuli can elicit myocardial cell hypertrophy by stimulating Ang II secretion from cardiomyocytes (1). It is thus conceivable that cardiac hypertrophy caused by mechanical (hemodynamic) load alone can be reduced by Ang II receptor antagonism.Dietary high-salt intake causes cardiac hypertrophy and hypertension in Dahl salt-sensitive (DS) rats and suppresses plasma renin activity (PRA). Thus, it appears that cardiac hypertrophy in saltloaded DS rats is induced mainly by hemodynamic load, with only a small contribution from the reninangiotensin system. However, if activation of a local renin-angiotensin system (RAS) is involved in cardiac left ventricular hypertrophy (LVH), blockade of the RAS could reduce LVH even in salt-loaded DS rats. We have previously demonstrated that angiotensin type I (AT1) receptor antagonists did not blunt hypertension or reduce LVH in DS rats fed a 4% NaCI diet (2, 3).Our findings suggest that sodium intake plays a major role in the development of LVH and hypertension in salt-loaded DS rats, and that the tissue RAS might not be activated in DS rats fed a 4% NaCI diet. It has been reported that an 8% sodium loading initially suppressed PRA and then increased its value after a 4-wk period of high-salt loading in DS rats (4). These findings suggest that the circulating RAS is activated even in DS rats given an 8% NaCI diet for a longer period, and suggest the possibility that the tissue renin-angiotensin system in DS...

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“…We also tested for heterogeneity of genotype distributions across ethnicities by the 2 test (3 d.f.). In both single-SNP and haplotype-based analyses, conditional multivariable logistic regression models were employed to estimate the odds ratios (ORs) (95% CI) for each genetic variant of type 2 diabetes risk with adjustments for multiple confounding variables including matching factors (age, clinical center, time of blood draw, and ethnicity), BMI, ln(fasting glucose), ln(fasting insulin), cigarette smoking (never, past, and current), alcohol intake (never, past, and current), postmenopausal hormone therapy (never, past, and current), type 2 diabetes family history (presence/absence), and total MET value (the energy expended by a person at rest; 1 MET ϭ 1 kcal ⅐ kg Ϫ1 body weight ⅐ h Ϫ1 [23]) from recreational physical activity per week at baseline. In single-SNP analyses, each SNP was coded as additive, dominant, and reces- …”

Section: Methodsmentioning

confidence: 99%

Genetic Variants in the UCP2-UCP3 Gene Cluster and Risk of Diabetes in the Women's Health Initiative Observational Study

et al. 2008

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OBJECTIVE-Mitochondrial uncoupling proteins (UCPs) are involved in body weight regulation and glucose homeostasis. Genetic variants in the UCP2-UCP3 gene cluster, located on chromosome 11q13, may play a significant role in the development of type 2 diabetes. RESEARCH DESIGN AND METHODS-We conducted a comprehensive assessment of common single nucleotide polymorphisms (SNPs) at the 70-kb UCP2-UCP3 gene cluster in relation to type 2 diabetes risk in a prospective, case-control study nested in the Women's Health Initiative Observational Study, an ethnically diverse cohort of postmenopausal women including Caucasian, African, Hispanic, and Asian American subjects. We genotyped 14 tag SNPs in 1,584 incident type 2 diabetes case and 2,198 control subjects matched by age, ethnicity, clinical center, time of blood draw, and length of follow-up. RESULTS-We identified a haplotype set (rs591758-rs668514-rs647126-rs1800006, spanning the UCP2-UCP3 intergenic and UCP3 regions) as significantly associated with greater type 2 diabetes risk (nominal P ϭ 0.0011, permutation P ϭ 0.046) in Caucasian women, especially among overweight Caucasians (BMI Ͼ25 kg/m 2 ) (nominal P ϭ 0.0006, permutation P ϭ 0.032). Compared with the most common haplotype (h1010 as the referent), haplotype h0001 (19.5% in control subjects) had odds ratios of 2.0 (95% CI 1.13-3.37) in in Caucasian overweight women. Similar haplotype-type 2 diabetes association was also observed among Hispanic women who were overweight. CONCLUSIONS-These findings suggest a role of UCP2-UCP3 gene cluster haplotypes in diabetes; in particular, the effects of the high-risk haplotypes were more apparent in overweight Caucasian women. These data warrant further confirmation in future prospective and experimental studies.

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Correlates of left ventricular mass in a population sample aged 36 to 37 years. Focus on lifestyle and salt intake.

Cited by 114 publications

References 46 publications

Myocardial collagen turnover in normotensive obese patients: relation to insulin resistance

Myocardial collagen turnover in normotensive obese patients: relation to insulin resistance

Effects of Renin-Angiotensin System Blockade and Dietary Salt Intake on Left Ventricular Hypertrophy in Dahl Salt-Sensitive Rats.

Genetic Variants in the UCP2-UCP3 Gene Cluster and Risk of Diabetes in the Women's Health Initiative Observational Study

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