Impact of Obesity on Left Ventricular Mass and Function in Subjects With Chronic Volume Overload

Ballo, Piercarlo; Motto, Andrea; Mondillo, Sergio; Faraguti, Sergio Antonio

doi:10.1038/oby.2007.241

Cited by 14 publications

(8 citation statements)

References 24 publications

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“…One major mechanism by which obesity may influence LV geometry and the subsequent development of eccentric hypertrophy is through the enlargement of the left ventricle [36]. This process may be influenced by increased hemodynamic load [37], decreased LV myocardial contractility, and inflammatory activity that promotes cardiac remodeling [38]. In comparison with eccentric LV hypertrophy, concentric LV hypertrophy is most often associated with increased pressures primarily from hypertension rather than obesity [39].…”

Section: Discussionmentioning

confidence: 99%

Which measures of adiposity predict subsequent left ventricular geometry? Evidence from the Bogalusa Heart Study

Gustat

et al. 2015

Nutrition, Metabolism and Cardiovascular Diseases

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Background and aims Left ventricular (LV) hypertrophy increases the risk of future cardiovascular events. The relationship between obesity in young adulthood and later LV geometry is unknown. We examined the association between long-term changes in measures of adiposity and subsequent LV geometry among 1073 young adults from the Bogalusa Heart Study. Methods and results Echocardiography-measured LV geometry was classified into normal (N = 796), concentric remodeling (N = 124), eccentric hypertrophy (N = 99), and concentric hypertrophy (N = 54) by integrating relative wall thickness and LV mass index. The mean age of our population was 38 years when the LV geometry was measured. Body mass index (BMI) increased by a mean of 4.9 kg/m2 over a median of 20 years, waist circumference (WC) by 10.9 cm over 17 years, waist/hip ratio by 0.02 over 10 years, waist/height ratio by 0.06 over 17 years, abdominal height by 0.9 cm over 10 years, body fat (BF) percentage by 12.7% over 20 years, and Visceral Adiposity Index by 0.30 over 17 years. In polytomous logistic regression models corrected for multiple comparisons, participants with one-standard-deviation increases in BMI,WC, waist/height ratio, and BF had 2.00 (95% confidence interval (CI): 1.53–2.61), 1.33 (1.06–1.68), 1.35 (1.07–1.70), and 1.60 (1.26–2.03) times the risk of eccentric hypertrophy, respectively, after adjustment for demographic, lifestyle, metabolic risk factors, and follow-up time. Likewise, the rates of change in BMI, WC, waist/height ratio, and BF were associated with eccentric hypertrophy. There was no association with concentric remodeling or concentric hypertrophy. Conclusions Our findings suggest that increases in BMI, WC, waist/height ratio, and BF were strong predictors of eccentric hypertrophy in middle age.

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Section: Discussionmentioning

confidence: 99%

Which measures of adiposity predict subsequent left ventricular geometry? Evidence from the Bogalusa Heart Study

Gustat

et al. 2015

Nutrition, Metabolism and Cardiovascular Diseases

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“…Obesity is a complex disease state that is accompanied by a number of cardiac disease risk factors including hypertension and metabolic dysregulation (glucose intolerance, insulin resistance, dyslipidemia)[54] that are associated with pathologic changes in the heart (ventricular hypertrophy, heart failure)[6, 16, 34, 65] and in the vasculature (atherosclerosis, microvascular dysfunction)[8, 31, 60]. In prospective clinical studies, overweight or obese individuals have increased rates of cardiovascular diseases [1, 3, 41], contributing to a 2–3 fold increase in overall mortality relative to normal weight individuals[1, 7, 15, 32, 49, 51].…”

Section: Introductionmentioning

confidence: 99%

Obesity alters molecular and functional cardiac responses to ischemia/reperfusion and glucagon-like peptide-1 receptor agonism

et al. 2016

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This study tested the hypothesis that obesity alters the cardiac response to ischemia/reperfusion and/or glucagon like peptide-1 (GLP-1) receptor activation, and that these differences are associated with alterations in the obese cardiac proteome and microRNA (miR) transcriptome. Ossabaw swine were fed normal chow or obesogenic diet for 6 months. Cardiac function was assessed at baseline, during a 30-min coronary occlusion, and during 2 hours of reperfusion in anesthetized swine treated with saline or exendin-4 for 24 hours. Cardiac biopsies were obtained from normal and ischemia/reperfusion territories. Fat-fed animals were heavier, and exhibited hyperinsulinemia, hyperglycemia, and hypertriglyceridemia. Plasma troponin-I concentration (index of myocardial injury) was increased following ischemia/reperfusion and decreased by exendin-4 treatment in both groups. Ischemia/reperfusion produced reductions in systolic pressure and stroke volume in lean swine. These indices were higher in obese hearts at baseline and relatively maintained throughout ischemia/reperfusion. Exendin-4 administration increased systolic pressure in lean swine but did not affect blood pressure in obese swine. End-diastolic volume was reduced by exendin-4 following ischemia/reperfusion in obese swine. These divergent physiologic responses were associated with obesity-related differences in proteins related to myocardial structure/function (e.g. titin) and calcium handling (e.g. SERCA2a, histidine-rich Ca2+ binding protein). Alterations in expression of cardiac miRs in obese hearts included miR-15, miR-27, miR-130, miR-181, and let-7. Taken together, these observations validate this discovery approach and reveal novel associations that suggest previously undiscovered mechanisms contributing to the effects of obesity on the heart and contributing to the actions of GLP-1 following ischemia/reperfusion.

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“…A previous study had already shown that longitudinal, but not radial, systolic myocardial deformation properties of the right ventricle and LV were altered in obese children, and thus, prevention of obesity is important even in children (31). Another study of hypertension patients found that there is an earlier longitudinal systolic dysfunction compared with the circumferential impairment, dependent on the effect of LV mass, LV geometry, and LV wall stress (32). This probably reflects longitudinal fibers' vulnerability to ischemia, hypertrophy, or abnormalities in LV activation.…”

Section: Discussionmentioning

confidence: 99%

Subclinical Regional Left Ventricular Dysfunction in Obese Patients With and Without Hypertension or Hypertrophy

Santos

Salemi

Picard

et al. 2011

Obesity

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We investigated the impact of obesity on the abnormalities of systolic and diastolic regional left ventricular (LV) function in patients with or without hypertension or hypertrophy, and without heart failure. We studied 120 individuals divided into 6 groups of 20 patients (42 ± 6 years, 60 females) using standard and pulsed‐wave tissue Doppler imaging (TDI) echocardiography, and heterogeneity index (HI): nonobese (I: no hypertension, no hypertrophy, control group; II: hypertension, no hypertrophy; III: hypertension and hypertrophy) and obese (IV: no hypertension, no hypertrophy; V: hypertension, no hypertrophy; VI: hypertension and hypertrophy). The criterion for obesity was BMI ≥30 kg/m2, for hypertension was blood pressure ≥140/90 mm Hg, for hypertrophy in nonobese was LV mass/body surface area (BSA) >134 g/m2 (men) and >110 mg/m2 (women), and in obese was LV mass/height(2.7) >50 (men) and >40 (women). Obese groups had normal LV ejection fraction compared with nonobese groups, but decreased longitudinal and radial systolic myocardial peak velocities (S'), and early diastolic myocardial peak velocity (E'). Also, a great variability of E' and late diastolic myocardial peak velocity (A') from the longitudinal basal region was observed in obese groups (E'basal nonobese: 11 ± 7 vs. obese 19 ± 11, P < 0.001, A'basal nonobese: 7 ± 4 vs. obese 11 ± 7, P < 0.001). Our findings were more evident when comparing groups IV with V and VI, with the latter having concentric hypertrophy and obvious segmental systolic and diastolic dysfunctions. Subclinical myocardial alterations and increased variability of the velocities were observed in obese groups, especially with hypertension and hypertrophy, reflecting impaired regional LV relaxation, segmental atrial, and systolic dysfunctions.

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Impact of Obesity on Left Ventricular Mass and Function in Subjects With Chronic Volume Overload

Cited by 14 publications

References 24 publications

Which measures of adiposity predict subsequent left ventricular geometry? Evidence from the Bogalusa Heart Study

Which measures of adiposity predict subsequent left ventricular geometry? Evidence from the Bogalusa Heart Study

Obesity alters molecular and functional cardiac responses to ischemia/reperfusion and glucagon-like peptide-1 receptor agonism

Subclinical Regional Left Ventricular Dysfunction in Obese Patients With and Without Hypertension or Hypertrophy

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