Obesity As A Causal Risk Factor For Aortic Valve Stenosis

Kaltoft, Mikkel; Langsted, Anne; Nordestgaard, B.G.

doi:10.1016/j.atherosclerosis.2019.06.197

Cited by 10 publications

(16 citation statements)

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“…Abdominal obesity (waist circumference ≥102 cm for men and ≥88 cm for women) was tightly correlated with a 30% higher occurrence rate of AVS ( 292 ). Later the Denmark group including 108,304 individuals revealed similar results with risk of AVS and aortic valve replacement much greater those with both high BMI and high waist-hip ratio or waist circumference ( 293 ). At this point, the precise mechanism behind AVS risk in obesity is unclear although structural or metabolic changes in the heart may play a role.…”

Section: Cardiac Remodeling In Obesitymentioning

confidence: 87%

“…Earlier studies have shown conflicting results with regards to the relationship between BMI and aortic valve stenosis (AVS) ( 289 – 291 ). However, recent large cohort observational studies have depicted an association between increased adiposity and AVS risk ( 292 , 293 ). A Swedish study including 71,817 individuals found a positive relationship between obesity and risk of AVS.…”

Section: Cardiac Remodeling In Obesitymentioning

confidence: 99%

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Obesity cardiomyopathy: evidence, mechanisms, and therapeutic implications

Ren

Wang

et al. 2021

Physiological Reviews

207

120

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The prevalence of heart failure is on the rise and imposes a major health threat, in part, due to the rapidly increased prevalence of overweight and obesity. To this point, epidemiological, clinical and experimental evidence supports the existence of a unique disease entity termed "obesity cardiomyopathy", which develops independent of hypertension, coronary heart disease and other heart diseases. Our contemporary review evaluates the evidence for this pathological condition, examines putative responsible mechanisms, and discusses therapeutic options for this disorder. Clinical findings have consolidated the presence of left ventricular dysfunction in obesity. Experimental investigations have uncovered pathophysiological changes in myocardial structure and function in genetically-predisposed and diet-induced obesity. Indeed, contemporary evidence consolidates a wide array of cellular and molecular mechanisms underlying the etiology of obesity cardiomyopathy including adipose tissue dysfunction, systemic inflammation, metabolic disturbances (insulin resistance, abnormal glucose transport, spillover of free fatty acids, lipotoxicity, and amino acid derangement), altered intracellular especially mitochondrial Ca2+ homeostasis, oxidative stress, autophagy/mitophagy defect, myocardial fibrosis, dampened coronary flow reserve, coronary microvascular disease (microangiopathy), and endothelial impairment. Given the important role of obesity in the increased risk of heart failure, especially that with preserved systolic function and the recent rises in COVID-19-associated cardiovascular mortality, this review should provide compelling evidence for the presence of obesity cardiomyopathy, independent of various comorbid conditions, underlying mechanisms, and offer new insights into potential therapeutic approaches (pharmacological and lifestyle modification) for the clinical management of obesity cardiomyopathy.

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Section: Cardiac Remodeling In Obesitymentioning

confidence: 87%

Section: Cardiac Remodeling In Obesitymentioning

confidence: 99%

Obesity cardiomyopathy: evidence, mechanisms, and therapeutic implications

Ren

Wang

et al. 2021

Physiological Reviews

207

120

View full text Add to dashboard Cite

show abstract

“…Obesity has been associated with poor outcomes related to cardiovascular disease and health in general, often attributed to the higher rates of comorbidities in this population. 3,[5][6][7][8][9][10][11] VHD is another common condition. It is estimated that VHD has a worldwide prevalence of 2.5%, and approximately 250 000 heart valve replacements are performed worldwide each year, with this number expected to reach 850 000 by 2050.…”

Section: Introductionmentioning

confidence: 99%

Heart valve surgery and the obesity paradox: A systematic review

et al. 2021

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Obesity has been associated with increased incidence of comorbidities and shorter life expectancy, and it has generally been assumed that patients with obesity should have inferior outcomes after surgery. Previous literature has often demonstrated equivalent or even improved rates of mortality after cardiac surgery when compared to their lower-weight counterparts, coined the obesity paradox. Herein, we aim to review the literature investigating the impact of obesity on surgical valve interventions. PubMed and Embase were systematically searched for articles published from

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“…Both aortic and mitral valve calcifications may impact risk of heart valve disease and death [3][4][5][6][7]. Risk factors for aortic valve calcification and disease include male sex, smoking, age, blood pressure, low-density cholesterol, chronic kidney disease and body mass index whereas risk factors for mitral valve calcification and disease are less studied [8][9][10][11][12][13][14][15].…”

Section: Introductionmentioning

confidence: 99%

Elevated lipoprotein(a) in mitral and aortic valve calcification and disease: The Copenhagen General Population Study

et al. 2022

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Background and aims: We tested the hypotheses (i) that elevated lipoprotein(a) is causally associated with both mitral and aortic valve calcification and disease, and (ii) that aortic valve calcification mediates the effect of elevated lipoprotein(a) on aortic valve stenosis. Methods: From the Copenhagen General Population study, we included 12,006 individuals who underwent cardiac computed tomography to measure mitral and aortic valve calcification and 85,884 to examine risk of heart valve disease. Participants had information on plasma lipoprotein(a) and genetic instruments associated with plasma lipoprotein(a) to investigate potential causality. Results: At age 70-79 years, 29% and 54% had mitral and aortic valve calcification, respectively. For 10-fold higher lipoprotein(a) levels, multifactorially adjusted odds ratios for mitral and aortic valve calcification were 1.26 (95% confidence interval: 1.13-1.41) and 1.62 (1.48-1.77). For mitral and aortic valve stenosis, corresponding hazard ratios were 0.93 (95%CI:0.40-2.15, 19 events) and 1.54 (1.38-1.71, 1158 events), respectively. For ≤23 versus ≥36 kringle IV type 2 number of repeats, the age and sex adjusted odds ratios for mitral and aortic valve calcification were 1.53 (1.18-1.99) and 2.23 (1.81-2.76). For carriers versus non-carriers of LPA rs10455872, odds ratios for mitral and aortic valve calcification were 1.33 (1.13-1.57) and 1.86 (1.64-2.13). For aortic valve stenosis, 31% (95%CI:16%-76%) of the effect of lipoprotein(a) was mediated through calcification. Conclusions: Elevated lipoprotein(a) was genetically and observationally associated with mitral and aortic valve calcification and aortic valve stenosis. Aortic valve calcification mediated 31% of the effect of elevated lipoprotein(a) on aortic valve stenosis.

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Obesity As A Causal Risk Factor For Aortic Valve Stenosis

Cited by 10 publications

References 0 publications

Obesity cardiomyopathy: evidence, mechanisms, and therapeutic implications

Obesity cardiomyopathy: evidence, mechanisms, and therapeutic implications

Heart valve surgery and the obesity paradox: A systematic review

Elevated lipoprotein(a) in mitral and aortic valve calcification and disease: The Copenhagen General Population Study

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