Key result
Obesity drives adverse cardiovascular remodeling and heart failure via neurohormonal activation and increased plasma volume.
Answers are grounded in this paper and cite their sources.
Reveals how adipose neurohormonal activity drives hypertension and ventricular remodeling, highlighting key pathophysiological mechanisms linking obesity to congestive heart failure.
Controversy exists regarding the amount of risk caused by obesity, but there is general consensus that it is associated with many serious disorders, mostly cardiovascular and neoplastic. Obesity is clearly associated with hypertension, ventricular remodeling with subsequent congestive heart failure, sleep-disordered breathing, and sudden death. The physiologic alterations associated with establishing and perpetuating the obese state are complex but are becoming clear. In discussing the cardiovascular consequences of obesity, the implications and mechanism of the associated hypertension need to be understood. There is growing recognition that adipose tissue is a very active in the neurohormonal axis and is not simply a passive storage depot. Among other things, adipocyte-related hormonal activity and resistance to feedback mechanisms are associated with increased plasma volume and increased sympathetic tone.
No takes yet. Share an insight, caveat, or question.
Good et al. (2008) conducted a review in Obesity and hypertension. Obesity was evaluated. Obesity is associated with hypertension, ventricular remodeling, heart failure, sleep-disordered breathing, and sudden death via neurohormonal activity increasing plasma volume and sympathetic tone.
Synapse has enriched 10 related papers. Consider them for comparative context: