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Obesity and hypertension. Hemodynamic aspects
1Alton Ochsner Medical Foundation, New Orleans, LA 70121.
Insights
Obesity-hypertension causes heart strain via increased blood volume and resistance, leading to cardiac hypertrophy. Weight loss can reverse these harmful hemodynamic changes, improving cardiovascular health.
Area of Science:
- Cardiovascular Physiology
- Nephrology
- Metabolic Disorders
Background:
- Obesity-hypertension presents complex cardiovascular challenges.
- Elevated arterial pressure in obese patients involves increased cardiac output and peripheral resistance.
- This leads to dual ventricular overload, promoting cardiac hypertrophy.
Purpose of the Study:
- To elucidate the hemodynamic and cardiac structural alterations in obesity-hypertension.
- To explore the impact on renal hemodynamics and function.
- To assess the potential for reversal of these derangements with weight reduction.
Main Methods:
- The study describes physiological mechanisms and observed changes in patients with obesity-hypertension.
- It analyzes the interplay between intravascular volume, cardiac output, and vascular resistance.
- Pathophysiological consequences on cardiac and renal systems are discussed.
Main Results:
- Obesity-hypertension is linked to expanded intravascular volume, increased cardiac output, and elevated total peripheral resistance.
- This results in left ventricular hypertrophy (both concentric and eccentric) due to volume and pressure overload.
- Renal blood flow is increased, but a higher filtration fraction may promote glomerulosclerosis, exacerbated by diabetes risk.
Conclusions:
- The hemodynamic derangements in obesity-hypertension significantly strain the cardiovascular system, increasing risks of cardiac insufficiency and failure.
- Renal complications, including glomerulosclerosis, are a concern.
- Weight reduction offers a potential therapeutic strategy to reverse these adverse hemodynamic and cardiac changes.
Abstract:
Elevated arterial pressure in patients with obesity-hypertension is associated with an increased cardiac output and total peripheral resistance. The elevated output is related to expanded intravascular volume that increases cardiopulmonary volume, venous return, and left ventricular preload; the elevated pressure and total peripheral resistance increase afterload. This dual ventricular overload promotes a dimorphic, concentric, and eccentric hypertrophy in response to the volume and pressure overload. Increased myocardial oxygen demand results from the elevated tension in the left ventricular wall, reflecting its increased diameter and pressure, and provides physiologic rationale for the greater potential of coronary arterial insufficiency and cardiac failure. There are greater renal blood flow and lower renal vascular resistance in patients with obesity-hypertension at any level of arterial pressure. This may be offset by an increased renal filtration fraction that may favor protein deposition and glomerulosclerosis, and predisposition of obese patients for diabetes may aggravate this problem. With weight reduction, these hemodynamic derangements may be reversed: intravascular volume contracts, cardiac output decreases, and arterial pressure falls.