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Published on: February 25, 2016
Obesity is associated with lower coronary microvascular density
Duncan J Campbell1, Jithendra B Somaratne, David L Prior
1St. Vincent's Institute of Medical Research, Fitzroy, Australia ; Department of Medicine, The University of Melbourne, St. Vincent's Health, Fitzroy, Australia.
Insights
Obesity is linked to reduced coronary microvascular density and increased left ventricular filling pressure. This may explain heart issues like diastolic dysfunction and higher heart failure risk in obese individuals.
Area of Science:
- Cardiology
- Obesity Medicine
- Cardiovascular Pathology
Background:
- Obesity is a known risk factor for diastolic dysfunction, reduced myocardial blood flow, impaired metabolism, and heart failure.
- The relationship between obesity, left ventricular filling pressure, and myocardial structure requires further investigation.
Purpose of the Study:
- To investigate the association between obesity, left ventricular filling pressure, and myocardial structure.
- To determine how obesity impacts coronary microvascular density and cardiac function.
Main Methods:
- Histological analysis of non-ischemic myocardium from 57 patients undergoing coronary artery bypass graft surgery.
- Comparison of myocardial structure and microvasculature between obese (BMI >30 kg/m²) and non-obese (BMI ≤30 kg/m²) individuals.
Main Results:
- Obese patients exhibited lower capillary length density and higher diffusion radius compared to non-obese patients.
- Increased Body Mass Index (BMI) correlated with elevated pulmonary capillary wedge pressure (PCWP).
- Lower capillary length density was associated with both increased BMI and elevated PCWP.
Conclusions:
- Obesity and elevated left ventricular filling pressure are linked to reduced coronary microvascular density.
- This reduction in microvascular density may contribute to diastolic dysfunction, impaired myocardial metabolism, and an increased risk of heart failure in obese individuals.
Background:
Obesity is associated with diastolic dysfunction, lower maximal myocardial blood flow, impaired myocardial metabolism and increased risk of heart failure. We examined the association between obesity, left ventricular filling pressure and myocardial structure.
Methods:
We performed histological analysis of non-ischemic myocardium from 57 patients (46 men and 11 women) undergoing coronary artery bypass graft surgery who did not have previous cardiac surgery, myocardial infarction, heart failure, atrial fibrillation or loop diuretic therapy.
Results:
Non-obese (body mass index, BMI, ≤ 30 kg/m(2), n=33) and obese patients (BMI >30 kg/m(2), n=24) did not differ with respect to myocardial total, interstitial or perivascular fibrosis, arteriolar dimensions, or cardiomyocyte width. Obese patients had lower capillary length density (1145 ± 239, mean ± SD, vs. 1371 ± 333 mm/mm(3), P=0.007) and higher diffusion radius (16.9 ± 1.5 vs. 15.6 ± 2.0 μm, P=0.012), in comparison with non-obese patients. However, the diffusion radius/cardiomyocyte width ratio of obese patients (0.73 ± 0.11 μm/μm) was not significantly different from that of non-obese patients (0.71 ± 0.11 μm/μm), suggesting that differences in cardiomyocyte width explained in part the differences in capillary length density and diffusion radius between non-obese and obese patients. Increased BMI was associated with increased pulmonary capillary wedge pressure (PCWP, P<0.0001), and lower capillary length density was associated with both increased BMI (P=0.043) and increased PCWP (P=0.016).
Conclusions:
Obesity and its accompanying increase in left ventricular filling pressure were associated with lower coronary microvascular density, which may contribute to the lower maximal myocardial blood flow, impaired myocardial metabolism, diastolic dysfunction and higher risk of heart failure in obese individuals.
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