Abstract 14813: The Cardiac Microvasculature in Heart Failure With Preserved Ejection Fraction: An Autopsy Study
Background: Patients with heart failure (HF) and preserved ejection fraction (HFpEF) have impaired left ventricular (LV) systolic and diastolic reserve function in the absence of epicardial coronary artery stenosis. Reduced microvascular density (MVD) may limit myocardial perfusion with stress and contribute to the pathophysiology of HFpEF.
Hypotheses: We hypothesized that MVD is decreased in HFpEF as compared to Controls without HF and that reduction in MVD is associated with LV hypertrophy and fibrosis.
Methods: Patients with ante mortem diagnosis of HFpEF (HF hospitalization with EF > 40%; median EF = 60%) were identified and crossed to the Mayo Clinic Autopsy Tissue Registry (ATR) to identify HFpEF patients (n=159) with autopsy. Controls (n=123; ≥ 20 per 4th-9th decade ) with no ante mortem HF diagnosis and non-cardiac death were identified from the ATR. The density of vessels < 300 um2 was measured in full thickness LV sections (whole field digital microscopy, WFDM) with bright field immunohistochemistry (CD31 stain) using intensity histogram-based and homogeneity quantitative analysis (Definiens®). LV hypertrophy was assessed with heart weight. Percent myocardial fibrosis was quantified using WFDM and a customized stain (SAB) specific quantitative analysis algorithm (Definiens®).
Results: MVD was normally distributed in both groups. See Table. HFpEF patients were older with higher prevalence of hypertension and diabetes. Adjusting for age and sex, HFpEF patients had more hypertrophy and fibrosis and lower MVD than Controls. Adjusting for age, sex and presence of HFpEF, MVD was inversely associated with BSA adjusted heart weight (p=0.004) and fibrosis severity (p<0.0001) and was lower in diabetics (p=0.01).
Conclusion: MVD is reduced in HFpEF in association with hypertrophy and fibrosis.Reduction in MVD may contribute to the pathophysiology of HFpEF.
- © 2013 by American Heart Association, Inc.