A histological study of the atria in patients with isolated rheumatic mitral regurgitation with and without atrial fibrillation.

BACKGROUND: There is a high incidence of atrial fibrillation (AF) in patients with isolated rheumatic mitral regurgitation (MR). The histopathologic changes in the atria of patients with isolated rheumatic MR with and without AF are unknown. OBJECTIVES: We aimed to determine the histological findings in patients with isolated severe rheumatic MR with and without AF. METHODS: Patients with severe isolated rheumatic MR undergoing valve replacement surgeries underwent endocardial biopsies from right atrial appendage, left atrial appendage, right free wall, left free wall, left posterior wall, and mitral valve. Group I consisted of patients in sinus rhythm (SR), and Group II included patients with AF. We analyzed and compared these 10 histological features in the biopsies of patients in Groups I and II. RESULTS: Of the 25 patients, 12 were in Group I and 13 in Group II. In Group I, patients had severe myocyte hypertrophy (60% vs. 18%, p = .04) that was significantly more in the right atrium (22.7% vs. 11.4%, p = .059). Interstitial adipose tissue deposition was more common in Group I (30% vs. 25%, p = .06). Interstitial fibrosis was evenly distributed at all sites without significant difference between the two groups. Group II patients had a higher prevalence and severity of vacuolar degeneration (91% vs. 60%, p = .09). CONCLUSIONS: Patients with isolated severe rheumatic MR and AF have more vacuolar degeneration in the atrial tissue. Patients with SR have myocyte hypertrophy and interstitial adipose tissue deposition. Interstitial fibrosis is uniformly distributed in patients in SR and AF.

The prevalence of enteroviral RNA and protein in mitral valves of chronic rheumatic heart disease.

INTRODUCTION: Acute Rheumatic Fever/ Rheumatic Heart Disease (ARF/RHD), a sequel of group A streptococcal (GAS) infection, even today constitutes a public health issue in developing countries including India. Differences in the prevalence of ARF/RHD in countries with a similar prevalence of GAS infections indicate the role of other cofactors in pathogenesis of RHD. METHODOLOGY: We investigated the prevalence of enterovirus (EV) in RHD by probing for both EV RNA and VP1 protein using Nonisotopic In Situ Hybridization (NISH) and Immunohistochemistry (IHC) respectively in 75 valvectomy specimens obtained from RHD cases. RESULTS: Twenty-eight (37%) of the valves showed tissue inflammation with lymphocytic infiltration in a majority of the cases. Twenty-six and 27 (38% and 40%) of the 68 valves showed the presence of EV by IHC and NISH respectively, indicating a very good association between the two tests; however, only about 46 to 48% of them exhibited tissue inflammation. In eight cases (12%) the EV genome was detectable in absence of VP1 protein perhaps indicating a latent viral infection. CONCLUSIONS: Due to a high degree of endemicity of EV in India, we are tempted to speculate that EV may be responsible for the severity and rapid progression of RHD. The virus could either be working synergistically with GAS or could be an opportunist infecting damaged valves.