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Background: Mitral regurgitation (MR) burdens the left and right ventricles with a volume or pressure overload that leads to a series of compensatory adaptations that eventually lead to ventricular dysfunction, and it is well known that in rheumatic heart disease (RHD) that the inflammatory process not only occurs in the valve but also involves the myocardial and pericardial layers. However, whether the inflammatory process in rheumatic MR is associated with ventricular function besides hemodynamic changes is not yet established. Purpose: Evaluate whether rheumatic etiology is associated with ventricular dysfunction in patients with chronic MR. Methods: The study population comprised patients aged 18 years or older included in the registry who had echocardiography performed at the National Cardiovascular Center Harapan Kita in Indonesia during the study period with isolated primary MR due to rheumatic etiology and degenerative process with at least moderate regurgitation. Results: The current study included 1,130 patients with significant isolated degenerative MR and 276 patients with rheumatic MR. Patients with rheumatic MR were younger and had a higher prevalence of atrial fibrillation and pulmonary hypertension, worse left ventricle (LV) ejection fraction and tricuspid annular plane systolic excursion (TAPSE) value, and larger left atrium (LA) dimension compared to patients with degenerative mitral regurgitation (MR). Gender, age, LV end-systolic diameter, rheumatic etiology, and TAPSE were independently associated with more impaired LV ejection fraction. Whereas low LV ejection fraction, LV end-systolic diameter, and tricuspid peak velocity (TR) peak velocity >3.4 m/s were independently associated with more reduced right ventricle (RV) systolic function (Table 3). Conclusions: Rheumatic etiology was independently associated with more impaired left ventricular function; however, rheumatic etiology was not associated with reduced right ventricular systolic function in a patient with significant chronic MR.

IntroductionDespite advances in diagnostic and treatment, morbidity and mortality due to infective endocarditis (IE) has not decreased. There is a discrepancy in epidemiology of IE between developed and developing countries. Over the last years, increased early detection and consequently prevalence of rheumatic heart disease (RHD) and congenital heart disease (CHD) which are considered predisposing conditions for IE, is noted. Here, we present a review of literature on IE in developing countries.MethodsWe conducted a systematic literature search of IE studies in developing countries through PubMed and Embase. We have divided the studies into two groups: studies published before 2015 (group 1) and studies ≥ 2015 (group 2). The outcome was defined as a difference in epidemiology, microbiology, treatment, and mortality over time. The Scale for Assessment of Narrative Review Articles guidelines was applied.FindingsIn total, 16 studies were included. The total number of IE cases was 1,098 and 1,505 in groups 1 and 2, respectively. We compared 4/7 cohorts from group 1 (n = 789) with 5/9 cohorts from group 2 (n = 636). Six studies were not included in the comparison because they were interacting between the two cohorts. Males predominated in all studies. Rheumatic heart disease was higher in group 1 than in group 2 (42.3% vs. 30.3%, p < 0.001) while for CHD there was no change (17.6% vs. 16.7%, p = 0.672). Streptococci infections was lower in group 1 than group 2 (26.2% vs. 37.7%, p < 0.001). The proportion of Staphylococcus aureus was 15.3% in group 1 and 23.6% in group 2, p < 0.001. Negative blood culture (NBC) was higher in group 1 than in group 2 (42.2% vs. 34.1%, p = 0.002). Patients in group 1 received more surgery than in group 2 (38.8% vs. 28.8%, p < 0.001). Mortality was similar in the two groups (20.9% vs. 22.3%, p = 0.518).ConclusionThis review shows a scarcity of studies on IE in developing countries. Rheumatic heart disease and congenital heart disease are common predisposing conditions. Other risk factors are prosthetic valves, degenerative valve disease (DVD), intravenous drug use, and human immunodeficiency virus infection. While the proportion of IE cases caused by Streptococcus and Staphylococcus has increased, the number of NBC and patients getting surgery has decreased. Mortality has not changed over time. Timely diagnosis and management of patients with RHD and CHD and comprehensive management of IE are warranted.

Rheumatic heart disease (RHD) is common in developing countries and poses a big medical challenge and burden. The pathogenesis of RHD is influenced by the triad of host, agent, and environment. Autoantigens generated from Group A Streptococcus (GAS) infection are captured by the resident dendritic cells (DCs) in the heart's valvular endothelium. DCs differentiate into antigen presenting cells (APC) in the valve interstices. APC induces activation of autoreactive T cells, which triggers inflammation and tissue fibrosis. Cardiac fibrosis is promoted through the activation of Mitogen activated protein kinases (MAPKs) and its downstream signaling, including its interaction with transforming growth factor-β (TGF-β) and Smad proteins. TGF-β-induced phosphorylation of Smad2 complexes with Smad3 and Smad4, and translocates into the nucleus. Angiotensin II enhances the migration, maturation, and presentation of DC. In RHD, Angiotensin II induces fibrosis via the stimulation of TGF-β, which further increases the binding of IL-33 to sST2 but not ST2L, resulting in the upregulation of Angiotensin II and progression of cardiac fibrosis. This cascade of inflammation and valvular fibrosis causes calcification and stiffening of the heart valves in RHD. Angiotensin converting enzyme inhibitors (ACEIs) inhibit Angiotensin II production, which in turn decreases TGF-β expression and the onset of overt inflammatory response. This condition leads to a reduction in the sST2 as the decoy receptor to “steal” IL-33, and IL-33 binds to ST2L and results in cardioprotection against cardiac fibrosis in the pathogenesis of RHD.

Abstract Background The assessment of outcomes of interventions based on the patient’s perspective using patient-reported outcome measures (PROMs) has been increasingly highlighted in clinical practice. However, health related quality of life (HRQoL), one of the common constructs measured by PROMs remain unknown among patients after heart valve replacement (HVR) in Tanzania. Objectives To assess the HRQoL amongst patients operated on for rheumatic mitral stenosis at Jakaya Kikwete Cardiac Institute (JKCI). Methods A prospective study of patients operated on due to rheumatic mitral stenosis at JKCI from January 2020 to April 2021 was undertaken. The HRQoL was assessed by using the MacNew questionnaire, addressing three domains (physical, emotional, and social function); the score ranges from 0 to 7. We categorized HRQoL as low (mean score ≤ 4.9), moderate (5–6) and high (> 6). We analysed several sociodemographic and clinical variables for HRQoL. Results Out of 54 patients, there were 34 females and 20 males. Their mean (± SD) age was 37.98 (± 12.58) years. The reliability of translated Kiswahili version of MacNew was good. The mean (± SD) global scores were 3.47 ± 0.59, 4.88 ± 0.71 and 6.14 ± 0.50 preoperatively, at 3 months and 6 months respectively (p-values