The aim of the study is to investigate the association between the severity of rheumatic mitral valvular disease (RMVD) and the neutrophil-lymphocyte ratio (NLR). A total of 227 patients were enrolled in the study and divided into 3 groups. Patients in group 1 had rheumatic mitral stenosis (RMS), those in group 2 had RMVD without stenosis, and those in group 3 served as the control group. Group 1 was further divided into 2 groups, severe mitral stenosis (MS) and mild to moderate MS. The NLR was significantly higher in patients with severe MS when compared to those with mild to moderate MS (P = .002) while lymphocyte count was lower (P = .034). Using a cutoff level of 2.56, the NLR predicted severe RMS with a sensitivity of 75% and specificity of 74%. In conclusion, as an inexpensive, simple, and accessible marker of inflammation, the NLR may be useful in predicting the presence and severity of MS in patients with RMVD.

https://journals.sagepub.com/doi/pdf/10.1177/1076029613514131

Association of neutrophil-lymphocyte ratio with the presence and severity of rheumatic mitral valve stenosis.

Background— At present, no medical therapy is known to affect the progression of rheumatic mitral stenosis (MS). We sought to assess the effect of statin treatment on long-term progression of MS in a large population. Methods and Results— From our 20-year database, we identified all patients with rheumatic MS with ≥2 echocardiographies ≥1 year apart. Exclusion criteria were previous intervention on the mitral valve, more than moderate aortic regurgitation, or symptoms at first examination. The study sample included 315 patients (mean age, 61±12 years; 224 women); 35 patients (11.1%) were treated with statins, and 280 (88.9%) were not. Mean follow-up period was 6.1±4.0 years (range, 1 to 20). The rate of decrease in mitral valve area was significantly lower in the statin group compared with the untreated group (0.027±0.056 versus 0.067±0.082 cm2/y; P=0.005). The annualized change in mean transmitral gradient was lower in statin-treated patients (0.20±0.59 versus 0.58±0.96 mm Hg/y; P=0.023). The prevalence ...

Effect of Hydroxymethylglutaryl Coenzyme-A Reductase Inhibitors on the Long-Term Progression of Rheumatic Mitral Valve Disease

Rheumatic heart valve disease (RHVD) is a post-infectious sequel of acute rheumatic fever resulting from an abnormal immune response to a streptococcal pharyngitis that triggers valvular damage. RHVD is the leading cause of cardiovascular death in children and young adults, mainly in women from low and middle-income countries. It is known that long-term inflammation and high degree of fibrosis leads to valve dysfunction due to anatomic disruption of the valve apparatus. However, since public and private investments in RHVD studies are practically inexistent the number of publications is scarce. This disease shows different natural history and clinical presentations as compared to other degenerative heart valve diseases. Although more than five decades passed after the pioneering studies on the pathogenesis of RHVD, it is still unclear how self-tolerance mechanisms fail in this disease, and how humoral and cellular inflammatory responses are interconnected. Despite that pathological mechanisms have been already proposed for RHVD, none of them are able to explain the preferential involvement of the mitral valve. This review focuses on pathophysiology and underlying mechanisms of RHVD.

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Rheumatic Heart Valve Disease Pathophysiology and Underlying Mechanisms.

The mitral valve is a living structure comprised of specific structural components which contain a heterogeneous population of cells. The cells include an amalgam of interstitial cells within the valve and a continuous covering of endothelial cells, each of which play a role in responding to the mechanical forces that the valve experiences, to maintain the function and durability of the valve. Attention on the characteristics and function of valve cells has focused mainly on those in the aortic valve, with relatively few studies addressing the role of these cells in the physiological and pathophysiological function of the mitral valve. This article reviews what is known about the function of cells within the mitral valve and how the changes in the physical and chemical environments can affect their function in the different types of mitral valve disease. Investigating the contribution of the cellular components of the mitral valve to valve function in health and disease will aid the understanding of how the durability and function of the valve are regulated, and possibly highlight molecular and pharmacological targets for the development of novel treatments for mitral valve disease.

Cellular Mechanisms in Mitral Valve Disease

Aim of the work To elucidate the hypothesis of ongoing inflammation in children with chronic rheumatic heart disease, and its possible consequences. Subjects and methods This study was conducted on 36 patients with a mean age of 12.63 years: six with acute rheumatic carditis, and 30 with chronic rheumatic heart disease. There were 15 age- and sex-matched children who served as a control group. All subjects underwent echocardiographic assessment of valvular involvement and left ventricular function. Laboratory investigations comprised lipid profile, high-sensitivity C-reactive protein, and homocysteine assay. Results High-sensitivity C-reactive protein was significantly elevated in patients with acute rheumatic carditis and in patients with chronic rheumatic heart disease (mean and standard deviation of 78.33, 156 micrograms per millilitre and 78.33, 23.17 micrograms per millilitre, respectively) as compared to the control group (mean and standard deviation of 5.83 and 2.79 micrograms per millilitre). High-sensitivity C-reactive protein correlated with the grade of mitral regurgitation (p less than 0.05). Homocysteine was significantly elevated in patients with acute carditis and patients with rheumatic heart disease as compared to the control group (their mean and standard deviation were 2.96, 0.476 nanograms per decilitre, 2.99, 1.48 nanograms per decilitre, and 1.717, 0.733 nanograms per decilitre, respectively), but did not show significant difference between the two studied groups of patients. Neither C-reactive protein nor homocysteine correlated with any of the studied parameters of lipid profile. Conclusion There is evidence of ongoing inflammation in children with rheumatic heart disease, which correlates with the degree of valvular involvement. This ongoing inflammation may put those children at risk for premature atherosclerosis.

Ongoing inflammation in children with rheumatic heart disease.

Rheumatic Heart Disease (RHD) is well known to be an active inflammatory process which develops progressive calcification and leaflet thickening over time The potential for statin therapy in slowing the progression of valvular heart disease is still controversial Retrospective studies have shown that medical therapy is beneficial for patients with calcific aortic stenosis and recently for rheumatic valve disease However, the prospective randomized clinical trials have been negative to date This article discusses the epidemiologic risk factors, basic science, retrospective and prospective studies in valvular heart disease and a future clinical trial to target RHD with statin therapy to slow the progression of this disease Recent epidemiological studies have revealed the risk factors associated with valvular disease include male gender, smoking, hypertension and elevated serum cholesterol and are similar to the risk factors for vascular atherosclerosis An increasing number of models of experimental hypercholesterolemia demonstrate features of atherosclerosis in the aortic valve (AV), which are similar to the early stages of vascular atherosclerotic lesions Calcification, the end stage process of the disease, must be understood as a prognostic indicator in the modification of this cellular process before it is too late This is important in calcific aortic stenosis as well as in rheumatic valve disease There are a growing number of studies that describe similar pathophysiologic molecular markers in the development of rheumatic valve disease as in calcific aortic stenosis In summary, these findings suggest that medical therapies may have a potential role in patients in the early stages of this disease process to slow the progression of RHD affecting the valves This review will summarize the potential for statin therapy for this patient population

Margaret A Lloyd

Papers

Medical therapy for rheumatic heart disease: is it time to be proactive rather than reactive?