PH is common in patients with mitral valve disease. The present study demonstrated that 37.4% of patients with moderate to severe mitral valve disease had PH, while an incidence of 23–33% was reported in previous studies [1–4]. LA volume index and a severe clinical disease are both independent determinants of PH in patients with mitral valve disease and in the subgroups of MS and MR. Furthermore, the present study demonstrated the importance of significant right-sided valvular regurgitation as an independent determinant of PH in patients with mitral valve disease and the subgroup of MR.
Significance Of Pulmonary Hypertension In Mitral Valve Disease
The presence of PH in patients with mitral valve disease adversely affects the clinical symptoms and it is a predictor of poor long-term outcome, including event-free survival, even after successful corrective interventions [13, 14]. Patients with mitral valve disease and PH are vulnerable to right heart failure and/or pulmonary edema, which greatly contribute to the morbidity and mortality. The current guidelines on treatments of valvular heart disease recommend valvular intervention for asymptomatic patients with mitral valve disease and pulmonary artery systolic pressure > 50 mmHg [6, 7].
Pathophysiological Consequences of Mitral Valve Disease in Association with Pulmonary Hypertension
The initial insult leading to PH in chronic mitral valve disease differs between MS and MR. MS leads to LA pressure overload imposed by the stenotic mitral valve, while MR leads to volume overload from significant regurgitation. Despite these different pathophysiological mechanisms, the common anatomical and physiologic changes include an increased LA pressure, LA enlargement, a passive backward transmission of pressure to the pulmonary vessels, pulmonary vasoconstriction, irreversible vascular remodeling of pulmonary arterial wall, an increased pulmonary vascular resistance, and eventually PH [5, 15–17]. Among patients with mitral valve disease in the present study, dyspnea, LA volume index, significant regurgitation of right-sided heart valves, severe disease and stenotic lesion were independent determinants of PH. These findings emphasize the importance of the pathophysiological alterations of mitral valve disease, such as the severity of clinical disease, LA remodeling and stenotic lesion, leading to PH. The relationship between New York Heart Association functional class and PH in patients with mitral valve disease has previously been reported [2, 18]. The more severe the mitral valve disease, the greater is the expected LA dilatation and the higher pulmonary pressure. The present study showed that MS was a more significant determinant of PH than MR, regardless of clinical symptoms, cardiac rhythm, and the severity of mitral valve disease. As previously recognized, LA volume index and the severity of MR were identified as the independent determinants of PH and had prognostic implications in patients with MR [1, 2, 19]. However, less has been reported with regard to patients with MS. The present study showed that LA volume index and severe disease were important determinants of PH both in patients with MS and those with MR. Our findings confirm the importance of LA remodeling to the development of PH in patients with mitral valve disease, and supported the fundamental relationship in term of pathophysiological mechanisms.
Study Limitations
The present study has some limitations. Similar to several previous studies, the majority of patients in the present study had a severe disease and the results may not be applicable to patients with milder disease. The present study focused on the determinants of PH in patients with mitral valve disease and the outcome data are not available. The assessment of pulmonary artery pressure in the present study was achieved solely by Doppler echocardiography, not by right heart catheterization. However, the echocardiographic estimation of pulmonary artery pressure has been well-validated and reinforced by the current guideline for the routine clinical practice [11].