Abstract
In patients with mitral stenosis, there is poor correlation between the severity of mitral stenosis, as measured by the mitral valve area and the magnitude of pulmonary hypertension. We tested the hypothesis that left atrial compliance is a major factor determining the height of pulmonary artery pressure in patients with pure mitral stenosis and sinus rhythm. The right sided and left atrial trans-septal catheterization data was analyzed in 84 patients (67 females, 17 males) with pure MS and sinus rhythm. Pulmonary artery peak systolic, diastolic and mean pressures were obtained through right sided catheterization. The magnitude of the LA a and v waves and the mean (m) LA pressure were measured directly through trans-septal catheterization. A non-compliant LA was considered to exist if the LA v_m pressure difference equaled to or exceeded 10 mmHg. The mitral valve area was determined by echocardiographic and Doppler methods, as were the LA size, LV systolic and diastolic dimensions, and the LV ejection fraction. Multiple regression analysis was performed to determine the most important factor in the determination of pulmonary artery pressure. Fifty four patients had PAPs≥50 mmHg, 41 of whom had non- compliant LA. Of the 30 patients with PAPs
Highlights
Pulmonary hypertension develops in patients with mitral stenosis and may dominate the clinical picture of these patients
Relation between pulmonary arterial systolic pressure (PAPs) and measures of mitral stenosis severity: there was a strong correlation between the severity of pulmonary hypertension and peak left atrial v-wave pressure, mean left atrial pressure and mean pressure gradient through the mitral valve by catheterization (P
In the current study, we have confirmed other investigator’s findings that in patients with mitral stenosis, the development of pulmonary hypertension is largely independent of the mitral valve area[1,7,12,13]
Summary
Pulmonary hypertension develops in patients with mitral stenosis and may dominate the clinical picture of these patients. It has adverse effect on the functional status, exercise tolerance and prognosis[1]. The mechanism of pulmonary hypertension with mitral stenosis is known to be a complex process. Pulmonary hypertension may result from: 1- Passive backward transmission of the elevated LA pressure; 2- Pulmonary arterial constriction, which presumably is triggered by LA and pulmonary venous hypertension (reactive pulmonary hypertension); 3- Organic obliterative changes in the pulmonary vascular bed[2 ]. Vasoactive substances like endothelin and adrenomedullin have been linked to the development of pulmonary hypertension[3,4]. It is generally thought that the severity of mitral stenosis and the resultant increase in the left atrial pressure are important
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