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JACC Cardiovasc Imaging. 2011 Sep;4(9):946-54. doi: 10.1016/j.jcmg.2011.06.017.

Contribution of ventricular diastolic dysfunction to pulmonary hypertension complicating chronic systolic heart failure.

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Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota, USA.



The aim of the study is to clarify the clinical role of Doppler-echocardiographic parameters of left ventricular diastolic dysfunction (LVDD) as determinants of pulmonary hypertension in patients experiencing left ventricular systolic dysfunction (LVSD) with and without the presence of functional mitral valve regurgitation (FMR).


Pulmonary hypertension (pulmonary venous or mixed pulmonary venous-arterial hypertension) complicating LVSD is associated with poor outcomes beyond that of LVSD alone. The view of the contribution of LVDD as a determinant of pulmonary hypertension is controversial and not well defined as a tool in clinical practice.


Data from patients with LVEF ≤40% undergoing Doppler-echocardiography evaluations during the period from August 2001 to December 2004 were analyzed. Pulmonary systolic pressure (PSP), parameters of diastolic function (mitral valve [MV] transmitral flow velocity [E]/mitral annular diastolic velocity [e'] ratio, MV deceleration time [DT]), quantitated effective regurgitant orifice area (EROA) of FMR, and clinical characteristics were evaluated. Pulmonary hypertension was defined as an estimated PSP ≥45 mm Hg.


Criteria were met in 1,541 patients; one-third (n = 533) demonstrating PSP ≥45 mm Hg (58 ± 10 mm Hg, range 45 to 102 mm Hg). Patients with pulmonary hypertension were older with higher E/e' ratio, EROA, and lower DT and LVEF. In multivariate analysis, pulmonary hypertension was independently predicted not only by severity of FMR (EROA ≥20 mm(2), odds ratio: 3.8, p < 0.001) but also by parameters of LVDD (E/e' ratio ≥15, odds ratio: 3.31, p < 0.001; DT ≤150 ms, odds ratio: 3.8, p < 0.001). Receiver-operating characteristics curve analysis showed that EROA, E/e' ratio, and DT provided significant incremental value in predicting pulmonary hypertension (c-statistic 0.830, p < 0.001).


Patients with LVSD commonly have secondary pulmonary hypertension, which is largely determined by the severity of LVDD even with adjustment for FMR and low LVEF. Thus, measures of LVDD in routine clinical practice where PSP may not be estimated are important physiologic descriptors of hemodynamic status and are cumulatively linked in the prediction of pulmonary hypertension.

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