Pulmonary artery pressure and diastolic dysfunction in normal left ventricular systolic function☆
Introduction
Diastolic heart failure is caused by the inability to produce an adequate cardiac output at normal left ventricular (LV) filling pressure despite the presence of normal ventricular systolic function [1]. A normal forward cardiac output in these patients can only be maintained by a compensatory elevation of left ventricular filling pressure [2]. This state is associated with a marked increase in morbidity [3] and all-cause mortality [4]. With the aid of echocardiography, based on the pattern of diastolic left ventricular filling velocities, diastolic failure can be subgrouped into 3 major stages: 1. impaired relaxation, in which myocardial stiffness is evident but left atrial pressure is not yet elevated, 2. pseudo normal filling pattern; in which there is already a modest increase in left atrial pressure, and 3. restrictive pattern; where left atrial pressure is markedly elevated [2]. It has been shown that progression in the degree of diastolic dysfunction is associated with worsening of the prognosis of heart failure patients [4], [5]. Pulmonary hypertension complicating left ventricular systolic dysfunction is also associated with an increased incidence of mortality [6]. Several studies have demonstrated an association between abnormal mitral inflow patterns consistent with diastolic dysfunction and increased pulmonary artery pressure (PAP) in subjects with concomitant LV dysfunction [7], [8], [9]. Enriquez-Sarano et al. have demonstrated that pulmonary hypertension is not independently related to the degree of LV systolic dysfunction but is strongly associated with diastolic dysfunction in patients with LV systolic dysfunction [10]. In their study, a restrictive mitral inflow pattern was found to be the major marker of pulmonary hypertension. Moller et al. have recently shown that the degree of diastolic dysfunction is an independent predictor of pulmonary hypertension in a population of patients with acute myocardial infarction [11]. However, this association has never been studied systematically in patients with normal systolic function.
Therefore we performed a retrospective analysis of Doppler echocardiographic studies of subjects with normal LV wall motion, to assess the correlation of the degree of diastolic dysfunction with the magnitude of PAP. Patients with other co-morbidities that could have affected PAP by mechanisms other than LV diastolic dysfunction were excluded. We hypothesized that 1. PAP is higher in patients with pure diastolic dysfunction compared to cases with both normal systolic and diastolic function. 2. The magnitude of PAP is positively correlated to the degree of diastolic dysfunction.
Section snippets
Methods
The study was approved by the Institutional Review Board.
Results
Four hundred and seventy seven patients were enrolled in the study of whom 298 (62.5%) were in-hospital patients and 179 (37.5%) out patients. Their mean age was 64.7 ± 17.1 years and 211 (44.2%) of them were males. Patients were divided into 4 groups based on their diastolic dysfunction stage. One hundred and ten patients were graded as having normal diastolic function (grade 0), 256 as grade 1 diastolic dysfunction, 102 as grade 2 and 9 had grade 3 dysfunction. Their baseline characteristics
Discussion
In this study, we have demonstrated that PAP is positively correlated with the degree of diastolic dysfunction in patients with normal LV systolic function. For any increment in diastolic dysfunction grade, a statistically significant increase in pulmonary artery systolic pressure was observed. All patients analyzed in the study had normal LV systolic function and none showed any other cardiac pathology (i.e. mitral stenosis or regurgitation, congenital heart disease or systemic disorder) that
Conclusions
Pure left ventricular diastolic dysfunction is associated with an increase in PAP. There is a significant increase in PAP for any increase in the diastolic dysfunction stage. We suggest that diastolic dysfunction should be included in the differential diagnosis of pulmonary hypertension and therefore diastolic function should be carefully examined when evaluating a patient with this disorder.
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No conflict of interest to disclose. The expenses of this study were covered by personal resources. No outside sponsorship was obtained.