Correlation Study Of Pulmonary Arterial Hypertension And Left Ventricular Diastolic Dysfunction

Background: Pulmonary hypertension (PH) refers to a well-known sequel to theprogressive increase of pulmonary vascular resistance caused by the injury ofpulmonary vascular bed, which finally resulted in right heart failure. Pulmonaryhypertension induced by left heart diseases was mainly related with the pulmonaryvenous connection and increase of pulmonary circulation pressure caused by the leftheart failure and restrictive left heart filling. To date, left heart failure has beenconsidered as the leading cause for PH. Left ventricular failure and/or heart valvedisorders may induce the increase of left atrial pressure, leading to the subsequentincrease of pulmonary artery pressure. On this occasions, the pulmonary vascularresistance (PVR) is≤3wood, while the pressure gradient between mean pulmonaryartery pressure (mPAP) and pulmonary capillary wedge pressure (PWCP) was in itsnormal range (＜12mmHg). For those with left ventricular disorders, the major mainfor the increase of pulmonary artery pressure was the increase of pulmonary venouspressure, during which the PWCP was>15mmHg. Previous study indicated that a strictcorrelation was noted between PCWP and PASP using right heart catheterization.Moreover, controlled trials indicated that E/E’ was correlated with left ventricular fillingpressure (LVFP) and PCWP. Currently, E/E’ has been applied in the evaluation ofLVFP. In this study,Objective: To investigate the correlation between E/E’ and pulmonary arterialsystolic pressure (PASP). Additionally, to investigate the effects of PH on the outcomesof patients with left ventricle diastolic dysfunction.Methods: One hundred and sixty-three patients with hypertrophic cardiomyopathy(HCM) refered to our hospital between January2010and December2011were includedin this study. Fifty healthy subjects (46%male mean age69.6±8.9years,) were enrolled as control group. Fifty patients with diastolic heart failure were divided intonon-pulmonary hypertension group (n=30,56%male, mean age61.7±9.5years) andpulmonary group (n=20,45%male, mean age69.5±13.8years). Two-dimensional andcolor Doppler, tissue Doppler echocardiography as well as serum N-terminal pro-brainnatriuretic peptide (NT-proBNP) detection were performed. The end-diastolic leftventricular posterior wall thickness (LVPWd), interventricular septal thickness (IVSd),and left ventricular end-diastolic dimension (LVDd) were measured at the level of leftventricular long axis using VIVID-7ultrasonoscope. In addition, the left ventricularejection fraction (LVEF) was measured at the apical four-chamber view. Thefollowing variables including peak velocity of early mitral inflow (E), late filling peakfrom atrial contraction (A), and deceleration time of the E wave velocity (EDT) weredetermined at the apical four-chamber view using pulsed wave Doppler system. Earlydiastolic mitral annular velocity (E’) was measured with myocardial tissue dopplerimaging, based on which the ratio of E/E’ was calculated. Tricuspid regurgitation peakvelocity (TRV) was detected with the pattern of tricuspid regurgitation which wasdetermined at the apical four-chamber view. The pulmonary artery systolic pressure(PASP) was calculated according to the following formula:PASP=RVSP=4(TRV)2+right artial pressure (RAP), where RVSP stands for the rightventricular systolic pressure. Inter and intra-group comparison of E/E’ and PASP wasevaluated in all the patients of the three groups. Additionally, the pearson correlationbetween E/E’ and PASP was analyzed.Results:1. No statistical difference was noted in the gender among the three groups(P>0.05). Significant decrease was noted in the patient ages in group2compared withthose of group1and3(P<0.05). For the blood level of NT-proBNP, remarkableincrease was noted in the patients of group2and3(P<0.05). Moreover, significantincrease was noted in the level of NT-proBNP in patients of group3compared withthose of group2(P<0.05).2. Statistical difference was noted in the IVSd, LVPWd, LADs, LVDd, peakvelocity of A and EDT (P<0.05). Significant increase was noted in IVSd, LVPWd,LADs and LVDd in the patients of group2and3(P<0.05). The EDT obtained in group2was higher than those obtained in group1(P<0.05). Significant increase was noted inE/A in group3compared with that of group1(P<0.05). Additionally, remarkabledecrease was noted in the peak velocity of A (P<0.05). 3. The peak value of E’ showed significant decrease in the patients of group2and3(P<0.05). Significant increase was observed in the E/E’ in the patients of group2and3(P<0.05). Remarkable decrease of peak value of E was observed in group3comparedwith that of group2(P<0.01). Additionally, remarkable increase of E/E’ was noted ingroup2compared with that of group3(P<0.01).4. Weak correlation was detected between E/E’and PASP among all the patients（r=0.472，P <0.01）. No correlation in group2, however, a strict correlation wasdetected between between E/E/and PASP in group3(r=0.876，P<0.001).Conclusions: PH was an important clinical complication for those with diastolicheart failure. There was significant correlation between E/E′and PASP in patients withdiastolic heart failure and pulmonary arterial hypertension, So, the increase of PH wasassociated with the degree of left ventricular diastolic dysfunction. Since the increase ofpulmonary artery pressure may lead to the deterioration of heart function, PASP couldbe used as an indicator for the outcome of those with diastolic heart failure.