Influence Factors Analysis Of Pulmonary Hypertension Secondary To Dilated Cardiomyopathy

Objective: This trial is aimed at analyzing clinical risk factors of Dilated Cardiomyopathy(DCM) patients secondary to pulmonary hypertension(pulmonary arterial hypertension, PAH).Methods: Patients who were diagnosed with DCM in the Second Hospital of Hebei Medical University from February 2015 to February 2016 were enrolled. Echocardiographic examination was performed within 24 hours on admission. On basis of echocardiography pulmonary artery pressure(pulmonary artery pressure PAP), The patients were divided into dilated cardiomyopathy secondary pulmonary hypertension group(DCM-PAH) and dilated pulmonary artery pressure normal group(DCM). Baseline clinical datas of both groups were recorded, including Age, sex, body mass index, heart rate, smoking history, drinking history, history of hypertension, history of diabetes, stroke history, cardiac function. Meanwhile, Blood, B-type natriuretic peptide(BNP) and endothelin 1(ET-1), uric acid(UA), homocysteine(HCY) and other biochemical indexes were detected. Echocardiographic parameters of both groups were recorded,including left ventricular ejection fraction(LVEF), left ventricu- lar(LV), left atrial(LA), tricuspid regurgitation velocity(TR), systolic pulmonary artery pressure(SPAP), left ventricular end-diastolic volume(EDV), left ventricular systolic volume(ESV), early diastolic mitral flow velocity and early diastolic mitral annulus velocity ratio(E/e ').arrhythmia was recorded by Holter. The risk factors of PAH were analyzed by multiple Logistic regression. All clinical data were analyzed with SPSS 20.0. P Value less than 0.05 was considered to be statistically significant.Results: A total of 68 patients were enrolled and divided into DCM-PAH group(30 cases) and DCM group(38 cases).1.There were no significant differences between both groups in baseline characteristics, including Age, sex, smoking history, drinking history, history of hypertension, history of diabetes, stroke history, body mass index(BMI), heart rate, atrial fibrillation, nonsustained ventricular tachycardia and complete left bundle branch block( P>0.05).2.HCM-PAH serum ET-1(95.2�13.4 VS 81.0�8.1 pg/m L,P=0.000), BNP(2352.9�1335.7 VS 606.3�551.9 pg/m L, P=0.000),UA(526.1�122.5 VS 361.8�104.4 umol/L,P=0.002), HCY(18.7�5.4 VS 11.2�6.0umol/L, P=0.001) were higher compared with HCM group.Hemoglobin, red blood cell distribution width,lipids,creatinine, urea nitrogen, transaminases bet- wee n both groups were not significantly different(P>0.05).3.Echocardiographic parameters comparision found that, LA in HCM-PAH group was significantly higher than that in HCM group(45.2�7.7 vs 40.9�5.5 mm,P =0.008).However, other parameters such as LV, LVEF, EDV, ESV, E/e' were not statistical different(P > 0.05).4.Pulmonary artery pressure level rised with deterioration of cardiac function. PAP of patients with NYHA I was 22 � 2.8mm Hg. PAP of patients with NYHA II was 27.6 � 7.3mm Hg. PAP of patients with NYHA III was 42.2 � 10.3mm Hg. PAP of patients with NYHA IV was 62 � 17.4mm Hg. comparsions of Pulmonary artery pressure level between any random groups were found significantly different(P<0.001) except for that between class I and class II patients(P> 0.05). ET-1 levels increased with deterioration of cardiac function,that of patients with NYHA I was 70.9 � 0.84pg/m L, that of patients with NYHA II was 76.5 � 7.36pg/m L, that of patients with NYHA III was 87.3 � 2.81pg/m L, that of patients with NYHA IV was 95.8 �3.36pg/m L.comparsions between any random groups were statistically significant(p<0.05); BNP levels increased with impaired cardiac function.BNP in patients with NYHA I was 175� 131pg/m L, in patients with NYHA II was 247 � 148pg/m L, in patients with NYHA III was 1506�797pg/m L, in patients with NYHA IV was 2865�1619pg/m L. Comparisions between any two classes were demonstrated to be significantly different except for that between class I and class II(P> 0.05).5.ET-1 levels increased with the increasing grade of pulmonary arterial pressure. ET-1 in the DCM group was 81.1� 8.1pg/m L. ET-1 of PAH I group was 89.2�6.1pg/m L. ET-1 of PAH II group was 103.2 � 1 6.5pg/m L.pairwise comparisons for those parameters were statistically significant(p <0.05).UA levels increased with increase in pulmonary artery pressure grading, UA in normal group was 361.8�104.3 umol/L, UA of PAH I group was 476.9�114.7umol/L, UA of PAH II group was 559.4�11 9.7umol/L.Among subgroups, pairwise comparisons of the parameters were found statistically significant(p <0.05). BNP levels increased with increased grade of pulmonary arterial pressure.BNP of the normal group was 606.3�551.9pg/m L, that of PAH I group 1772.1�771.3pg/m L,that of PAH II group 3112.5�1554.2pg/m L.pairwise comparisons were statistically significant(p <0.05); HCY levels increased with increased grade of pulmonary arterial pressure.HCY of the normal group was 11.2 � 6.0 umol/L, that of PAH I group 16.5� 4.7 umol/L, that of PAH II group 21.6�5.1 umol/L.Among subgroups, pairwise comparisons were statistically significant(p <0.05).6. levels of ET-1,BNP,UA,HCY and LA were positively correlated with pulmonary arterial pressure(r = 0.786,P = 0.000; r = 0.767,P = 0.000; r = 0.651,P = 0.000; r = 0.422,P = 0.011; r = 0.235, P=0.038).7. Binary Logistic regression analysis showed that ET-1(OR = 1.272,95%Cl =1.002-1.614,P = 0.048), UA(OR = 1.003,95%Cl =1.001-1.005,P = 0.011), HCY(OR = 1.375, 95%Cl =1.089-1.736, P = 0.007), LA(OR = 1.305, 95%Cl =1.080-1.578,P = 0.006) were independent risk factors of pulmonary hypertension secondary to dilated cardiomyopathy.Conclusion:1 Endothelin-1, uric acid,homocysteine, B-type natriuretic peptide and left atrium diameter in patients with pulmonary artery secondary to dilated cardiomyopathy were significantly increased.2 Level of pulmonary artery pressure, endothelin-1 and B-type natriuretic peptide increased with deterioration of cardiac function.3 endothelin-1, uric acid, homocysteine, B-type natriuretic peptide increased with rise in pulmonary artery pressure.4 endothelin-1, uric acid, homocysteine, left atrial diameter in dilated cardiomyopathy patients were independent risk factors of secondary pulmonary hypertension.