The Echocardiography Evaluation And Clinical Analysis Of Mixed Pulmonary Hypertension Due To Primary Dilated Cardiomyopathy With Heart Failure

Objective: To understand the characteristics and pathogenesis of the differenttypes pulmonary hypertension from primary dilated cardiomyopathy (DCM) with leftventricular systolic dysfunction by echocardiography evaluation and clinical analysis,and compared with passive pulmonary hypertension, if mixed pulmonary hypertensionwould cause a worse clinical outcome.Methods: Twenty-five healthy subjects and seventy-eight DCM patients withsystolic heart failure (SHF) whose NYHA II-III、tricuspid regurgitation were mild tomoderate and right ventricular systolic function were normal had been collected.Two-dimensional and color Doppler, tissue Doppler echocardiography detection wereperformed. We collected RAP(right atrial pressure), TRVmax(tricuspid regurgitationmaximum velocity), PRVmax(pulmonic regurgitation maximum velocity), RVOTTVI(right ventricular outflow tract of time velocity integral), E(peak velocity of earlymitral inflow), E’(early diastolic mitral annular velocity), and then calculated thefollowing variables: PASP(pulmonary artery systolic pressure)=4TRVmax2+RAP(rightatrial pressure)， PADP(artery diastolic pressure)=4PRVmax2+RAP, mPA(meanpulmonary artery pressure)=PADP+1/3(PASP-PADP)， PVR(pulmonary vascularresistance)=（TRVmax/RVOTTVI）×10+0.16，PWCP（pulmonary capillary wedgepressure）=1.3(E/E’)+2，TPG（trans-pulmonary gradient）=mPAP-PCWP. Accordingto whether these patients had Pulmonary arterial hypertension and elevated pulmonaryvascular resistance, one hundred and three cases were divided into group1(healthysubjects, n=25), group2(DCM with SHF, but no Pulmonary arterial hypertension,mPAP<25mm Hg, PVR <3WU, n=30), group3(DCM with SHF, who had Pulmonaryarterial hypertension but the pulmonary vascular resistance were normal, mPAP>25mm Hg, PVR <3WU, n=23), group4(DCM with SHF, who had Pulmonary arterialhypertension and the pulmonary vascular resistance were higher than3WU, mPAP>25mm Hg, PVR>3WU, n=25). We would mainly analysis the changes of PASP, MPAP,PCWP, TPG, PVR,6-minute walk test (6MWT), B-type natriuretic peptide (BNP) andmechanism in the four groups.Results:1. The difference of the four groups in hemodynamic parameters(1) Compared with group1, SBP, DBP, CO, CI, LVEF of the group2wereobviously reduced, and PASP, PCWP, RAP were obviously increased, but the PVR (1.0±0.5WU vs0.6±0.4WU, P>0.05) had no significant difference. However, there werestatistical difference between group2and group3in PVR(1.0±0.5WU vs2.2±0.7WU, P <0.05).(2) There were statistical difference between the group4and the group3in PASP(56.3±8.4mmHg vs45.2±7.9mmHg, P <0.05) and PVR (4.3±1.3WU vs2.2±0.7WU, P <0.05)，but no significant difference in PCWP (19.9±1.8mmHg vs18.9±1.8mmHg, P>0.05).(3) The hemodynamic consequences of the group3patients were MPAP (29.3±3.7mmHg), PCWP (18.9±1.8mmHg), TPG (10.1±1.7mmHg), PVR (2.2±0.7WU),which match the characteristics of passive pulmonary hypertension, and the results ofthe group4patients were MPAP (36.2±1.5mmHg), PCWP (19.9±1.8mmHg), TPG(16.6±1.7mmHg), PVR (4.3±1.3WU), which match the characteristics of mixedpulmonary hypertension.(4) Although there were no significant difference in PCWP and6-minute walkdistance, dyspnea score and quality of life score between the group4and the group3,compared with group3, the left ventricular function (LVEF, CO, CI) and rightventricular function (RVEF, TAPSE, S’) in the group4were significantly lower (P<0.05), and BNP was significantly higher, which indicated that mixed pulmonaryhypertension patients had worse condition.(5) The correlation between PASP and PCWP in the group3was r2=0.806(P<0.001), the consequences in the group4was r3=0.838(P <0.001), and in allpulmonary hypertension patients(groups3and group4) the result was r1=0.747(P<0.001).(6) From group1to group4the right ventricular indicators RVEF (45.0±1.2%vs42.2±0.9%vs39.3±0.7%vs35.5±0.5%), TAPSE (22.9±1.3mm vs20.1±0.8mm vs18.5±0.6mm vs16.5±0.4mm), S ’(16.5±2.3cm/s vs14.3±1.4cm/s vs12.3±1.0cm/s vs10.4±0.4cm/s) was gradually reduced, and there were statistical difference inthe four groups.2. The difference of the four groups in clinic outcome(1) There were no significant difference in age, sex, and body mass index of thefour groups(P>0.05).(2)6-minute walk test distance, dyspnea score and quality of life rating: comparedwith group1, there were obviously difference in group2～4(p<0.05),and comparedwith group2, there also had statistical difference in group3～4(p<0.05), however, noobvious difference of these paraments between the group3and the group4can befound(p>0.05).(3) Significant difference can be seen in course of disease and BNP of the fourgroups(p<0.05).Conclusion:1. In the process of gradually increased pulmonary artery pressure which caused byleft ventricular systolic dysfunction, there were no significant changes in pulmonaryvascular resistance without pulmonary hypertension, however, when PASP>35mm Hg,the pulmonary vascular resistance had been significantly increased.2. Pulmonary hypertension caused by left ventricular systolic dysfunction was asequential process, in the early time there was only high pulmonary artery systolicpressure (PASP>35mmHg), but PVR did not obviously increase and lower than3WU,so in the early time of increased pulmonary artery pressure caused by left heart disease,if pulmonary vascular resistance had significantly greater than3WU, we should highlyalert to if we neglected other diseases, such as lung disease which lead to elevatedpulmonary vascular pressure and resistance.3. Compared with passive pulmonary hypertension caused by left ventricularsystolic heart failure, the PASP of mixed pulmonary hypertension patients wasobviously increased, but there was no outstanding difference in PCWP, which indicatedthe degree of pulmonary arterial pressure and left ventricular filling pressure were notcompletely consistent in the pathological process of pulmonary hypertension caused byleft ventricular systolic heart failure.4. There were high correlation between PASP and PCWP in the patients withpulmonary hypertension caused by left ventricular systolic heart failure, the correlationof PASP and PCWP in patients with passive pulmonary hypertension was r2=0.806(P<0.001), and the result in patients with mixed pulmonary hypertension was r3=0.838 (P<0.001). The correlation of PASP and PCWP in all pulmonary hypertensionpatients(groups3and group4) was r1=0.747(P<0.001), which indicated pulmonaryhypertension caused by left ventricular systolic function was mainly related with leftventricular filling pressure.5. There were no obvious difference between passive pulmonary hypertensionpatients and mixed pulmonary hypertension patients in6MWT, Dyspnea score, The qualityof life score and PCWP, however, the left ventricular function (LVEF, CO, CI) and rightventricular function (RVEF, TAPSE, S’) were significantly lower, and BNP indicatorswas significantly higher, which indicated mixed pulmonary hypertension patients hadworse condition.