| Background: Pulmonary arterial hypertension was a pathologic state associated with many disease. It was characterized by pulmonary artery vasospasm, intimal hyperplasia and remodeling. The right ventricular deal with large capacity, low pressure, which had a better tolerance to ischemia. It was important to explore the influence of pulmonary arterial hypertension on right ventricular function and contraction synchrony because it would help us judge the prognosis and treatment. Pulmonary arterial hypertension resulted in right ventricular pressure overload, right heart dysfunction or even right heart failure. Right ventricular inflow tract and outflow tract were not at the same level, so it was difficult to evaluate the right heart function for its infundibulum and special flow distribution.Objective: It was unclear whether right ventricular with pressure overload and remodeling had contraction asynchrony. It was important to the prognosis assessment and the therapy by evaluating the right ventricular function and asynchrony in the pulmonary arterial hypertension patients.Methods: Thirty-five patients with pulmonary hypertension (mean age 60.5±16.4years, 15males) and 35 normal controls (mean age 57.9±12.9years, 15males) were investigated. Pulmonary arterial hypertension with using tricuspid regurgitation were divided into mild (10cases) and moderate-severe (25cases) groups, and the difference between control group and pulmonary arterial hypertension group were compared. All images were recorded by GE Vingmed Vivid 7 system trasthoracic echocardiography. The evaluation of right ventricular size and function was performed in Standard real-time two-dimensional echocardiographic images . Right ventricular end-diastolic and end-systolic areas were measured from the apical 4-chamber view to calculate right ventricular fractional area change. In addition, the tissue Doppler imaging was also obtained to assess time-to-peak (TTP) recorded by longitudinal peak systolic strain and the interval from the onset of echocardiography Q-wave to the peak velocity of right ventricular wall, interventricular septum, and lateral wall of the left ventricle. The time differences between interventricular septum and the right ventricular wall TTP We compared. The time differences between interventricular septum and the right ventricular wall TTP in the strain were also compared. The isovolumic contraction acceleration was calculated by the measured peak isovolumic contraction velocity and time to peak. The following regional parameters were evaluated by pulse doppler (pw-TVI) echocardiography in different myocardial segments (right ventricular wall, interventricular septum, and left ventricular wall) on apical 4-chamber view including systolic myocardial velocity (Sm), early-and late-diastolic myocardial velocity (Em and Am).Results:1. Compared with the control group, patiens with moderate-severe pulmonary arterial hypertension showed increased right ventricular end-systolic and end-diastolic areas (RVESA 6.1±1.7cm2 vs. 12.3±4.0cm2; RVEDA 11.5±2.4cm2 vs. 19.2±4.1cm2, p<0.01), and reduced right ventricular fractional area change (47.1±11.7% vs. 36.7±13.6%, p<0.01). Patiens with mild pulmonary arterial hypertension also showed increased right ventricular end-systolic and end-diastolic areas (RVESA 6.1±1.7cm2 vs. 8.6±3.2cm2; RVEDA 11.5±2.4cm2 vs. 15.6±3.7cm2, p<0.05 or p<0.01), and reduced right ventricular fractional area change (47.1±11.7% vs. 44.1±9.9%, p=0.534).2. The moderate-severe pulmonary arterial hypertension group showed lower interventricular septum and right ventricular wall systolic myocardial velocity, and late diastolic myocardial velocity compared with the control group; early diastolic myocardial velocity of interventricular septum was lower than the control group (p<0.05 or p<0.01). The mild pulmonary arterial hypertension group showed lower right ventricular wall systolic myocardial velocity, and late diastolic myocardial velocity compared with the control group; systolic myocardial velocity of interventricular septum was lower than the control group (p<0.05 or p<0.01).3. Right ventricular wall myocardial systolic activation was delayed significantly in the pulmonary hypertension group. The difference between the right ventricular wall and interventricular septum TTP obtained by TVI and strain image increased significantly (26.7±22.8ms vs. 51.8±24.8ms and 33.8±51.8ms vs. 136.1±46.2ms, p<0.05 or p<0.01). Right ventricular myocardial contraction was delayed in the mild pulmonary arterial hypertension patients compared with the control group, the difference between the right ventricular wall and interventricular septum TTP was increased in the TVI (85.5±56.0ms vs. 33.8±51.8ms, p<0.01).4. The moderate-severe pulmonary arterial hypertension group showed decreased isovolumic contraction acceleration compared with the controlled group (0.9±0.3m/s2 vs. 1.6±0.3m/s2, p<0.01).5. Right ventricular myocardial contraction was markedly delayed in the moderate-severe pulmonary arterial hypertension patients compared with the mild pulmonary arterial patients (p<0.05or p<0.01). The difference between the right ventricular wall and interventricular septum TTP was increased in the TVI and strain image (33.0±18.3ms vs. 51.8±24.8ms and 85.5±56.0ms vs. 136.1±46.2ms, p<0.05or p<0.01). The difference between the right ventricular wall TTP was increased in the TVI image (157.4±26.1ms vs. 170.4±26.3ms , p<0.05).Conclusions: Pulmonary arterial hypertension not only leads to right ventricular remodeling, but also induces myocardial systolic asynchron. The pathophysiologic significance of contraction asynchron should be discussed further. |
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