Background: Some studies have evaluated the right ventricular (RV) function in volume-overload and pressure-overload conditions and have always categorized pulmonary arterial hypertension (PAH) in the latter group. However, PAH and pulmonary stenosis (PS) are two frequent diseases, both resulting in the RV pressure overload.

Objectives: The aim of this study was to evaluate the RV response to two causes of the RV pressure overload: severe PAH and PS.

Patients and Methods: Eighteen patients with PAH at a mean age of 43 ± 12 years (66.6% female) and 16 patients with PS at a mean age of 33 ± 17 years (56.35% female) were enrolled. Standard echocardiography, tissue Doppler, and longitudinal strain imaging at the base, mid, and apical levels of the RV free wall were done.

Results: Significant tricuspid regurgitation was more prevalent in the PAH group than in the PS group (61% vs. 18.5%; P < 0.001). The abnormalities in the RV myocardial performance index, RV areas, and RV fractional area change were significantly more robust in the PAH group (all Ps < 0.05) despite the higher net RV systolic pressure in the PS group as compared to the PAH group (121 ± 39 vs. 88 ± 26 mmHg; P < 0.001).

Conclusions: It seems that severe PAH aggravates the RV function more severely.

Once the right ventricle (RV) was called “the forgotten ventricle” (1); and with the progressive rate of atherosclerosis and its complications, most of the studies were focused on the left ventricle (LV). Nevertheless, the RV has a complex shape complicating the objective and precise assessment of the RV systolic function by echocardiography. The normal RV is a crescent-shaped structure wrapped around the LV and cannot be completely assessed in any single two-dimensional (2D) view. So, the assessment of the RV structure and function remains mostly qualitative and many clinicians rely on the visual assessment of the RV size and function (2, 3). Some studies have evaluated the RV function in volume-overload and pressure-overload conditions and have always tended to classify pulmonary arterial hypertension (PAH) in the latter group (4, 5). PAH and pulmonary stenosis (PS) are two frequent diseases, both resulting in the RV pressure overload.

The aim of this study was to determine whether the RV function is similarly influenced by PAH and PS or whether one is more compromising than the other, keeping in mind that both conditions elevate the RV systolic pressure.

3.1. Patients

Eighteen patients with severe mostly idiopathic PAH, defined as the RV systolic pressure (pulmonary arterial pressure) ≥ 60 mmHg estimated by echocardiography, were enrolled. The PS group included 16 patients with severe valvular and/or subvalvular stenosis and RV systolic pressure ≥ 60 mmHg.

The exclusion criteria were comprised of:

Given the possibility of coronary artery disease in older age, all the controls > 40 years underwent exercise electrocardiography or stress echocardiography and the negative ones were enrolled.

The study protocol was approved by the institutional review board. All the subjects provided written informed consent before participation.

The demographic and echocardiographic data in the PAH and PS patients are listed in Table 1.

The mean ± SD of the pulmonary valve gradient was (91.12 ± 13.76) in the PS group. The data of the most important associated abnormalities in the PS group are illustrated in Table 2.

The PAH patients were about a decade older than the PS patients, and 66.6% of the PAH patients were female versus 56.3% of the PS group. Significant tricuspid regurgitation was more prevalent in the PAH group as compared to the PS group (61% vs. 18.5%; P < 0.001). The RV systolic pressure was significantly higher in the PS group than in the PAH group (121 ± 39 vs. 88 ± 26 mmHg; P < 0.001), but it was totally discordant with the RV areas, RVFAC, and RVMPI changes between the two groups.

Among the strain and strain rate parameters (Table 1), the systolic strain rate at the RV apex was the only index which was significantly different between the patients with PAH and PS (-1.18 ± 0.83 vs. -0.80 ± 0.20; P = 0.022; respectively).

Table 1. Demographic and Echocardiographic Data in the PAH and PS Groups and Their Age-Matched Control Groups a, b

Table 2. Associated Abnormalities in the PS Group (n= 16) a

Table 3. Results from the Multivariate Logistic Regression Analysis Performed on Patients in the PAH and PS Groups a

Although there are many reports about the differences of the LV remodeling in response to various pathologies that put pressure overload on this chamber, similar studies about the RV are rare. In the present research, we sought to compare how the RV acts in the presence of pressure overload compared to normal individuals and also to find out whether there are any differences between the different pathologies that cause pressure loading on this chamber. The most important tissue Doppler imaging characteristics of PAH should be strain, systolic and diastolic SR (S, E) reduction and significant prolongation of IVRT over the tricuspid annulus. These have been confirmed by several other investigators (5-9), but this was confirmed for PS as well by a study conducted by Sutherland et al. (10). It is notable that in the ASE guideline (11), RVFAC < 35% and RVMPI > 0.55 are considered abnormal. According to our results, the PAH patients had lower RVFAC (36 ± 11% vs. 43 ± 9%; P = 0.039) and higher RVMPI (0.65 ± 0.19 vs. 0.43 ± 0.11; P = 0.001) as compared to the PS patients. Similar findings were reported in a nearly recent study by Jurcut et al. who concluded that at similar levels of pressure overload, the RV is less dilated and performs better in patients with PS compared with those with PAH (12). This suggests that the RV could activate intrinsic mechanisms that allow it to cope with increased afterload. They also noticed that although some RV functional parameters were comparable with those of healthy individuals, SR showed lower values, suggesting subclinical longitudinal dysfunction in patients with PS. However, the systolic strain rate at the apex was the only tissue-Doppler derived index which was significantly different between our PAH and PS patients. Tricuspid regurgitation severity was greater in the patients with PAH, which can expose this group of patients to some degree of RV volume overload. This volume overload could relatively be involved in the worse condition of the RV in the PAH group, which is compatible with the study of Gondi et al. (13). The presence of some chemical mediators could also be responsible for the worse RV function in these patients.

We gratefully acknowledge the generous assistance provided by the staff of the Echocardiography Department of Rajaei Cardiovascular, Medical and Research Center throughout this project.