Pulmonary arterial hypertension (PAH) includes a group of chronic lung vascular diseases frequently complicated by right ventricle (RV) dysfunction and failure (1, 2). Under physiological conditions, the RV interacts with a low-pressure, low-resistance pulmonary circulation (3). However, under pathological conditions such as PAH, the RV is—at least initially—capable of adapting to the increase in pressure overload with remarkable hypertrophy in both humans and animals (4, 5). Although the mechanisms by which pressure overload induces RV hypertrophy are partially understood, the mechanisms whereby adaptive hypertrophy becomes maladaptive are still incomplete (4, 6). Puzzling examples are the patients with Eisenmenger’s syndrome (EMS). The “resilient” RV of patients with EMS appears to be better adapted to increased pressure overload compared with the RV of patients with idiopathic PAH (IPAH) or other forms of PAH (7). Moreover, whereas most patients with IPAH frequently present with decreased cardiac output at the time of diagnosis (2), patients with EMS maintain a normal cardiac output and right atrial pressure in spite of a similar degree of pressure overload (8), at least until later stages of the disease (8). Interestingly, whereas the hemodynamic differences between patients with IPAH and those with EMS have long been recognized (8), and some structural differences of the RV have been described by cardiac tomography (7), an anatomopathological comparison between the hearts of patients with EMS and IPAH has so far not been reported. In the present study, we performed a postmortem morphometric analysis of the left ventricles (LVs) and RVs of patients with IPAH (n= 6) or EMS (n= 6) who died from RV failure. All patients with EMS had a patent ductus arteriosus as the systemic-to-pulmonary shunt. Age-matched patients who died from noncardiac, nonpulmonary disease were used as control subjects (n= 6). The majority of patients died before any PAH-specific therapies were available. However, we excluded any patient that had been treated with a PAH-specific drug later in time. Informed consent was obtained from the family of each patient. The study protocol conformed to the ethical guidelines of the 1975 Declaration of Helsinki and was approved by the Instituto Nacional de Cardiologıa “Ignacio Chávez” Institutional Review Board. We measured the anterior-to-posterior and septum-to-free-wall diameters, as well as RV and LV wall thickness at the base, middle, and apex levels (Figures 1A and 1B). Annular dimensions of tricuspid and mitral valves were also measured. Using the RV diameters, we estimated the RV-chamber area using the formula A=(p 3 dAP 3 dSW)/4, where A represents the RV-chamber area, dAP represents the anterior-to-posterior diameter, and dSW represents the septumto-free-wall diameter. This formula was derived from the formula to calculate the area of a circle. All results are reported as mean 6 standard deviation. Differences between groups were assessed by oneway or two-way analysis of variance, and Bonferroni’s post hoc test was used to assess significant differences between groups. A P value less than 0.05 was accepted as significant. Correlation analysis was done using a Spearman’s test. The mean age for all groups was 28 6 10 years. Both patients with EMS and those with IPAH had severe pulmonary hypertension (56 6 14 mm Hg in IPAH vs. 78 6 14 mm Hg in EMS, P= 0.023). Figures 1C–1E illustrate that the RV in both groups of patients responded to pressure overload with significant hypertrophy as evidenced by increased RV wall thickness. Interestingly, patients with EMS also …