Diameter and shunt act as an alleviator of pulmonary hypertension: an echocardiography assessment of patients with ostium secundum atrial septal defect

Background Ostium-secundum atrial septal defect (OS-ASD) increases pulmonary arterial systolic pressure (PSAP) and eventually leads to pulmonary hypertension (PH). Nevertheless, whether the characteristics of OS-ASD could serve as an alleviator within chronic-volume overload in the right atrium (RA) is unclear. Aims To evaluate a potential interaction of OS-ASD diameter and the shunt (Qp/Qs ratio) on PSAP values in patients with secondary PH. Methods We designed a cross-sectional study of 63 adult patients with OS-ASD. A conventional transthoracic echocardiography was performed using Vivid 9X-clear equipment (GE Vingmed Ultrasound, Horten, Norway) to evaluate the OS-ASD diameter and the Qp/Qs ratio. The PSAP was calculated by tricuspid regurgitation velocity with continuous-wave Doppler in the apical four-chamber view. Polynomic adjusted correlations were performed between the RA volume and the PSAP; we evaluated a double and triple interaction-effect of the OS-ASD diameter and Qp/Qs ratio, respectively adjusted for age, sex and body surface area. Results In our study population, 78% (n=49) were female, with a mean age of 41.8 (±15) years. 44% (n=28) with mild-PH, 38% (n=24) with moderate-PH and 17% (n=11) with severe-PH. Mean echocardiographic parameters were: RA volume 58.8 (±26.4) mL, PSAP of 55.9 (±20.7) mmHg, OS-ASD diameter 30.1 (±7.8) mm and Qp/Qs 2.9 (±0.9). We observed a cubic relationship between RA volume and PSAP (r=0.354, p=0.006; Figure 1A). ASD-Diameter had a negative interaction effect (β=−0.0231 95% CI: −0.043 to −0.003, p=0.03) of the relationship between RA volume and PSAP (Figure 1B). Furthermore, the addition of Qp/Qs ratio displayed a positive triple interaction effect (β=0.021 95% CI: 0.001–0.043, p=0.048) on the previously mentioned variables (Figure 1C) after adjusting for covariates. Conclusions The increase in OS-ASD diameter and shunt decreases PSAP values. Our results could indicate that OS-ASD could potentially ameliorate chronic-volume overload in patients with secondary PH. FUNDunding Acknowledgement Type of funding sources: None. Figure 1

Effects of Trandolapril on Structural, Contractile and Electrophysiological Remodeling in Experimental Volume Overload Heart Failure

Chronic volume overload induces multiple cardiac remodeling processes that finally result in eccentric cardiac hypertrophy and heart failure. We have hypothesized that chronic angiotensin-converting enzyme (ACE) inhibition by trandolapril might affect various remodeling processes differentially, thus allowing their dissociation. Cardiac remodeling due to chronic volume overload and the effects of trandolapril were investigated in rats with an aortocaval fistula (ACF rats). The aortocaval shunt was created using a needle technique and progression of cardiac remodeling to heart failure was followed for 24 weeks. In ACF rats, pronounced eccentric cardiac hypertrophy and contractile and proarrhythmic electrical remodeling were associated with increased mortality. Trandolapril substantially reduced the electrical proarrhythmic remodeling and mortality, whereas the effect on cardiac hypertrophy was less pronounced and significant eccentric hypertrophy was preserved. Effective suppression of electrical proarrhythmic remodeling and mortality but not hypertrophy indicates that the beneficial therapeutic effects of ACE inhibitor trandolapril in volume overload heart failure might be dissociated from pure antihypertrophic effects.