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Abstract:

Background: atrial septal defect (ASD) is characterized by a progressive increase in pulmonary vascular resistance and, accordingly, pressure in small circulation circle. It is noteworthy that these hemodynamic changes go in parallel with morphofunctional changes in small vessels of pulmonary artery system. At the same time, changes in hemodynamics of small circulatory circulation after endovascular closure in this category of patients and reversibility of pulmonary hypertension are not fully studied.

Aim: was to assess clinical course, indicators of cardiac chamber geometry and hemodynamics of small circulation circle after transcatheter closure of secondary ASD in adult patients with moderate and significant pulmonary hypertension in immediate and long-term periods.

Material and methods: from 2009 to 2020, 103 patients (mean age 48,3 ± 15,3 years) with secondary ASD underwent endovascular transcatheter closure of the defect. 60 (58,3%) patients had pulmonary hypertension. Depending on systolic pulmonary arterial pressure (SPAP), patients were divided into 3 groups: the first group consisted of 41 (68,3%) patients with mild PH (from 40 to 49 mm Hg); the second group included 10 (16,6%) patients with moderate PH (50 to 59 Hg); and the third group consisted of 9 (15%) patients with high SPAP (? 60 mm Hg). Average pulmonary artery systolic pressure in groups was: 43,6 ± 2,9 mm Hg; 52,1 ± 2,5 mm Hg; 64,4 ± 5,2 mm Hg, respectively. Average sizes of ASD (according to Pre-TEE data) were 18,7 + 6,1 mm; 22,1 ± 7,5 mm and 21,3 ± 5,3 mm, respectively. In all cases, echocardiographic signs of the right heart volume overload were detected. Follow-up was performed on an outpatient basis with an assessment of the clinical status and TTE in the long-term period.

Results: technical success of endovascular defect closure was 100%. Average size of the occluder was 26,3 + 6,96 (from 12 to 40) mm. Immediately after implantation of device, complete closure of ASD was observed in 55 (91,7%) cases. Residual flow (<3 mm) was observed in 5 cases (2 cases in the first group, 1 case in second group, and 2 cases in third group, (p >0,05)). In the vast majority of cases - 54 (90%) hospital period proceeded smoothly. All patients were examined in the long-term period (on average 12,5 + 6,5 months). The survival rate in groups was 100%. In the long- term follow-up remodeling of the right heart was observed in all patients. In the first group the size of RA decreased from 6,0 ± 0,5 cm to 3,3 ± 0,4 cm, RV size decreased from 4,7 ± 0,5 to 3,1 ± 0,4 cm; in the second group RA from 5,7 ± 0,7 cm to 3,8 ± 0,5 cm, RV - from 4,7 ± 0,9 to 3,8 ± 0,6 cm; in the third group RA - from 5,5 ± 0,6 cm and 4,2 ± 0,5 cm, the size of RV decreased from 4,5 ± 0,6 4,0 ± 0,5 cm, respectively. In all patients, significant decrease in SPAP was observed, in some cases up to normalization. In the first group, SPAP decreased from 43,7 ± 2,9 to 32,1 ± 2,6 mmHg, in the second group - from 52,1 ± 2,5 to 34,3 ± 2,6 mmHg; in the third group - from 64,4 ± 5,2 to 50,3 ± 4,8 mmHg. The most expressed decrease of pressure occurred in the second group of patients. At the same time, in the third group, dynamics of pressure reduction was significantly less expressed in comparison with the other two groups. At the same time in two patients of third group high PH remained in the long-term period, despite the successful closure of the defect.

Conclusion: results show that in case of left-right shunt in the absence of hypoxemia, transcatheter closure of ASD in adult patients with moderate and significant pulmonary hypertension is a pathophysiologically and clinically justified, is a highly effective treatment method that allows achieving significant improvement of both clinical manifestations and intracardiac and systemic hemodynamics. In patients with a significant degree of pulmonary hypertension and a high probability of the latter, the following tactical approaches may be considered:

1. primary closure of defect with further drug therapy;

2. primary drug therapy aimed on regulating of the anatomic-functional state of the arterial bed of the small circulation and hence reducing pulmonary vascular resistance followed by endovascular ASD-closure;

3. closure of the defect with a fenestrated occluder (in case of a negative test for temporary balloon occlusion), followed by drug therapy. This assumption can be considered in future research.

 

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