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Case Reports
. 2023 Apr 20:13:100458.
doi: 10.1016/j.ijcchd.2023.100458. eCollection 2023 Sep.

Percutaneous coronary intervention combined with treat-repair-treat strategy in a patient with pulmonary arterial hypertension associated with atrial septal defect and left main coronary compression syndrome

Yuan He  1 , Chen Zhang  1 , Qiangqiang Li  1 , Lixia Yang  2 , Dongmei Shi  2 , Bradley B Keller  3 , Hong Gu  1
Affiliations
Case Reports

Percutaneous coronary intervention combined with treat-repair-treat strategy in a patient with pulmonary arterial hypertension associated with atrial septal defect and left main coronary compression syndrome

Yuan He et al. Int J Cardiol Congenit Heart Dis. .

Erratum in

Abstract

Compression of left main coronary artery is a severe complication in PAH and the treatment strategy is tricky and should be individualized. We presented a patient with large atrial septal defect (ASD) and non-Eisenmenger pulmonary arterial hypertension (PAH). Right heart catheterization (RHC) showed the defect was non-correctable due to a pulmonary vascular resistance (PVR) of 9.49 Wood Units. EKG suggested myocardial ischemia and coronary angiography and coronary CTA confirmed proximal left main coronary artery was compressed by extremely dilated pulmonary arterial trunk, which is named left main coronary compression syndrome (LMCS). Percutaneous coronary intervention (PCI) using drug-eluting stent was performed and combined PAH-specific medications was prescribed simultaneously. At 6-month following the PCI procedure, PVR had decreased to 3.43 Wood Units, and percutaneous ASD closure procedure was performed. A 6-month follow-up the patient was asymptomatic and had significantly improved pulmonary hemodynamics. LMCS is rare among patients with ASD-PAH. PCI combined with PAH-specific medications allowed the closure of ASD, resulting in clinical improvement.

Keywords: Atrial septal defect; Case report; Left main coronary compression syndrome; Pulmonary arterial hypertension.

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Conflict of interest statement

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Figures

Fig. 1
Fig. 1
Chest radiograph. A: Chest radiograph at diagnosis. B: Chest radiograph after PCI and 6 months of PAH targeted therapy. C: Chest radiograph at 6-month follow up after ASD closure.
Fig. 2
Fig. 2
Echocardiographic examinations, 1: Parasternal long-axis image; 2. Apical four-chamber image; A: Echocardiography at diagnosis; B: Echocardiography after PCI and 6 months of PAH targeted therapy; C: Echocardiography immediately after ASD closure; D: Echocardiography at 6-month follow up after ASD closure.
Fig. 3
Fig. 3
Electrocardiogram examinations. A: Electrocardiogram at diagnosis. B: Electrocardiogram after PCI and 6 months of PAH targeted therapy. C: Electrocardiogram immediately after ASD closure. D: Electrocardiogram at 6-month follow up after ASD closure.
Fig. 4
Fig. 4
A: Coronary angiography and intravascular ultrasound (insert 1) at diagnosis; B: Coronary angiography and intravascular ultrasound (insert 2) after PCI; C: Coronary angiography 6 months after PCI and 6 months of PAH targeted therapy. D: Coronary angiography at 6-month follow up after ASD closure.
Fig. 5
Fig. 5
A: Coronary computed tomography angiography at dignosis; B: Coronary computed tomography angiography after PCI and 6 months of PAH targeted therapy. C: Coronary computed tomography angiography at 6-month follow-up after ASD closure.
See this image and copyright information in PMC

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