Major aortopulmonary collateral artery (MAPCA) with diminutive pulmonary artery (PA) is a complex and rare form of congenital heart disease. The most important consideration in this disease is how to facilitate pulmonary arterial growth. Generally, a surgical strategy involving unifocalization of the MAPCAs or rehabilitation of the native PA is used. We report two rare cases of complete transcatheter rehabilitation of the native PA without surgery in patients with MAPCAs and diminutive pulmonary antegrade flow, using balloon valvuoplasty and embolization. The important factors in this strategy were a sufficient dual supply from the native PA and the MAPCAs, as well as a subarterial ventricular septal defect. This strategy can be a useful option as a bridge to definitive repair for this particular patient group, and therefore palliative surgery in early infancy, which is associated with a relatively high mortality, can be avoided.

A 12 month-old boy with tricuspid atresia underwent cardiac catheterization prior to undergoing a bidirectional Glenn shunt (BDG) procedure. A late-phase aortography image showed retrograde blood flow through the left superior vena cava, and selective coronary angiography revealed coronary sinus ostial atresia (CSOA). CSOA associated with single ventricle physiology is a potentially fatal condition because of the resultant disturbance of coronary circulation. An accurate evaluation of angiographic findings is necessary to identify CSOA.

Clinical recognition of the rarely occurring forms of syndromic congenital heart defects is not always straightforward. Chromosomal microarray testing is known to play promising roles in the diagnosis of congenital disorders presenting with multiple anomalous features. Herein, chromosomal microarray testing proved effective in establishing the molecular diagnosis of Mowat–Wilson syndrome, one of the under-recognized, phenotypically variable genetic syndromes often presenting with a congenital heart defect. Taking advantage of the increasingly available genetic diagnostic tools may aid in paving our way through the complicated differential diagnoses in such unexplained syndromic congenital heart defect circumstances.

Microvascular angina is defined as angina-like chest discomfort with normal epicardial coronary arteries, which is due to coronary microvascular dysfunction. The condition is most prevalent in perimenopausal or postmenopausal women, but is rare in young women. Here, we report the case of a 16-year-old female who complained of chest discomfort during exercise and was diagnosed with microvascular angina. Exercise stress-induced chest discomfort was not relieved by nitroglycerin treatment. Exercise thallium-201 myocardial scintigraphy showed a perfusion defect in the anteroseptal wall. Although there was no significant stenosis or vasospasm in the epicardial coronary arteries on angiography, an ergonovine spasm stimulation test induced chest discomfort and delayed distal vessel opacification in the left anterior descending coronary artery. Concomitant treatment using carvedilol and diltiazem in addition to exercise limitation reduced the frequency of chest pain. Improvement was also seen in exercise scintigraphy perfusion defects. Recent evidence challenges the assumption that microvascular angina is a benign condition; therefore, early treatment may be particularly important in young patients. Physicians who examine young patients with angina-like chest discomfort should consider a possible diagnosis of microvascular angina.