We report 2 cases of postinfarction ventricular septal perforation (VSP) attributable to obstruction of the right coronary artery. Case 1 was a 63-year-old man in whom VSP developed after percutaneous coronary angioplasty for complete obstruction of the right coronary artery. He developed papillary muscle rupture intraoperatively, requiring mitral valve replacement and subsequent treatment for right-side heart failure. He was discharged l7 weeks after surgery. Case 2 was a 77-year-old man. During catheterization following the detection of 99% obstruction of the #2 segment of the right coronary artery, VSP was found and the patient underwent emergency surgery. Postoperative echocardiography and ventriculography did not reveal a residual shunt or mitral regurgitation (MR). However, he suddenly developed acute MR in the 4th postoperative week and died of acute heart failure. VSP attributable to obstruction of the right coronary artery is difficult to repair surgically because of its anatomical location, among other reasons, and mitral valve replacement is sometimes needed if VSP is accompanied by necrosis of the mitral valve papillary muscle. Appropriate care is therefore needed in this case.

A 54-year-old woman underwent abdominal aortic replacement for abdominal aortic aneurysm in March 2012. Approximately 6 months after surgery, she was taken by ambulance to hospital due to thoracodorsal pain, lower limb paralysis and pain. Emergency computed tomography indicated acute aortic dissection involving the ascending aorta, aortic arch, and descending aorta. The outline of the prosthesis implanted in the abdominal aorta was absent, and emergency surgery was performed immediately by median sternotomy to treat suspected complete obstruction. Following confirmation of brachiocephalic artery dissection, extracorporeal circulation was started with drainage of blood from the vena cava and the return via left axillary artery, plus perfusion in both lower limbs. However, the level of regional oxygen saturation declined as the flow of extracorporeal circulation increased. To solve this problem, an incision was made in the ascending aorta, and an aortic cannula was inserted directly into the true lumen. Aortic arch replacement was then performed, but this central repair failed to improve blood flow in both the left and right femoral artery. Proximal thrombectomy successfully removed a large amount of thrombi, but did not improve blood circulation. Left axillobifemoral bypass was subsequently performed, and improved lower limb blood circulation, but with residual motor impairment. Since the patient regained somatosensory sensation and was able to perform simple exercises, rehabilitation was started. Hemodialysis was required after abnormal increases in muscle enzyme levels and white blood cell count, but this was later discontinued following improvement of renal function. The patient was transferred to a rehabilitation clinic 54 days after surgery.

Primary aldosteronism (PA) is the most common cause of secondary hypertension, and is associated with an increased incidence of cardiovascular events. PA itself is clinically classified into the following two types: unilateral PA, mostly composed of aldosteroneproducing adenoma (APA); and bilateral hyperaldosteronism, consisting of multiple aldosterone-producing micronodules (APMs) and aldosterone-producing diffuse hyperplasia. Histopathologically, those disorders above are all composed of compact and clear cells. The cellular morphology in the above-mentioned aldosterone-producing disorders has been recently reported to be closely correlated with patterns of somatic mutations of ion channels including KCNJ5, CACNA1D, ATP1A1, ATP2B3, and others. In addition, in non-pathological adrenal glands, APMs are frequently detected regardless of the status of the renin-angiotensin-aldosterone system (RAAS). Aldosterone-producing nodules have been also proposed as non-neoplastic nodules that can be identified by hematoxylin and eosin staining. These non-neoplastic CYP11B2-positive nodules could represent possible precursors of APAs possibly due to the presence of somatic mutations. On the other hand, aging itself also plays a pivotal role in the development of aldosterone-producing lesions. For instance, the number of APMs was also reported to increase with aging. Therefore, recent studies indicated the novel classification of PA into normotensive PA (RAAS-independent APM) and clinically overt PA.