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Coronary artery disease (CAD) remains a leading cause of mortality and morbidity in developed countries. Although urgent revascularization is the cornerstone of management of acute coronary syndrome (ACS), for patients with stable CAD recent large-scale clinical trials indicate that a mechanical 'fix' of a narrowed artery is not obviously beneficial; ACS and stable CAD are increasingly recognized as different clinical entities. We review the perspectives on (1) modifying the diagnostic pathway of stable CAD with the incorporation of modern estimates of pretest probability, (2) non-imaging evaluations based on their availability, (3) the optimal timing of invasive coronary angiography and revascularization, and (4) the implementation of medical therapy during the work-up.

Sitosterolemia is a rare, inherited, autosomal recessive disorder of lipid metabolism characterized by increased levels of plant sterols, such as sitosterol and campesterol, xanthomas, and accelerated atherosclerosis. In a 15-year-old boy exhibiting ST-elevation acute myocardial infarction, lipid panels, including plant sterol, and genetic testing for the ATP-binding cassette sub-family G member 5 (ABCG5) gene mutation, confirmed the diagnosis of sitosterolemia. A comprehensive lipid panel and genetic testing should be considered in patients with premature coronary artery disease to prevent disease progression through dietary and pharmacologic interventions specific to sitosterolemia. Résumé: La sitostérolémie est une maladie génétique rare à transmission autosomique récessive touchant le métabolisme des lipides, qui est caractérisée par une augmentation des taux de stérols végétaux comme le sitostérol et le campestérol, la présence de xanthomes et une athérosclérose accélérée. Chez un garçon âgé de 15 ans ayant subi un infarctus aigu du myocarde avec élévation du segment ST, le diagnostic de sitostérolémie a été confirmé par un bilan lipidique comprenant un dosage des stérols d'origine végétale et un test génétique de dépistage de la mutation du gène ABCG5 (ATP-binding cassette sub-family G member 5). Un bilan lipidique exhaustif et un test génétique doivent être envisagés chez les patients présentant une coronaropathie prématurée afin de prévenir la progression de la maladie grâce à des interventions d'ordre tant diététique que pharmacologique propres à la sitostérolémie.

OBJECTIVES We evaluated the operative and long-term outcomes of the frozen elephant trunk (FET) technique for acute type A aortic dissection. METHODS This study evaluated 426 consecutive patients who underwent aortic repair for acute type A aortic dissection from June 2007 to December 2018 at our centre. Of these, 139 patients underwent total arch replacement with FET (FET group), and 287 underwent other procedures (no FET group). Ninety-two patients in the FET group were matched to 92 patients in the no FET group by using propensity score matching analysis. RESULTS Thirty-day mortality and neurological dysfunction were not significantly different between the FET and no FET groups (1.4% vs 2.4%, P = 0.50 and 5.0% vs 6.3%, P = 0.61, respectively). Long-term survival was better in the FET group than in the no FET group (P = 0.008). Freedom from distal thoracic reintervention was similar in the FET and no FET groups (P = 0.74). In the propensity-matched patients, freedom from aortic-related death was better in the FET group than in the no FET group (P = 0.044). CONCLUSIONS Operative outcomes showed no significant difference between the 2 groups. FET contributes to better long-term survival in patients with acute type A aortic dissection.

Eosinophilic myocarditis (EM) is a rare condition characterized by myocardial eosinophilic infiltration due to various underlying etiologies. The patient with EM may benefit from appropriate use of mechanical circulatory support (MCS) that acts as a bridge to myocardial recovery in response to effective immunosuppressive therapy. A 16-year-old boy presented with cardiogenic shock due to fulminant myocarditis, for which a percutaneous ventricular assist device (PVAD) was immediately inserted. Based on the histological diagnosis of EM, immunosuppressive therapy was immediately commenced, leading to improvement of left-ventricular ejection fraction (27% to 47%). The PVAD was successfully removed on day 7. Cardiac magnetic resonance imaging and dual-tracer myocardial scintigraphy suggested limited extent of irreversible myocardial damage. For fulminant EM, the short-term use of PVAD, together with immunosuppressive therapy guided by an immediate histological investigation, may be an effective bridging strategy to myocardial recovery.

The management of chronic disseminated intravascular coagulation (DIC) caused by aortic dissection has not yet been established. Even in cases where surgical correction is performed, therapeutic control of systemic hemorrhaging is still required. We herein report the successful treatment of a case of aortic dissection with a patent false lumen using tranexamic acid for acute exacerbation of chronic DIC. Oral administration of 1,500 mg tranexamic acid per day stabilized the coagulative and fibrinolytic parameters and relieved bleeding tendencies with no side effects. Heparin was administered periodically for the management of hemodialysis. This favorable result continued for up to 3 years.

A 69-year-old man was admitted to our hospital with cardiopulmonary arrest. Percutaneous cardio-pulmonary support (PCPS) using the right femoral artery and vein was initiated, because ventricular fibrillation continued. Although we succeeded in defibrillation after percutaneous coronary intervention (PCI), a chest radiograph indicated a pneumothorax in the right lung and a pulmonic contusion in the left lung caused by cardiopulmonary resuscitation. Two days after PCI, partial pressure of arterial oxygen (PaO2) from the right radial artery suddenly decreased, and his cardiac function showed improvement on an echocardiogram. To avoid additional brain damage, we converted the treatment to veno-venous extracorporeal membrane oxygenation by changing the blood returning site of PCPS from the right femoral artery to the right jugular vein. Thereafter, the patient's PaO2 level gradually improved.

In peripheral arterial disease (PAD) of the lower extremities, the presence of flow-limiting stenoses can be objectively detected by the ankle-brachial index (ABI). However, the severity of ischemic symptoms is not necessarily associated with the ABI value. Atherosclerotic plaque in lower extremity PAD induces ankle arterial stiffness and reduces ankle vascular resistance, which may decrease ankle blood flow and cause ischemic symptoms. We hypothesized that the ankle hemodynamic index (AHI), defined as the ratio of ankle arterial stiffness to ankle vascular resistance, could be used to assess the blood supply deficiency in a diseased lower limb in patients with PAD. The 85 consecutive patients with PAD who were retrospectively analyzed in this study had Rutherford grade 1 to grade 6 ischemia diagnosed as PAD and significant stenotic lesions (>50% diameter stenosis) of the lower extremity on contrast angiography. The AHI was calculated as the product of the ankle pulse pressure and the ratio of heart rate to ankle mean arterial pressure (ankle pulse pressure × heart rate/ankle mean arterial pressure). The Rutherford grade was significantly correlated with the AHI (r = 0.50, P < 0.001), but not with the ABI (r = 0.07, P = 0.52). Multiple ordinal regression analysis showed that anemia (odds ratio 0.66, P = 0.002) and AHI (odds ratio 1.04, P = 0.02) were independently associated with Rutherford grade. Our study shows that AHI, a novel parameter based on the ABI measurement, is well correlated with ischemic symptoms, and may be a useful means to assess the arterial blood supply of the lower extremities of patients with PAD.