Su-Kiat Chua

Acute ST-elevation myocardial infarction in young patients: 15 Years of experience in a single center

There have been few studies done regarding young patients with ST‐elevation myocardial infarction (STEMI). The purpose of this study was to investigate the clinical characteristics and coronary angiographic features in young patients with STEMI.

Renal artery stent fracture with refractory hypertension: a case report and review of the literature.

A 73‐year‐old man with resistant hypertension and impaired renal function underwent stenting for right renal artery (RRA) stenosis. Two years later, he presented with uncontrolled hypertension and worse renal function. Renal arteriogram revealed RRA stent fracture with in‐stent restenosis. Another stent was deployed. Four months later, however, renal arteriogram revealed in‐stent restenosis again. This time, balloon angioplasty alone was performed. He had been symptom‐free with stable condition at 2‐year follow‐up. A literature review disclosed six renal artery stent fracture cases, including the present one, who developed in‐stent stenosis resulted from stent fracture. Two major anatomy features of renal artery stenosis were suggestive for development of stent fracture: (1) renal artery entrapment by diaphragmatic crus, and (2) mobile kidney with acute angulation at proximal segment of the renal artery. It is important to detect this etiology of renal artery stenosis because stenting in these vessels may contribute to in‐stent restenosis or stent fracture. Management of renal artery stent fracture, including endovascular treatment or aortorenal bypass, should be considered on a case‐by‐case basis in relation to clinical settings.

Real-World Experience with Idarucizumab to Reverse Anticoagulant Effect in Dabigatran-Treated Patients: Report of 11 Cases from Taiwan

BACKGROUNDnThis study aims to observe the effectiveness and safety of idarucizumab in dabigatran-treated patients with severe bleeding or requiring surgery in Taiwan.nnnMETHODS AND RESULTSnIn Taiwan, 11 dabigatran-treated patients developed severe bleeding, fracture that needed surgery, and acute ischemic stroke requiring thrombolysis. These patients were treated with idarucizumab and obtained adequate hemostasis. Our experiences reconfirmed the efficacy and safety of idarucizumab in Asian patients.nnnCONCLUSIONSnIdarucizumab improves safety in dabigatran-treated patients. Continued education about the availability and appropriate use of idarucizumab is necessary in Asia.

Atorvastatin alleviates cardiomyocyte apoptosis by suppressing TRB3 induced by acute myocardial infarction and hypoxia

BACKGROUND/PURPOSEnTRB3 (tribbles 3), an apoptosis-regulated gene, increases during endoplasmic reticulum stress. Hypoxia can induce inflammatory mediators and apoptosis in cardiomyocytes. However, the expression of TRB3 in cardiomyocyte apoptosis under hypoxia is not thoroughly known. We investigated the regulation mechanism of TRB3 expression and apoptosis induced by hypoxia in cardiomyocytes.nnnMETHODSnAn inxa0vivo model of acute myocardial infarction (AMI) was applied in adult Wistar rats to induce myocardial hypoxia. Rat neonatal cardiomyocytes were subjected to 2.5% O2 to induce hypoxia.nnnRESULTSnThe expression of TRB3 was evaluated in cultured rat neonatal cardiomyocytes subjected to hypoxia. Hypoxia significantly enhanced TRB3 protein and mRNA expression. Adding c-jun N-terminal kinase (JNK) inhibitor SP600125, JNK small interfering RNA (siRNA), tumor necrosis factor-α (TNF-α) antibody, and atorvastatin 30xa0minutes before hypoxia reversed the induction of TRB3 protein. A gel-shift assay showed the DNA-binding activity of growth arrest and DNA damage-inducible gene 153 (GADD153), which increased after hypoxia. Hypoxia increased, whereas the TRB3-mut plasmid, SP600125, and TNF-α antibody abolished the hypoxia-induced TRB3 promoter activity. Hypoxia increased the secretion of TNF-α from cardiomyocytes. Exogenous administration of TNF-α recombinant protein to the cardiomyocytes without hypoxia increased TRB3 protein expression, similar to that observed after hypoxia. Hypoxia-induced cardiomyocyte apoptosis is inhibited by TRB3 siRNA, the TNF-α antibody, and atorvastatin. Atorvastatin reduced the TRB3 expression and cardiomyocyte apoptosis induced by AMI. Hypoxia induces TRB3 through TNF-α, JNK, and the GADD153 pathway.nnnCONCLUSIONnTreatment of atorvastatin inhibits the expression of TRB3 and cardiomyocyte apoptosis induced by AMI and hypoxia.