No abstract

It has been extensively verified that inflammation and oxidative stress play important roles in the pathogenesis of cardiovascular diseases (CVDs). Curcuminoids, from the plant Curcuma longa, have three major active ingredients, which include curcumin (curcumin I), demethoxycurcumin, and bisdemethoxycurcumin. Curcuminoids have been used in traditional medicine for CVDs' management and other comorbidities for centuries. Numerous studies had delineated their anti‐inflammatory, antioxidative, and other medicinally relevant properties. Animal experiments and clinical trials have also demonstrated that turmeric and curcuminoids can effectively reduce atherosclerosis, cardiac hypertrophy, hypertension, ischemia/reperfusion injury, and diabetic cardiovascular complications. In this review, we introduce and summarize curcuminoids' molecular and biological significance, while focusing on their mechanistic anti‐inflammatory/antioxidative involvements in CVDs and preventive effects against CVDs, and, finally, discuss relevant clinical applications.

Congenital absence of the right coronary artery (RCA) is a rare coronary anomaly. Few cases of this condition have been reported. Congenital absence of the RCA is considered as a benign anomaly. However, in certain cases, these patients may develop life-threatening clinical complications that include acute myocardial infarction, stroke, or sudden death. We report two patients who were diagnosed with congenital absence of the RCA and presented with acute myocardial infarction. We discuss our experience in diagnosis and treatment of this disease. Congenital absence of the RCA with acute myocardial infarction is an uncommon clinical emergency. Therefore, early detection, correct diagnosis, and appropriate treatment are important.

Solitary fibrous tumours are unusual neoplasms that develop from mesenchymal cells, usually originating from the pleura. A pericardial solitary fibrous tumour is an extremely rare occurrence. We report a 64-year-old woman who presented to the hospital with chief complaints of dyspnoea and abdominal distension. Echocardiography and enhanced computed tomography revealed an intrapericardial tumour with local invasion to the right atrium. Histopathological examination of a biopsy specimen showed a patternless distribution of spindle-shaped cells in a collagen stroma, with a high mitosis rate. Immunohistochemistry was positive for vimentin, CD34, and Bcl-2. The final diagnosis was a pericardial malignant solitary fibrous tumour with right atrial invasion. Surgical resection of the tumour was not performed because of its invasion into the myocardium. We systematically reviewed the literature on cardiac solitary fibrous tumours up to 2019.

AimDiabetic cardiomyopathy is an independent cardiac injury that can develop in diabetic individuals. Our previous study showed that C66, a curcumin analogue, protects against diabetes‐induced cardiac damage. The present study sought to reveal the underlying mechanisms of C66‐mediated cardioprotection.MethodsAn experimental diabetic model was established using JNK2−/− and wild‐type (WT) mice. C66 (5 mg/kg) was administered orally every other day for 3 months. Body weight, plasma glucose levels, cardiac function, and structure were measured. Masson trichrome and TUNEL staining were used to assess myocardial fibrosis and apoptosis, respectively. mRNA and protein levels of inflammation, fibrosis, oxidative stress, and apoptosis molecules were measured by quantitative PCR and Western blot, respectively.ResultsNeither C66 treatment nor JNK2 knockout affected body weight or plasma glucose levels. Cardiac inflammation, fibrosis, oxidative stress, and apoptosis were increased in WT diabetic compared to WT control mice, all of which were attenuated by C66 treatment. However, these pathological and molecular changes induced by diabetes were eliminated in JNK2−/− diabetic mice compared to JNK2−/− control mice, and C66 treatment did not further affect these parameters in JNK2−/− diabetic mice.ConclusionsOur results indicate that C66 ameliorates diabetic cardiomyopathy by inhibiting JNK2 relative pathways.