Simultaneous coronary thrombosis with multisite myocardial infarction and complex malignant arrhythmia: A case report.

INTRODUCTION: Acute myocardial infarction with simultaneous coronary thrombosis has been rarely reported. This combination induces various arrhythmias and is a high-risk factor for cardiogenic shock. PATIENT CONCERNS: A 65-year-old man presented with sweating and a 3-h abrupt persistent back pain that radiated to the anterior. DIAGNOSIS: Multisite myocardial infarction, coronary thrombosis with and complex malignant arrhythmia INTERVENTIONS:: Prompt intervention includes cardiac pacing, percutaneous coronary intervention (PCI), thrombus aspiration and intra-aortic balloon pump (IABP). OUTCOMES: The patient was successfully rescued after PCI and thrombus aspiration. CONCLUSIONS: Recognition of dynamic electrocardiographic changes enhances our understanding of the pathogenesis of myocardial infarction.

Attitudes towards acceptance of an innovative home-based and remote sensing rehabilitation protocol among cardiovascular patients in Shantou, China.

BACKGROUND: Cardiac rehabilitation (CR) protocols have diversified to include home-based cardiac tele-rehabilitation (HBCTR) as an alternative to hospital-based or center-based CR. To adopt the use of home-based cardiac tele-rehabilitation, it is necessary to assess cardiac patients' attitudes towards acceptance of such e-health technology, especially in China where knowledge of such technology is deficient. METHODS: Interviews were conducted in the First Affiliated Hospital of Shantou University Medical College, Shantou, China. After percutaneous coronary interventional (PCI) surgery, patients completed the survey. RESULTS: Among the 150 patients, only 13% had ever heard of HBCTR. After an introduction of our HBCTR program, 60% of patients were willing to participate in the program. From our multivariate analysis of questionnaire data, age (OR: 0.92, 95% CI: 0.86-0.98; P = 0.007), average family monthly income (OR: 0.13, 95% CI: 0.05-0.34; P < 0.001), education level (OR: 0.24, 95% CI: 0.10-0.59; P = 0.002) and physical exercise time (OR: 0.19, 95% CI: 0.06-0.56; P = 0.003) were independent predictors for acceptance of HBCTR. From the reasons for participation, patients selected: enhanced safety and independence (28.3%), ability to self-monitor physical conditions daily (25.4%), and having automatic and emergency alert (23.1%). Reasons for refusal were: too cumbersome operation (34.3%) and unnecessary protocol (19.4%). CONCLUSIONS: Most patients lacked knowledge about HBCTR but volunteered to participate after they have learned about the program. Several personal and life-style factors influenced their acceptance of the program. These indicate that both improvement of technology and better understanding of the program will enhance active participation.

The mechanism underlying vascular smooth muscle cell apoptosis induced by atorvastatin may be mainly associated with down-regulation of survivin expression.

PURPOSE: Studies have shown that statins may induce vascular smooth muscle cells (VSMCs) apoptosis. But its mechanisms are incompletely understood. In this study, we investigate the effects of atorvastatin and survivin antisense oligonucleotides (ASODN) on VSMCs apoptosis and the relation between survivin and VSMCs apoptosis. MATERIALS AND METHODS: Cultured VSMCs were treated with atorvastatin and vascular endothelial grow factor (VEGF). Apoptosis of VSMCs at 6-72 h after treatment with atorvastatin was detected by means of Hoechst33258 staining. Survivin and Fas factors expression were detected by means of immunohistochemistry. Survivin and Fas mRNA expression were detected by means of RT-PCR. In order to determine the relations between survivin and VSMCs apoptosis, we also performed transfection of VSMCs with survivin ASODN using GenePORTER Transfection Reagent and studied the survivin protein expression by means of western blotting. RESULTS: VSMCs apoptosis after treatment with atorvastatin was increased in a dose- and time-dependent manner. The expression of survivin and survivin mRNA in VSMCs was significantly down-regulated at 24 h and disappeared at 48-72 h after treatment with atorvastatin. Fas and Fas mRNA in VSMCs could only be detected at 72 h and not at 6-48 h after treatment with atorvastatin. We did not observe any effects of VEGF on VSMCs apoptosis, on survivin and survivin mRNA expression, and on Fas and Fas mRNA expression in VSMCs after treatment with atorvastatin. At 48 hours after the start of transfection, survivin protein expression was significantly reduced after transfection with 0.5, 1.0 and 2.0 microg/ml of survivin ASODN and there was no survivin protein expression after transfection with 3.0 and 4.0 microg/ml of survivin ASODN. In contrast, in the GenePORTER only and SODN studies, survivin protein expression was observed with western blotting. Hoechst33258 staining showed that treatment of VSMCs with survivin ASODN resulted in VSMCs apoptosis. CONCLUSIONS: Atorvastatin induces VSMCs apoptosis in a dose- and time-dependent manner. Transfection of survivin ASODN can directly induce VSMCs apoptosis. The mechanisms of VSMCs apoptosis induced by atorvastatin may be mainly associated with down-regulation of survivin expression in VSMCs. Up-regulation of Fas in VSMCs may play a role in later stages following atorvastatin treatment.