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SUMMARYThis study attempts to compare the risks and benefits of provisional stenting with drug eluting stents and bypass surgery for left main coronary artery (LMCA) stenosis.Recent improvements in interventional technologies have increased interest in percutaneous treatment of LMCA stenosis. However, application of percutaneous techniques to LMCA has been sporadic and controversial.In-hospital and one year outcomes of coronary artery bypass graft (CABG) and percutaneous coronary intervention (PCI) cases were compared. From September, 2003 to June, 2005, a total of 59 consecutive patients with de novo unprotected LMCA stenosis were treated with either CABG or PCI. Twenty patients received non-intravascular ultrasound-guided PCI with a stent in the LMCA. Thirty-nine patients underwent CABG.At 30-day follow-up, the major adverse cardiac and cerebrovascular event (MACE) rates of mortality, myocardial infarction, cerebral vascular accident, and target vessel revascularization were 25.6% in the CABG group and 5% in the PCI group (P = 0.054).At one year follow-up, the MACE rates were 33.3% in the CABG group and 5% in the PCI group. One year MACE for the CABG group significantly differed from that of the PCI group (P = 0.015). The odds ratio (OR) of one year MACE-free survival was 0.75 (P < 0.001) in the CABG group versus the PCI group. Further analysis demonstrated there was a significant difference in in-hospital MACE and one year MACE between the elective CABG group and elective PCI group (P = 0.045). However, there was no significant difference between the emergent CABG group and emergent PCI group (P = 1.000 for in-hospital MACE; P = 0.486 for one year MACE).PCI on unprotected LM offers an alternative option in patients with high surgical risk and appropriate lesion morphology. (Int Heart J 2008; 49: 355-370)

SUMMARYAcute pulmonary embolism continues to cause significant morbidity and mortality despite advances in diagnosis and treatment. This retrospective analysis aimed to determine whether the combination of elevated troponin I and right ventricular dilatation (RVD) could provide a more powerful predictor for risk evaluation.The study data comprised records of 110 patients with either high-probability ventilation/perfusion lung scan or positive spiral computed tomography. All cause 100-day mortality was 18.2%. The hypotension and RVD variables significantly influenced 100-day mortality. For the combination of RVD and raised troponin I, the 100-day mortality rate was 31%. Notably, the group with elevated troponin I and no RVD had a 100-day mortality rate of only 3.7%. The combination of RVD and elevated troponin had a positive predictive value of 31% and a negative predictive value of 88% for 100-day mortality. Compared with existing reports, conflicting conclusions for the individual prognostic role of elevated troponin I, cancer, and heart failure were obtained. These conflicting conclusions most likely resulted from inappropriate cut-off troponin I values and the modest sample size.In conclusion, the combination of elevated troponin and RVD was able to identify a subset of patients most likely to benefit from aggressive therapy. (Int Heart J 2006; 47: 775-781) Key words: Pulmonary embolism, Right ventricular dilatation, Troponin I PULMONARY embolism (PE) remains a major cause of morbidity and mortality among the general population, with an estimated incidence of 0.5 per 1000 people 1) and a case-fatality rate of 15% at 3 months.2) Patients with pulmonary embolism present with a wide range of clinical acuity, thus necessitating different therapeutic strategies. Shock or systemic hypotension with systolic BP < 90 mmHg are the generally accepted indications for urgent thrombolysis in patients with acute PE.

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SUMMARYMost tumor invasion into the heart is nonspecific and clinically silent. Myocardium metastasis rarely mimics a myocardial infarction. In this case, a cardiac metastasis from a squamous cell carcinoma presented with both persistent ST elevation and paroxysmal supraventricular tachycardia. The secondary lesion was located in the anterior wall and lateral wall of the left ventricle and induced electrocardiographic changes imitating an acute myocardial infarction. (Int Heart J 2007; 48: 399-405)

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The most common ventricular premature contractions (VPCs) originate from the right ventricular outflow tract (RVOT), but the molecular mechanisms of altered cytoskeletons of VPC-induced cardiomyopathy remain unexplored. We created a RVOT bigeminy VPC pig model (n = 6 in each group). Echocardiography was performed. The histopathological alternations in the LV myocardium were analyzed, and next generation sequencing (NGS) and functional enrichment analyses were employed to identify the differentially expressed genes (DEGs) responsible for the histopathological alternations. Finally, a cell silencing model was used to confirm the key regulatory gene and pathway. VPC pigs had increased LV diameters in the 6-month follow-up period. A histological study showed more actin cytoskeleton disorganization and actin accumulation over intercalated disc, Z-line arrangement disarray, increased β-catenin expression, and cardiomyocyte enlargement in the LV myocardium of the VPC pigs compared to the control pigs. The NGS study showed actin cytoskeleton signaling, RhoGDI signaling, and signaling by Rho Family GTPases and ILK Signaling presented z-scores with same activation states. The expressions of Rac family small GTPase 2 (Rac2), the p-cofilin/cofilin ratio, and the F-actin/G-actin ratio were downregulated in the VPC group compared to the control group. Moreover, the intensity and number of actin filaments per cardiomyocyte were significantly decreased by Rac2 siRNA in the cell silencing model. Therefore, the Rac2/cofilin pathway was found to play a crucial role in the sarcomere morphology and Z-line arrangement disarray induced by RVOT bigeminy VPCs.