Despite the higher STS PROM in TMVR patients, there was no difference in 1-year mortality between the TMVR and SMVR groups. Echocardiographic findings after TMVR were similar to SMVR at 30 days. There was a statistically significant difference in mitral gradient at 1 year, though this is likely not clinically important. TMVR may be an alternative to SMVR in patients with previous mitral bioprosthetic valves.
Accordingly, the first objective was to evaluate the association between intensive statin therapy and new-onset diabetes Background-Practice guidelines recommend intensive-dose statins for patients with acute coronary syndrome, but recent data about the risk of new-onset diabetes mellitus have raised concerns about its use. Our main objective was to evaluate the association between intensive statin therapy and new-onset diabetes mellitus in patients with myocardial infarction and to evaluate the association of intensive statin therapy with long-term adverse clinical outcomes. Methods and Results-A propensity score-matched cohort was created consisting of 17 080 patients with myocardial infarction aged >65 years old, hospitalized in Ontario, Canada, from 2004 to 2010. Clinical outcomes were compared in patients prescribed intensive-dose versus moderate-dose statins at hospital discharge. At 5 years, 13.6% of patients receiving intensive-dose statins and 13.0% of patients receiving moderate-dose statins had new-onset diabetes, which was not significantly different (P=0.19). By contrast, the 5-year rate of death or acute coronary syndrome was significantly lower at 44.8% in the intensive-dose statin group compared with 46.5% in the moderate-dose group (P=0.044). The reduction in combined clinical outcome was driven mainly by a significantly lower rate of acute coronary syndrome (P=0.039) associated with intensive-dose statins. No significant difference in mortality rates (34.8% in both groups) was observed between the treatment groups during the study period (P=0.89). Conclusions-In older patients with myocardial infarction, we found intensive-dose statin therapy to be effective in reducing repeat hospitalization for acute coronary syndrome.
Methods
Data SourcesOMID was created by linking together several healthcare administrative databases in Ontario. 17,18 Residents with myocardial infarction admitted to any acute care hospitals in Ontario were identified using the International Classification of Disease, 10th Revision code (I21) in the Canadian Institute for Health Information discharge abstract database. OMID excluded patients aged <20 years or >105 years, those with an invalid health card, and those who had an infarction caused by a complication from other conditions. The first myocardial infarction during the study period was considered as the index event, and subsequent hospitalizations were considered as outcomes. The rationale for these inclusion and exclusion criteria is detailed elsewhere.
17,18The diagnostic accuracy of myocardial infarction in OMID has been demonstrated to be >94%.17,18 The OMID information was then linked to the following: (1) the Ontario Registered Persons Database, which contains information on the vital status of all Ontario residents; (2) the Canadian Institute for Health Information discharge abstract database, which contains information on all repeat hospitalizations; and (3) the Ontario Drug Benefit prescription claims database, which contains information on outpatient prescri...
Coronary revascularization remains the standard treatment for obstructive coronary artery disease and can be accomplished by either percutaneous coronary intervention (PCI) or coronary artery bypass graft surgery. Considerable advances have rendered PCI the most common form of revascularization and improved clinical outcomes. However, numerous challenges to modern PCI remain, namely, in-stent restenosis and stent thrombosis, underscoring the importance of understanding the vessel wall response to injury to identify targets for intervention. Among recent promising discoveries, endothelial progenitor cells (EPCs) have garnered considerable interest given an increasing appreciation of their role in vascular homeostasis and their ability to promote vascular repair after stent placement. Circulating EPC numbers have been inversely correlated with cardiovascular risk, while administration of EPCs in humans has demonstrated improved clinical outcomes. Despite these encouraging results, however, advancing EPCs as a therapeutic modality has been hampered by a fundamental roadblock: what constitutes an EPC? We review current definitions and sources of EPCs as well as the proposed mechanisms of EPC-mediated vascular repair. Additionally, we discuss the current state of EPCs as therapeutic agents, focusing on endogenous augmentation and transplantation.
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