Among patients with unstable angina or myocardial infarction without ST-segment elevation, prasugrel did not significantly reduce the frequency of the primary end point, as compared with clopidogrel, and similar risks of bleeding were observed. (Funded by Eli Lilly and Daiichi Sankyo; TRILOGY ACS ClinicalTrials.gov number, NCT00699998.).
The National interventional council of Cardiological Society of India has conventionally been presenting the data on various forms of cardiac interventions performed in the previous year at its annual meeting. Here we are reporting the data on coronary interventions done in India during the year 2011.
Glycoprotein IIb/IIIa inhibitor PCI Safety a b s t r a c t Aims: The aim of the study was to assess the safety and efficacy of Bivalirudin þ Glycoprotein (Gp) IIb/IIIa inhibitor as compared to unfractionated Heparin (UFH) þ Gp IIb/IIIa inhibitor in high risk patients undergoing elective percutaneous coronary intervention (PCI). The primary end point was time to sheath removal and ambulation where as periprocedure myocardial damage, access site bleeding and major adverse cardiac events (MACE) rates were secondary end points.Methods: One hundred and one high risk patients undergoing elective PCI were randomly assigned to either Bivalirudin þ GpIIb/IIIa inhibitor or UFH þ Gp IIb/IIIa inhibitor. PCI was performed by standard technique and activated clotting time was monitored immediately on arrival to recovery area and every 60 min thereafter. Sheath were pulled out once ACT was below 150 seconds and patients were mobilized 6hrs after sheath were removed. Periprocedure myocardial damage was assessed by serial Trop I levels.Results: Patient assigned to Bivalirudin þ Tirofiban has significantly reduced time to sheath removal and ambulation as compared to those who received UFH þ tirofiban (p < 0.0001) although peak Act did not differ in the groups. Peak Trop I levels were significantly lower in Bivalirudin þ Tirofiban group (p ¼ 0.023) and peri-procedure Trop I elevation occurred in significantly lower number of patients treated with Bivalirudin þ Tirofiban (p ¼ 0.029).
Conclusions:The combination of Bivalirudin þ Tirofiban was safe and effective as compared to UFH þ Tirofiban in high risk patients undergoing elective PCI.
Atherosclerotic peripheral arterial disease is a common medical problem worldwide and portends a poor prognosis because of increased cardiovascular morbidity and mortality. Regular exercise, weight loss, and aggressive risk factor modification, including treatment of dyslipidemia and complete cessation of smoking, is extremely important in this high-risk cohort. Vascular surgery in these patients, who often have concomitant coronary or cerebrovascular atherosclerosis, is associated with significant risk. Steady improvements in endovascular revascularization techniques have made this a safe and effective alternate revascularization modality. Percutaneous peripheral vascular interventions have increased dramatically in recent years, from 90,000 in 1994 to more than 200,000 in 1997, and endovascular techniques may soon replace up to 50% of traditional vascular operations. In this article, the authors review the current state of interventional treatment for peripheral arterial disease.
Acute coronary occlusion, causing a heart attack, is best treated by prompt intervention and re-opening of the blocked artery. Such acute reperfusion, although saving many threatened heart cells from death, also paradoxically causes lethal reperfusion injury due to calcium overload in the mitochondria. There are protective molecular rescue paths that lessen the extent of such reperfusion injury. We discuss the evolution of these pathways during primitive times when heart attacks were rare. We believe that these paths evolved to counter acute stress situations in our ancestors when stimulated by intense physical effort, environmental conditions or hunting hazards, often accompanied by blood loss and hypotension. To test our hypothesis, we developed an underperfused model of acute heart failure with low perfusion pressure in the isolated rat heart to simulate the hypotensive response. We also increased the contents of free fatty acids (FFA) in the perfusate to supraphysiological levels to mimic the rapid fear-driven elevation of FFA in the hunter. FFA have a deleterious effect on a failing heart while glucose is proposed as protecting the acutely failing heart. We found that glucose given to the acutely failing heart improved the functional recovery by increasing the heart rate and contractility. We hypothesise that similar metabolic principles may protect against acute heart failure as against regional ischemia with lethal injury. We further suggest that the requirement for protection against acute stress in primitive persons led to the evolution of the molecular pathways now known to protect from lethal reperfusion injury.
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