Search

There are many published articles on the effects of the antithrombolytic function of platelet glycoprotein IIb/IIIa inhibitors (GP IIb/IIIa inhibitors) in myocardial infarction. However, few studies have explored the effects and optimal concentration of tirofibans in diminishing the extent of myocardial reperfusion injury (RI).Rats received 120 minutes of coronary ligation and 180 minutes of reperfusion. The rats were then divided into 7 groups based on the concentration of tirofiban administered intravenously 30 minutes prior to coronary reperfusion to the end of reperfusion. The ratio of myocardial necrotic area to area at risk (AAR), and myocardial malondialdehyde (MDA) and plasma myeloperoxidase (MPO) activities were measured. The apoptotic index (AI) was the percentage of myocytes positive for terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) out of all myocytes stained by 4', 6-diamidino-2-phenylindole (DAPI).The ratio of myocardial necrotic area to AAR significantly decreased in all tirofiban subgroups. The MDA activity for tirofiban concentrations of 2 and 5 ug/kg/minute showed a slight reduction. MPO activity was significantly decreased at a tirofiban concentration of 2 ug/kg/minute. The AI was significantly decreased at a tirofiban concentration of ≥ 0.4 ug/kg/minute.The results indicate that a tirofiban can significantly ameliorate the cardiac RI and myocyte apoptosis in rats.

This study analyzed the corrected QT dispersion (cQTd) before and at 24 hours after successful primary percutaneous coronary intervention (PCI) in 81 patients with single coronary artery disease and acute ST elevation myocardial infarction. Major cardiovascular events (MACE) at 1 year were defined as death, nonfatal myocardial infarction, life-threatening arrhythmias, and heart failure hospitalization. The cQTd before primary PCI was significantly longer in patients without MACE than in patients with MACE (73.1 ± 29.3 versus 56.3 ± 25.2 msec, P = 0.026). The cQTd at 24 hours after primary PCI was significantly shorter in patients without MACE than in patients with MACE (38.4 ± 20.8 versus 50.8 ± 28.7 msec, P = 0.045). Thus, the absolute cQTd change was significantly higher in patients without MACE compared to patients with MACE (P = 0.001). By multivariate analysis, absolute cQTd change was an independent predictor for the development of MACE, with an odds ratio of 1.498 for each 10-msec decrement in absolute cQTd change (95 percent confidence interval, 1.157 to 1.939, P = 0.002). In conclusion, the absolute cQTd change after primary PCI was an independent predictor of the development of MACE in patients with single vessel disease and acute ST elevation myocardial infarction.

This 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.

Most 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.

Acute 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.

No-reflow phenomenon is frequently observed during percutaneous coronary intervention in patients with acute coronary syndrome. It may jeopardize hemodynamic status or result in ischemic chest pain in these patients. Currently, there is no adequate solution for this problem. We report our experience with an acute coronary syndrome patient who developed no-reflow phenomenon associated with ST segment elevation and shock after percuteneous coronary balloon dilatation and stent deployment. Intracoronary administration of tirofiban immediately restored the coronary flow of the target vessel, and the disastrous condition reversed. Our experience suggests that intracoronary administration of tirofiban can be considered as an option in case of no-reflow phenomenon during percutaneous coronary intervention.