Clopidogrel, prasugrel or ticagrelor in patients with acute coronary syndromes undergoing percutaneous coronary intervention.

BACKGROUND: Guidelines recommend prasugrel or ticagrelor instead of clopidogrel in patients with acute coronary syndromes (ACS) undergoing percutaneous coronary interventions (PCI). AIM: We sought to describe the trends in uptake of the newer agents and analyse the clinical characteristics and short-term outcomes of patients treated with clopidogrel, prasugrel or ticagrelor. METHODS: We analysed the temporal trends of antiplatelet use since the availability of prasugrel (2009-2013) in patients with ACS from the Melbourne Interventional Group registry. To assess clinical characteristics and outcomes, we included 1850 patients from 2012 to 2013, corresponding to the time all three agents were available. The primary outcome was major adverse cardiovascular events (MACE). The safety end-point was in-hospital bleeding. RESULTS: For the period of 2009-2013, the majority of patients were treated with clopidogrel (72%) compared with prasugrel (14%) or ticagrelor (14%). There was a clear trend towards ticagrelor by the end of 2013. Patients treated with clopidogrel were more likely to present with non-ST-elevation ACS, be older, and have more comorbidities. There was no difference in unadjusted 30-day mortality (0.9 vs 0.5 vs 1.0%, P = 0.76), myocardial infarction (2 vs 1 vs 2%, P = 0.52) or MACE (3 vs 3 vs 4%, P = 0.57) between the three agents. There was no difference in in-hospital bleeding (3 vs 2 vs 2%, P = 0.64). CONCLUSION: Prasugrel and ticagrelor are increasingly used in ACS patients treated with PCI, predominantly in a younger cohort with less comorbidity. Although antiplatelet therapy should still be individualised based on the thrombotic and bleeding risk, our study highlights the safety of the new P2Y12 inhibitors in contemporary Australian practice.

Trends in door-to-balloon time and outcomes following primary percutaneous coronary intervention for ST-elevation myocardial infarction: an Australian perspective.

BACKGROUND: Guidelines for patients with ST-elevation myocardial infarction include a door-to-balloon time (DTBT) of ≤90 min for primary percutaneous coronary intervention. AIM: The aim of this study was to assess temporal trends (2006-2010) in DTBT and determine if a reduction in DTBT was associated with improved clinical outcomes. METHODS: We compared annual median DTBT in 1926 STEMI patients undergoing primary percutaneous coronary intervention from the Melbourne Interventional Group registry. ST-elevation myocardial infarction presenting >12 h and rescue percutaneous coronary intervention was excluded. Major adverse cardiac events were analysed according to DTBT (dichotomised as ≤90 min vs >90 min). A multivariable analysis for predictors of mortality (including DTBT) was performed. RESULTS: Baseline demographics, clinical and procedural characteristics were similar in the STEMI cohort across the 5 years, apart from an increase in out-of-hospital cardiac arrest (3.6% in 2006 vs 9.4% in 2010, P < 0.0001) and cardiogenic shock (7.7-9.6%, P = 0.07). The median DTBT (interquartile range) was reduced from 95 (74-130) min in 2006 to 75 (51-100) min in 2010 (P < 0.01). In this period, the proportion of patients achieving a DTBT of ≤90 min increased from 45% to 67% (P < 0.01). Lower mortality and major adverse cardiac event rates were observed with DTBT ≤90 min (all P < 0.01). Multivariable analysis showed that a DTBT of ≤90 min was associated with improved clinical outcomes at 12 months (odds ratio 0.48; 95% confidence interval 0.33-0.73, P < 0.01). CONCLUSION: There has been a decline in median DTBT in the Melbourne Interventional Group registry over 5 years. DTBT of ≤90 min is associated with improved clinical outcomes at 12 months.

Clinical risk prediction model for 30-day all-cause re-hospitalisation or mortality in patients hospitalised with heart failure.

BACKGROUND: This study aimed to develop a risk prediction model (AUS-HF model) for 30-day all-cause re-hospitalisation or death among patients admitted with acute heart failure (HF) to inform follow-up after hospitalisation. The model uses routinely collected measures at point of care. METHODS: We analyzed pooled individual-level data from two cohort studies on acute HF patients followed for 30-days after discharge in 17 hospitals in Victoria, Australia (2014-2017). A set of 58 candidate predictors, commonly recorded in electronic medical records (EMR) including demographic, medical and social measures were considered. We used backward stepwise selection and LASSO for model development, bootstrap for internal validation, C-statistic for discrimination, and calibration slopes and plots for model calibration. RESULTS: The analysis included 1380 patients, 42.1% female, median age 78.7 years (interquartile range = 16.2), 60.0% experienced previous hospitalisation for HF and 333 (24.1%) were re-hospitalised or died within 30 days post-discharge. The final risk model included 10 variables (admission: eGFR, and prescription of anticoagulants and thiazide diuretics; discharge: length of stay>3 days, systolic BP, heart rate, sodium level (<135 mmol/L), >10 prescribed medications, prescription of angiotensin converting enzyme inhibitors or angiotensin receptor blockers, and anticoagulants prescription. The discrimination of the model was moderate (C-statistic = 0.684, 95%CI 0.653, 0.716; optimism estimate = 0.062) with good calibration. CONCLUSIONS: The AUS-HF model incorporating routinely collected point-of-care data from EMRs enables real-time risk estimation and can be easily implemented by clinicians. It can predict with moderate accuracy risk of 30-day hospitalisation or mortality and inform decisions around the intensity of follow-up after hospital discharge.

Neurochemical evidence of cardiac sympathetic activation and increased central nervous system norepinephrine turnover in severe congestive heart failure.

OBJECTIVES: The aim of this study was to characterize cardiac sympathetic nervous function in patients with severe heart failure and to investigate the influence of the cause of heart failure, hemodynamic variables and central nervous system catecholamine release on cardiac sympathetic tone. BACKGROUND: Although heart failure is generally accompanied by sympathoexcitation, the integrity of cardiac sympathetic nerve function in heart failure remains controversial, particularly in relation to nerve firing activity and to the capacity of sympathetic nerves to recapture norepinephrine. Additionally, the location of the afferent and central neural pathways implicated in heart failure-induced sympathoexcitation remains unclear. METHODS: Radiotracer techniques were applied in 41 patients with severe heart failure and 15 healthy control subjects to study the biochemical aspects of whole body and cardiac sympathetic activity. Hemodynamic indexes of cardiac performance were measured in the heart failure group, and their association with sympathetic activity was studied. Jugular venous catechol spillover was measured to study the central noradrenergic control of sympathetic outflow. RESULTS: Sympathoexcitation was evident in the heart failure group, reflected by a 62% increase (p < 0.001) in total body and a 277% increase (p < 0.001) in cardiac norepinephrine spillover rates. These changes were accompanied by significant increases in the cardiac spillover of the norepinephrine precursor dihydroxyphenylalanine, the sympathetic cotransmitter neuropeptide Y and the extraneuronal metabolite 3-methoxy-4-hydroxyphenylglycol. The level of cardiac sympathetic activity was significantly correlated (r = 0.59, p < 0.001) with the mean pulmonary artery pressure. An increase in the spillover of dihydroxyphenylalanine and 3-methoxy-4-hydroxyphenylglycol from the brain was present, suggesting activation of central noradrenergic neurons. CONCLUSIONS: Cardiac sympathetic activation is present in severe heart failure, bearing a close relation with pulmonary artery pressures, independent of heart failure etiology. Activation of noradrenergic neurons in the brain is also present and may be the underlying central nervous mechanism of the sympathoexcitation observed in heart failure.

Adverse consequences of high sympathetic nervous activity in the failing human heart.

OBJECTIVES: In view of previous experimental evidence relating sympathetic nervous overactivity in the heart to myocardial necrosis and ventricular arrhythmias, we prospectively examined the hypothesis that heightened cardiac sympathetic nervous activity is associated with an adverse outcome in patients with moderate to severe heart failure. BACKGROUND: Despite recent therapeutic advances, patients with heart failure continue to have high mortality from progressive hemodynamic decompensation and lethal ventricular arrhythmias. It is believed that initially compensatory increases in sympathetic nervous system activity may ultimately be maladaptive, potentially contributing to subsequent adverse events. METHODS: Sixty patients with moderate to severe heart failure (left ventricular ejection fraction 18.9 +/- 0.9% [mean +/- SE]) were studied prospectively. In addition to the compilation of a hemodynamic, biochemical and electrocardiographic profile for each patient, whole-body and cardiac sympathetic activity were determined by isotope dilution. The relation of these variables to outcome was determined by Cox proportional hazards analysis. RESULTS: The mean follow-up period of the study group was 7 +/- 1 months (range 1 to 24) with a 12-month actuarial survival of 75%. Deaths (14 in all) were accounted for either by sudden death or progressive heart failure in equal numbers. The rate of release of norepinephrine from the heart was significantly higher in patients with heart failure than in healthy subjects (402 +/- 37 vs. 105 +/- 19 pmol/min, p < 0.01), although the values for heart failure ranged widely from normal to 10 times normal. By univariate Cox proportional hazards analysis, pulmonary capillary wedge pressure (p < 0.01), mean pulmonary artery pressure (p < 0.001), serum sodium levels (p < 0.01) and cardiac norepinephrine spill-over rate (p < 0.001) were identified as significant prognostic markers. In a multivariate analysis, cardiac norepinephrine spillover rate was identified as the most powerful prognostic marker (p = 0.0006) of those evaluated in this study. CONCLUSIONS: These results suggest that activation of the sympathetic nervous system in patients with heart failure, specifically the cardiac sympathetic nerves, may contribute to the poor prognosis associated with severe heart failure. The data therefore provide a rationale for the use of drugs such as beta-adrenergic blocking agents in the management of patients with heart failure.

Dietary supplementation with L-arginine fails to restore endothelial function in forearm resistance arteries of patients with severe heart failure.

OBJECTIVES: We sought to examine the efficacy of dietary supplementation of L-arginine on endothelium-dependent vasodilation in patients with congestive heart failure. BACKGROUND: Endothelial dysfunction, as evidenced by a diminished response to such vasodilators as acetylcholine, is well defined in patients with heart failure. These responses are improved by intraarterial infusion with L-arginine. Because L-arginine is a semi-essential amino acid, we investigated the effects of dietary L-arginine on endothelium-dependent vasodilation in these patients. METHODS: Twenty patients with heart failure (New York Heart Association functional class III/IV, mean [+/- SE] age 51.3 +/- 1.7 years) and seven healthy control subjects (mean age 52.6 +/- 3.3 years) were studied. All patients continued taking their usual treatment. Responses to acetylcholine and sodium nitroprusside were determined using forearm plethysmography. Patients with heart failure received either L-arginine (20 g/day every day for 28 days) or placebo (vehicle syrup in equal amounts) in a double-blind protocol. The calculated power of the study was between 62% and 80% to detect a 30% to 40% change in area under the dose-response (forearm vascular resistance) curve. RESULTS: Responses to acetylcholine, but not to sodium nitroprusside, were significantly attenuated in patients with heart failure compared with control subjects (mean area under curve [AUC], control subjects vs. patients with heart failure: 1,125.4 +/- 164.5 vs. 617.3 +/- 116.6 U, p < 0.05, by Student t test). A significant increase in urea and aspartate transaminase levels in patients receiving active L-arginine treatment was observed. Responses to acetylcholine (AUC; before vs. after L-arginine: 641.5 +/- 126.7 vs. 695.9 +/- 151.9 U) and sodium nitroprusside were not affected by either L-arginine or placebo. CONCLUSIONS: Endothelial dysfunction was apparent in patients with heart failure despite rigorous vasoactive treatment. Oral administration with L-arginine was ineffective in influencing endothelial function in these patients.

Selective inhibition of factor Xa is more efficient than factor VIIa-tissue factor complex blockade at facilitating coronary thrombolysis in the canine model.

OBJECTIVES: We determined the effect of adjunctive inhibition of the extrinsic coagulation pathway by factor VIIa-tissue factor complex inhibitors, DEGR VIIa and tissue factor pathway inhibitor (TFPI), and the selective factor Xa inhibitor, tick anticoagulant peptide (TAP), after thrombolytic therapy with tissue-type plasminogen activator (t-PA) in a canine model of electrically induced coronary thrombosis. BACKGROUND: Ongoing thrombin generation is considered an important component of the heightened thrombin activity associated with thrombolytic therapy and may be responsible for reperfusion failure and reocclusion. METHODS: Forty-two dogs with electrically induced coronary thrombus undergoing thrombolysis with t-PA (1 mg/kg over 20 min) were randomly assigned to one of the following adjunctive regimens: TAP (30 micrograms/kg body weight per min for 90 min, n = 10); TFPI (100 to 150 micrograms/kg per min for 90 min, n = 10); DEGR VIIa (1- to 2-mg/kg bolus, n = 10) and saline control (n = 12). The dogs were observed for 120 min after thrombolysis for reocclusion. RESULTS: All three active study agents accelerated the time to reperfusion by an average of 12 min (all p < 0.05). Duration of reflow was greatest with TAP (117 +/- 8 min, p < 0.05 compared with saline control), whereas DEGR VIIa and TFPI did not prolong the duration of reflow. Reocclusion rates were similar among control, DEGR VIIa and TFPI groups (70%, 78% and 67%, respectively). Tick anticoagulant peptide reduced the occurrence of reocclusion (0%, p < 0.05 compared with saline control). CONCLUSIONS: In this experimental model, during systematic blockade of various extrinsic coagulation pathway proteins, we demonstrated that whereas acceleration of thrombolysis occurs with factor VIIa-tissue factor complex inhibition, optimal enhancement of thrombolysis was achieved through specific factor Xa blockade.

Increased risk of non-Q wave myocardial infarction after directional atherectomy is platelet dependent: evidence from the EPIC trial. Evaluation of c7E3 for the Prevention of Ischemic Complications.

OBJECTIVES: We sought to determine the effects of platelet glycoprotein IIb/IIIa receptor blockade on adverse outcomes, especially non-Q wave myocardial infarction, in patients undergoing directional atherectomy in the Evaluation of c7E3 for the Prevention of Ischemic Complications (EPIC) trial. BACKGROUND: Randomized trials comparing directional atherectomy with percutaneous transluminal coronary angioplasty (PTCA) have demonstrated modest benefits favoring atherectomy but at a cost of increased acute ischemic complications, notably non-Q wave myocardial infarction. The mechanism for this excess risk is unknown. METHODS: Of 2,038 high risk patients undergoing coronary intervention in the EPIC trial, directional atherectomy was performed in 197 (10%). Patients randomly received the chimeric glycoprotein IIb/IIIa antibody 7E3 (c7E3), as a bolus or a bolus and 12-h infusion or placebo. Study end points included death, myocardial infarction, repeat intervention or bypass surgery. RESULTS: Patients undergoing directional atherectomy had a lower baseline risk for acute complications but had a higher incidence of any myocardial infarction (10.7% vs. 6.3%, p = 0.021) and non-Q wave myocardial infarction (9.6% vs. 4.9%, p = 0.006). Bolus and infusion of c7E3 reduced non-Q wave myocardial infarctions by 71% after atherectomy (15.4% for placebo vs. 4.5% for bolus and infusion, p = 0.046). Non-Q wave myocardial infarction rates after PTCA were not affected by c7E3, although Q wave myocardial infarctions were reduced from 2.6% to 0.8% (p = 0.017). CONCLUSIONS: The EPIC trial confirmed the increased risk of non-Q wave myocardial infarction with directional atherectomy use compared with PTCA. A bolus and 12-h infusion of the glycoprotein IIb/IIIa receptor inhibitor c7E3 abolished this excess risk. Directional atherectomy-related non-Q wave myocardial infarction appears to be platelet aggregation dependent.

Coronary stenting in diabetic patients: Results from the ROSETTA registry.

OBJECTIVE: Diabetes mellitus is associated with high rates of restenosis and adverse outcomes after percutaneous transluminal coronary angioplasty (PTCA). It is unclear whether coronary stenting reduces adverse events in diabetic patients after PTCA. Our purpose was to determine whether coronary stenting improves clinical event rates in diabetic patients after PTCA. METHODS: The Routine Versus Selective Exercise Treadmill Testing After Angioplasty (ROSETTA) registry was a prospective multicenter observational study examining functional testing and adverse outcomes after successful PTCA. RESULTS: Among the 791 patients enrolled, 180 were diabetic. A total of 90 diabetics received stents while the remaining 90 patients did not. Baseline clinical characteristics were similar between the 2 groups of patients. However, patients with stents were more likely to have complex lesions, whereas those without stents were more likely to undergo atherectomy and have greater residual coronary stenosis. At 6-month follow-up, the composite end point defined as cardiac death, unstable angina, myocardial infarction, need for repeat PTCA, or coronary artery bypass graft surgery (CABG) occurred in 25.0% of stented and 22.2% of nonstented diabetic patients (P not significant [NS]). A multivariate logistic regression analysis showed that coronary stenting was not associated with a reduced incidence of the composite end point among diabetic patients (odds ratio 0.97, 95% CI 0.46-2.05, P NS). CONCLUSION: Coronary stenting does not improve clinical event rates in diabetic patients after PTCA.

Effects of platelet glycoprotein IIb/IIIa receptor blockade by a chimeric monoclonal antibody (abciximab) on acute and six-month outcomes after percutaneous transluminal coronary angioplasty for acute myocardial infarction. EPIC investigators.

Percutaneous transluminal coronary angioplasty (PTCA) for acute myocardial infarction is an attractive alternative to thrombolysis, but is still limited by recurrent ischemia and restenosis. We determined whether adjunctive platelet glycoprotein IIb/IIIa receptor blockade improved outcomes in patients undergoing direct and rescue PTCA in the Evaluation of c7E3 for Prevention of Ischemic Complications (EPIC) trial. Of the 2,099 patients undergoing percutaneous intervention who randomly received chimeric 7E3 Fab (c7E3) as a bolus, a bolus and 12-hour infusion, or placebo, 42 underwent direct PTCA for acute myocardial infarction and 22 patients had rescue PTCA after failed thrombolysis. The primary composite end point comprised death, reinfarction, repeat intervention, or bypass surgery. Outcomes were assessed at 30 days and 6 months. Baseline characteristics were similar in direct and rescue PTCA patients. Pooling the 2 groups, c7E3 bolus and infusion reduced the primary composite end point by 83% (26.1% placebo vs 4.5% c7E3 bolus and infusion, p = 0.06). No reinfarctions or repeat urgent interventions occurred in c7E3 bolus and infusion patients at 30 days, although there was a trend toward more deaths in c7E3-treated patients. Major bleeding was increased with c7E3 (24% vs 13%, p = 0.28). At 6 months, ischemic events were reduced from 47.8% with placebo to 4.5% with c7E3 bolus and infusion (p = 0.002), particularly reinfarction (p = 0.05) and repeat revascularization (p = 0.002). We conclude that adjunctive c7E3 therapy during direct and rescue PTCA decreased acute ischemic events and clinical restenosis in the EPIC trial. These data provide initial evidence of benefit for glycoprotein IIb/IIIa receptor blockade during PTCA for acute myocardial infarction.

Impact of early percutaneous coronary intervention on short- and long-term outcomes in patients with cardiogenic shock after acute myocardial infarction.

This study assesses the impact of early percutaneous coronary intervention in patients presenting with cardiogenic shock after acute myocardial infarction. Predictors of in-hospital death include the need for intubation, cardiopulmonary resuscitation, and angiographic failure; long-term outcomes at 2 years in hospital survivors are favorable.

Selective inhibition of factor Xa during thrombolytic therapy markedly improves coronary artery patency in a canine model of coronary thrombosis.

The success of current thrombolytic strategies is undermined by ongoing thrombin activity, but it is uncertain whether prevention of thrombin generation or direct thrombin antagonism is effective in achieving more optimal thrombolysis. To address this question, 24 dogs with electrically induced coronary thrombus undergoing thrombolysis with tissue-type plasminogen activator (1 mg/kg) over 20 min, were given one of the following adjunctive regimens in a random fashion. Twelve dogs received saline, and served as the control group; a direct thrombin antagonist, hirudin, was given at a dose of 20 micrograms/kg/min for 90 min to six dogs, and a selective factor Xa inhibitor, tick anticoagulant peptide (TAP), was administered to six dogs at a dose of 30 micrograms/kg/min for 90 min. The time to reperfusion was similar in the saline and hirudin groups (34 +/- 4 vs 37 +/- 7 min; P = NS) but shorter in the TAP group (21 +/- 4 min; P < 0.05). Coronary blood flow was restored to 100% of its baseline value for 7 +/- 2 min in control dogs, and for 20 +/- 6 min in the hirudin group (P < 0.05). In the TAP group, coronary blood flow was restored to 100% of its baseline value for more than 120 min in all dogs (P < 0.01 vs others treatments). Reocclusion occurred in 89% and 50% of dogs receiving saline and hirudin, respectively (P = NS), but in none of the TAP-treated dogs (P < 0.01). Plasma fibrinopeptide A (FpA) and thrombin-antithrombin III complex (TAT) levels were determined in all dogs as indicators of thrombin activation. In the saline group, FpA and TAT during reperfusion were 19 +/- 2 ng/ml and 104 +/- 24 ng/ml respectively (P < 0.02 vs baseline) indicating high thrombin activity. In contrast, during reperfusion in hirudin-treated dogs FpA and TAT remained similar to baseline (10 +/- 3 ng/ml and 53 +/- 4 ng/ml respectively; both P < 0.05 vs saline). Reperfusion in TAP-treated dogs did not alter FpA and TAT in plasma, which remained similar to baseline (9 +/- 1 ng/ml and 39 +/- 5 ng/ml respectively; both P < 0.05 vs saline). Scanning electron microscopy of coronary arteries showed residual thrombi with intense platelet and fibrin deposition adherent to the deendothelialized surface of the vessels following saline and hirudin therapy. In contrast, TAP-treated arteries were characterized by the absence of fibrin and minimal platelet deposition. In conclusion, these hemodynamic, biochemical and morphologic data suggest that adjunctive treatment with a higher tier blockade of the coagulation cascade is superior to direct thrombin inhibition in maintaining coronary artery patency following thrombolysis in the experimental canine electrolytic model. These findings highlight the potential adverse effects of unchecked thrombin generation in the setting of thrombolytic therapy.

Antiplatelet and anticoagulant use after myocardial infarction.

Coronary thrombosis leading to myocardial infarction is a complex process involving the interaction of the arterial wall, the coagulation cascade, and platelets. Increased understanding of the molecular biology of thrombosis has prompted an evolution in antithrombotic therapy, from the early use of warfarin following myocardial infarction to agents targeting specific receptors or modulators in the thrombotic process. The complexity of thrombosis allows for numerous sites of pharmacologic intervention; the multiple pathways leading to platelet aggregation and thrombin formation provide the opportunity for combined therapies. This review presents the current clinical data on antiplatelet, anticoagulant, and specific antithrombin therapies following myocardial infarction.

The clinical role of platelet glycoprotein IIb/IIIa receptor inhibitors in ischemic heart disease.

The platelet glycoprotein (GP) IIb/IIIa receptor antagonists are powerful new antiplatelet drugs that show promise in reducing complications of coronary angioplasty and acute coronary syndromes.

Clinical outcomes of drug-eluting stent use in patients with ST elevation myocardial infarction.

AIM: Randomised trials using drug-eluting stents (DES) in ST elevation myocardial infarction (STEMI) have shown mixed results, and excluded patients at the highest risk of adverse outcomes. We aimed to determine the real world clinical outcomes of DES and compare these with bare-metal stents (BMS) in an unrestricted observational study of patients presenting with STEMI. METHODS: 564 consecutive patients undergoing primary PCI for STEMI were prospectively enrolled in the Melbourne Interventional Group registry (August 2004 to May 2006). The choice of using DES was at the operator's discretion, yet restricted to patients considered at highest risk of restenosis [e.g. diabetes, long lesions (>20 mm) and small target vessels (<2.5 mm)]. Clinical, procedural, and 12-month outcomes of patients receiving DES were evaluated and compared to BMS. RESULTS: DES were used in 45% of patients presenting with STEMI. The rates of cardiogenic shock were similar in the DES and BMS groups (10.2 vs. 11%, p=0.71). In-hospital outcomes were not significantly different with respect to death (4.7 vs. 7.2%, p=0.23), major adverse cardiac events (MACE) (10.6 vs. 11.3%, p=0.80) or stent thrombosis (1.7 vs. 0.3%, p=0.71). At 12 months, target vessel revascularisation (TVR) in patients with DES was 10.2% vs. 7.2% in BMS (p=0.22). On propensity score adjusted multivariate analyses, the only independent predictor of 12-month MACE was presentation with cardiogenic shock (OR 2.59, 95% C.I 1.04-6.45), and the only predictor of 12-month TVR was reference vessel diameter ≤2.5 mm (OR 2.16, 95% C.I 1.06-4.33). DES use was not independently predictive of lower TVR, MACE rates or mortality. Late stent thrombosis rates were similar (DES 3.2 vs. BMS 3.8%, p=0.65). CONCLUSIONS: Drug-eluting stents are frequently used in Australia in the high-risk setting of STEMI. While target vessel revascularisation rates were moderate in this high-risk group, there was no increased mortality, reinfarction or stent thrombosis compared to bare-metal stents.

The foundation and launch of the Melbourne Interventional Group: a collaborative interventional cardiology project.

The Melbourne Interventional Group (MIG) is a voluntary collaborative venture of interventional cardiologists practicing at 12 major public and private hospitals in Victoria, designed to record data pertaining to percutaneous coronary interventions (PCI) and perform long-term follow-up. The potential advantages of collaboration involve large-scale analysis of current interventional strategies (e.g. drug-eluting stents, evaluation of new technologies and cost-effective analysis), provide a basis for multi-centred clinical trials and allow comparison of clinical outcomes with cardiac surgery. The established registry documents demographic, clinical and procedural characteristics of consecutive patients undergoing PCI and permits analysis of those characteristics at 30 days and 12 months. The registry is co-ordinated by the Centre of Clinical Research Excellence (CCRE), a research body within the Department of Epidemiology and Preventive Medicine (Monash University, Melbourne). The eventual goal of MIG is to provide a contemporary appraisal of Australian interventional cardiology practice, with opportunities to improve in-hospital and long-term outcomes of patients with coronary artery disease.

Platelet glycoprotein IIb/IIIa receptor inhibitors in ischemic heart disease.

The key role of platelets in the pathogenesis of ischemic heart disease has led to the development of new classes of agents to control platelet function. The platelet glycoprotein IIb/IIIa receptor mediates the final common pathway to platelet aggregation. Drugs that block the glycoprotein IIb/IIIa receptor potently inhibit platelet aggregation. Monoclonal antibodies, cyclic peptides, and peptide-derivative glycoprotein IIb/IIIa inhibitors have been developed. The monoclonal antibody Fab fragment, chimeric 7E3, has been shown to significantly reduce ischemic complications and clinical restenosis after high-risk angioplasty in the large-scale Evaluation of 7E3 for the Prevention of Ischemic Complications (EPIC) trial. A number of glycoprotein IIb/IIIa inhibitors have been tested in patients with unstable angina with similarly positive results, and initial trials in patients with acute myocardial infarction are also encouraging. Further evaluation of these agents in large scale trials is currently underway and should help determine the place and appropriate use of these agents in the clinical arena.