AstraZeneca, Biosensors, and The Medicines Company.

Many changes occur during reperfusion of the myocardium after ischemic damage. Necrosis and apoptosis appear to be ongoing during ischemia, while apoptosis is boosted by the reperfusion event. In the past 10 years, distinct intracellular pathways important for hypertrophy, apoptosis, cardiac failure, ischemic preconditioning and reperfusion damage have been recognized. The eventual response of the cardiomyocyte will depend on energy and time available as well as changes in pH and ion handling and the delicate balance of activation of signaling molecules and transcription factors. There is agreement on the central role of mitochondria and nitric oxide (NO) in programmed cell death. However, although many groups analyzed the contribution of NO to cell death, still the circumstances and levels required for cardioprotection or death are unclear. Growth factors, cytokines, and downstream signaling molecules have been shown to influence programmed cell death through mechanisms reminiscent of preconditioning. Here, the role of apoptosis in ischemia reperfusion-related cell death is reviewed. Important data have been obtained in isolated cells, intact hearts and intact animals. Both pharmacological as well as genetic interventions are discussed. Proof for apoptosis in man post-myocardial infarction (MI) treated through primary Percutaneous Trans-luminal Coronary Angioplasty or other reperfusion therapy is reviewed. Finally, the currently available quantification methods for apoptosis post-MI are mentioned.

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Abstract Background The utility of the PRECISE-DAPT score in predicting short-term major bleeding, either alone, or in comparison with the CRUSADE and ACUITY scores, has not been investigated. This analysis compared the predictive performances of the three bleeding scores in stratifying the risk of 30-day major bleeding postpercutaneous coronary intervention in patients with dual-antiplatelet therapy. Methods In this post hoc subanalysis of the GLOBAL LEADERS trial, the primary safety objective (bleeding according to the Bleeding Academic Research Consortium [BARC] criteria [type 3 or 5]) was assessed at 30 days according to the three scores in the overall population, and in patients with acute (ACS) and chronic coronary syndrome (CCS). Results In a total of 15,968 patients, we calculated all three scores in 14,709 (92.1%). Irrespective of clinical presentation, the PRECISE-DAPT (c-statistics: 0.648, 0.653, and 0.641, respectively), CRUSADE (c-statistics: 0.641, 0.639, and 0.644, respectively), and ACUITY (c-statistics: 0.633, 0.638, and 0.623, respectively) scores were no significant between-score differences in discriminatory performance for BARC 3 or 5 bleeding up to 30 days, and similarly the PRECISE-DAPT score had a comparable discriminative capacity according to the integrated discrimination improvement when compared with the other scores. In ACS, the CRUSADE score had a poor calibration ability (Hosmer–Lemeshow goodness-of-fit [GOF] chi-square = 15.561, p = 0.049), whereas in CCS, the PRECISE-DAPT score had poor calibration (GOF chi-square = 15.758, p = 0.046). Conclusion The PRECISE-DAPT score might be clinically useful in the overall population and ACS patients for the prediction of short-term major bleeding considering its discriminative and calibration abilities.

SUMMARY The diagnostic accuracy of the following methods of analysing exercise tests were evaluated: (a) the cumulative area of ST segment depression during exercise normalised for workload and heart rate (exercise score); (b) discriminant analysis of electrocardiographic exercise variables, workload, and symptoms; and (c) ST segment amplitude changes during exercise adjusted for heart rate. Three hundred and forty five men without a history of myocardial infarction were studied. One hundred and twenty three were apparently healthy. Less than half (170)

Isolated left ventricular noncompaction in a patient presenting with a subacute myocardial infarctionIsolated left ventricular noncompaction is a rare cardiomyopathy that is often not recognised. So far, it is not well established how best to manage this abnormality. We describe a patient in whom the diagnosis of isolated left ventricular noncompaction was made after presentation with a subacute myocardial infarction. Because of nonsustained ventricular tachycardias during hospitalisation, which were inducible and deteriorated into ventricular fibrillation on electrophysiological examination after coronary artery bypass grafting, he received an implantable defibrillator. Whether the ventricular tachycardias were due to the myocardial infarction or to the noncompacted myocardium remains uncertain. (Neth Heart J 2007; 15:109-11.) Keywords: noncompaction (isolated), cardiomyopathy, echocardiographyA 73-year-old man without a cardiac history presented to the Emergency Department because of chest pain radiating to the throat for two days. On physical examination he measured 1.70 m and weighed 58 kg. His blood pressure was 110/60 mmHg and the pulse regular at a rate of 70 beats/min. The jugular venous pressure appeared normal. Cardiac auscultation revealed normal heart sounds without murmurs. The lungs were clear to auscultation. The electrocardiogram showed sinus rhythm with right bundle branch block, 1 mm ST-segment elevation in leads I, II, aVL and V 3 to V 6 , and slightly terminally negative T waves in leads V 3 to V 6 . The chest X-ray was normal with a cardiothoracic ratio of 43%. Creatine kinase (CK) and CK-MB were increased at presentation (2263 and 356 U/l, respectively). The diagnosis of subacute anterolateral myocardial infarction was made and the patient received aspirin, clopidogrel, lowmolecular-weight heparins, nitrates, β-blockers and a statin. The next day, the CK and CK-MB had fallen and transthoracic echocardiography revealed akinetic anterolateral wall segments, a left ventricular ejection fraction of 35 to 40%, no significant valve disease, and prominent trabeculation of the apex of the left ventricular myocardium consistent with noncompaction. The presence of noncompaction was confirmed by contrast echocardiography (1.5 ml SonoVue intravenously), showing direct communication between the left ventricular cavity and the deep intertrabecular recesses (figure 1). The patient's convalescence was complicated by the occurrence of recurrent nonsustained ventricular tachycardia from the fourth day after admission, and ST depression (without chest pain) during bicycle ergometry on the fifth day after admission. Coronary angiography showed significant two-vessel disease of the left anterior descending (LAD) and left circumflex (LCX) coronary artery. Three weeks after admission, the patient underwent coronary artery bypass grafting (CABG). The left internal mammary artery was anastomosed with the LAD, and a venous jump graft was anastomosed with the obtuse marginal branch of the LCX via the anterolateral br...

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