What is the optimal postconditioning algorithm?

Ischemic postconditioning has emerged as a clinically feasible intervention for limiting infarction in the setting of percutaneous intervention. In ischemic postconditioning, a number of cycles of a brief period of reperfusion followed by a brief period of occlusion are applied immediately upon reperfusion of the ischemic heart. Although ischemic postconditioning is protective in both animals and man, the animal studies reveal that the algorithm used in selecting the duration of the occlusion and reperfusion periods is critical to the degree of protection realized and it varies with species. The question then arises what is the best algorithm for man? The available animal and clinical data are examined in an attempt to shed light on this perplexing problem

Sertraline for the treatment of depression in coronary artery disease and heart failure

Depression is a common co-morbid condition in patients with cardiac disease and has been identified as an independent risk factor for increased morbidity and mortality. SSRIs are established agents for the treatment of depression and are well tolerated in patients with cardiac disease. SSRIs are a heterogeneous group of antidepressants, which apart from their common mechanism of action, differ substantially in their chemical structure, metabolism and pharmacokinetics. This article reviews experimental and clinical evidence on the safety and efficacy of the most extensively studied SSRI, sertraline, in depressed patients with coronary artery disease and heart failure. Intervention with sertraline has the potential to provide depressed patients with cardiac disease relief from their depressive symptoms, improvement in quality of life and a potential benefit in their cardiovascular risk profile. © 2007 Informa UK Ltd

Inflammatory and non-invasive vascular markers: The multimarker approach for risk stratification in coronary artery disease

Current thinking supports the notion that several inflammatory proteins intervene with endothelium and haemostatic factors leading to plaque formation and rupture. Of these, C-reactive protein (CRP), monocyte/macrophage colony-stimulating factor (MCSF) and interleukin-6 (IL-6) promote atherogenesis by inducing monocyte-macrophage activation, foam cell formation, platelet activation, tissue factor expression, release of other procoagulant cytokines or downregulation of atheroprotective cytokines such as interleukin 10 and transforming growth factor b-1 (TGFb-1). CRP, MSCF and IL-6 are interrelated and have been found in increased blood concentrations in CAD. Increased levels of CRP and IL-6 predict a higher cardiovascular event rate in the general population and in addition to high MCSF or low TGFb-1 predict adverse outcome in CAD patients independently of traditional risk factors. Moreover, in CAD patients, the predictive value of MCSF is additive and beyond that of CRP suggesting the need of a "multimarker approach" in assessing cardiovascular risk. Accumulating evidence supports the utility of non-invasive markers of subclinical atherosclerosis, namely carotid intimal media thickness, flow mediated dilatation of the brachial artery, augmentation index or pulse wave velocity, in the prediction of cardiovascular risk particularly in primary prevention settings. The combination of these non-invasive tests has been shown to improve their prognostic accuracy compared to each other alone. Although several therapeutic strategies like vaccination against antigens promoting atherogenesis, cyclooxygenase inhibitors, statins, and ACE inhibitors may reduce the levels of these inflammatory markers and improve the non-invasive markers of subclinical atherosclerosis, the impact on cardiovascular risk resulting from these changes is unknown. The combination of an established inflammatory marker such as CRP or a vascular marker such as IMT with novel biochemical and vascular markers of cardiovascular disease may offer additive prognostic information for adverse outcome. © 2008 Elsevier Ireland Ltd. All rights reserved

Background dietary habits are strongly associated with the development of myocardial infarction at young ages: A case-control study

Background: We investigated whether dietary habits can discriminate young individuals with myocardial infarction (MI) from age-sex-matched controls. Methods: We enrolled 100 consecutive patients who had survived their first MI before the age of 36 years and 100 age- and sex-matched controls without a history of cardiovascular disease. Dietary habits were assessed through a semi-quantitative food frequency questionnaire, and a diet score that evaluates quality of diet was developed (ranging 14-60). Smoking habits, physical activity status, body mass index, clinical history and blood lipid levels were also measured. Results: Data analysis revealed that MI patients had less healthy dietary as compared to their matched controls (23 ± 4 vs. 31 ± 4; p < 0.001). Multi-adjusted logistic regression analysis showed that 1-unit increase in the diet score (i.e., better dietary habits) decreased by 40% (95% CI 15%-57%) the odds of having a MI, after controlling for smoking habits, body mass index, cholesterol levels, presence and management of hypertension and diabetes, physical activity status, and family history of coronary heart disease (CHD). Discriminant analysis showed that diet score was the strongest discriminator for MI, followed by cholesterol levels and pack-years of smoking. Conclusions: The present work provides scientific evidences that promotion of healthy eating from the youth may prevent the development of CHD. © 2008 European Society for Clinical Nutrition and Metabolism

Novel biologic mechanisms of levosimendan and its effect on the failing heart

Background: Calcium sensitizers belong to a new class of cardiac enhancers that stimulate cardiac contractility without causing intracellular calcium overload or increasing myocardial oxygen demand. Levosimendan, the most well-studied calcium sensitizer in the real clinical practice, produces greater hemodynamic and symptomatic improvement in patients with acute heart failure than traditional inotropes. Objective: To review the recent experimental and clinical evidence on novel biologic mechanisms explaining the pleiotropic effects of levosimendan on the falling heart. Methods: A systematic search of peer-reviewed publications was performed on Medline and EMBASE from January 1995 to December 2007. The results of unpublished trials were obtained from presentations at national and international meetings. Results: Levosimendan has a unique dual mechanism of action by enhancing cardiac contractility and causing peripheral vasodilatation. Immunomodulatory and antiapoptotic properties of levosimendan may be an additional biologic mechanism that prevents further cytotoxic and hemodynamic consequences of abnormal immune and neurohormonal respones in acute heart failure, leads to cardioprotection and beneficially intervenes in the progression of syndrome. Experimental data show that levosimendan exerts its cardioprotective effects through its antioxidant properties and seems to be a potent inhibitor of H2O2-induced cardiomyocyte apoptotic cell death. Clinical data demonstrate that levosimendan does not increase markers of oxidative and nitrosative stress, in contrast to placebo treatment, in advanced chronic heart failure patients. Levosimendan has also been shown to activate mitoKATP channels which are important mediators of ischemic preconditioning. Pharmacological modulation of KATP channels may prove beneficial in patients at risk of myocardial ischemia, particularly those requiring inotropic support. Conclusion: Pleiotropic effects of levosimendan appear to have important clinical and prognostic implications in acute heart failure syndromes and ischemic heart disease. © 2008 Informa UK Ltd