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Background. Despite recent advances in stent design and constantly improving protective pharmacological strategies, complications and adverse events following percutaneous coronary interventions (PCI) are still major factors influencing morbidity and mortality. Therefore, predicting secondary vascular occlusions represents an unmet medical need.Aim. To triage clinical and laboratory predictors of major adverse clinical events (MACE) following coronary stenting.Material and methods. This was a prospective, case-controlled, single-center study, which included 94 consecutive patients with documented ischemic heart disease (IHD) who underwent PCI with drug-eluting stent implantation. All patients received dual antiplatelet therapy with acetyl salicylic acid and clopidogrel. Numerous clinical characteristics and laboratory biomarkers were assessed before stenting, as well as CYP2C19 genotyping after patient’s discharge and were correlated with poststenting MACE over the mean follow-up of 28 months. MACE included death, nonfatal myocardial infarction, target vessel revascularisation, stroke, stent thrombosis, angina recurrence and in-stent restenosis.Results. Twenty-three patients experienced MACE. According to univariate regression analysis we found following MACE predictors after PCI: diabetes mellitus (p=0.049), P2Y12 Reaction Units (PRU) according to VerifyNow® (p=0.01), number of stented arteries more than 2 (p=0.01), number of implanted stents more than 2 (p=0.01), baseline levels of plasminogen activator inhibitor-1 (PAI-1) (p=0.03) and von Willebrand activity (vWF) (p=0.01). Using multivariate analysis we demonstrated that concomitant diabetes mellitus, PRU ≥202, PAI-1 level ≥75.95 ng/ml, von Willebrand factor activity ≥155.15% are independent predictors of adverse cardiac events after PCI in stable IHD patients. Other clinical characteristics and laboratory indices, including CYP2C19*2 carriage, showed no significant impact on outcomes after elective PCI. Conclusions. Background diabetes mellitus, high on-treatment platelet reactivity (according to VerifyNow®), PAI-1 and vWF presenting activity may be useful for MACE prediction over 28 months of follow-up after PCI with drug-eluting stent implantation.

The abrupt cessation of effective cardiac function that is generally due to heart rhythm disorders can cause sudden and unexpected death at any age and is referred to as a syndrome called "sudden cardiac death" (SCD). Annually, about 400,000 cases of SCD occur in the United States alone. Less than 5% of the resuscitation techniques are effective. The prevalence of SCD in a population rises with age according to the prevalence of coronary artery disease, which is the most common cause of sudden cardiac arrest. However, there is a peak in SCD incidence for the age below 5 years, which is equal to 17 cases per 100,000 of the population. This peak is due to congenital monogenic arrhythmic canalopathies. Despite their relative rarity, these cases are obviously the most tragic. The immediate causes, or mechanisms, of SCD are comprehensive. Generally, it is arrhythmic death due to ventricular tachyarrythmias - sustained ventricular tachycardia (VT) or ventricular fibrillation (VF). Bradyarrhythmias and pulseless electrical activity account for no more than 40% of all registered cardiac arrests, and they are more often the outcome of the abovementioned arrhythmias. Our current understanding of the mechanisms responsible for SCD has emerged from decades of basic science investigation into the normal electrophysiology of the heart, the molecular physiology of cardiac ion channels, the fundamental cellular and tissue events associated with cardiac arrhythmias, and the molecular genetics of monogenic disorders of the heart rhythm (for example, the long QT syndrome). This review presents an overview of the molecular and genetic basis of SCD in the long QT syndrome, Brugada syndrome, short QT syndrome, catecholaminergic polymorphic ventricular tachycardia and idiopathic ventricular fibrillation, and arrhythmogenic right ventricular dysplasia, and sudden cardiac death prevention strategies by modern techniques (including implantable cardioverter-defibrillator).