[Cardiovascular screening for recreational, leisure, vigorous and competitive sport activities over 35 years]. / Kardiovaskuläre Vorsorge im Breitensport, ambitionierten Freizeitsport und Wettkampfsport über das 35. Lebensjahr hinaus.

Particularly among over 30 years old ambitious hobby- and competitive athletes arrhythmias and even sudden cardiac deaths occur again and again. The spectacular sudden deaths during marathon, football and, just recently, in the trend discipline triathlon seem to support that view. Reports about the "athlete`s heart" and complications in the elderly causes uncertainty among athletes, fitness fans and sports physicians. The question arises, how to avoid complications caused by ambitious sporting activity in the elderly and how to screen hobby- and ambitious athletes between the age of 35 and 75 years. For athletes > 35 years old besides medical history and physical examination basic examinations including resting ECG, echocardiography and exercise ECG/stress echocardiography are mandatory. Further examinations, if clinically necessary, should be spiroergometry, Holter ECG or magnetic resonance tomography and Carotis-Duplex or Cardio-CT for the purpose of arteriosclerosis screening. In suspicious inflammation a further extended laboratory testing may become necessary (incl. viral/bacterial antibodies) or even a multidisciplinary approach (immunological, neurological, dental or orthodontic examination).

Prasugrel vs clopidogrel in cardiogenic shock patients undergoing primary PCI for acute myocardial infarction. Results of the ISAR-SHOCK registry.

There is limited clinical data comparing different P2Y12-receptor inhibitors in patients with acute myocardial infarction (AMI) complicated by cardiogenic shock. The aim of the ISAR-SHOCK registry was to compare the clinical outcome of patients treated with clopidogrel vs prasugrel in this setting. Patients (n=145) with AMI complicated by cardiogenic shock and undergoing primary PCI in two centres (Deutsches Herzzentrum München and Klinikum rechts der Isar, Technical University Munich) between January 2009 and May 2012 were included in this registry. The use of prasugrel for patients within this registry reflected co-morbidities and platelet function testing results during the acute AMI phase. Early outcome at 30-days was reported with regard to all-cause mortality, myocardial infarction (MI), stent thrombosis (ST) and bleeding events. With regard to antiplatelet treatment in the 145 cardiogenic shock patients, 50 patients were initially treated or immediately switched to prasugrel while 95 patients were treated with clopidogrel. All-cause mortality was lower in prasugrel- vs clopidogrel-treated patients (30 % vs 50.5%, HR: 0.51, 95% CI [0.29-0.92], p=0.025). No significant differences in prasugrel- vs clopidogrel-treated patients were observed for the occurrence of MI (p=0.233), ST (p=0.306) or TIMI major bleedings (p=0.571). Results of the ISAR-SHOCK registry suggest that the use of prasugrel in AMI patients complicated by cardiogenic shock might be associated with a lower mortality risk as compared to clopidogrel therapy without increasing the risk of bleeding. These findings, however, need confirmation from specifically designed randomised studies in this high-risk cohort of patients.

Randomised trial of three rapamycin-eluting stents with different coating strategies for the reduction of coronary restenosis: 2-year follow-up results.

BACKGROUND: Drug-eluting stent (DES) platforms devoid of durable polymer have potential to enhance long-term safety outcomes. The ISAR-TEST-3 study was a randomised trial comparing three rapamycin-eluting stents with different coating strategies. The present study examined 2-year outcomes of these patients and is the first large-scale trial to report longer-term outcomes with biodegradable polymer and polymer-free DES. METHODS: Patients with de novo coronary lesions in native vessels were randomly assigned to receive biodegradable polymer (BP; n = 202), permanent polymer (PP; Cypher; n = 202) and polymer-free (PF; n = 201) stents. The 2-year endpoints of interest were target lesion revascularisation (TLR), death/myocardial infarction (MI), stent thrombosis and delayed angiographic late luminal loss (LLL) between 6-8 months and 2 years. RESULTS: There were no significant differences in TLR (8.4%, 10.4% and 13.4% for BP, PP and PF stents, respectively; p = 0.19), death/MI (5.9%, 6.4% and 6.5% with BP, PP and PF respectively; p = 0.97) or stent thrombosis (definite/probable 0.5%, 1.0% and 1.0% with BP, PP and PF, respectively; p = 0.82). Paired angiographic follow-up at 6-8 months and 2 years was available for 302 patients (69.0% of eligible patients). Delayed LLL was significantly different across the treatment groups: 0.17 (0.42) mm, 0.16 (0.41) mm and -0.01 (0.36) mm for BP, PP and PF stents, respectively (p<0.001). CONCLUSION: Clinical antirestenotic efficacy was maintained with all three platforms between 1 and 2 years, although angiographic surveillance showed ongoing delayed LLL with both BP and PP stent platforms. At 2 years there was no signal of a differential safety profile between the three stent platforms.

P27 and P53 gene polymorphisms and restenosis following coronary implantation of drug-eluting stents.

OBJECTIVE: Drug-eluting stents (DES) have reduced restenosis rates compared with bare-metal stents. P27 and P53 play important roles in the signal transduction leading to neointimal growth inhibition and induction of apoptosis of smooth muscle cells due to rapamycin and paclitaxel. We hypothesized that genetic variants of P27 and P53 influence the development of restenosis and the clinical outcome of patients receiving DES. METHODS: Polymorphisms in the genes encoding for P27 and P53 were tested for their association with restenosis and major adverse cardiac events. P27 C-79T and P53 G72C polymorphism genotypes were determined in a series of 433 consecutive patients receiving DES. Follow-up angiography after 6 months was performed in 87% of the patients. Genotyping was performed with PCR-based methods. RESULTS: For patients with the respective P27 C-79T and P53 G72C genotypes, the angiographic restenosis rates were between 5.0 and 22.0%, and the clinical restenosis rates were between 0.0 and 16.3%, without significant differences for the studied genotypes (p > 0.19). There was no association of the studied genotypes with the 1-year incidences of death and myocardial infarction. CONCLUSION: This study could not demonstrate a clinically relevant role of P27 and P53 polymorphisms in the processes leading to in-stent restenosis.

Interferon-gamma and interferon-gamma receptor 1 and 2 gene polymorphisms and restenosis following coronary stenting.

In a recent study, analysis of gene expression in atherectomy specimens derived from restenotic coronary lesions revealed 223 differentially expressed genes. Thirty-seven of these genes indicated activation of interferon- (IFN-) gamma signaling in neointimal smooth muscle cells. Moreover, genetic disruption of IFN-gamma signaling in a mouse model of restenosis significantly reduced the vascular proliferative response. Thus, IFN-gamma is assumed to play an important role in the control of tissue proliferation during neointima formation. We hypothesized that genetic variants of IFN-gamma and its receptor subunits are involved in upregulation of IFN-gamma related genes in neointimal tissue of patients that develop in-stent restenosis. Polymorphisms in the genes encoding for IFN-gamma (IFNG T874A) and its receptors 1 (IFNGR1 C-56T) and 2 (IFNGR2 A839G) were tested for their association with restenosis. IFNG T874A, IFNGR1 C-56T and IFNGR2 A839G genotypes were determined in a consecutive series of patients (n=2591) that had been treated with coronary stents. Follow-up angiography 6 months after stent implantation was performed in 76.8% of the patients. Genotyping was performed with PCR-based methods. IFNG T874A, IFNGR1 C-56T and IFNGR2 A839G genotypes were not associated with the incidence of angiographic and clinical restenosis (P>0.23). Moreover, there was no association between IFNG, IFNGR1 and IFNGR2 genotypes and the combined incidence of death form any cause and non-fatal myocardial infarction during the first 12 months following the intervention (P>0.61). Thus, this study does not support a clinically relevant role of the studied polymorphisms in the processes leading to in-stent restenosis.