Sports-Related Sudden Cardiac Arrest in Germany

BackgroundKnowledge about causes of sports-related sudden cardiac arrest (SrSCA) may influence national strategies to prevent such events. Therefore, we established a prospective registry on SrSCA to estimate the incidence and in particular describe the etiologies of SrSCA in the general population in Germany.MethodsThe registration of SrSCA based upon 4 pillars: a web-based platform to record SrSCA cases in competitive and recreational athletes, media-monitoring, cooperation with the German Resuscitation Registry, and 15 institutes of forensic medicine.ResultsAfter an observation period of 6 years, a total of 349 cases was recorded (mean age 48.0 ± 12.7 years); 109 subjects survived. Most of the cases occurred during nonelite competitive or recreational sports. Bystander cardiopulmonary resuscitation (CPR) was initiated in 262 cases (75%); however, rhythm analysis and defibrillation (if indicated) was mainly performed by medical services. In patients ≤ 35 years of age, premature coronary artery disease (CAD) and sudden arrhythmic death syndrome (SADS) prevailed, followed by myocarditis. In athletes ≥ 35 years of age, CAD predominated.ConclusionsCountry-specific registries are necessary to define the national screening and prevention strategy optimally. In Germany, premature CAD, SADS, and myocarditis are the leading causes of SrSCA in young athletes, reinforcing the great disparity of the prevalence of cardiac diseases among different countries. Extension of on-site SCD-prevention campaigns, with training of CPR and explanation of the efficient use of automated external defibrillators (AEDs), may decrease the burden of SrSCD.     

A novel approach for transtunnel puncture in a patient with atrial tachyarrhythmias and Fontan circulation

Journal of Interventional Cardiac Electrophysiology -     

Intravascular ultrasonic comparative analysis of degree of intimal hyperplasia produced by four different stents in the coronary arteries

Intravascular ultrasound studies were performed at angiographic follow-up on 121 native coronary lesions treated with 1 bare metal stent (n = 50), high-dose dexamethasone-eluting stents (n = 18), non-polymer-based paclitaxel-eluting stents (n = 18), or sirolimus-eluting stents (n = 35). Paclitaxel- and sirolimus-eluting stents reduced mean intimal hyperplasia thickness compared with bare metal stents by 49% and 90% (p = 0.048 and p <0.001), respectively, whereas mean intimal hyperplasia thickness treated with dexamethasone-eluting stents was similar to those lesions treated with bare metal stents.     

Determinants of target vessel failure in chronic total coronary occlusions after stent implantation. The influence of collateral function and coronary hemodynamics

OBJECTIVES: The goal of this study was to assess the influence of collateral function, coronary hemodynamics, and the angiographic result on the risk of target vessel failure (TVF) after recanalization of a chronic total coronary occlusion (CTO). BACKGROUND: Collaterals may have an adverse effect on TVF. METHODS: In 111 consecutive patients, a CTO (duration >2 weeks) was successfully recanalized with stent implantation. Collateral function was assessed by intracoronary Doppler flow velocity and pressure recordings distal to the occlusion. Baseline collateral function was determined before the first balloon inflation, and recruitable collateral function after stenting during a balloon reocclusion. Finally, the coronary flow velocity reserve (CFVR) and the fractional flow reserve (FFR) were measured. RESULTS: Angiographic follow-up after 5 +/- 4 months in 106 patients showed a reocclusion in 17% and a restenosis in 36%. The major determinants of TVF were the stent length (p < 0.01) and number of implanted stents (p < 0.01). No difference was observed in baseline or recruitable collateral function between patients with and without TVF; 52% of patients had a CFVR >or= 2.0, and only 18% a CFVR >or=2.5 after percutaneous transluminal coronary angioplasty, but neither cutoff-value predicted TVF. A low FFR discriminated patients with reocclusion (0.81 +/- 07 vs. 0.86 +/- 08, p < 0.05) but not with restenosis (0.87 +/- 0.06). CONCLUSIONS: This study showed that there is no relation between a well-developed collateral supply and the risk of TVF in recanalized CTOs. This was rather determined by the stented segment length. There was also no adverse effect of the frequently observed impaired CFVR on TVF, whereas a low FFR was associated with a higher risk of reocclusion.     

Pathophysiology of Stroke: Lessons from Animal Models

The current pathophysiological understanding of stroke is substantially based on experimental studies. Brain injury after cerebral ischemia develops from a complex signaling cascade that evolves in an at least partially unraveled spatiotemporal pattern. Early excitotoxicity can lead to fast necrotic cell death, which produces the core of the infarction. The ischemic penumbra that surrounds the infarct core suffers milder insults. In this area, both mild excitotoxic and inflammatory mechanisms lead to delayed cell death, which shows biochemical characteristics of apoptosis. While brain cells are challenged by these deleterious mechanisms, they activate innate protective programs of the brain, which can be studied by means of experimentally inducing ischemic tolerance (i.e., ischemic preconditioning). Importantly, cerebral ischemia not only affects the brain parenchyma, but also impacts extracranial systems. For example, stroke induces a dramatic immunosuppression via an overactivation of the sympathetic nervous system. As a result, severe bacterial infections such as pneumonia occur. Complex signaling cascades not only decide about cell survival, but also about the neurological deficit and the mortality after stroke. These mechanisms of damage and endogenous protection present distinct molecular targets that are the rational basis for the development of neuroprotective drugs.     

Diagnostik und Indikation zum Klappenersatz bei asymptomatischer und symptomatischer Aorteninsuffizienz

Chronic volume overload is associated with dilatation and eccentric hypertrophy of the left ventricle (=ventricular remodeling). With the dilatation of the left ventricle and the shift of the pressure-volume-relationship to the right, the filling pressures can be kept normal despite severe regurgitation. Therefore, the patient with aortic regurgitation can remain asymptomatic over many years. Thus, the indication for aortic valve replacement in patients with severe aortic regurgitation is sometimes difficult and may lead to problems to choose the optimal time point for operation. As a general rule, symptomatic patients with severe aortic regurgitation should be operated as soon as possible. In asymptomatic patients with significant dilatation of the left ventricle and reduction of systolic pump function the therapy of choice is aortic valve replacement. Asymptomatic patients with normal left ventricular function have usually a good prognosis with a yearly mortality rate of approximately 0.04%. However, in the presence of significant dilatation of the left ventricle, i. e. enddiastolic chamber diameter more than 70 mm respectively endsystolic diameter more than 50 mm, patients have to be checked on a regular basis, i. e. in yearly intervals to detect left ventricular dysfunction in due time. According to the literature, asymptomatic patients with severe aortic regurgitation develop left ventricular dysfunction in a yearly rate of 4%. However, approximately 50% of all patients are even after 10 years asymptomatic. The indication for aortic valve replacement is given when the patient shows a deterioration of left ventricular function or becomes symptomatic. Valve replacement is also indicated in patients with an ejection fraction below 50% and/or endsystolic chamber diameter of more than 55 mm. Therapy of choice in symptomatic patients with severe aortic regurgitation is aortic valve replacement. In asymptomatic patients, operation depends on the degree of chamber dilatation respectively the severity of left ventricular dysfunction. In patients with severe aortic regurgitation but without clinical symptoms and moderate enlargement of the left ventricle regular check-ups in yearly intervals are indicated. In the presence of severe left ventricular dilatation check-ups should be performed on a half-year basis to prevent irreversible damage to the heart muscle.