Combined effect of acute altitude exposure and vigorous exercise on platelet activation.

Exposure to high altitudes and exercise alters body's physiology and may cause acute cardiovascular events. Platelet activation is one of the key players in these events. Therefore, we investigated the effect of vigorous exercise at higher altitude (2650 m) on platelet aggregation and serum markers of platelet activation. 14 healthy subjects performed a step incremental ergometer test until exhaustion at the Environmental Research Station (UFS, 2650 m) at Zugspitze. Platelet aggregation and serum levels of endothelin-1, soluble p-selectin, platelet factor 4 and Chromogranin A were measured. Platelet activation was significantly enhanced after exercise at high altitude compared to measures immediately prior exercise. We detected significantly enhanced serum levels of endothelin-1 and soluble p-selectin whereas chromogranin A and platelet factor 4 remained unchanged. This effect might be due to increased endothelin-1 levels causing pulmonary vasoconstriction, rheological changes and direct platelet activation. This might be of clinical relevance, especially in patients with pre-existing diseases.

Postmortem interrogation of cardiac implantable electrical devices may clarify time and cause of death.

BACKGROUND: Postmortem interrogation of cardiac implantable electrical devices (CIED) in autopsy is not routinely performed. Thus, it remains unclear whether an interrogation might clarify time and cause of death. METHODS: Seventy of 4401 patients (1.6%) undergoing autopsy in 2014 and 2015 presented with a CIED. The explanted CIED were interrogated with respect to time and possible cause of death. Battery and lead parameters, clinical and technical alerts, and arrhythmia episodes were reviewed and afterwards correlated with the results of autopsy and clinical data. RESULTS: Twenty-five implantable cardioverter defibrillators (ICD) and 45 pacemaker (PM) devices were analyzed. Death was classified as cardiac by autopsy in 17 of 70 patients. Accordingly, presumably lethal ventricular arrhythmias were documented in six patients (8.6%; 5 ICD, 1 PM). In two of 30 patients with unknown cause of death after autopsy (6.7%), interrogation revealed ventricular tachycardia as potential reason for decease (1 ICD, 1 PM). Postmortem CIED interrogation additionally allowed to make a statement regarding the day of death in 36 patients (51%; 13 ICD, 23 PM). This was in accordance with clinical data or the results of autopsy in nine patients (25%; 3 ICD, 6 PM) or could even clarify the time of death in six patients (16.7%; 4 ICD, 2 PM). CONCLUSION: Interrogation of CIED revealed potentially lethal ventricular arrhythmias in 9 of 70 patients investigated and enabled valid estimation of the day of death in 15 patients. We therefore conclude that routinely performed postmortem CIED interrogation may clarify time and cause of death.

Clinical management of clopidogrel inefficiency by point of care platelet function testing and individual adjustment of anti-platelet therapy--initial experiences.

Insufficient inhibition of ADP dependent platelet aggregation by clopidogrel is associated with an increased risk for adverse coronary events, such as stent thrombosis, after percutaneous coronary intervention. Here, we describe an approach to the clinical management of patients with insufficient inhibition of ADP dependent platelet aggregation by clopidogrel involving dose adjustment or switching of the thienoyridine. We put special emphasize on a patient who experienced recurrent acute myocardial infarction due to stent thrombosis associated with severe clopidogrel non response following elective coronary drug eluting stent implantation. In this patient, an inadequate clopidogrel effect at maintenance doses was confirmed by repeated platelet function assessment with a multiple electrode impedance point of care platelet function test. Subsequent dose adjustments still did not result in sufficient inhibition of ADP dependent platelet aggregation. Only after switching to the then shortly available new thienopyridine prasugrel could a sufficient platelet inhibition be obtained. However, our data from further patients show that although this may overcome inadequate clopidogrel efficiency in many cases, even under prasugrel suboptimal platelet inhibition may occur.