Unusual cause of exercise-induced ventricular fibrillation in a well-trained adult endurance athlete: a case report

<p>Abstract</p> <p>Introduction</p> <p>The diseases responsible for sudden deaths in athletes differ considerably with regard to age. In young athletes, congenital malformations of the heart and/or vascular system cause the majority of deaths and can only be detected noninvasively by complex diagnostics. In contrast, in older athletes who die suddenly, atherosclerotic disease of the coronary arteries is mostly found. Reports of congenital coronary anomalies as a cause of sudden death in older athletes are rare.</p> <p>Case presentation</p> <p>A 48-year-old man who was a well-trained, long-distance runner collapsed at the finish of a half marathon because of a myocardial infarction with ventricular fibrillation. Coronary angiography showed an anomalous origin of the right coronary artery from the left sinus of Valsalva with minimal wall alterations. Multislice computed tomography of the coronary arteries confirmed these findings. Cardiomagnetic resonance imaging demonstrated a mild hypokinesia of the basal right- and left-ventricular posterior wall. An electrophysiological study showed an inducible temporary polymorphic ventricular tachycardia and an inducible ventricular fibrillation. The athlete was subsequently treated by acetylsalicylic acid 100 mg (0-1-0), bisoprolol 2.5 mg (1-0-0) and atorvastatin 10 mg (0-0-1) and was instructed to keep his training intensity under the 'individual anaerobic threshold'. Intense and long-lasting exercise under extreme environmental conditions, particularly heat, should also be avoided.</p> <p>Conclusion</p> <p>This case report presents a coronary anomaly as the most likely reason for an exercise-induced myocardial infarction with ventricular fibrillation in a well-trained 48-year-old endurance athlete. Therefore, coronary anomalies have also to be considered as a possible cause of cardiac problems in older athletes.</p

Effect of physical exercise on pain thresholds and plasma beta-endorphins in patients with silent and symptomatic myocardial ischaemia

In a double-blind study, eight patients with symptomatic myocardial ischaemia and nine with asymptomatic myocardial ischaemia were compared during physical exercise under naloxone (6 mg i.v.) or placebo. Plasma beta-endorphin, cortisol and catecholamines were measured before exercise, during maximal exercise, and 10, 20 and 60 min after exercise. A tourniquet pain test (on the forearm, under control of transcutaneous PO2), and an electrical pain test (intracutaneous electrode placed in the finger with the electrical stimulus under computer control and two-interval forced-choice psychophysical technique) were performed before exercise as well as immediately after, and 60 min after exercise. Plasma beta-endorphin levels increased significantly (P < 0.01) during exercise in symptomatic and asymptomatic patient groups; every patient showed an increase on betaendorphins during and after exercise. However, the increase found in beta-endorphins during and after exercise was significantly larger (P < 0.01) in asymptomatic than in symptomatic patients. After naloxone, this difference was no longer evident. Angina pectoris during exercise was reported with less latency in symptomatic patients (P < 0.05) and occurred in two of nine asymptomatic patients following naloxone. The time course of plasma cortisol levels exhibited the same pattern as beta-endorphins with the same significant differences between symptomatic and asymptomatic groups. Electrical pain thresholds, though on average higher in asymptomatic patients (2.21 mA vs. 0.79 mA), were not affected by exercise or naloxone. Asymptomatic patients required more time to reach pain thresholds in the tourniquet pain test (P < 0.02). After exercise, tourniquet pain thresholds were significantly lower (P < 0.01) under naloxone compared with placebo. The results suggest that there arequantitative differences in the endorphinergic regulation of pain in patients with symptomaticand asymptomatic myocardial ischaemia

Reduced pain during baroreceptor stimulation in patients with symptomatic and silent myocardial ischaemia

Objective: Baroreceptor activation has been shown to reduce pain, and the accumulation of such pain reduction has been implicated in the operant learning (under certain circumstances) of hypertension. The current study is an examination of differences in the pain dampening effects of baroreceptor activity in patients with symptomatic and asymptomatic myocardial ischaemia. The objective was to determine whether there are differences between patients with symptomatic and silent myocardial ischaemia with respect to their antinociceptive response to baroreceptor stimulation, and, if so, whether these differences could be related to the absence of angina pectoris pain in patients with silent myocardial ischaemia. Methods: Sensory detection and electrical pain thresholds were compared in nine symptomatic and 10 asymptomatic patients with replicable myocardial ischaemia during PRES (phase related external suction) carotid baroreceptor manipulation in which the pressure inside a neck cuff was phase locked in time to the R wave of the ECG and negative pressure was applied during either systole or diastole. Tourniquet pain thresholds were also determined. Results: It was found that (1) external baroreceptor manipulation had no effect on detection thresholds; (2) painful stimuli were judged by both symptomatic and asymptomatic patients as less intense when delivered during maximum baroreceptor activity, (3) symptomatic and asymptomatic patients did not differ in their sensory detection thresholds; and (4) asymptomatic patients had significantly higher ischaemic (tourniquet) pain thresholds than symptomatic patients. Conclusions: The results indicate that baroreceptor activity can modify the intensity of painful stimuli. The degree to which baroreceptor manipulation affects pain does not appear to differ between patients with painful and silent myocardial ischaemia. Thus the baroreceptor dependent pain inhibition effects seems not to be responsible for the higher ischaemic pain threshold found in the silent myocardial ischaemia group

EFFECT OF BREATHING RATE ON OXYGEN SATURATION AND EXERCISE PERFORMANCE IN CHRONIC HEART FAILURE

none4L. BERNARDI; BELLWON J.; ROSKAMM H; FREY A.W.Bernardi, Luciano; Bellwon, J.; Roskamm, H; Frey, A. W