1st degree av block12/11/2023 ![]() 5 Increased vagal tone and enlarged cardiac chambers help accommodate the increased demand in cardiac output. Individuals who regularly engage in at least 4 h of physical activity per week undergo structural, functional, and electrical adaptations in the heart collectively known as the athlete’s heart. Based on this comprehensive evaluation, no medical treatment was necessary so far. Since his evaluation, he has not had any recurrence of his symptoms and is training normally. This tallied with the acute increase in training volume in preparation for the competition at the time. His initial symptoms were attributed to vasovagal syncope in the context of overtraining. He was reassured and was advised to undergo biannual surveillance with echocardiography and ambulatory ECG monitoring. Atrioventricular block improved with rapid atrial pacing and after administering isoprenaline infusion, effectively ruling out infranodal block. No His signal was recorded when in AVB, confirming the presence of intranodal physiological AVB ( Figure 4). This improved to 320 ms (188 b.p.m.) following the administration of isoprenaline. Atrioventricular Wenckebach was achieved by pacing the atrium at 740 ms (81 b.p.m.). Baseline sinus node recovery time was measured at 231 ms, baseline AH interval at 307 ms and an HV interval measured at 38 ms. He was referred for an EPS for better risk stratification and phenotypic characterization, a pre-requisite prior to giving full clearance for competitive sports. The presence of symptoms increased the suspicion of conduction disease in the context of early dilated cardiomyopathy. In the absence of a definite clinical phenotype, the team opted against referral.Īll these secondary investigations failed to confirm the presence of a definite cardiac phenotype. The pros and cons of genetic testing were also discussed. Family screening of both his parents and his two siblings was negative. No macroscopic fibrosis was present on late enhancement sequences. This revealed a low–normal LV and RV ejection fraction (LVEF 52%, RVEF 51%), with normal chamber dimensions. Cardiac magnetic resonance (CMR) imaging was also performed because of possible arrhythmic symptoms in the context of conduction abnormalities and ventricular function towards the lower limits of normal. There was no objective evidence of cardiac or ventilatory limitation to exercise (heart rate recovery at 1 min was 28 b.p.m., O2/Pulse 17.1 mL/beat which was 104% of predicted). ![]() Atrioventricular conduction was also normal throughout the test, with PQ prolongation again seen in recovery. There was a normal blood pressure response. Ventilatory efficiency was normal (VE/VCO2 28.4). Holter monitoring showing 2:1 atrioventricular block.Ĭardiopulmonary exercise testing (CPET) was normal with a VO 2MAX of 42.5 mL/kg/min (93% of predicted). He did not report any symptoms during ambulatory ECG monitoring. Nocturnal episodes of 2:1 AVB in the context of Wenckebach were also recorded ( Figure 3). Diastolic parameters 24-h ambulatory ECG monitoring revealed prolonged periods of sinus bradycardia, 1st-degree AVB and intermittent 2nd-degree Mobitz I (Wenckebach) AVB ( Figure 2). Diastolic parameters were normal with the left atrium mildly dilated. The systolic function of both ventricles was also towards the lower limits of normal, with an LV and RV ejection fraction of 53% and 52%, respectively. The LV and right ventricular (RV) volumes were at the upper limits of normal. A transthoracic echocardiogram was consistent with an athletic heart. QRS duration and axis were normal, with no evidence of QRS fragmentation. The QRS satisfied voltage criteria for left ventricular (LV) hypertrophy. The presence of symptoms in the context AVB prompted referral.Ī 12-lead ECG revealed sinus bradycardia with profound 1st-degree AVB ( Figure 1). The patient was eventually referred to the Sports Cardiology Clinic months later after having discussed this with his family doctor during his routine yearly screening appointment. There was no family history of sudden cardiac death. He was never symptomatic before that point. Physical examination was largely unremarkable, with sinus bradycardia (50 b.p.m.), normal blood pressure, and no added heart sounds. He was referred to hospital and all investigations including blood tests, telemetry, and a computerized tomography pulmonary angiogram were normal. He was fully oriented and recovered spontaneously a few minutes later. It was preceded with lightheadedness and nausea, lasting ∼30 s. This had occurred soon after the patient came out of the pool at the end of the race. A 19-year-old male Caucasian competitive waterpolo player, engaging in 20 h of moderate- to high-intensity physical activity on a weekly basis was referred for cardiovascular assessment follow an isolated episode of syncope 1 year previously during competition.
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