Exercise-induced Ventricular Arrhythmias Research Articles

Electrophysiological Characteristics and Ablation Outcomes in Patients With Catecholaminergic Polymorphic Ventricular Tachycardia.

Catheter ablation of premature ventricular contractions (PVCs) that trigger polymorphic ventricular tachycardia (PVT) or ventricular fibrillation has been reported as a novel therapy to reduce the syncope events in patients with catecholaminergic PVT, whereas the long-term ablation outcome and its value in improving exercise-induced ventricular arrhythmias remain unclear. Fourteen consecutive selected patients with catecholaminergic PVT (mean±SD age, 16±6 years; 43% male patients) treated with maximum β-blockers with no possibility of adding flecainide were prospectively enrolled for catheter ablation. The primary end point was syncope recurrence, and the secondary end point was the reduction of the ventricular arrhythmia score during exercise testing. Twenty-six PVT/ventricular fibrillation-triggering PVCs were identified for ablation. The trigger beats arose from the left ventricle in 50% of the cases and from both ventricles in 36% of the cases. Purkinje potentials were observed at 27% of the targets. After a mean follow-up of 49 months after ablation, 8 (57%) patients were free from syncope recurrence. Ablation of trigger beat significantly reduced the syncope frequency (mean±SD, 4.3±1.6 to 0.5±0.8 events per year; P<0.001) and improved the ventricular arrhythmia scores at the 3-month (5 [range, 3-6] to 1.5 [range, 0-5]; P=0.002) and 12-month (5 [range, 3-6] to 2 [range, 0-5]; P=0.014) follow-ups. The induction of nontriggering PVCs postablation was closely associated with syncope recurrence (hazard ratio, 6.8 [95% CI, 1.3-35.5]; P=0.026). Catheter ablation of PVT/ventricular fibrillation-triggering PVCs in patients with catecholaminergic PVT who cannot receive flecainide treatment seems to be a safe and feasible adjunctive treatment that may reduce the syncope burden and improve exercise-related ventricular arrhythmias. Induction of nontriggering PVCs after ablation is associated with a higher risk of syncope recurrence.

Cardiovascular Effects of Chronic Hormone Therapy: Study on Olympic Female Athletes

Female physiology is regulated after puberty by the menstrual cycle, whose hormonal fluctuations create a multitude of effects on several systems, including the cardiovascular one. The use of hormone therapy (HT) is quite common in female athletes and data on cardiovascular effects in this population are lacking. We sought to investigate the effects of HT in highly trained athletes to assess any difference associated with HT on cardiac remodelling, exercise capacity and clinical correlates. We studied 380 female elite athletes (mean age 25.5 ± 4.8) competing in endurance and mixed sports. 67 athletes (18%) were in chronic HT therapy. All athletes underwent baseline ECG, exercise ECG stress test, transthoracic echocardiogram, complete blood tests including lipid profile and inflammation indexes. The echocardiographic study showed a characteristic left ventricular (LV) remodelling, defined by lower LV mass index (86.2 vs. 92.5 g/m2, p<0.006), end-diastolic LV diameter (28.3 vs. 29.4 mm/m2, p<0.004) and end-diastolic LV volume (61.82 vs. 67.09 mL/m2, p<0.010) compared to controls, without changes in systolic function and diastolic relaxation/filling indexes. A lower burden of ventricular arrhythmias on exercise was observed in HT athletes (1.5% vs 8.6% in those without therapy, p=0.040). Linear regression analysis showed that HT had independent effect on LVEDDi (p=0.014), LVEDVi (p=0.030) and LVMi (p=0.020). In conclusion, chronic treatment with HT in female athletes is associated with less cardiac remodelling, including a lower LV cavity, volume and mass, with preserved systolic and diastolic function, and decreased burden of exercise-induced ventricular arrhythmias. HT, therefore, appears to be responsible for a more economic, but equally efficient, cardiac adaptation to intensive athletic conditioning.

A Novel Ryr2 Mutation in an Adult Patient with Cardiac Arrest Caused by Ventricular Arrhythmia Suspected to be Catecholaminergic Polymorphic Ventricular Tachycardia: A Case Report

Inherited arrhythmia syndromes remain an important and increasingly recognized cause of ventricular tachycar dia (VT) and sudden cardiac death. Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a rare but potentially lethal, heritable cardiac arrhythmia that occurs in response to physical or emotional stress, it often manifests as exercise-induced ventricular arrhythmias, syncope, or sudden death. If untreated, catecholaminergic polymorphic ventricular tachycardia is a highly lethal condition: About 80% of affected individuals experience recurrent syncope, and 30% experience cardiac arrest. CPVT is caused by mutations in genes encoding proteins involved in calcium handling in cardiomyocytes, such as the cardiac ryanodine receptor (RyR2). RyR2 mutations impair the regulation of calcium release from the sarcoplasmic reticulum, leading to delayed afterdepolarizations and triggered arrhythmias. Here, we report a case of CPVT in a patient with RyR2 gene mutation, causing sudden cardiac arrest.

The Fragmented QRS Complex in Lead V1: Time for an Update of the Athlete’s ECG?

Differentiating between ECG patterns related to athletes' heart remodeling and pathological findings is a challenge in sports cardiology. As the significance of fragmented complex in athletes remains uncertain, this study aimed to assess the presence of fragmented QRS in lead V1 (fQRSV1) among young athletes and its association with heart adaptations and arrhythmias. Young athletes referred for annual pre-participation screening receiving a maximal exercise testing and transthoracic echocardiography from January 2015 to March 2021 were included. The study included 684 young athletes. The prevalence of fQRSV1 was 33%. Subjects with fQRSV1 had higher exercise capacity and indexes of right ventricular function and remodeling. Among highly trained athletes, the fQRSV1 group demonstrated also increased left ventricular wall thickness. No significant association existed between fQRSV1 and exercise-induced arrhythmias, even in highly trained athletes. The high prevalence of fQRSV1 in young athletes is associated with training-induced heart adaptations but not exercise-induced ventricular arrhythmias.Graphical The fragmented QRS complex in lead V1 in young athletes. PPS = preparticipation screening; EST = exercise stress test; fQRSV1 = fragmented QRS in lead V1; PSBs = premature supraventricular beats; PVBs = premature ventricular beats.

Evolving spectrum of arrhythmogenic cardiomyopathy: Implications for Sports Cardiology.

Arrhythmogenic cardiomyopathy (ACM) is a genetic heart muscle disease, structurally characterized by progressive fibro-fatty replacement of the normal myocardium and clinically by ventricular arrhythmias (VAs). Predominantly thanks to the use of cardiac magnetic resonance, we have learnt that the spectrum of the disease encompasses not only the classical right ventricular phenotype, but also biventricular and left dominant variants.Sport activity contributes to the phenotypic expression and progression of ACM and may trigger life-threatening VAs and sudden cardiac death (SCD).We conducted a review of the literature about ACM and its implications in Sport Cardiology and summarized the main findings in this topic.Early identification of affected athletes through preparticipation screening (PPS) is fundamental but, while classical right-ventricular or biventricular phenotypes are usually suspected because of electrocardiogram (ECG) and echocardiographic abnormalities, variants with predominant left ventricular involvement are often characterized by normal ECG and unremarkable echocardiography. Usually the only manifestations of such variants are exercise-induced VAs and for this reason exercise testing may empower the diagnostic yield of the PPS.Patients with ACM are not eligible to competitive sports activity, but low-to-moderate intensity physical activity under medical supervision is possible in most cases.

PO-04-222 OUTFLOW TRACT VERSUS NON-OUTFLOW TRACT VENTRICULAR ARRHYTHMIAS IN ATHLETES: MYOCARDIAL SUBSTRATE AND LONG-TERM CLINICAL OUTCOMES

Outflow tract ventricular arrhythmias (OT-VA) are common in healthy subjects without structural heart disease (SHD), and are generally considered benign. However, athlete-specific data on the clinical meaning of different ventricular arrhythmia (VA) morphologies are scarce. To assess the prevalence of SHD as well as long-term clinical and sports medicine outcomes in a cohort of athletes with OT-VA undergoing a comprehensive diagnostic assessment, by comparing them with athletes with non-outflow tract VAs (nOT-VA). We conducted a multi-center, observational, retrospective study enrolling athletes who were referred because of complex VAs (>500 PVCs/24 h, exercise-induced VAs, nonsustained or sustained ventricular tachycardia). Athletes were categorized into two groups: OT-VA, in case of monomorphic ventricular arrhythmias of left bundle branch block and inferior axis morphology; nOT-VA, in case of polymorphic VAs or monomorphic VAs of right bundle branch block or left bundle branch block and superior/intermediate axis. The two co-primary outcomes were survival free from all-cause death or sustained VAs and sports practice at last follow-up. 175 athletes with complex ventricular arrhythmias (OT-VA,n=82; nOT-VA,n=93) were included in the present analysis; clinical characteristics are resumed in the Table. Remarkably, the prevalence of signs of SHD was higher in nOT-VA compared to OT-VA (Table). A final diagnosis of idiopathic VA was more common in OT-VA compared to nOT-VA and, accordingly, catheter ablation was more commonly performed in the former group. Over a median follow-up of 61(43-85) months, there were 2 cardiac arrests and 1 appropriate ICD shock, all occurring in athletes in the nOT-VA group with in vivo evidence of SHD and polymorphic VAs, for an overall prevalence of a primary outcome event of 0 and 3% in the OT-VA and the nOT-VA groups, respectively (p=0.25). At last follow-up, 31 athletes (18%) practiced competitive sports (OT-VA vs. nOT-VA,p=0.23), while 92 (53%) were leisure-time athletes (OT-VA vs. nOT-VA,p=0.91). Our data confirm that the prevalence of an underlying SHD substrate is lower in athletes with OT-VA than in athletes with nOT-VA, and that all major adverse cardiac events occurred in athletes with polymorphic VAs. Nevertheless, a comprehensive workup with liberal use of cardiac magnetic resonance allowed the identification of SHD in a substantial minority of athletes with OT-VA, with clear implications for sports eligibility assessment.

Reproducibility of ventricular arrhythmias at exercise testing for prediction of non-ischaemic left ventricular scar in athletes.

The non-ischaemic left ventricular scar (NILVS) is an emerging substrate of ventricular arrhythmias (VA) in the athlete. We tested the diagnostic value of VA reproducibility at repeated exercise testing (ET). We included consecutive athletes who underwent cardiac magnetic resonance (CMR) for evaluation of VA and two consecutive ET off-therapy within 12 months. Those with a positive family history of premature sudden death/cardiomyopathy, syncope/pre-syncope, ECG or echocardiography abnormalities, or low-risk VA (exercise-suppressed infundibular or fascicular VA) were excluded. The NILVS was defined as subepicardial/midmyocardial stria of late gadolinium enhancement involving >5% of the LV mass. Reproducibility was defined as the occurrence of VA with the same pattern and behaviour during repeated ET. Of 325 athletes who underwent CMR for evaluation of VA, 75 were included, and 30 showed NILVS involving three [2-4] LV segments. At first ET, athletes with NILVS showed a higher prevalence of exercise-induced VA (93% vs. 53%, P < 0.001), while other VA characteristics did not differ between groups. At repeated ET, reproducibility was observed in 97% of athletes with vs. 13% without NILVS (P < 0.001). The remaining 87% of athletes with normal CMR either did not show any VA at repeated ET (59%) or showed arrhythmias with different patterns, mostly infundibular. Reproducibility yielded a positive predictive value for NILVS of 83% and a negative predictive value of 98%. VA reproducibility at repeated ET predicted an underlying NILVS in athletes with VA and otherwise normal clinical work-up. This finding may improve risk stratification and appropriate CMR referral of athletes with apparently idiopathic VA.

Algorithm for the management of patients with ventricular arrhythmias recorded during wakefulness

Aim. To study the clinical and electrocardiographic characteristics of exerciseinduced arrhythmias and develop an algorithm for managing patients with exerciseinduced ventricular arrhythmias (VA).Material and methods. For the period from 2015 to 2019 203 patients with VA during periods of wakefulness were selected from the database of patients who performed Holter monitoring; 167 of them were selected, who underwent a treadmill test (TT) according to the standard Bruce protocol. During TT, the qualitative and quantitative characteristics of VA were assessed. Further examination and treatment were carried out according to the proposed algorithm.Results. In 80 patients (48% of all those who underwent TT), regardless of VA presence in the pretest, arrhythmias had an exercise nature and appeared and/or progressed during exercise. These patients were included in the present study to assess the causal relationship of VA with any disease. Following the algorithm, coronary artery disease was verified in 15 people, stage I-II hypertension — in 25, and minor heart defects — in 21. Of the remaining 19 patients without association of exercise-induced VA with any disease during the initial examination, 5 patients were diagnosed with arrhythmogenic cardiomyopathy/right ventricular dysplasia during prospective follow-up. In the remaining 14, VAs were considered idiopathic.Conclusion. The presented algorithm can accelerate both the search for the causes of exercise-induced VA and the choice of personalized treatment.

Prevalence of exercise-induced arrhythmias in young athletes with fragmented QRS pattern in lead V1

Abstract Funding Acknowledgements Type of funding sources: None. Background Resting 12-lead electrocardiogram (ECG) in apparently health athletes has specific pattern, typically associate to heart remodelling in response to regular exercise. (1,2) Moreover, these adaptations were correlated to typical ventricular arrhythmias, not associated with underlying cardiac abnormalities.(3) Recently, also fragmented QRS complex in lead V1 (fQRSV1), representing right ventricular (RV) activation, seems related to training-induced RV remodelling in athletes, where its prevalence is greater.(4) Purpose Evaluate presence of fQRSV1pattern at resting ECG in a population of young athletes and its relationship with training-associated structural heart adaptations and exercise-induced ventricular arrhythmias. Methods This study retrospectively enrolled subjects who consecutively undergo to annual pre-participation screening and also to transthoracic echocardiography assessment, from January 2015 to September 2020. For each participant, medical history, physical examination, resting ECG, maximal standardized exercise test and echocardiographic evaluation were collected. All ECG were reviewed by two independent physicians to evaluate fQRSV1 pattern. Results 684 young athletes (mean age 14.87±1.96 years, 36% female) were included and the overall prevalence of fQRSV1was 27%. Figure 1 shows an example of fQRSV1 pattern. Principal subject characteristics and evaluations data are shown in Table 1. fQRSV1 subjects presented a significantly wider QRS interval (p=0.004) and lower heart rate at rest (p=0.001). Exercise workload expressed in METs and exercise duration were higher in subjects with fQRSV1 (p=0.002 and p=0.023, respectively). Echocardiographic data showed that subjects with fQRSV1differ in morphological and functional right ventricular (RV) characteristics, especially had a higher indexed RV end diastolic diameter (p=0.019) and higher TAPSE (p=0.013). Patients with fQRSV1did not show an increased occurrence of supraventricular or ventricular arrhythmias, regardless of morphology, neither for isolated nor for repetitive events. Conclusion Overall prevalence of fQRSV1 pattern in young athletes is comparable with the one studied in other population of adult athletes in previous studies. Adolescent athletes with fQRSV1 present structural heart characteristic that differ from subjects without this ECG pattern, especially in RV feature. No differences in prevalence of any type of exercise-induced arrhythmias was shown, especially in common ventricular arrhythmias consistent with origin from the right ventricular outflow tract, previously described in healthy athletes.

Prevalence and clinical significance of isolated low QRS voltages in young athletes.

AimsLow QRS voltages (peak to peak <0.5 mV) in limb leads (LQRSV) on the athlete’s electrocardiogram (ECG) may reflect an underlying cardiomyopathy, mostly arrhythmogenic cardiomyopathy (ACM) or non-ischaemic left ventricular scar (NILVS). We studied the prevalence and clinical meaning of isolated LQRSV in a large cohort of competitive athletes.Methods and resultsThe index group included 2229 Italian competitive athletes [median age 18 years (16–25), 67% males, 97% Caucasian] without major ECG abnormalities at pre-participation screening. Three control groups included Black athletes (N = 1115), general population (N = 1115), and patients with ACM or NILVS (N = 58). Echocardiogram was performed in all athletes with isolated LQRSV and cardiac magnetic resonance (CMR) in those with ventricular arrhythmias or echocardiographic abnormalities. The isolated LQRSV pattern was found in 1.1% index athletes and was associated with increasing age (median age 28 vs. 18 years; P < 0.001), elite status (71% vs. 34%; P < 0.001), body surface area, and body mass index but not with sex, type of sport, and echocardiographic left ventricular mass. The prevalence of isolated LQRSV was 0.2% in Black athletes and 0.3% in young individuals from the general population. Cardiomyopathy patients had a significantly greater prevalence of isolated LQRSV (12%) than index athletes, Black athletes, and general population. Five index athletes with isolated LQSRV and exercise-induced ventricular arrhythmias underwent CMR showing biventricular ACM in 1 and idiopathic NILVS in 1.ConclusionsUnlike cardiomyopathy patients, the ECG pattern of isolated LQRSV was rarely observed in athletes. This ECG sign should prompt clinical work-up for exclusion of an underlying cardiomyopathy.

Prevalence and clinical correlates of exercise-induced ventricular arrhythmias in arrhythmogenic right ventricular cardiomyopathy.

Exercise has a deleterious effect on the phenotypic expression of arrhythmogenic right ventricular cardiomyopathy (ARVC) and increases the risk of sudden death. The aim of the study was to determine the prevalence and correlates of exercise-induced arrhythmias during exercise tolerance test (ETT) in patients with ARVC. Between 2010 and 2019, 30 (47% males, mean age 42 ± 12years) consecutive patients with a definite diagnosis of ARVC underwent a full genotypic and phenotypic characterization at our center. Exercise-induced arrhythmic response (EIAR) was defined by the development of complex or repetitive ventricular arrhythmias after stage 2 of exercise. A heart rate ≥ 85% of predicted was achieved by 23 (77%) patients. In 16 (53%) cases, a desmosomal pathogenic variant was found [most commonly PKP2 (n = 7) and DSP (n = 3)]. In 12 (40%) cases, an EIAR was observed. In 2 (6%) patients, ETT was interrupted due to the onset of ventricular tachycardia (sustained with a LBBB/inferior axis pattern in one case, and non-sustained LBBB/superior axis pattern in the other). Mean body surface area (BSA)-indexed left ventricular (LV) end-diastolic volumes (EDV) were higher in the EIAR group (92 ± 12ml/m2 vs 80 ± 7ml/m2, p = 0.002), as well as right ventricular EDV/BSA (110 ± 18ml/m2 vs 91 ± 27ml/m2, p = 0.04). Subepicardial/mid-wall LV late gadolinium enhancement (LGE) was more common in the EIAR group (67% vs 22%, p = 0.01). ARVC patients commonly exhibit exercise-induced ventricular arrhythmias. Patients with more significant RV remodeling and LV involvement (based on the presence of LV dilatation and LGE) appear more susceptible to exercise-induced arrhythmias.

Catecholaminergic polymorphic ventricular tachycardia complicated by dilated cardiomyopathy: a case report.

Background Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a severe genetic arrhythmogenic disorder characterized by adrenergically induced ventricular tachycardia manifesting as stress-induced syncope and sudden cardiac death. While CPVT is not associated with dilated cardiomyopathy (DCM) in most cases, the combination of both disease entities poses a major diagnostic and therapeutic challenge.Case summary We present the case of a young woman with CPVT. The clinical course since childhood was characterized by repetitive episodes of exercise-induced ventricular arrhythmias and a brady-tachy syndrome due to rapid paroxysmal atrial fibrillation and sinus bradycardia. Medical treatment included propranolol and flecainide until echocardiography showed a dilated left ventricle with severely depressed ejection fraction when the patient was 32 years old. Cardiac magnetic resonance imaging revealed non-specific late gadolinium enhancement. Myocardial inflammation, however, was excluded by subsequent endomyocardial biopsy. Genetic analysis confirmed a mutation in the cardiac ryanodine receptor but no pathogenetic variant associated with DCM. Guideline-directed medical therapy for HFrEF was limited due to symptomatic hypotension. Over the next months, the patient developed progressive heart failure symptoms that were finally managed by heart transplantation.Discussion Management in patients with CPVT and DCM is challenging, as Class I antiarrhythmic drugs are not recommended in structural heart disease and prophylactic internal cardioverter-defibrillator implantation without adjuvant antiarrhythmic therapy can be detrimental. Regular echocardiographic screening for DCM is recommendable in patients with CPVT. A multidisciplinary team of heart failure specialists, electrophysiologists, geneticists, and imaging specialists is needed to collaborate in the delivery of clinical care.

Yield and clinical significance of genetic screening in elite and amateur athletes.

The purpose of this study was to assess the value of genetic testing in addition to a comprehensive clinical evaluation, as part of the diagnostic work-up of elite and/or amateur Italian athletes referred for suspicion of inherited cardiac disease, following a pre-participation screening programme. Between January 2009-December 2018, of 5892 consecutive participants, 61 athletes were investigated: 30 elite and 31 amateur athletes. Elite and amateur athletes were selected, on the basis of clinical suspicion for inherited cardiac disease, from two experienced centres for a comprehensive cardiovascular evaluation. Furthermore, the elite and amateur athletes were investigated for variants at DNA level up to 138 genes suspected to bear predisposition for possible cardiac arrest or even sudden cardiac death. Of these 61 selected subjects, six (10%) had diagnosis made possible by a deeper clinical evaluation, while genetic testing allowed a definite diagnosis in eight (13%). The presence of >3 clinical markers (i.e. family history, electrocardiogram and/or echocardiographic abnormalities, exercise-induced ventricular arrhythmias) was associated with a higher probability of positive genetic diagnosis (75%), compared with the presence of two or one clinical markers (14.2%, 8.1%, respectively, p-value = 0.004). A combined clinical and genetic evaluation, based on the subtle evidence of clinical markers for inherited disease, was able to identify an inherited cardiac disease in about one-quarter of the examined athletes.

P6327Non-terminating ventricular arrhythmias during exercise testing reflect poorer prognosis and advanced disease severity in heart failure regardless of ejection fraction

Abstract Introduction Electrocardiography is an integral component of cardiopulmonary exercise testing (CPET), a standard of care in patients with heart failure (HF). We hypothetized that ventricular arrhythmias during CPET that do not meet test-termination criteria (NTVA) set forth by current guidelines may help in phenotyping disease severity and prognosis in HF with either reduced (rEF), and mid-range (mrEF)/preserved (pEF) left ventricular (LV) ejection fraction. Methods 319 patients with HF (199 HFrEF; 80 HFmrEF; 41 HFpEF) underwent CPET. Tricuspid annular plane systolic excursion (TAPSE) and pulmonary artery systolic pressure (PASP) were measured by echocardiography. B-type natriuretic peptide (BNP) at rest and peak exercise were also determined. The patients were tracked for the primary [cardiac death] and secondary composite outcome [all-cause death, heart transplantation/left ventricular assist device implantation, hospitalization for cardiac reasons]. Results 47 (15%) of the patients demonstrated NTVA during CPET, regardless of coronary artery disease prevalence. Patients without arrhythmias had a significantly higher LVEF (p&lt;0.05), TAPSE/PASP ratio (p&lt;0.001), peak oxygen consumption (p&lt;0.01), lower resting and peak BNP (p&lt;0.001) and the minute ventilation/carbon dioxide production slope (p&lt;0.001) compared to those with NTVA. 71 patients died during the tracking period, 54 for cardiac reasons. NTVA during CPX were a significant predictor of primary and secondary outcome in all patients with HF (HR: 5.3, 3.7; 95% CI: 3.1–9.1, 2.4–5.5, p&lt;0.001, respectively) as well as in subgroups categorized according to reduced, middle range and preserved LVEF (p&lt;0.001). Conclusion These results indicate that exercise-induced ventricular arrhythmias not reaching criteria for test termination are nonetheless indicative of an advanced disease severity phenotype and worse prognosis.

4252Additional value of stress testing for evaluation of ventricular arrhythmias in athletes undergoing preparticipation screening

Abstract Introduction The optimal protocol of athletes pre-participation screening is a matter of debate. The aim of this study is to test the additional value of exercise testing (ET) for evaluation of ventricular arrhythmias (VA) in athletes with otherwise normal findings. Methods The study included 10,975 competitive athletes who underwent preparticipation screening including ECG and stress testing. Athletes with ≥3 isolated premature ventricular beats or ≥1 repetitive VA underwent second-line investigations (echocardiography and 24-hour ambulatory ECG monitoring with a training session) and, in case of frequent, complex or exercise-induced VA or echocardiographic abnormalities, also cardiac magnetic resonance (CMR). Results 451 (4,1%) athletes were excluded for abnormalities at history, physical examination and baseline ECG. Among the remaining 10524 athletes, 524 (5%)showed VA at ET, 87 of whom underwent CMR.Echocardiography identified major cardiac abnormalities in 5 athletes and regional ventricular systolic dysfunction in 7, which were confirmed by CMR in 6. Other 12 patients with normal echocardiography had a positive CMR. In particular, in 16 subjects the CMR showed left ventricular late gadolinium enhancement suggesting myocardial fibrosis with a non-ischemic distribution. At multivariate analysis, VA observed at high work load at ET, the presence of complex VA at ET and the presence of a morphology other than infundibular or fascicular predicted an underlying pathological myocardial substrate while the presence of frequent (&gt;500/24-hour) premature ventricular beats did not. Predictors of underlying pathological myocardial substrate Substrate Univariate Multivariable YES (n=23) NO (n=501) OR (95% IC) P OR (95% IC) P Age 17 [13–43] 15 [14–17] 1.03 [0.98 -1.06] 0.18 – Male gender 15 (65%) 184 (37%) 3.2 [1.3–7.7] &lt;0.001 1.6 [0.7–4.8] 0.28 &gt;500 PVBs/24-hour 7 (30%) 98 (20%) 1.8 [0.7–4.5] 0.21 – VA at high work-load 10 (44%) 78 (16%) 4.2 [1.8–9.8] &lt;0.001 1.6 [1.1–4.7] 0.02 Couplets/NSVT at ET 14 (61%) 117 (23%) 6.2 [2.5–15] &lt;0.001 8.5 [2.5–29] 0.01 PVBs other than infundibular/fascicular 17 (74%) 118 (24%) 6.1 [2.4–16] &lt;0.001 3.9 [1.4–11] 0.008 Conclusions VA at ET may represent the only sign of a pathological myocardial abnormalities, such as the “isolated nonischemic left ventricular scar”, that could be the substrate for life-threatening ventricular arrhythmias. Addition of ET to baseline ECG may increase the sensitivity of PPE of competitive athletes.

P359A very unusual cause of exercise-induced ventricular arrhythmias in the athlete

P359A very unusual cause of exercise-induced ventricular arrhythmias in the athlete

Subclinical coronary artery disease in veteran athletes: is a new preparticipation methodology required?

ObjectivePreparticipation evaluation of veteran athletes should focus on accurate cardiovascular (CV) risk stratification and subclinical detection of coronary artery disease (CAD), which is the main cause of sudden cardiac death...

SEARCH OF THE STRESS INDUSED VENTRICULAR TACHICARDIA REASONS — THE METABOLIC THERAPY OPPORTUNITIES

A clinical case of a 56-year-old man is presented in which only ventricular tachycardia without clinical and ECG criteria of myocardial ischemia is recorded on the exercise test. The ventricular tachycardia was the only reason for stopping the test. This clinical case demonstrates all the difficulties in determining the genesis of ventricular arrhythmias induced by exercise. The purpose of the work was to show all the difficulties in determining the genesis of exercise-induced ventricular arrhythmia. The literature references related to the exercise-induced ventricular arrhythmia differentiation is rather poor. It is only known that if a patient develops and progresses ventricular arrhythmia, a tredmill test is considered questionable. Exerciseinduced ventricular arrhythmias especially ventricular tachycardia, are the most dangerous. Therefore, additional diagnostic methods were used to reveal the main disease as the background of ventricular tachycardia. Results of pharmacological test with nitroglycerine were the indication of the ischemic origin of ventricular tachycardia. Coronary angiography did not reveal coronary artery stenoses. Positron emission tomography revealed coronary microcirculation disturbance after which a decision about metabolic therapy with Mexicor was made. The correct choice of the drug (Mеxisor) was confirmed by the results of control studies — improvement of metabolism and antiarrhythmic effect. The article concludes that the choice of the treatment exercise-induced ventricular arrhythmia in patients with stable coronary artery disease should be individual and pathogenetic.

Predictive value of exercise testing in athletes with ventricular ectopy evaluated by cardiac magnetic resonance

Exercise-induced ventricular arrhythmias (EIVA) in young athletes raise the suspicion of an underlying heart disease at risk of sudden death. We aimed to assess the prevalence and determinants of abnormal cardiac magnetic resonance (CMR) findings in athletes referred for EIVA vs non-EIVA with negative or inconclusive echocardiography. We performed CMR in a consecutive series of athletes aged 15-50 years referred for frequent (>500 per day) or repetitive premature ventricular beats. Clinical and CMR findings were compared between athletes with EIVA and those with non-EIVA, and predictors of abnormal CMR were assessed. We included 36 athletes with EIVA (median age 25 years; 27 (75%) males) and 24 with non-EIVA (median age 17 years; 18 (75%) males). CMR revealed cardiac abnormalities in 20 athletes with EIVA (56%) and in 5 with non-EIVA (21%) (P = .004). In particular, left ventricular late gadolinium enhancement was identified in 17 athletes with EIVA (47%) and in 3 with non-EIVA (13%) (P = .006), mostly with a nonischemic pattern. Predictors of abnormal CMR were T-wave inversion on electrocardiography (ECG) (odds ratio [OR] 5.2; 95% confidence interval [CI] 1.0-27.1; P = .05), complex ventricular arrhythmias on 24-hour ambulatory ECG monitoring (OR 4.5; 95% CI 1.1-18.7; P = .04), and complex EIVA with a right bundle branch block or polymorphic morphology on exercise testing (OR 5.3; 95% CI 1.4-19.4; P = .01). Pathological myocardial substrates on CMR were observed significantly more often in athletes with EIVA than in those with non-EIVA. Repolarization abnormalities on baseline ECG and complex EIVA with a right bundle branch block or polymorphic morphology identified the subgroup of athletes with the highest probability of CMR abnormalities.

Divergent effects of adrenaline in human induced pluripotent stem cell-derived cardiomyocytes obtained from hypertrophic cardiomyopathy

ABSTRACTHypertrophic cardiomyopathy (HCM) is a common inherited cardiac disease that affects the heart muscle with diverse clinical outcomes. HCM can cause sudden cardiac death (SCD) during or immediately after mild to rigorous physical activity in young patients. However, the mechanism causing SCD as a result of exercise remains unknown, but exercise-induced ventricular arrhythmias are thought to be responsible for this fatal consequence. To understand the disease mechanism behind HCM in a better way, we generated patient-specific induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) from HCM patients carrying either the MYBPC3-Gln1061X or TPM1-Asp175Asn mutation. We extensively investigated the effects of low to high concentrations of adrenaline on action potential characteristics, and the occurrence of arrhythmias in the presence of various concentrations of adrenaline and in wash-out condition. We classified and quantified different types of arrhythmias observed in hiPSC-CMs, and found that the occurrence of arrhythmias was dependent on concentrations of adrenaline and positions of mutations in genes causing HCM. In addition, we observed ventricular tachycardia types of arrhythmias in hiPSC-CMs carrying the TPM1-Asp175Asn mutation. We additionally examined the antiarrhythmic potency of bisoprolol in HCM-specific hiPSC-CMs. However, bisoprolol could not reduce the occurrence of arrhythmias during administration or during the wash-out condition of adrenaline in HCM-specific hiPSC-CMs. Our study demonstrates hiPSC-CMs as a promising tool for studying HCM. The experimental design used in this study could be suitable and beneficial for studying other components and drugs related to cardiac disease in general.