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Sporcu Kalbi
- 1. Atlet Kalbi Görüntülemesi ve EKG Bulguları Dr. Selcen Yakar Tülüce İKÇÜ Atatürk Eğitim ve Araştırma Hastanesi Kardiyoloji Bölümü
- 3. 35 y, E sporcu, FHLP (+)artık daha kısa mesafede yoruluyor L.V.
- 4. 22 y, E, spor yapabilir mi diye değerlendirme isteniyor
- 5. 19 y, profesyonel yüzücü, EKG değişikliği nedeniyle refere
- 6. Hangi bulgu gri bölgede?
- 7. 17 y, K sporcu, EKG anormalliği nedenli yönlendirilmiş
- 9. 29y, profesyonel futbolcu, şikayeti yok 14 yaşında, lise basketbol takımında
- 11. Hangi sporcularda görüntüleme gerekli? Anamnez: Ailede AKÖ, KMP öyküsü Çarpıntı Senkop Göğüs ağrısı Fizik muayene: Kardiyak üfürüm Anormal ek ses Marfanoid görünüm 12 derivasyonlu EKG: T dalga negatifliği ST segment depresyonu Patolojik q Komplet LBBB Bifasiküler blok Nonspesifik İVİD LVH,RVH lehine minör nonvoltaj Anormal efor testi
- 12. Egzersize kardiyak adaptasyon Kardiyak output ↑ PVR↑↑↑ Basınç yüklenmesi Kardiyak output ↑↑ PVR↓ Volüm yüklenmesi↑
- 13. Atlet kalbi Spor yapmayan bireylerden farklı değil Duvar kalınlıkları <13 mm, LV kavitesi genişlememiş Duvar kalınlıkları <13 mm, LV kavitesi hafif genişlemiş Duvar kalınlıkları LV kavitesi orantılı olarak artmış European Heart Journal 2017
- 14. Sporcu kalbinde ekokardiyografik bulgular
- 15. Atlet kalbi • Elit atletlerin %45’inde LV dilatasyonu vardır • %14’ünde LVEDD >60mm’dir • %40’ında RV dilatasyonu vardır • LV ve RV dilatasyonu simetriktir • Dilatasyonun miktarı atletin fitness düzeyi ( VO2max) ile orantılıdır • LV EF normal veya hafif düşük olabilir (Daha yüksek LV EDV istirahat esnasında gerekli atım hacminin sağlanması için daha az kontraktilite gerektirir) • Egzersiz ekokardiyografi ile LVEF’nin normalize olduğu görülür
- 16. Sporun tipi ve LV yeniden şekillenmesi
- 17. Fransa Bisiklet Turu Atletlerinin %11’inde LVEF≤ % 52 23 yaşında sedanter birey 23 yaşında olimpik atlet (bisikletçi)
- 18. Atletlerde diastolik fonksiyonlar normal/supra normaldir • E/A >2 • Increased e’ • Decreased E/e’
- 19. Atletlerde atriyal remodelling-LA genişlemesi • %18 atlette hafif LA dilatasyonu (>40mm),%2 olguda belirgin LA dilatasyonu (>45mm) vardır • LA genişlese de , atrial disfonksiyon yoktur • Atriyal rezervuar ve kondüit fonksiyonları normal, atrial kontraktil fonksiyonları düşüktür. Bu düşüklük supernormal LV diastolik fonksiyonlara ve LV dolumunun erken diastole kaymasına bağlıdır • AF sıklığı bu nedenle X5 kat artmıştır ve çoğunlukla artan vagal tonusa bağlıdır
- 20. Hipertrofik kardiyomiyopati mi? Sporcu kalbi mi? • Beyaz atletlerin %2’sinde, siyah atletlerin %12’sinde 13-15mm düzeyinde ciddi LVH mevcut • Ayırıcı tanıda tek başına en iyi parametre: LV-diyastol sonu çapı LVED-çap> 54 mm RWT 0.3-0.45 Caselli S, Am J Cardiol 2014
- 22. Anormal LV kavite geometrisi ve/veya segmental LV hipertrofisi Apikal anevrizma ile birlikte midventriküler hipertrofiAsimetrik septal hipertrofi Apikal HKM Konsantrik HKM
- 23. HKM mi? Sporcu Kalbi mi? Caselli S. J Am Soc Echocardiogr 2015 Pelliccia A. European Heart Journal 2017
- 24. HKM mi? Sporcu Kalbi mi? LA paradoksu
- 25. Kardiyak MR
- 26. Ayırt etmek önemli çünkü…. Reggie Lewis, antreman sırasında arrest otopsi ile HKM nedenli ex olduğu anlaşıldı Mark Vivien Foe, 28 y, 2003 FİFA Kamerun-Kolombia maçının 72. dakikasında ani kollaps Otopsi ile HKM Hank Gather,23y, Maç esnasında arrest Otopsi HKM ile uyumlu
- 27. Egzersize bağlı yeniden şekillenme mi? LVNC mi? Journal of Biomechanical Engineering, 2017
- 28. • >1000 atlet Chin ve Jenni kriterine göre % 8.1’inde LVNC, 415 sedanterde % 7.0¹ • >2500 olimpik atlet % 1.4 LVNC kriteri (+) ancak semptom, aile öyküsü, LV sistolik ve diast fonk.ları, aritmiler ve CMR bulguları % 0.1’i LVNC tanısı almış² • Hamilelikte artan trabekülasyon • 4 profesyonel basketbolcu Egzersize bağlı yeniden şekillenme mi? LVNC mi? ¹Gati S, Heart. 2013 ² Caselli S, Int J Cardiol. 2016
- 29. 28y, K, amatör sporcu sporcu EKG:LBBB LVEF:%48 SolV sistolik fonksiyonda bozukluk, Apikal ve lateral duvarda trabekülasyon artışı Non-kompakte alan > 2.5 Kompakte alan
- 30. Atlette aşırı trabekulasyon varsa… • KY semptomları? • Senkop, çarpıntı, nörolojik/nöromusküler semptomlar, tromboembolik olay? • Ailede kardiyomiyopati/AKÖ öyküsü • Sol dal bloğu gibi ileti sistemi hastalığı, patolojik T dalga negatifliği gibi repolarizasyon anormalliği • Egzersiz testinde veya Holter EKG de ventriküler aritmi • Kardiyopulmoner testte düşük zirve oksijen tüketimi • Orta düzeyde egzersizle (HKH nın %70) LVEF’yi %20 den az arttırabilme • Orta veya ciddi LV sistolik disfonksiyon, diyastolik disfonksiyon, BDHK • Kardiyak MR’da LGE tutulumu • Sistolde kompakte alan < 8 mm
- 31. Sporcu kalbi mi? ARVD mi? • Yoğun ve uzun süreli egzersiz hem RV kavitesini genişletir, hem de RV kitlesini arttırır • EKO’da ARVD kriterlerinde atletler yok
- 32. • Olimpik atletlerin %16’sı majör kriterin üzerinde , %41’i minör kriterin üzerinde RVOT/BSA oranına sahip¹ • RV diskinezi, hipokinezi! • CMR Erkek ≥110mL/m² Kadın ≥100mL/m² , RVEDV/LVEDV >1.2 • EKO’da AP4 RV inflow çapı/LV end-diastolik çap (PLAX) >0.9 Sporcu kalbi mi? ARVD mi? ¹D’Ascenzi F, J Am Coll Cardiol Img 2017;10:385–93.
- 33. ARVD
- 34. Antonio Puerta, İspanyol futbolcu, Cennetin en pahalı futbol transferi! 2007 bu görüntü sonrası soyunma odasından entübe çıktı, ARVD’ye bağlı VT nedenli 22 yaşında ex oldu
- 36. Dilate Kardiyomiyopati mi? Sporcu Kalbi mi? • Sıklığı az • Elit atletlerin %15’inde LVEDD> 60 mm • Bir süre dekondüsyon sonrası (ne kadar süre??) LVEDD > 60 mm LVEF ↓ (özellikle < %45) • Kardiyak MR • Stress EKO • Stress kardiyak MR: egzersiz ile LVEF’de >% 11 artış Dilate KMP lehine DKM aleyhine
- 38. Kardiyak MR’da fibrosis • Atletlerde özellikle RV insersiyon noltalarında minör miyokardial fibrozis görülebilmekte (%40-45 in athlete karşı kontrollerin %10’unda) • Major fibrozis veteran atletlerin %11’inde saptanmıştır • Ağır egzersiz sonrası oluşan tekrarlayan kardiyak hasara bağlanmıştır • Bu atletlerde AKÖ riski artmış olabilir Elit maraton koşucusu
- 40. Teşekkürler
Editor's Notes
- Electrocardiogramof a 29-year-old male asymptomatic soccer player showing sinus bradycardia (44 bpm), early repolarization in I, II, aVF, v5–V6 (arrows), voltage criterion for left ventricular hypertrophy (S-V1þR-V5> 35mm), and tall, peaked T waves (circles). These are common, training related findings in athletes and do not requiremore evaluation. Figure
- the European Society of Cardiology, , and the International Olympic Committee (“Lausanne Recommendations”) recommend the 12-lead ECG screening as a part of pre-participation screening of competitive athletes , whereas within the US cardiology and sport medicine community there is no consensus , and the routine use of 12-lead ECG screening in both competitive and leisure athletes remains controversial. Although there is general agreement that ECG screening improves the sensitivity for detecting unsuspected cardiac disease amongasymptomatic athletes, arguments against universal ECG screening include the low prevalence of disease in a very large population with an expected high false-positive rate,financial sustainability, the potentially difficult interpretation that requires specific expertise, the logistical challenges and costs related to second-tier confirmatory screening with imaging, and/or other testing should primary evaluations raise the suspicion of cardiac disease
- Usually, in professional athletes, training schedules involve >10–15 h/week of intensive exercise conditioning. In detail, isotonic (dynamic) exercise is associated with a substantial increase in cardiac output and reduction in peripheral vascular resistance; therefore, endurance training mainly results in volume overload; conversely, isometric (static) exercise is characterized by less increase in cardiac output and by a transient increase in peripheral resistances; therefore, it training is characterized by a pressure overload. Most sports disciplines are characterized by a varying degree of both isometric and isotonic components, and therefore the original dichotomic classification in strength (isometric) or endurance (isotonic) disciplines is not applicable for most athletes. Therefore, we suggest a simple classification of sports in four majör groups based on the main physiologic characteristics of the exercise training: endurance, power, skill, and mixed
- HCM is believed to be the most usual cause of death in young athletes, responsible for about one-third of sports related SCD in this population [51]. Patients with HCM are discouraged from participating in competitive sports, as the risk of ventricular arrhythmias and SCD may increase during exercise [52]. However, exercise may not necessarily be harmful for HCM patients, and has been found to be associated with potential beneficial effects [1, 53]. Accordingly, previous reports have indicated adverse clinical outcome in overweight HCM patients, highlighting the importance of avoiding the adverse effects of a sedentary
- Twenty-two years-old male competitive endurance athlete (swimmer). Panel A: Apical 4-chamber and (Panel B) parasternal short-axis views, showing left ventricular (LV) hypertrophy, with symmetric increase of both wall thickness and LV internal cavity diameters. Panel C: Standard Doppler transmitral inflow pattern, showing a ‘supranormal’ early-diastolic function, with increased E velocity and E/A ratio. Panel D: Pulsed Tissue Doppler pattern of LV lateral wallmyocardial function, i.e. increased e’ velocity.A total of 1,145 Olympic athletes (61% men), and 154 controls, free of cardiovascular disease, underwent two-dimensional echocardiography, Doppler echocardiography, and Doppler tissue imaging. E/A ratios in athletes and controls. Histogram shows the distribution of transmitral PW Doppler–derived E/A ratio in E/A ratios in athletes and controls. Histogram shows the distribution of transmitral PW Doppler–derived E/A ratio inE/A ratios in athletes and controls. All subjects in the study population had E/A ratios > 1.0, and the upper limit was 2.6 in controls and 4.8 in athletes. Septal DTI e0 velocity. The graph shows the relation between maximal LV wall thickness (represented as a categorical variable) and DTI-derived septal e0 velocity in athletes; circles represent single values and dotted line represents the reference value of 8 cm/sec. As demonstrated by the regression analysis, increase in maximal LV wall thickness showed only a modest association with a decrease in septal e0 velocity (R = 0.356, R2 = 0.127, P < .001). All athletes showed e0 values $ 8 cm/sec. Athletes with substantial LV hypertrophy ($13 mm) showed mild reductions in septal e0 velocity (12.5 6 1.9 vs 13.96 2.2 cm/sec, P = .001) compared with the remaining athletes. The two athletes with LV wall thicknesses of 14 and 15 mm had e0 velocities of 11.3 and 8.2 cm/sec, respectively.
- LGE images in 4-chamber (A,C,E) and 2-chamber views (B,D,F) of athletes with HCM. Concentric HCM with no LGE (A,B), asymmetric form with pronounced midmyocardial patchy LGE (C,D) and apical HCM with mild LGE in the hypertrophic segments (D-F). In this setting, LGE imaging provides robust diagnostic and prognostic information, though present in only about 50% of HCM patients, so that the absence of LGE does not exclude HCM. On the other hand, non-specific small clustered patches of LGE are frequently encountered in the hearts of otherwise healthy athletes, especially after long-standing endurance training [7]. Of note, the presence of balanced remodeling (specifically assessed based on sexspecific reference values of RV/LV end-diastolic volume ratio and LV end-diastolic volume/mass ratio [59]), and a LV diastolic wall-to-volume ratio < 0.15 mm × m2 × ml(− 1) have been shown to accurately confirm physiologic rather than pathologic LVH [
- Human hearts were obtained postmortem within 24 h of death from six male organ donors who died suddenly. LVNC için:The first echocardiographic criteria were proposed by Chin et al. are also known as the California criteria . These were based on a case series of eight, predominantly paediatric patients and generated a Chin X/Y ratio, measuring the epicardial distance to the trabeculation trough against the epicardial distance to the trabeculation peak in a long-axis, diastolic view, though many have subsequently applied this method to short-axis images. Jenni et al. proposed the second set of criteria [18], also known as the Zurich or Swiss criteria. The investigators highlighted that measurement was often difficult in diastole and the boundary between myocardial layers more easily distinguished in systole. These were derived from 34 adult patients, collected over a 13-year period with 7 having histopathological examination providing anatomical correlation. Moreover, rather than comparing “LVNC cases” with healthy controls, patients harbouring other disease pathologies associated with prominent trabeculations (dilated cardiomyopathy and hypertensive LV hypertrophy) were used for comparison. A maximal, end-systolic,short-axis trabeculated layer thickness at least twice that of the adjacent compacted layer was felt to discriminate LVNC from other pathologies. In addition to this 2:1 ratio, it was emphasised that additional conditions must be met for the diagnosis of “isolated LVNC”, including the absence of any coexisting cardiac anomaly, and that colour Doppler imaging must demonstrate that blood from the ventricular cavity perfuses the intertrabecular recesses directly. Stollberger et al. proposed a third set of criteria, also known as the Vienna criteria . Acknowledging that end-systolic, short-axis images employed in the Jenni criteria are vulnerable to erroneous inclusion of papillary muscles, aberrant bands and false tendons in the trabecular layer, the investigators favoured long-axis, end-diastolic images for measurement. Stollberger et al. also undertook a different approach, instead of drawing upon collected “LVNC cases” to define what is “abnormal”, they began by utilising autopsy data to define the extent of normal trabeculation in human hearts. Of 474 hearts studied previously, 68% showed prominent trabeculation but only in 4% could more than three trabeculae be counted apically to the papillary muscles, with no heart possessing more than five trabeculae. The Stollberger criteria moved away from “isolated LVNC” to favour “LV hypertrabeculation (LVHT)”, aiming to include cases with additional cardiac anomalies and stipulated that (1)> 3 trabeculations protruding from the LV wall, apically to the papillary muscles, visible in one imaging plane and (2) perfusion of intertrabecular spaces from the ventricular cavity visualised on colour Doppler were required for the diagnosis. The investigators originally resisted the inclusion of a trabeculated to compacted layer ratio, taking the view that any ratio could be compatible with the diagnosis of LVNC ; however, they later incorporated the end-systolic 2:1 ratio from the Jenni criteria. Despite amalgamation of echocardiographic criteria, expert observers, with 20–29 years’ experience in assessing LVHT, found low interobserver agreement with disagreement in 35% of cases, which even after mutual review remained unresolved in 11%. CMR has seen a similar proliferation in LVNC criteria. Petersen et al. proposed the first, which remains one of the most frequently used in clinical practice due to the ease of measurement without the need for additional analysing software. Similar to the Jenni criteria, the investigators compared 7 “LVNC cases” with a variety of conditions associated with prominent trabeculations, including athletes, hypertrophic cardiomyopathy, dilated cardiomyopathy, hypertensive heart disease and aortic stenosis patients in addition to healthy controls. They concluded that a trabeculated to compacted layer ratio of 9 2.3, measured in an end-diastolic long axis view but excluding the apex (segment 17), provided the best sensitivity and specificity for identifying the “LVNC cases” [26]. They were also aware of the potential for over-diagnosis if applying this threshold to a population with a low pre-test probability of cardiomyopathy, suggesting that the findings were only useful in the context of clinical suspicion such as heart failure, arrhythmia, systemic thromboembolism, family history of LVNC, associated muscular disorders or regional wall motion abnormalities.
- A case series of four professional basketball players with excessive LV trabeculation were evaluated with echocardiography at the beginning of the training season, during training and after a period of detraining. These athletes developed increased trabeculation, which was reportedly most pronounced in the peak-training period and associated with athletic ECG repolarization changes . The series was limited by the small size and lack of trabeculation quantification, though highlights the risk of LVNC overdiagnosis in a low risk population with a likely alternative mechanism for excessive trabeculation than cardiomyopathy
- Ancak ilk defa 2002 Sydney Olimpiyat Oyunlarında, Olimpik spor olarak kabul edilen Triatlon’ un Olimpiyatlarda kabul gördüğü şekli yüzme, bisiklet ve koşu disiplinlerinden oluşmaktadır.
- DCM is characterized by increased LVEDD, LV, and possibly RV volumes, in addition to an impaired overall systolic function. DCM is relatively rare in competitive athletes as compared with other cardiomyopathies due to the fact that systolic function impairment preventing adequate cardiac output during exercise is not generally compatible with professional sports practice. A structural overlap between early-stage DCM and endurance AH phenotype according to the Morganroth hypothesis does exist. In this regard, it was reported that more than 10% of elite cyclists competing in the Tour de France fulfilled the diagnostic criteria for DCM. However, as morpho-functional adaptations typical of the AH have been described to persist over the long term, a brief period of detraining may not be sufficient to achieve a clear differential diagnosis. Preliminary data showed that native T1, ECV, and T2 relaxation times were significantly higher in DCM patients as compared with healthy subjects and athletes, with native T1 and ECV providing better discrimination between DCM patients and athletes. Of note, low-normal native T1 values have been also associated with increased VO2max. However, CMR during the resting condition sometimes cannot be sufficient in case of LV dilation associated with mildly reduced LVEF and absence of LGE. This scenario may require downstream evaluation by stress imaging,nor repeated assessment after detraining. Stress echocardiography and CMR are often effective in identifying abnormalities of both systolic and diastolic function that become more apparent on exercise, and to detect abnormal tissue characterization, i.e., replacement scar, increased extracellular volume. Furthermore, it has been shown that real-time CMR imaging performed during exercise can be used to quantify cardiac function—including biventricular and biatrial function—with very high accuracy and reproducibility [58]. Exercise CMR appears promising for becoming the gold standard for ventricular volume quantification during high-intensity exercise in order to investigate differences in contractile reserve between normal and early diseased myocardium
- Phidippides was a Greek messenger who experienced sudden death after running more than 175 miles intwo days. Cardiac magnetic resonance imaging with late gadolinium enhancement demonstrating a small patch of scar in the interventricular septum consistent with a focus of cardiac fibrosis.