Περίπτωση συγκοπής κατά τη διάρκεια άσκησης. Ποια είναι η ενδεδειγμένη προσέγγιση;
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1 Περίπτωση συγκοπής κατά τη διάρκεια άσκησης. Ποια είναι η ενδεδειγμένη προσέγγιση; Dr H. Θ. Ζάρβαλης Καρδιολόγος Διευθυντής ΕΣΥ Καρδιολογική Κλινική Γ. Ν. Παπαγεωργίου Θεσσαλονίκη
2 ELPIDOFOROS S. SOTERIADES et al. N Engl J Med 2002
3 ELPIDOFOROS S. SOTERIADES et al. N Engl J Med 2002
4 Janneke Berecki-Gisolf,et al. PLoS One. 2013; 8(9): e75255
5 exertional syncope appears to have a higher association with cardiovascular disease, including, but not limited to hypertrophic cardiomyopathy, long QT syndrome, CPVT coronary anomalies, and arrythmogenic right ventricular cardiomyopathy
6 case report A 31-year-old male runner presented to our ED for syncope during a 5-km running race The patient reported that he was running at a fast pace without any complaint during the first 3 km, while afterwards he experienced dizziness, blurred vision, fatigue and then lost consiousness The athlete recovered gradually in the supine position, and he was able to stand up and walk unaided He had been training systematically for this running race the last 5 months, while he exercised recreationally and only occasionally before this period. His training regimen consisted of 2-h aerobic training 3 days per week He reported no previous episodes of syncope, and he had no family history of cardiac disease or unexplained sudden death.
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9 Exercise associated collapse (EAC) Exercise associated collapse (EAC) is a common term utilized in the sports medicine community and occurs when an athlete is unable to stand or walk as a result of lightheadedness, faintness, dizziness, or syncope. EAC usually occurs immediately after completing a race or stopping exercise and is commonly observed at endurance events. Victims of EAC are often able to assist in their own recovery while affected, as opposed to the abrupt and complete loss of consciousness that may be seen in an ERS event secondary to a pathologic arrhythmia ERS victim from an arrhythmic event may have a rapid spontaneous recovery, the EAC victim may have persistent symptoms for longer periods of time, often exceeding 1 hour
10 Exercise associated collapse (EAC) The mechanism for collapse is the abrupt decrease in venous return due to the relaxation of the muscular pump when activity is stopped. Given the typical degree of vasodilatation seen in prolonged exertion, this sudden loss in the pressure exerted by the skeletal muscles on blood volumes and venous return often results in the loss of postural tone, leading to collapse there is a possibility that a modifiable noncardiac condition during exercise, such as hyperthermia, hypoglycemia or hyponatremia, may have caused discomfort, prompting the cessation of exercise, with syncope eventually occurring immediately after the sudden termination of exercise There can be considerable crossover between EAC and ERS
11 History the history surrounding a syncopal episode is of paramount importance provide a general direction to the clinical evaluation and possibly also yield a final diagnosis in the athlete precipitating events, presence or absence of a prodrome such as chest pain or palpitations, post-recovery phenomenon (post-ictal state, loss of bowel or bladder control) and any precedent trauma (commotio cordis) or associated motions and positions Signs and symptoms that may be suggestive of significant underlying pathology Symptoms that tend to be more correlated with a benign etiology include collapse after exercise, and the presence of prodromal symptoms prior to collapse such as lightheadedness, diaphoresis, tunnel vision or nausea family history Constructing a family tree can be useful in revealing overlooked cases of sudden or unexplained death.
12 Exercise-Related NCS in Athletes Distinguishing if the syncopal event occurred during or after exercise is crucial since it will lead to direct implications in evaluation and management however, in real practice, the distinction of whether syncope occurred during or after exercise may be quite difficult, or even impossible, for sports characterized by rapid starts and stops, such as soccer, volleyball or basketball
13 Initial testing Physical examination was normal A subsequent blood examination 5 hours after the race revealed complete normal biochemical parameters exept for increased serum levels of creatine kinase The resting electrocardiogram was normal
14 Initial Diagnostic Testing many of the undiagnosed and underlying causes of syncope in athletes are suspected in analysis of ECG There is some value in a normal electrocardiogram (ECG) if the history is consistent with a non-cardiac etiology Likewise, many of the pathologic conditions associated with ERS have characteristic ECG findings, and a clearly abnormal ECG in the face of a suggestive history is equally helpful in determining treatment options and prognosis
15 important to recognize that a prominent subset of conditions will defy these general rules For example, coronary artery anomalies, the second most prevalent finding among sudden death in American athletes, typically show no abnormalities on a resting ECG In contrast, many findings associated with pathologic conditions in the general population may be considered normal in athletes These can include sinus bradycardia, first and second degree heart block, early repolarization, and voltage criteria for left ventricular hypertrophy.
16 Echocardiography HCM RVC Valvular diseases ( aortic stenosis) The resting transthoracic echocardiography was normal without left ventricular (LV) hypertrophy or dilatation
17 monitoring 24-h ambulatory electrocardiographic monitoring SR bpm with no conduction abnormalities. Only rare isolated monomorphic premature ventricular beats without pairs or episodes of ventricular tachycardia. Duration of pauses during sleep was not greater than 1.5 s. monitoring include Holter monitors, event monitors, and continuous loop recorders The estimated diagnostic yield in syncope is 1 5% for a h standard Holter monitor; 5 10% for a 3 7 day patch/external loop recorder/mcot; 15 25% for a 1 4 week patch/external loop recorder/mcot; and 30 50% for a 36 month ICM
18 stress test A maximal exercise treadmill test with BRUCE protocol was performed, which showed a normal rise in heart rate up to 205 bpm and BP up to 160/80 mm Hg The test was stopped at min (19.6 Mets) due to exhaustion The athlete did not experience syncope or any chest discomfort during the exercise test or recovery phase There were no abnormal electrocardiographical changes indicating myocardial ischemia during the exercise test or the recovery phase.
19 stress test stress testing typical protocols (Bruce, modified Bruce, Ramp, etc) for exercise stress testing are designed to use low intensity exertion to elicit ischemic manifestations While these protocols may be appropriate for older athletes who have additional risk factors for ischemic cardiac disease, they may not produce the intensity or the duration required to elicit findings in younger or more highly trained athletes. In such cases, a test that is designed to reproduce the demands and specific characteristics of the sporting activity can be very useful
20 Lars Lindholm Sorensen et al. Am Heart J We find exercise testing capable of providing potentially important information in a substantial amount (19%) of patients with high gradient HCM.
21 CPVT
22 long QT QT interval during the recovery phase (3-4 minutes) may reveal a diagnostic QT prolongation in LQTS cases with borderline QTc interval at baseline,
23 a negative even maximal-effort stress ECG does not exclude a potentially lethal coronary anomaly
24 CTA
25 cardiac MRI cardiac magnetic resonance imaging (MRI) with delayed enhancement imaging after injection of gadolinium investigation for smaller structural defects myocardial fibrosis from myocarditis hypertrophic cardiomyopathy
26 Tilt table testing
27 Tilt table testing tilt table testing has significant limitations in its utility for the evaluation of athletes. Much of the concern is related to the increased susceptibility that athletes may have to orthostatic hypotension.
28 at least four factors associated with athletic training may contribute to orthostatic intolerance: (1) increased limb compliance (2) eccentric left ventricular hypertrophy (3) increases in total blood volume which presumably attenuate cardiovascular baroreflex responsiveness and (4) independent effects on carotid and aortic baroreflex responsiveness. This increases the likelihood for false positive findings and may provide inappropriate confidence in returning athletes to activity Europace (2000) 2, 77 82
29 A 31-year-old male recreational runner with Syncope during exercise Minimal prodromal symptoms Apparently normal heart after a complete workup and A mixed response positive Tilt Test Is it possible to have a non cardiac etiology in syncope during exercise? Prognosis?
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31 conclusions syncope occurring during exercise indicates a possible cardiac etiology and dictates the performance of an extensive diagnostic workup to confirm the diagnosis of cardiac syncope he threshold for finally reaching a definite diagnosis of NCS in these situations should be high enough, in order to not miss the diagnosis of a potentially life-threatening cardiac disorder It is important also to recognize that the abnormalities found during cardiovascular testing may not have a causal relationship to syncope itself Determining the significance of such abnormalities, their causality, and whether subsequent treatment is merited requires clinical judgment and appropriate selection of cardiovascular testing Post exercise syncope has almost always a benign etiology However, the distinction between syncope occurring during and after exercise may be challenging enough
32 It is important also to recognize that the abnormalities found during cardiovascular testing may not have a causal relationship to syncope itself Determining the significance of such abnormalities, their causality, and whether subsequent treatment is merited requires clinical judgment and appropriate selection of cardiovascular testing
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35 ROBERT SHELDON et aljournal of Cardiovascular Electrophysiology Vol. 21, No. 12, December 2010
36 Symptoms/signs that warrant referral include: syncope during exertion; palpitations preceding syncope; abrupt syncope without prodromal symptoms; syncope in the supine position; athletes with known underlying cardiovascular disease (particularly known reduced ejection fraction); family history of sudden cardiac death (HCM, RVC, LQTS); syncope induced by loud noises, or diving into a swimming pool; older age (.35), or other risk factors for ischemic heart disease
37 Physical
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39 Abnormal blood pressure responses during exercise in hypertrophic cardiomyopathy patients Symptoms of impaired consciousness occur in 15 25% of the patients with HCM. that approximately one-third of patients had an ABPR on exercise ABPR may, in most cases, be at least in part due to an exaggerated fall in systemic vascular resistance related to inappropriate vasodilatation or a failure of vasoconstriction in non-exercising vascular beds
40 Left ventricular outflow tract obstruction in hypertrophic cardiomyopathy no association between ABPR and resting LV outflow tract obstruction (LVOTO) has been found, this does not exclude dynamic LVOTO as an important mechanism, and in our clinical experience, we have certainly encountered some patients in whom cardiac output limitation was the dominant mechanism of ABPR during exercise recent studies have reported a normalization of ABPR following alcohol septal ablation for LVOTO However, in our experience, an exaggerated fall in systemic vascular resistance appears to be a major component in a substantial proportion of patients
41 Investigation of recurrent syncope in hypertrophic cardiomyopathy Detailed investigations identify a probable mechanism in a minority of these, usually paroxysmal AF or VT. In the majority of cases, however, no likely mechanism is found despite repeated 24-h ambulatory ECG or patient-activated monitoring, exercise testing, and invasive electrophysiological testing
42 Hypertrophic cardiomyopathy (HCM) remains the most common cardiomyopathy causing SCD in athletes, accounting for 36% of all such cases. In a retrospective analysis of patients with HCM-related deaths, 16% died during moderate or severe physical exertion. Thus, historical guidelines have advocated for aggressive restriction of exercise to low and some moderate intensity sports. However, recent studies suggest that arrhythmic events during exercise may be much less common. In a cohort of 1380 patients with HCM, only 24 patients (1.7%) developed ventricular arrhythmias during exercise testing, highlighting a subpopulation which tended to have a worse prognosis
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45 NCS during exercise, the better described cases refer to older individuals with sympathetic dysfunction, where blood pressure (BP) fails to increase during exercise due to impairment of sympathetic vasoconstriction
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47 in general, athletes are defined as those who participate in sports requiring intense systematic training and regular competition against others in an organized team or individual sport. 8,9 Young competitive athletes (aged <35 years) are widely regarded as a special subgroup of healthy individuals with a unique lifestyle, who are seemingly invulnerable and capable of extraordinary physical achievement.
48 Over follow-up, the recurrence rate of syncope was 20 per 1000 subject-years, whereas the rate of new syncopal episodes was 2.2 per 1000 subject-years. Athletes with exercise-unrelated events had a diagnosis of either vasovagal or situational syncope Unlike postexertional syncope, 50% of syncopal episodes occurring during exertion were cardiogenic (2 of 4) and caused by either hypertrophic cardiomyopathy or ventricular tachycardia
49 BS
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52 Although the typical form of postexercise NCS occurs when the subject is in an upright posture after exercise, there is a possibility of postexercise NCS in the seated position, such as in rowers
53 Runners participating in endurance events collapse more frequently near cut-off times for medals or race closure, implying that extreme physical effort beyond the athlete s capability may induce undue stress to the athlete s circulatory system that could predispose to syncope
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55 F. Colivicchi et al. European Heart Journal (2002) 23,
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