2Cardiology, Fellow , University of Florida , College of Medicine, Jacksonville, FL, USA
3Professor of Medicine, Mayo College of Medicine, Rochester, MN, USA
4Professor of Adult and Pediatric Cardiology, Emeritus Nasseff Professor of Cardiology, Mayo Clinic, Rochester MN, USA
5Professor of Cardiology, Pediatrics and Adult Congenital Heart Disease, Aurora St. Luke’s Medical Center, Milwaukee WI, USA
A solution will languish until the expert community takes direct action to embrace 21st century systems based medicine, causality, and digital technology [7,9,10]. The first step is to break the code of silence by open public discourse (publish and speak about the transformative attributes of systems based medicine).The second step is to make everyone accountable (causal prediction and prevention must be 100%). The third and final step is to focus on how to define the components of systems based medicine, determine how these components interact with one another, and delineate the dynamics of these components in determining pre-emergent disease states [10].
How? Every essential screening test must detect normality, and on the other hand alert the presence and intensity of a potential life threatening abnormality with a very low rate of false positives. An essential screening exam should emphasize prognostication and not the permutations of disease detection [12]. Athletes are known to have normal to hyper-normal physiology, while life-threatening diseases have distinctly abnormal physiology.
Echo/Doppler screening should be looked upon as a strategy used in a select population of healthy, asymptomatic individuals to identify pre-emergent disease. Using focused echo/Doppler screening the incidence of a cardiovascular finding in athletes has been reported to be roughly one case in every 170 athletes screened with a "false positive" finding in only 8 of 508 athletes [2, 10, 13-15]. We describe how to provide a highest quality, exceptionally low cost pathophysiologic athletic screening test, which is validated to differentiate the status of a normal state from an abnormal life-threatening pathophysiologic state.
Matching pre-emergent disease (without phenotypic expression) "associated" with sudden death through diastolic parameters is the key to differentiating normal from abnormal pathophysiology [5, 9, 16-24]. These data are focused on two principal objectives: detect an imminent life-threatening state at a time when the opportunity for prevention is optimal [25, 26], and define the magnitude of imminent risk that enlightens physician decision making and management [23, 26-28].
The most optimal screening test for a large, asymptomatic athletic population prioritizes testing to confirm wellness and rule out disease. An abnormality in screening would be referred for comprehensive evaluation. The rule out principle is important because the penalty for missing a disease has the potential for athletic death. This principle reduces the number of specific diseases to be considered during screening. All cardiomyopathies are grouped as having abnormal diastolic tissue Doppler examination. Conversely, ruling in a disease is more applicable when confirming a high frequency disease. Confirming wellness and ruling out disease is most applicable to large, asymptomatic athletic population [5, 6].
The testing that depicts pre-clinical disease is diastolic function [29]. Primary diastolic dysfunction occurs early in the emergence of cardiomyopathies, hypertension, valvular, and ischemic heart disease Table 4. Doppler-echocardiography is recognized as the most useful tool to routinely and economically quantify diastolic and systolic function [29-34].
Asymptomatic diastolic myocyte dysfunction followed by systolic myocyte dysfunction and microvascular ischemiaemerge early in the pathophysiologic continuum, while structuraland electrical remodeling (electrical heterogeneity, arrhythmogenesis, and fibrosis) and symptoms occur later [60]. The prognostic importance of asymptomatic pre-emergent pathophysiology has only recently been realized [61, 62]. Asymptomatic athletes commonly engage in activities that can accentuate pre-emergent pathophysiology that could be acutely detrimental to myocardial function. For screening purposes "cardiomyopathy" can theoretically apply to almost any disease affecting the heart in which the heart muscle is structurally abnormal. Essential screening should be focused on prognostication of risk ,and not detection, or characterization of a disease type [12, 63]. An essential examrequires the acquisition of a small number of essential data, which define the presence and intensity ofemergent cardiac dysfunction Table 1. Disease risk is always defined by more than one datum feature. Hypertrophic cardiomyopathy (HCM) is an exemplary candidate for pathophysiologic screening. HCM rarely has any premonitory symptoms [35], even under exertion [35], ECG has a high rate of false positives [64-67], ejection fraction (EF) is rarely abnormal,[32]and anatomic remodeling is variable, and typically occurs late in the pathophysiologic cascade [68]. However, associated diastolic dysfunction can be detected and measured early in the HCM cascade [68-70] and is capable of detecting pre-clinicalHCM risk [68, 69, 71]. An essential screening exam is the one designed to affirm the existence of anormal physiologic profile, and identify individuals with an abnormal risk profile, independent of morphology Table 2 [9, 21, 28, 72].The algebraic summation of a small aggregate of related data (E/A, DT, e’, E/e’)define causality [28, 41] which mirrors the status of an individual’s risk state in both a positive and negative direction during serial screening, management, and follow-up [7, 8, 73].
Cardiomyopathy-screening needs to take a focused approach to potential emergent cardiac dysfunction and risk [36, 74]. Each cardiomyopathy disease(hypertrophic [68, 75], restrictive [76, 77], dilated[78], ischemic [79, 80], hypertensive [81, 82], arrhythmogenic right ventricular [83], myocarditis [84], left ventricular non-compaction [85, 86]) each has validated pathophysiologic features that can confirm a risk state [52, 87]. Averaged features have a very low incidence of false positives and false negatives results [9, 14, 48, 50].
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Diastolic Function |
Normal |
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Reference |
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Mitral inflow E (cm/s) |
60±12 |
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[47] |
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Diastolic velocity MV annulus |
Normal e’ by Age group (y) |
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16-20 |
21-40 |
41-60 |
>60 |
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Septal e’ (cm/s)! Lateral e’ (cm/s)! |
14.9 ± 2.4 20.6 ± 3.8 |
15.5 ± 2.7 19.8 ± 2.9 |
12.2 ± 2.3 16.1 ± 2.3 |
10.4 ± 2.1 12.9 ± 3.5 |
[30] |
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E/e’ |
NormalE/e’ (& Normal e’) |
Abnormal E/e’ (& Abnormal e’) |
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Septal E/e’ ratio Lateral E/e’ ratio |
7.05±6.0 6.18±1.53 |
8-10 >8-9 |
11-14 10-11 |
≥15 ≥12 |
[30, 47] |
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Average E/e’ ratio |
<8 |
9-12 |
>13 |
[30] |
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MV inflow E/A ratio if the e’ is normal |
>0.8 to <2* |
If e’ is abnormal these same data ranges would be abnormal (i.e. pseudonormal) |
[30] |
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MV inflow DT if the e’ is normal |
>140 to <240* |
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Left Atrial Morphology |
Normal |
LA overload |
[51] |
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LA Volume Index (mL/m2) |
16 to 28 22±6
|
Mild 29-33 |
Moderate 34-39 |
Severe ≥40 |
[52] |
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Benign if e’ is Normal |
[51, 53] |
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Malignant if e’ is Abnormal |
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Systolic Function |
Normal |
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EF % Artifactual EF %* |
≥55 50-55 |
Athletes with Large LV; EF can appear mildly reduced; if diastolic function is normal the low EF is likely an artifact |
[54] |
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Global Longitudinal Strain % |
-19.7 |
(As the negative number increases the function improves) |
[55, 56] |
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Tissue Doppler s’ (cm/s) Septal Lateral |
>7.5 10±1.5 |
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[57] |
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RV systolic Function (cm) Tricuspid Annular Displacement TAPSE (cm)
|
≥1.8 |
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[58] |
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*EF between 50-55% [54] (LV cavity enlargement in normal athletes can be associated with a modest lowering the EF).The presence of normal diastolic function would strongly suggest normal athletic CV remodeling and not physiologic dysfunction.
! GLS (Global Longitudinal Strain) is a measure of sub-clinical systolic function. There is a universal pathophysiologic cascade inprimary and secondary cardiomyopathies [39, 59]
There is controversy regarding the means of quantifying imminent CAD riskin asymptomatic athletes (92). At present, recommendations for the assessment of imminent risk are limited, inconsistent, or nonexistent [101, 108, 112]. However, echo/Doppler determination of an individual’s physiologic state is a logical general predictor of imminent risk, includingthe risk of ischemic heart disease. If the physiologic risk was sufficiently abnormal further assessment ofcoronary anatomy and physiology would be clinically indicated particularly in individual’s ≥35 years old. As the population ages, the incidence of pre-clinical risk associated diastolic dysfunction increases [61, 62]. This fact supports the use of essential screening in the general population just as screening is used withother disease processes (e.g., colonoscopy [113]; mammography [114]; and often CV disease [115]).
Proper recognition ofthesewarning signsmay significantly reduce primary electrical deaths and initiate amore comprehensive electrophysiology workup [65, 118]. Currently technical and logistical challenges preclude the use of ECG as a robust tool for universal screening in asymptomatic population [116,119]. One of the biggest challenges with ECG is the high incidence of false positive findings [66, 118]. Interestingly in recent research subclinical Doppler pathophysiologic changes were identified in nearly 20% of Long QT syndrome patients [120]. These findings prompt speculation that electrical dysfunction (abnormal cardiac repolarization and rhythm) may precipitate macroscopic structural and functional changes visible on focused echocardiograms [120, 121].
Measure |
Equivalent PAP |
Normal Values |
Reference |
TRv m/s |
(Systolic PAP) |
≤2.8 m/s (>31mmHg) |
[122] |
PRv m/s |
(End Diastolic PAP) |
≤1.1 m/s (≥5 mmHg) |
[122] |
Pulmonary AcT |
(Mean PAP) |
>100 ms (<20-39 mmHg) <75 ms (≥40 mmHg) |
[122-124] |
PRv: Pulmonary Regurgitant Velocity; AcT : Acceleration Time
A. Echocardiogram (135). Anomalous right coronary artery (RCA) arising from a common orifice with the left main coronary artery
Computed tomography [134]. Single right coronary artery with an inter arterial path of the left main coronary stem. Left coronary artery (white arrowheads) originates for the proximal part of the right coronary artery (black arrow) then follows an inter-arterial path between the ascending aorta and the pulmonary trunk. The white arrows indicate the inter-arterial part of the circumflex coronary artery. AO: Ascending Aorta; LA: Left Atrium LV: Left Ventricle.
Echocardiogram[135]. Anomalous origin of he left anterior descending (LAD) coronary from the proximal right coronary artery (RCA).
Shunt lesions are inferred in otherwise healthy individuals by increased pulmonary blood flow, asymmetric heart chamber enlargement, arrhythmias and increased pulmonary pressure.
Right panel: Bicuspid valve associated aortopathy
Complex lesions are recognized by pathognomonicstructural variations. Essential anatomic landmarks include[74, 135].
The internal cardiac crux is one of the most infallible cardiac landmarks (118). The apical 4-chamber view of the heart allows identification of the crux of the heart. The morphologic tricuspid valve consistently inserts lower on the ventricular and the morphologic mitral valve inserts higher. The internal crux anatomy unambiguously confirms the commitment of the morphologic tricuspid valve to the morphologic right ventricle. Many complex congenital anomalies distort the internal cardiac crux (Ebstein Anomaly, corrected transposition).The internal cardiac crux is one of the most infallible cardiac landmarks (118).
(Left panel) Normal internal cardiac crux of the heart: The morphologic tricuspid valve consistently inserts lower on the ventricular and the morphologic mitral valve inserts higher. The internal crux anatomy confirms the commitment of the morphologic tricuspid valve to the morphologic right ventricle. Many complex congenital anomalies distort the internal cardiac crux (e.g., Ebstein Anomaly, corrected transposition) (142,293). (Right panel) Abnormal Atrial-Ventricular Discordance:
(Reference) |
|
Abnormal (Athletic Aortopathy) |
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|
Normal |
Recommendation (130) |
||
[136] |
Very Low Risk |
Mild Restriction |
Moderate Restriction |
Consider Surgery |
Male Female |
≤40 mm ≤ 34 mm |
>40 mm >34 mm |
>45 mm To Be Determined |
≥50 mm |
[145-147] |
|
Risk of Aorta Rupture (Indexed Diameter cm/m2) |
||
Risk of Rupture
|
|
<2.75 cm/m2 ≈4% rupture/yr |
≥2.75 to 4.24 cm/m2 ≈8.5% /yr |
≥4.25 cm/m2 ≈20% /yr |
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