Criteria to distinguish athlete’s heart from HCM.
\\n\\n
Released this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\\n\\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
Note: Edited in March 2021
\\n"}]',published:!0,mainMedia:{caption:"Highly Cited",originalUrl:"/media/original/117"}},components:[{type:"htmlEditorComponent",content:'IntechOpen is proud to announce that 191 of our authors have made the Clarivate™ Highly Cited Researchers List for 2020, ranking them among the top 1% most-cited.
\n\nThroughout the years, the list has named a total of 261 IntechOpen authors as Highly Cited. Of those researchers, 69 have been featured on the list multiple times.
\n\n\n\nReleased this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\n\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
Note: Edited in March 2021
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Theory, TDDFT: Study of Ionization and Harmonic Generation in Linear Di-(N₂) and Tri-(CO₂, OCS, CS₂) Atomic Molecules with Ultrashort Intense Laser Pulses-Orientational Effects",slug:"non-perturbative-time-dependent-density-functional-theory-tddft-study-of-ionization-and-harmonic-gen",signatures:"Andre D Bandrauk and Emmanuel Penka Fowe",authors:[{id:"14146",title:"Dr.",name:"Andre D.",middleName:null,surname:"Bandrauk",fullName:"Andre D. Bandrauk",slug:"andre-d.-bandrauk"},{id:"14147",title:"Dr.",name:"Emmanuel",middleName:null,surname:"Penka Fowe",fullName:"Emmanuel Penka Fowe",slug:"emmanuel-penka-fowe"}]},{id:"12679",title:"Femtosecond Fabrication of Waveguides in Ion-Doped Laser Crystals",slug:"femtosecond-fabrication-of-waveguides-in-ion-doped-laser-crystals",signatures:"Andrey Okhrimchuk",authors:[{id:"13399",title:"Dr.",name:"Andrey",middleName:null,surname:"Okhrimchuk",fullName:"Andrey Okhrimchuk",slug:"andrey-okhrimchuk"}]},{id:"12573",title:"Heat Absorption, Transport and Phase Transformation in Noble Metals Excited by Femtosecond Laser Pulses",slug:"heat-absorption-transport-and-phase-transformation-in-noble-metals-excited-by-femtosecond-laser-puls",signatures:"Wai-lun Chan and Robert Averback",authors:[{id:"14122",title:"Dr.",name:"Wai-Lun",middleName:null,surname:"Chan",fullName:"Wai-Lun Chan",slug:"wai-lun-chan"},{id:"14123",title:"Prof.",name:"Robert S.",middleName:null,surname:"Averback",fullName:"Robert S. Averback",slug:"robert-s.-averback"}]},{id:"12574",title:"Probing Ultrafast Dynamics of Polarization Clusters in BaTiO₃ by Pulsed Soft X-Ray Laser Speckle Technique",slug:"probing-ultrafast-dynamics-of-polarization-clusters-in-batio-by-pulsed-soft-x-ray-laser-speckle-tech",signatures:"Kai Ji and Keiichiro Nasu",authors:[{id:"14564",title:"Dr.",name:"Kai",middleName:null,surname:"Ji",fullName:"Kai Ji",slug:"kai-ji"},{id:"14599",title:"Prof.",name:"Keiichiro",middleName:null,surname:"Nasu",fullName:"Keiichiro Nasu",slug:"keiichiro-nasu"}]},{id:"12575",title:"Two-Photon Polymerization of Inorganic-Organic Hybrid Polymers as Scalable Technology Using Ultra-Short Laser Pulses",slug:"two-photon-polymerization-of-inorganic-organic-hybrid-polymers-as-scalable-technology-using-ultra-sh",signatures:"Houbertz, Ruth, Steenhusen, Sönke, Stiche, Thomas1, and Sext, Gerhard",authors:[{id:"14099",title:"Dr.",name:"Ruth",middleName:null,surname:"Houbertz",fullName:"Ruth Houbertz",slug:"ruth-houbertz"}]},{id:"12576",title:"Several Diffractive Optical Elements Fabricated by Femtosecond Laser Pulses Writing Directly",slug:"several-diffractive-optical-elements-fabricated-by-femtosecond-laser-pulses-writing-directly",signatures:"Zhongyi Guo, Lingling Ran, Shiliang Qu and Shutian Liu",authors:[{id:"15733",title:"Dr.",name:"Zhongyi",middleName:null,surname:"Guo",fullName:"Zhongyi Guo",slug:"zhongyi-guo"}]},{id:"12577",title:"Sub-Wavelength Patterning of Self-Assembled Organic Monolayers via Nonlinear Processing with Femtosecond Laser Pulses",slug:"sub-wavelength-patterning-of-self-assembled-organic-monolayers-via-nonlinear-processing-with-femtose",signatures:"Nils Hartmann",authors:[{id:"13736",title:"Dr.",name:"Nils",middleName:null,surname:"Hartmann",fullName:"Nils Hartmann",slug:"nils-hartmann"}]},{id:"12578",title:"Application of Short Laser Pulses",slug:"application-of-short-laser-pulses",signatures:"S. Mehdi Sharifi and Abdossamad Talebpour",authors:[{id:"13471",title:"Dr.",name:"Seyed Mehdi",middleName:null,surname:"Sharifi Kalahroudi",fullName:"Seyed Mehdi Sharifi Kalahroudi",slug:"seyed-mehdi-sharifi-kalahroudi"}]},{id:"12579",title:"Ultrashort Laser Pulses Applications",slug:"ultrashort-laser-pulses-applications",signatures:"Ricardo Samad, Lilia Courrol, Sonia Baldochi and Nilson Vieira",authors:[{id:"13815",title:"Dr.",name:"Ricardo",middleName:null,surname:"Samad",fullName:"Ricardo Samad",slug:"ricardo-samad"},{id:"14327",title:"Dr.",name:"Lilia",middleName:null,surname:"Courol",fullName:"Lilia Courol",slug:"lilia-courol"},{id:"14328",title:"Dr.",name:"Sonia",middleName:null,surname:"Baldochi",fullName:"Sonia Baldochi",slug:"sonia-baldochi"},{id:"14329",title:"Dr.",name:"Nilson Dias",middleName:null,surname:"Vieira Junior",fullName:"Nilson Dias Vieira Junior",slug:"nilson-dias-vieira-junior"}]}]}],publishedBooks:[{type:"book",id:"1476",title:"Femtosecond-Scale Optics",subtitle:null,isOpenForSubmission:!1,hash:"54bc6a95c772396b46d9dc2ad127be5a",slug:"femtosecond-scale-optics",bookSignature:"Anatoli V. 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Duarte"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"5236",title:"High Energy and Short Pulse Lasers",subtitle:null,isOpenForSubmission:!1,hash:"481d4221e58d2c90fe398be93d898f43",slug:"high-energy-and-short-pulse-lasers",bookSignature:"Richard Viskup",coverURL:"https://cdn.intechopen.com/books/images_new/5236.jpg",editedByType:"Edited by",editors:[{id:"103742",title:"Dr.",name:"Richard",surname:"Viskup",slug:"richard-viskup",fullName:"Richard Viskup"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},onlineFirst:{chapter:{type:"chapter",id:"80652",title:"Pre-Sports Participation Cardiac Screening Evaluation—a Review",doi:"10.5772/intechopen.102942",slug:"pre-sports-participation-cardiac-screening-evaluation-a-review",body:'Sudden cardiac death (SCD) is defined as any death secondary to a cardiac cause within minutes to 24 h of the exercise activity [1, 2, 3]. The SCD may be associated with a rhythm disturbance or circulatory collapse. The prevalence of SCD in children is approximately 600 per annum in the USA [3]. By contrast, sudden infant death syndrome (SIDS) occurs in 7000–10,000 infants per year, and SCD in adults is seen in 300,000–400,000 subjects per year [3]. Consequently, the prevalence of SCD in childhood (and young adult) athletes is a lot less frequent than SIDS in babies and SCD in adults. The objectives of this presentation are to list the most frequent cardiac causes of sudden death in athletes, describe clinical features of more common cardiac disease entities causing SCD, and discuss methods of pre-sports participation screening. The discussion will not include SIDS and SCD without an antecedent exercise activity.
Disease processes causing SCD have changed remarkably over the years. In the 1970s, aortic valve stenosis, un-palliated cyanotic congenital heart defects (CHDs), and Eisenmenger’s syndrome were the major culprits. In the 1990s, hypertrophic cardiomyopathy (HCM), congenital anomalies of the coronary arteries (CAs), premature atherosclerosis, rupture of the aorta in Marfan’s syndrome, and arrhythmias were identified as major diseases entities causing SCD in athletes [2]. At the present time, HCM; congenital anomalies of the CAs; Marfan’s syndrome; structural cardiac defects, namely, repaired tetralogy of Fallot, repaired transposition of the great arteries by Mustard or Senning procedures, single ventricle lesions addressed by Fontan operation; CHD without prior surgery, including aortic is responsible for SCD [2, 3, 4]. Less common causes namely, acute or chronic myocarditis; complex forms of mitral prolapse, arrhythmogenic right ventricular cardiomyopathy (ARVC), Eisenmenger’s syndrome; long QT syndrome; other abnormalities of the coronary artery such as Kawasaki disease and familial hyperbeta hyperlipoproteinemia; commotio cordis; catecholaminergenic polymorphic ventricular tachycardia; and Brugada syndrome were also found to be responsible for SCD [4, 5, 6, 7]. Some of these entities will be reviewed in the ensuing paragraphs. In the US, SCD is seen more frequently following basketball and football than with other sports; this is likely to be related to the requirement for high level of physical activity in these sports [5, 6].
This condition has been called asymmetric septal hypertrophy (ASH), hypertrophic obstructive cardiomyopathy (HOCM), dynamic muscular subaortic stenosis, idiopathic hypertrophic subaortic stenosis (IHSS), diffuse muscular subaortic stenosis, Brock’s Disease, Teare’s Disease, and others, but is now best described as hypertrophic cardiomyopathy. HCM is a primary, often inherited, disease of the myocardium affecting the sarcomeric proteins. This results in hypertrophy and disorganization of myofibrils and fibrosis of interstitia. Autosomal dominant inheritance with a high degree of penetrance is noted. Matrilineal, X-linked, and autosomal-recessive inheritance patterns have also been described. One hundred or more different mutations in 10 genes have been discovered (chromosomes 1, 14 & 15). Troponin-T, beta myosin heavy chain, and alpha tropomyosin may also be involved.
HCM is characterized by hypertrophy of the left ventricle (more often) and/or right ventricle (RV). Concentric left ventricular (LV) hypertrophy is present without an identifiable hemodynamic reason. Frequently, there is asymmetric interventricular septal hypertrophy. Diastolic dysfunction including, delayed relaxation and increased muscle stiffness are present. LV outflow obstruction, which is dynamic is seen in 25% of cases. Systolic anterior motion (SAM) of the mitral valve may contribute to the LV outflow tract narrowing. RV outflow obstruction is rare but is more frequent in infants with HCM. There appear to be areas of localized hypertrophy in the LV muscle in addition to those in the septum and serve as potential arrhythmogenic foci.
There are usually no symptoms in infants and children; they are most often detected because of a cardiac murmur or family history of HCM. Symptoms in infancy usually indicate a poor prognosis. In early adulthood, the presenting symptoms are exertional dyspnea, lightheadedness, chest pain, syncope, or palpitations.
In the non-obstructive HCM, the findings are subtle with minimal or no increase in LV impulse. A third or fourth heart sound may be auscultated at the apex. There may either be a soft systolic murmur or no murmur. In the obstructive HCM, increased LV impulse, double or triple impulse may be felt. Pulses bisfiriens may be felt in some subjects. An ejection systolic murmur is heard at the left mid and right upper sternal borders. The murmur changes with postural maneuvers: decreases in intensity on squatting which may increase in a standing position. The murmur of HCM is usually auscultated at the left mid sternal border and increases in intensity with the Valsalva maneuver.
Chest X-ray is of limited value; the size of the heart may be normal or cardiomegaly may be present. The size of the heart may be normal even with marked LV hypertrophy. ECG is abnormal in 90% of patients; bizarre patterns are seen, but none are characteristic of HCM. Most commonly, increased LV voltages (deep S waves in V1 and V2 and tall R wave in V5 and V6) are detected. T wave inversion, deep q waves, and enlargement of the left atrium may be identified on the ECG in some patients. Unfortunately, the ECG pattern does not discriminate between obstructive and non-obstructive types or those at risk for sudden death. However, Holter monitoring is likely to detect arrhythmia [8, 9] and may help prognosticate [9].
Echocardiogram is the most useful test in the diagnosis of this condition. It demonstrates LV hypertrophy (Figure 1), asymmetric septal hypertrophy (Figures 1 and 2), and SAM of the mitral valve (Figure 3). The LV cavity is completely obliterated in systole (Figure 4). Doppler studies will detect abnormal mitral inflow Doppler patterns and mitral insufficiency and help to quantify LV outflow tract obstruction (Figures 5 and 6).
A. Parasternal long (A) and short (B) axis views of the left ventricle (LV) illustrating LV hypertrophy and strikingly thickened inter-ventricular septum (IVS). Ao, aorta; LVPW, LV posterior wall; RV, right ventricle. (reproduced from reference [
Parasternal short (left) and long (right) axis views of the left ventricle (LV) illustrating distinctly thickened inter-ventricular septum (arrows in both images). Ao, aorta; LA, left atrium.
Parasternal echocardiographic long axis views of the left ventricle (LV) and mitral valve illustrating systolic anterior motion (SAM) of the mitral valve (thick arrows in both ‘A’ and ‘B’). Note thickened inter-ventricular septum (thin arrows), particularly noticeable in ‘B’. Ao, aorta; LA, left atrium; RV, right ventricle.
Parasternal long-axis views of the left ventricle (LV) of a child with hypertrophic cardiomyopathy demonstrating total obliteration of the cavity of the LV (right image) in systole (arrows).
A. Parasternal long axis 2D and color doppler recording showing turbulent flow (TF) in the left ventricular (LV) outflow tract. B. Continuous-wave doppler indicates a gradient of 39 mmHg (the insert in B). The triangular pattern of the doppler recording is suggestive of subaortic narrowing. Ao, aorta. (reproduced from reference [
Apical five-chamber view with continuous-wave doppler across the left ventricular outflow tract demonstrating a peak gradient of 75 mmHg. The triangular pattern of the doppler recording is suggestive of subaortic narrowing.
Localized, atypical hypertrophy patterns as demonstrated in Figures 7–9 may also be detected.
Parasternal long-axis views of the left ventricle of a patient with hypertrophic cardiomyopathy showing marked inter-ventricular septal thickening (arrows). LA, left atrium.
Subcostal view of the left ventricle (LV) of a patient with hypertrophic cardiomyopathy showing marked inter-ventricular septal thickening (arrows).
Apical four-chamber view of the left ventricle (LV) of a patient with hypertrophic cardiomyopathy showing marked inter-ventricular septal thickening (arrows). RA, right atrium.
Some athletes develop LV hypertrophy and differentiation of this LV hypertrophy from that seen with HCM maybe not easy. Criteria that help differentiate these conditions [7] are listed in Table 1.
Parameter | Hypertrophic cardiomyopathy | Athlete’s heart |
---|---|---|
Unusual patterns of LVH on echo | Positive | Negative |
LV Cavity <45 mm | Positive | Negative |
LV Cavity >55 mm | Negative | Positive |
Left atrial enlargement | Positive | Negative |
Bizarre ECG patterns | Positive | Negative |
Abnormal LV filling | Positive | Negative |
Female gender | Positive | Negative |
Decreased LV muscle thickness with de-conditioning | Negative | Positive |
Family history of hypertrophic cardiomyopathy | Positive | Negative |
Criteria to distinguish athlete’s heart from HCM.
ECG, electrocardiogram; LV, left ventricle; LVH, left ventricular hypertrophy.
Yearly mortality rate in subjects with HCM is in the order of 2 to 4% of the HCM cases; this is largely based on patients cared for in large tertiary care centers. Consequently, the true population prevalence is unknown. Examination of SCD in competitive athletes revealed that HCM is the most frequent reason for SCD and accounted for 36% of deaths [5, 6, 7]. The mortality is largely confined to the 12-to-35-year age patient group. Most of these patients are asymptomatic or mildly symptomatic and therefore, risk stratification of HCM is difficult. In some investigations, risk factors for SCD in HCM patients have been identified and these include, a family history of sudden death related to HCM, history of syncope or pre-syncope, history of having survived sudden death episode, massive LV hypertrophy (> 30 mm), non-sustained ventricular tachycardia, unusual blood pressure (BP) response to exercise, and high LV outflow tract gradient [1, 2, 3, 4, 11, 12, 13].
The mechanism by which HCM results in SCD following exercise is not clearly understood, but the development of ventricular arrhythmia, leading to ventricular fibrillation is thought to be responsible for SCD [2]. Even at the present time, we have limited knowledge as to how to prevent SCD in HCM. We continue to lack sound criteria of individual severity and relative prognostic risk, in general, and especially in athletes. Early studies showed the usefulness of beta-blockers in reducing mortality, but recent studies did not corroborate the usefulness of beta-blocker usage in the prevention of mortality. Exercise limitation may be helpful in decreasing the probability of sudden death. Indeed, the athlete with HCM should not be permitted to take part in the strenuous sports activity. If non-sustained ventricular tachycardia is present, Amiodarone has been shown to be beneficial. Intra-cardiac defibrillators (ICDs) for high-risk patients with ventricular tachycardia induced by programmed ventricular stimulation may be helpful.
In normal subjects, the left and right coronary arteries (CAs) originate from left and right sinuses of Valsalva, respectively. The left main CA is short and divides into two branches, namely the left anterior descending (LAD) and circumflex. The LAD continues in the same course as the left main CA and traverses in the interventricular groove. The circumflex traverses perpendicular to the axis of the left main CA and keeps on going in the posterior atrioventricular groove. The left CA perfuses the LV and interventricular septum [14, 15]. The right CA originates from the right sinus of Valsalva and continues in the right atrioventricular sulcus and does not branch out similar to the left CA. The right CA supplies the RV [14, 15]. The site of origin and the course of the CAs proximally can easily be demonstrated in echocardiographic studies (Figures 10 and 11). Color flow mapping of the CAs (Figures 11 and 12) should also be undertaken concurrently to ensure that the parallel lines of the transverse sinus of the pericardium are not mistaken for CAs [16].
A short-axis view at the level of aortic sinuses demonstrating normal left and right (RC) coronary arteries and their branches. The left main coronary artery (LMC) continues in the same direction to become the left anterior descending (LAD) artery. The circumflex (CiR) and marginal (MR) branches traverse perpendicular to the axis of LMC. The aorta (AO) and pulmonary artery (PA) are also shown. Demonstration of color flow within the coronary arteries is required to ensure that these indeed are coronary arteries. (modified from reference [
The short-axis views at the level of aortic sinuses demonstrate the origin and course of the left (LCA) (A and B) and right (RCA) (C and D) coronary arteries. The LCA continues in the same direction to become the left anterior descending artery (LAD). The circumflex (CIRC) traverses perpendicular to the axis of LCA. Color flow within the coronary arteries is demonstrated in ‘B’ and ‘D’ and is required to ensure that these indeed are coronary arteries and not parallel lines of the transverse sinus of the pericardium. Ao, aorta.
A. a short-axis view at the level of aortic sinuses, similar to
The aberrant origin of the CA is a rare abnormality with its origin from the contralateral aortic sinus of Valsalva [16]. In aberrant left CA, the left CA originates from the right sinus of Valsalva (rarely from the right CA) with a short intramural (within the aortic wall) course and continues between the pulmonary trunk anteriorly and the aorta posteriorly. The ostium of the left CA is often Slit-like forming a potential site for obstruction to coronary blood flow. In aberrant right CA, the right coronary artery arises from the left sinus of Valsalva (less commonly from the left main CA). This is the counterpart of aberrant left CA. The right CA then traverses rightward with a short intramural course within the aortic wall and then traverses between the pulmonary artery and aorta to get to its usual course. There is adequate coronary flow at rest, but during exercise, ischemia may develop secondary to either partial or total occlusion of the CA [17, 18]. Several hypotheses have been proposed to elucidate the reason(s) for inadequate CA blood flow. One such hypothesis is compression of the CA (left or right) between the great arteries by the expansion of the aorta and pulmonary artery against each other during the exercise. Another hypothesis suggests that an angle is created between ostium of the CA and its main axis creating additional tension, during aortic expansion [19, 20, 21]. The intramural course of the coronary artery also contributes to the risk of SCD during exertion. Echocardiographic examples of aberrant left CA arising from the right sinus of Valsalva (Figure 13) and of aberrant right CA arising from the left sinus of Valsalva (Figures 14–16) are shown in Figures 13–16.
A short-axis view of the aorta demonstrating aberrant left coronary artery from the right sinus of Valsalva, traversing between the aorta (AO) and pulmonary artery (PA). (reproduced from reference [
The short-axis views of the aorta (Ao) demonstrate aberrant right coronary artery (RCA) from the left sinus of Valsalva by two-dimensional (A and B) and color flow (CF) (C) imaging. The intramural (IM) course of the right coronary artery is shown in ‘B’.
The short-axis views of the aorta (Ao) demonstrate aberrant right coronary artery (RCA) from the left sinus of Valsalva by two-dimensional (A) and color flow (B) imaging. Color flow (CF) at the origin of RCA (B) and intramural (IM) course of the RCA (A and B) are shown. PA. Pulmonary artery.
The short-axis views of the aorta (Ao) demonstrate aberrant right coronary artery (RCA) from the left sinus of Valsalva by two-dimensional (A) and color flow (B) imaging. Color flow acceleration (FA) at the origin of RCA (B) may suggest stenosis at the origin of RCA. The intramural (IM) course of the RCA (A and B) is seen. PA. Pulmonary artery.
The aberrant origin of the left CA is strongly associated with SCD [19, 20]. While not as common, aberrant right CA is also seen with SCD associated with exercise [21]. Aberrant CAs constitute 17% of all SCDs following exercise [5, 6, 7] and are next only to HCM with regard to frequency.
Often, the first presentation of most patients with aberrant coronary arteries is SCD with exercise. A few patients may present with symptoms of angina or syncope following exercise [22]. Some patients may be detected during echocardiograms performed for some other reason. Routine physical examination is completely normal. Patients with complaints of angina or syncope following exercise should be evaluated by a cardiologist. Stress testing, while routinely used for complaints of this nature, a regular stress test may not yield abnormal results in subjects with aberrant CAs particularly if the stress test is sub-maximal [16, 17]. If the stress test with maximal activity is performed, it may precipitate a coronary event or even sudden death. Instead, the author recommends echocardiographic studies, focusing on imaging of proximal CAs [16]. Reliable echocardiographic screening methods to identify aberrant CAs (Figure 17) have been described [23, 24] and may be used. However, normalcy (Figures 10–12) of the CAs or aberrancy (Figures 13–16) should be documented by direct visualization of the CAs by transthoracic echocardiographic studies. With the current state-of-the-art echocardiographic equipment, echo studies are the primary tools of investigation. If transthoracic echocardiographic images are not clear, especially in adolescents and adults with poor acoustic windows, other studies such as transesophageal echocardiography (TEE), computed tomography (CT) scan, or angiography may have to be performed to demonstrate the CA anatomy. Surgical re-implantation of the aberrant CAs along with enlarging the coronary ostium and un-roofing the intramural portion of the CA, as deemed appropriate, can be safely performed, and subsequent to recovery from surgery, participation in the full athletic activity is feasible.
Parasternal long-axis two-dimensional echo images of the left atrium (LA), left ventricle (LV) and aorta (AO) in a normal child are shown in A. A similar view of the heart in a child with an aberrant coronary artery (CA) is shown in B which demonstrated a cross-sectional image of the CA in the anterior wall of the AO (arrow in B). RV, right ventricle. Modified from Jureidini SB, Marino CJ, Singh GK, Balfour IC, Rao PS. J Am Society of Echocard 2003; 16: 756–763 [
Marfan’s syndrome is a disorder of the connective tissue with multisystem involvement, particularly of the musculoskeletal, ocular, and cardiovascular systems [25, 26]. Mutations of the fibrillin-1 gene are believed to be responsible for this syndrome. The overall prevalence is one in 10,000 to 20,000 individuals [27]. The inheritance pattern is autosomal dominant with variable expression. In approximately 15% of cases, it may manifest sporadically [25]. Several reviews of SCD in young athletes disclosed aortic rupture in Marfan’s syndrome patients (2 to 3%) as a causative factor [1, 5, 6, 7, 26, 28].
Clinical manifestations of Marfan’s syndrome are tall stature with arm span >105% of the height, scoliosis, arachnodactyly, pectus deformity, hyper-extensible joints, and dislocation of the lens. They may also have glaucoma and retinal detachment. Some of the clinical features are illustrated in Figure 18. Cardiovascular abnormalities include mitral valve prolapse (Figure 19) in almost 100% of patients, some with mitral regurgitation (Figure 19), and aortic root dilatation (Figures 20 and 21) in a high percentage of patients [26, 29]. The mitral prolapse and mitral regurgitation may be appreciated on careful auscultation and confirmed by echocardiography. However, echocardiography is necessary to detect aortic root dilatation [29]; the measurements are compared with normal subjects, and
A summary of clinical features of Marfan’s syndrome.
Selected video frames from apical four-chamber views demonstrating mitral valve prolapse (MP) and mitral regurgitation jet (MRJ) in a patient clinically diagnosed as Marfan’s syndrome. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
Selected video frame from parasternal long-axis view demonstrating measurements of the dilated aortic root in a patient clinically diagnosed as Marfan’s syndrome. Note the measurements are listed at the left bottom. The
Selected video frames from parasternal long-axis view demonstrating measurements of the dilated aortic root in a patient clinically diagnosed as Marfan’s syndrome. The measurements are listed at the left bottom in both ‘A’ and ‘B’. while the Z score of the aortic valve (AV) annulus was within normal limits, the Z score of the dilated aortic sinus was +5.5.
Congenital cardiac defects following repair (tetralogy of Fallot—total correction; transposition of the great arteries—Mustard or Senning operation, and single ventricle lesions—Fontan operation) in 2% and un-operated CHDs, including aortic stenosis in 3% have been reported as causative factors for SCD following exercise activity [4, 5, 6, 7]. The clinical features of these disease entities [32, 33, 34, 35, 36, 37] and their long-term squealae [38, 39] were reviewed elsewhere [32, 33, 34, 35, 36, 37, 38, 39] for the interested reader and will not be reviewed here.
Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a rare myocardial disorder inherited in an autosomal dominant pattern with an estimated prevalence of 1:1000–1:5000 [40]. It has been identified as a cause of SCD following sports participation in approximately 4% of cases [5, 6, 7]. Cardiomyopathic changes most frequently involve the right ventricular myocardium; however, cases involving the LV have also been reported. Exercise may be important in eliciting ventricular arrhythmias. The usual presenting symptoms are palpitations, syncope, or aborted cardiac arrest. Congestive heart failure may occur in the late stages. T-wave inversion in the right chest leads, indicative of repolarization abnormalities are seen in the ECG. However, the ECG is not sensitive in detecting ARVC [41]. The diagnosis is largely based on major and minor criteria in the echocardiographic and MRI studies, reviewed elsewhere [40, 42]. The mechanism for SCD following exercise is the development of ventricular arrhythmia 40].
There are number of other diseases/defects that have been known to have a causal relationship with SCD following exercise; the prevalence of each of these varied between 1 and 6% [5, 6, 7]. These are listed in Table 2. A detailed discussion of these entities is beyond the scope of this paper.
Disease entities | Percent prevalence | Comments |
---|---|---|
Myocarditis | 6% [5, 6, 7] | Early studies indicated a higher prevalence ranging from 18 to 29% [28, 43, 44] |
Complex Forms of Mitral Prolapse | 4% [5, 6, 7] | Family history of SCD and exercise-induced arrhythmias in mitral prolapse cases are likely to be related to SCD [2] |
Ion Channelopathies | 3 to 4% [5, 6, 7] | Long QT syndromes (Jervell and Lange-Nielson syndrome and Romano-Ward syndrome) and Brugada syndrome |
Myocardial Bridging of the Left Anterior Descending Coronary Artery | 3% [5, 6, 7] | Has also been reported in other studies [16, 45, 46] |
Atherosclerotic Coronary Artery Disease | 3% [5, 6, 7] | Premature atherosclerotic coronary artery disease secondary to hyperbeta hyperlipoprotenemia |
Dilated Cardiomyopathy | 2% [5, 6, 7] | — |
Wolf Parkinson White syndrome | 2% [7] | — |
Pulmonary Hypertension (Eisenmenger’s Syndrome), Sarcoidosis, Kawasaki Disease, Commotio Cordis | ∼1% each [2, 5, 6, 28, 47] | Pulmonary Hypertension (Eisenmenger’s Syndrome) [28], Sarcoidosis [5], Kawasaki Disease [2, 6], Commotio Cordis [6, 47] |
Other disease entities associated with SCD following exercise.
ECG, electrocardiogram; SCD, sudden cardiac death.
Pre-sports participation screening is commonly suggested by most medical societies [5, 48, 49, 50, 51, 52] including the American Academy of Pediatrics (AAP), American Heart Association (AHA), and the American College of Cardiology (ACC). Yet, the heart conditions which predispose to SCD happen in 5 in 100,000 persons and SCD occurs in 1 in 200,000 subjects. This degree of low risk makes the appraisal hard and the cost-effectiveness of screening techniques is low. The aim of any program is to discover individuals at risk for SCD during tough exercise without invasive testing and in a cost-effective manner. However, no generally established standards for screening are available at the present time. This issue was tackled differently in different countries. In the US, the pre-participation screening [5, 48, 51, 52] includes securing sports person’s personal and family history and complete physical examination (Tables 3 and 4) without an ECG or any other imaging studies and if abnormalities are detected in this initial screening process, further workup is pursued. In Italy [49, 53], Israel [54], and Japan [55], an ECG is also performed along with history and physical examination; this is mandated by the respective country’s laws. Screening of the athletes in other European countries is limited to the individuals participating in international, Olympic, or other professional sports [56]. Denmark, on the other hand completely rejected systematic screening for the athletes; their stated justification was a low event rate [57].
Personal history |
---|
1. Chest pain or discomfort during exertional activities |
2. Unexplained syncope or near-syncope |
3. Excessive exertional and unexplained dyspnea/fatigue or palpitations associated with exercise |
4. Previously recognized heart murmur |
5. Elevated systemic blood pressure |
6. History of prior restriction from participation in sports |
7. Results of prior testing of the heart by another physician/healthcare giver |
8. History of premature death (sudden and unexpected, or otherwise) prior to age 50 years secondary to a cardiac issue in more than 1 relative. |
9. Disability from heart disease in close relatives less than 50 years of age |
10. History of hypertrophic or dilated cardiomyopathy, long-QT syndrome or other ion channelopathies, Marfan’s syndrome, clinically significant arrhythmias, or genetic cardiac conditions in family members |
Physical examination |
---|
11. Complete physical examination including blood pressure in a sitting position* |
12. Palpation of femoral pulses to exclude coarctation of the aorta |
13. Look for physical stigmata of Marfan’s syndrome |
14. Careful auscultation to exclude left ventricular outflow tract obstruction** |
The numbering continues from Table 3.
Auscultation should be undertaken with the athlete in both the supine and standing positions (and with Valsalva maneuver) particularly to discover murmurs associated with HCM (dynamic left ventricular outflow tract obstruction).
Some investigators employed screening studies utilizing ECG [58, 59, 60, 61], echocardiogram [61, 62, 63, 64], or MRI [65], and these investigators demonstrated that the prevalence of high-risk cardiac condition that is likely to predispose to SCD following exercise is low: ECG—0.33 to 11.5%; echocardiogram—1.26 to 5.1%; and MRI—1.25% of the athletic population screened [58, 59, 60, 61, 62, 63, 64, 65].
The current recommendations by the AHA and ACC [5, 48, 51, 52] are to examine the personal history and family history (Table 3) and to carry out an orderly and complete physical examination (Table 4), whether it is undertaken in primary care doctors’ clinic or in mass pre-participation screening programs. The rationale of the pre-participation screening is not to exclude youths from participation in sports, but to enable as many of them as possible to participate in sports to their full potential.
As mentioned above, the present AHA/ACC suggestions are that screening assessments are executed by trained examiners. This appraisal should consist of the 14-key elements of personal and family history and physical examination (Tables 3 and 4). Such assessment should be carried out in a setting favorable for best auscultation of the heart. These all-inclusive screening assessments should be re-done in two years for high school athletes and in three years for the college student athletes. It is not realistic to presume that usual large-scale screening assessments are capable of excluding all clinically pertinent diseases. The writer of this chapter strongly believes that such appraisals should be undertaken by the primary care doctors (pediatricians, internists, family practitioners, and other primary care providers who care for children, adolescents and young adults) as a part of their annual regular physicals, but they should make sure that the AHA/ACC suggested 14-key elements of personal and family history and physical examination (Tables 3 and 4) are included.
If abnormalities are detected in the previously expressed, 14-Element AHA/ACC recommendations (Tables 3 and 4) for pre-participation cardiovascular screening, additional testing, as suitable, should be undertaken (Table 5).
1. Secure careful personal and family history (Table 3) |
2. Perform methodical pre-participation physical examination (Table 4) |
3. Obtain a 12-lead electrocardiogram if any abnormalities are detected during history and/or physical examination (items 1 and 2) |
4. If abnormalities are detected during history taking and physical examination or if unexplained ECG findings are seen, an echocardiogram should be performed. Particular focus should be paid to address the type of abnormality detected during items 1, 2, and 3 |
5. If problems are detected during items 1 through 4, additional studies, specifically addressing the detected abnormalities, are in order:
|
Stepwise approach to cardiac screening evaluation.
CT, Computed tomography; HCM, Hypertrophic cardiomyopathy; MRI, magnetic resonance imaging.
ECG is the first test that should be performed if any abnormalities are detected in the 14-element screening (Routine pre-participation screening ECG is not recommended in the US and the justification for such will be reviewed in the next section of this chapter). The ECG may identify patients with HCM because, as mentioned in the HCM section, many patients with HCM exhibit ECG abnormalities although the ECG abnormalities are not diagnostic of HCM. The value of ECG in identifying coronary abnormalities is limited. However, the ECG is useful in detecting long QT syndrome, Wolf-Parkinson-White (WPW) syndrome, atrioventricular block, and Brugada syndrome.
Echocardiogram should be performed to investigate abnormalities detected during history taking, performing a physical examination, or unexplained ECG findings. However, it is absolutely impracticable to use the echocardiogram as a screening tool for SCD [222]. Hypertrophic cardiomyopathy (Figures 1–9) and other types of cardiomyopathies can easily be diagnosed by echo-Doppler studies. Aberrant CAs should be specifically imaged in an attempt to document normalcy (Figures 10–12) or to establish aberrancy (Figures 13 through 17). Echo is also useful in quantifying dilatation of the aortic root (Figures 20 and 21) in Marfan’s syndrome. The presence of prolapse of the mitral valve and mitral valve insufficiency (Figure 19) can be detected easily in echo-Doppler studies.
A number of other studies may be useful in investigating these patients and they should focus on specific issues/concerns discovered during the screening process (Table 5). Exercise testing may help resolve the significance of exercise-induced symptoms. Holter or Event monitors may be used to document arrhythmias. An invasive electrophysiology study may be needed in some children. Genetic screening for HCM, Marfan’s syndrome, and long QT syndrome is currently available and may be performed as indicated for a given clinical scenario. MRI and CT scans may be employed in specific situations, not resolved by echocardiography. Cardiac catheterization and cineangiography are rarely needed.
Given the easy accessibility of echocardiography and its utility in the detection and quantification of causes of sudden death in athletes (as reviewed in Sections 2–8 of this chapter), echocardiography has become the primary mode of investigation to address issues identified during history, physical examination and ECG screening. However, in subjects with poor echo windows, noninvasive studies such as MRI and CT scans may be utilized. These studies are particularly useful in evaluating aortic arch and pulmonary artery anomalies. Another condition in which MRI is useful is arrhythmogenic right ventricular cardiomyopathy; indeed, MRI criteria forms the basis for diagnostic confirmation of ARVC. In patients with Marfan syndrome, aortic dilatation can be quantitated and aortic dissection detected by MRI. MRI and CT scans are also useful in evaluating anomalous origin and course of the coronary arteries as well in assessing other coronary artery abnormalities listed in Table 2.
The Task Force on Preparticipation Screening for Cardiovascular Disease in Competitive Athletes of AHA/ACC [5, 48, 51, 52] does not recommend routine ECGs and echocardiograms for pre-participation screening. On the other hand, the International Olympic Committee [66] and the European Society of Cardiology [67] guidelines recommend routine screening with a 12-lead ECG along with history and physical examination. Pre-participation screening ECG does not increase the diagnostic accuracy, is not practical, is not sensitive, and is not specific. In addition, both false positives and false negatives (5–20%) exist with the ECG [68]. However, it may detect patients with hypertrophic cardiomyopathy, WPW syndrome, atrioventricular block, long QT syndrome, and Brugada syndrome.
The justification for AHA/ACC guidelines for not recommending routine recording of ECGs as a part of pre-participation screening may be summarized as follows: 1. ECG is not sensitive and is not specific with false-positive ECGs taking place way above true-positive ECGs, 2. The incidence of cardiac conditions leading to sports-related deaths is rather low (5 out of 100,000 subjects), 3. The athlete group to be screened is of the considerable size (10 million in the USA and much larger worldwide), 4. Routine ECG screening will impose a large price tag of roughly 2 Billion dollars/year, and 5. There is no adequate physician pool to do and interpret this large number of ECGs. Furthermore, the subjects with undiagnosed cardiac abnormality may present with symptoms, namely chest pain, exertional dyspnea, or syncope which may be uncovered by the screening questionnaire. Since some of the entities have a genetic and familial origin, they may be discovered by the screening protocol. Finally, studies comparing the strategies with and without ECG during screening did not demonstrate a mortality benefit in the group with routine ECGs [52, 54, 69]. Based on these and other considerations, the author is in support of not performing ECG during pre-participation screening [3] and recommends careful attention to implementing the 14-point AHA/ACC pre-participation screening protocol.
Sudden death associated with sports participation often has a cardiovascular cause and the two most frequent etiologies are HCM and aberrant CAs. Clinical features of HCM, aberrant CAs, Marfan’s syndrome, and ARVC were reviewed and other entities responsible for SCD were listed/tabulated. The existing recommendations are a pre-spots participation review of full personal and family history and systematic physical examination, preferably in the primary care doctors’ office. Additional investigative studies should be undertaken if history or physical examination detect any abnormalities. Using ECG, echocardiogram, or MRI as routine screening techniques is contentious and is not currently recommended in the USA. The rationale of pre-sports participation evaluation is to allow as many athletes as feasible to partake instead of being excluded from sports participation.
The author declares no conflict of interest.
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Aronow"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}],booksByTopicTotal:7,seriesByTopicCollection:[],seriesByTopicTotal:0,mostCitedChapters:[{id:"43500",doi:"10.5772/54723",title:"Pharmacology of Arterial Grafts for Coronary Artery Bypass Surgery",slug:"pharmacology-of-arterial-grafts-for-coronary-artery-bypass-surgery",totalDownloads:3012,totalCrossrefCites:9,totalDimensionsCites:19,abstract:null,book:{id:"3542",slug:"artery-bypass",title:"Artery Bypass",fullTitle:"Artery Bypass"},signatures:"Oguzhan Yildiz, Melik Seyrek and Husamettin Gul",authors:[{id:"164299",title:"Prof.",name:"Oguzhan",middleName:null,surname:"Yıldız",slug:"oguzhan-yildiz",fullName:"Oguzhan Yıldız"},{id:"164968",title:"Dr.",name:"Melik",middleName:null,surname:"Seyrek",slug:"melik-seyrek",fullName:"Melik Seyrek"},{id:"164969",title:"Dr.",name:"Husamettin",middleName:null,surname:"Gul",slug:"husamettin-gul",fullName:"Husamettin Gul"}]},{id:"43514",doi:"10.5772/54418",title:"The Role of The Angiosome Model in Treatment of Critical Limb Ischemia",slug:"the-role-of-the-angiosome-model-in-treatment-of-critical-limb-ischemia",totalDownloads:3804,totalCrossrefCites:5,totalDimensionsCites:11,abstract:null,book:{id:"3542",slug:"artery-bypass",title:"Artery Bypass",fullTitle:"Artery Bypass"},signatures:"Kim Houlind and Johnny Christensen",authors:[{id:"165363",title:"Associate Prof.",name:"Kim",middleName:null,surname:"Houlind",slug:"kim-houlind",fullName:"Kim Houlind"},{id:"167383",title:"Dr.",name:"Johnny",middleName:null,surname:"Christensen",slug:"johnny-christensen",fullName:"Johnny Christensen"}]},{id:"43476",doi:"10.5772/54509",title:"Impact of Ischemia on Cellular Metabolism",slug:"impact-of-ischemia-on-cellular-metabolism",totalDownloads:2786,totalCrossrefCites:5,totalDimensionsCites:9,abstract:null,book:{id:"3542",slug:"artery-bypass",title:"Artery Bypass",fullTitle:"Artery Bypass"},signatures:"Maximilien Gourdin and Philippe Dubois",authors:[{id:"164978",title:"Prof.",name:"Philippe",middleName:"E",surname:"Dubois",slug:"philippe-dubois",fullName:"Philippe Dubois"},{id:"164982",title:"Dr.",name:"Maximilien",middleName:null,surname:"Gourdin",slug:"maximilien-gourdin",fullName:"Maximilien Gourdin"}]},{id:"61397",doi:"10.5772/intechopen.76844",title:"The Ethics in Repeat Heart Valve Replacement Surgery",slug:"the-ethics-in-repeat-heart-valve-replacement-surgery",totalDownloads:1190,totalCrossrefCites:4,totalDimensionsCites:7,abstract:"The treatment of patients with intravenous drug use (IVDU) has evolved to include a wide range of medications, psychiatric rehabilitation, and surgical interventions, especially for life-threatening complications such as infective endocarditis (IE). These interventions remain at the discretion of physicians, particularly surgeons, whose treatment decisions are influenced by several medical factors, unfortunately not without bias. The stigma associated with substance use disorder is prevalent, which leads to significant biases, even in the healthcare system. This bias is heightened when IVDU patients require repeat valve replacement surgeries for IE due to continued drug use. Patients who receive a valve replacement and continue to use illicit drugs intravenously often return to their medical providers, months to a few years later, with a reinfection of their bioprosthetic valve; such patients require additional surgeries which are at the center of many ethical discussions due to high mortality rates, for many complex medical and social reasons, associated with continuous chemical dependency after surgical interventions. This chapter examines the ethics of repeat heart valve replacement surgery for patients who are struggling with addiction. Considerations of justice, the fiduciary therapeutic relationship, and guiding ethical principles justify medically beneficial repeat heart valve replacement surgeries for IVDU patient populations.",book:{id:"6556",slug:"advanced-concepts-in-endocarditis",title:"Advanced Concepts in Endocarditis",fullTitle:"Advanced Concepts in Endocarditis"},signatures:"Julie M. Aultman, Emanuela Peshel, Cyril Harfouche and Michael S.\nFirstenberg",authors:[{id:"64343",title:"Dr.",name:"Michael S.",middleName:null,surname:"Firstenberg",slug:"michael-s.-firstenberg",fullName:"Michael S. Firstenberg"},{id:"227150",title:"Ms.",name:"Emanuela",middleName:null,surname:"Peshel",slug:"emanuela-peshel",fullName:"Emanuela Peshel"},{id:"229719",title:"Dr.",name:"Julie",middleName:"M.",surname:"Aultman",slug:"julie-aultman",fullName:"Julie Aultman"},{id:"232060",title:"Mr.",name:"Cyril",middleName:null,surname:"Harfouche",slug:"cyril-harfouche",fullName:"Cyril Harfouche"}]},{id:"43498",doi:"10.5772/54928",title:"Treatment of Coronary Artery Bypass Graft Failure",slug:"treatment-of-coronary-artery-bypass-graft-failure",totalDownloads:4819,totalCrossrefCites:4,totalDimensionsCites:7,abstract:null,book:{id:"3542",slug:"artery-bypass",title:"Artery Bypass",fullTitle:"Artery Bypass"},signatures:"M.A. Beijk and R.E. Harskamp",authors:[{id:"164896",title:"Dr.",name:"Marcel",middleName:"A.",surname:"Beijk",slug:"marcel-beijk",fullName:"Marcel Beijk"},{id:"165094",title:"Dr.",name:"Ralf",middleName:null,surname:"Harskamp",slug:"ralf-harskamp",fullName:"Ralf Harskamp"}]}],mostDownloadedChaptersLast30Days:[{id:"80213",title:"Evolution of Heart Transplantation Surgical Techniques",slug:"evolution-of-heart-transplantation-surgical-techniques",totalDownloads:277,totalCrossrefCites:0,totalDimensionsCites:0,abstract:"Organ transplantation has kindled the human imagination since the beginning of time. Prehistorically, transplantation appeared as mythological stories: from creatures with body parts from different species, the heart transplant between two Chinese soldiers by Pien Ch’iao, to the leg transplant by physician Saints Cosmas and Damian. By 19th century, the transplantation concept become possible by extensive contributions from scientists and clinicians whose works had taken generations. Although Alexis Carrel is known as the founding father of experimental organ transplantation, many legendary names had contributed to the experimental works of heart transplantation, including Guthrie, Mann, and Demikhov. The major contribution to experimental heart transplantation before the clinical era were made by a team lead by Richard Lower and Norman Shumway at Stanford University in the early 1960s. They played the vital role in developing experimental and clinical heart transplantation as it is known today. Using Shumway biatrial technique Christiaan Barnard started a new era of clinical heart transplantation, by performing the first in man human-to-human heart transplantation in 1967. The techniques of heart transplant have evolved since the first heart transplant. This chapter will summarize the techniques that have been used in clinical heart transplantation.",book:{id:"11236",slug:"heart-transplantation-new-insights-in-therapeutic-strategies",title:"Heart Transplantation",fullTitle:"Heart Transplantation - New Insights in Therapeutic Strategies"},signatures:"Samuel Jacob, Anthony N. Pham and Si M. Pham",authors:[{id:"439327",title:"Prof.",name:"Samuel",middleName:null,surname:"Jacob",slug:"samuel-jacob",fullName:"Samuel Jacob"},{id:"439329",title:"Prof.",name:"Si M.",middleName:null,surname:"Pham",slug:"si-m.-pham",fullName:"Si M. Pham"},{id:"451575",title:"Mr.",name:"Anthony N.",middleName:null,surname:"Pham",slug:"anthony-n.-pham",fullName:"Anthony N. Pham"}]},{id:"70032",title:"Coronary Artery Bypass Grafting: Surgical Anastomosis: Tips and Tricks",slug:"coronary-artery-bypass-grafting-surgical-anastomosis-tips-and-tricks",totalDownloads:1424,totalCrossrefCites:0,totalDimensionsCites:3,abstract:"The definite feature of coronary artery disease is the focal narrowing in the vascular endothelium, and this leads to the decrease in the flow of blood to the myocardium. Atherosclerotic plaque is the main lesion. These patients can present with chest pain (angina or myocardial infarction) and need further workup noninvasively and invasively for the management. The main reasons for myocardial revascularization can be: (1) relief from symptoms of myocardial ischemia; (2) reduce the risks of future mortality; (3) to treat or prevent morbidities such as myocardial infarction, arrhythmias, or heart failure. Coronary artery bypass grafting (CABG) is the surgical technique of cardiac revascularization. In 1910, Dr. Alexis Carrel described a series of canine experiments in which he devised means to treat CAD by creating a “complementary circulation” for the diseased native coronary arteries. No clinical translation occurred at the time, but he was awarded the Nobel Prize in Medicine. Experimental refinements of coronary arterial revascularization, including the use of internal thoracic artery (ITA) grafts, were later reported by Murray and colleagues, Demikhov, and Goetz and colleagues in the 1950s and early 1960s. Dr. Rene Favaloro performed his first coronary bypass operation in May 1967 with an interposed saphenous vein graft (SVG) and shortly thereafter used aortocoronary bypasses sutured proximally to the ascending aorta. The stenosed segment is bypassed using an arterial or venous graft. Left internal thoracic artery is the most commonly used artery, and long saphenous vein is the most commonly used vein for the coronary artery grafting to reestablish the blood flow to the compromised myocardium. This can be performed with or without the help of cardiopulmonary bypass machine and also with or without arresting the heart. These techniques are called as on-pump beating or on-pump arrested and off-pump beating coronary artery bypass grafting surgery. Distal and proximal anastomoses are usually performed in an end-to-side manner, but in the case of doing sequential grafting, side-to-side anastomosis is also performed proximal to the end-to-side anastomosis. In this chapter we are going to discuss the coronary artery bypass grafting tips and tricks in details.",book:{id:"9060",slug:"the-current-perspectives-on-coronary-artery-bypass-grafting",title:"The Current Perspectives on Coronary Artery Bypass Grafting",fullTitle:"The Current Perspectives on Coronary Artery Bypass Grafting"},signatures:"Mohd. Shahbaaz Khan",authors:[{id:"278633",title:"Dr.",name:"Mohd. Shahbaaz",middleName:null,surname:"Khan",slug:"mohd.-shahbaaz-khan",fullName:"Mohd. Shahbaaz Khan"}]},{id:"65984",title:"Low Flow Low Gradient Severe Aortic Stenosis: Diagnosis and Treatment",slug:"low-flow-low-gradient-severe-aortic-stenosis-diagnosis-and-treatment",totalDownloads:2301,totalCrossrefCites:0,totalDimensionsCites:0,abstract:"Approximately 40% of patients with aortic stenosis (AS) show discordant Doppler-echocardiographic parameters with aortic valve area (AVA) <1 cm2 and/or index iAVA <0.6 cm2/m2 (consistent with severe AS) and the mean gradient (MG) <40 mmHg, consistent with mild/moderate AS. Accurate diagnosis of true severe low flow low gradient AS versus pseudo-severe aortic stenosis is important for prognosis and optimal timing for intervention. Doppler echocardiography using intravenous low dose dobutamine challenge is widely used for differentiating pseudo-severe from true severe aortic stenosis. However, relying on echocardiography alone may have limitations in accurate diagnosis. Reliable diagnosis using echocardiography is dependent on multiple factors like the angle of interrogation of the aortic jet, the assumption that the LVOT area is circular in cross section, optimal echo windows, the presence of underlying subclinical coronary artery disease prior to dobutamine challenge etc. In this chapter, we describe non-invasive and invasive strategies to assess the aortic valve using dobutamine stress. Direct measurement of gradients across the aortic valve while estimating the change in cardiac output and aortic valve area with increments of dobutamine infusion dose is complementary, safe and useful when conventional echocardiography techniques are inconclusive. Finally, the chapter describes effective strategies of treatment for low gradient severe aortic stenosis, including the role for diagnostic balloon valvuloplasty, in the era of transcatheter valve replacement (TAVR).",book:{id:"8218",slug:"aortic-stenosis-current-perspectives",title:"Aortic Stenosis",fullTitle:"Aortic Stenosis - Current Perspectives"},signatures:"Faeez Mohamad Ali, Vindhya Wilson and Rajesh Nair",authors:[{id:"280651",title:"Dr.",name:"Rajesh",middleName:null,surname:"Nair",slug:"rajesh-nair",fullName:"Rajesh Nair"},{id:"280829",title:"Dr.",name:"Faeez",middleName:null,surname:"Mohamad Ali",slug:"faeez-mohamad-ali",fullName:"Faeez Mohamad Ali"},{id:"290351",title:"Dr.",name:"Vindhya",middleName:null,surname:"Wilson",slug:"vindhya-wilson",fullName:"Vindhya Wilson"}]},{id:"59547",title:"Left Ventricular Assist Device Infections",slug:"left-ventricular-assist-device-infections",totalDownloads:1480,totalCrossrefCites:0,totalDimensionsCites:0,abstract:"Left ventricular assist device (LVAD) infections are important causes of morbidity and mortality in patients who receive these mechanical circulatory supports as a bridge to transplantation (BTT) or as destination therapy (DT) (for individuals who are not candidates for cardiac transplant). Infections are more common among persons who received pulsatile flow LVADs as opposed to newer continuous flow (CF) devices. Other risk factors for infection include obesity, renal failure, depression and immunosuppression. An LVAD infection increases the risk of infections in persons who undergo cardiac transplantation. Infections include percutaneous site, driveline, pump pocket and pump/cannula infections; sepsis, bacteremia, mediastinitis and endocarditis. Diagnosis is achieved by monitoring LVAD flow parameters and observing typical clinical and laboratory manifestations of infection. Imaging such as PET-CT or SPECT-CT imaging can be helpful to establish a diagnosis of pump pocket infection. Echocardiography may aid in detecting native valve endocarditis and thrombus associated with the LVAD. The most common pathogens include Staphylococcus, Corynebacterium, Enterococcus, Pseudomonas and Candida spp. Treatment requires targeted antimicrobials plus surgical debridement of infected tissue and device components. In cases of pump/cannula/LVAD endocarditis, especially if fungal pathogens or Mycobacterium chimaera are involved, LVAD removal/reimplantation vs. transplant is necessary, combined with extended antimicrobial therapy.",book:{id:"6556",slug:"advanced-concepts-in-endocarditis",title:"Advanced Concepts in Endocarditis",fullTitle:"Advanced Concepts in Endocarditis"},signatures:"Marion J. Skalweit",authors:[{id:"186717",title:"Associate Prof.",name:"Marion",middleName:null,surname:"Skalweit",slug:"marion-skalweit",fullName:"Marion Skalweit"}]},{id:"60658",title:"Humoral Rejection in Cardiac Transplantation: Management of Antibody-Mediated Rejection",slug:"humoral-rejection-in-cardiac-transplantation-management-of-antibody-mediated-rejection",totalDownloads:1097,totalCrossrefCites:0,totalDimensionsCites:0,abstract:"After a successful heart transplantation, fundamental keys to achieve good results in the long term are to establish immunosuppressive therapy in the postoperative period in an appropriate manner and to ensure continuity of follow-ups. Despite the fact that these stages are maintained perfectly, patients may face one or more rejection episodes. T-cell-mediated acute cellular rejection of the cardiac allograft has well-established treatment algorithms, whereas antibody-mediated rejection (AMR) is challenging to diagnose, and its treatment varies between centers. Investigators reported that AMR is among the most important factors to improving long-term outcomes. Improved understanding of the roles of acute and chronic AMR has evolved in recent years following a major progress in the technical ability to detect and quantify recipient antihuman leukocyte antigen (HLA) antibody production. Recently, a study of the immunobiology of B cells and plasma cells that pertains to allograft rejection and tolerance has emerged. There are some questions regarding the classification of AMR, the diagnostic approaches, and the treatment strategies for managing. In this chapter, we are discuss the effector mechanisms that are used by antibodies to eliminate antigens and clinical experience about AMR and its treatment with a discussion about the latest articles.",book:{id:"6558",slug:"heart-transplantation",title:"Heart Transplantation",fullTitle:"Heart Transplantation"},signatures:"Umit Kervan, Dogan Emre Sert and Nesrin Turan",authors:[{id:"227772",title:"Prof.",name:"Umit",middleName:null,surname:"Kervan",slug:"umit-kervan",fullName:"Umit Kervan"},{id:"243592",title:"Dr.",name:"Dogan Emre",middleName:null,surname:"Sert",slug:"dogan-emre-sert",fullName:"Dogan Emre Sert"},{id:"243593",title:"Dr.",name:"Nesrin",middleName:null,surname:"Turan",slug:"nesrin-turan",fullName:"Nesrin Turan"}]}],onlineFirstChaptersFilter:{topicId:"984",limit:6,offset:0},onlineFirstChaptersCollection:[],onlineFirstChaptersTotal:0},preDownload:{success:null,errors:{}},subscriptionForm:{success:null,errors:{}},aboutIntechopen:{},privacyPolicy:{},peerReviewing:{},howOpenAccessPublishingWithIntechopenWorks:{},sponsorshipBooks:{sponsorshipBooks:[],offset:8,limit:8,total:0},allSeries:{pteSeriesList:[{id:"14",title:"Artificial Intelligence",numberOfPublishedBooks:9,numberOfPublishedChapters:90,numberOfOpenTopics:6,numberOfUpcomingTopics:0,issn:"2633-1403",doi:"10.5772/intechopen.79920",isOpenForSubmission:!0},{id:"7",title:"Biomedical Engineering",numberOfPublishedBooks:12,numberOfPublishedChapters:107,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2631-5343",doi:"10.5772/intechopen.71985",isOpenForSubmission:!0}],lsSeriesList:[{id:"11",title:"Biochemistry",numberOfPublishedBooks:33,numberOfPublishedChapters:330,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2632-0983",doi:"10.5772/intechopen.72877",isOpenForSubmission:!0},{id:"25",title:"Environmental Sciences",numberOfPublishedBooks:1,numberOfPublishedChapters:19,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2754-6713",doi:"10.5772/intechopen.100362",isOpenForSubmission:!0},{id:"10",title:"Physiology",numberOfPublishedBooks:14,numberOfPublishedChapters:145,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2631-8261",doi:"10.5772/intechopen.72796",isOpenForSubmission:!0}],hsSeriesList:[{id:"3",title:"Dentistry",numberOfPublishedBooks:9,numberOfPublishedChapters:140,numberOfOpenTopics:2,numberOfUpcomingTopics:0,issn:"2631-6218",doi:"10.5772/intechopen.71199",isOpenForSubmission:!0},{id:"6",title:"Infectious Diseases",numberOfPublishedBooks:13,numberOfPublishedChapters:123,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2631-6188",doi:"10.5772/intechopen.71852",isOpenForSubmission:!0},{id:"13",title:"Veterinary Medicine and Science",numberOfPublishedBooks:11,numberOfPublishedChapters:112,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2632-0517",doi:"10.5772/intechopen.73681",isOpenForSubmission:!0}],sshSeriesList:[{id:"22",title:"Business, Management and Economics",numberOfPublishedBooks:1,numberOfPublishedChapters:22,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2753-894X",doi:"10.5772/intechopen.100359",isOpenForSubmission:!0},{id:"23",title:"Education and Human Development",numberOfPublishedBooks:0,numberOfPublishedChapters:11,numberOfOpenTopics:1,numberOfUpcomingTopics:1,issn:null,doi:"10.5772/intechopen.100360",isOpenForSubmission:!0},{id:"24",title:"Sustainable Development",numberOfPublishedBooks:1,numberOfPublishedChapters:19,numberOfOpenTopics:5,numberOfUpcomingTopics:0,issn:"2753-6580",doi:"10.5772/intechopen.100361",isOpenForSubmission:!0}],testimonialsList:[{id:"6",text:"It is great to work with the IntechOpen to produce a worthwhile collection of research that also becomes a great educational resource and guide for future research endeavors.",author:{id:"259298",name:"Edward",surname:"Narayan",institutionString:null,profilePictureURL:"https://mts.intechopen.com/storage/users/259298/images/system/259298.jpeg",slug:"edward-narayan",institution:{id:"3",name:"University of Queensland",country:{id:null,name:"Australia"}}}},{id:"13",text:"The collaboration with and support of the technical staff of IntechOpen is fantastic. 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\r\n\tEducation and Human Development is an interdisciplinary research area that aims to shed light on topics related to both learning and development. This Series is intended for researchers, practitioners, and students who are interested in understanding more about these fields and their applications.
",coverUrl:"https://cdn.intechopen.com/series/covers/23.jpg",latestPublicationDate:"August 12th, 2022",hasOnlineFirst:!0,numberOfPublishedBooks:0,editor:{id:"280770",title:"Dr.",name:"Katherine K.M.",middleName:null,surname:"Stavropoulos",slug:"katherine-k.m.-stavropoulos",fullName:"Katherine K.M. Stavropoulos",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRdFuQAK/Profile_Picture_2022-05-24T09:03:48.jpg",biography:"Katherine Stavropoulos received her BA in Psychology from Trinity College, in Connecticut, USA and her Ph.D. in Experimental Psychology from the University of California, San Diego. She completed her postdoctoral work at the Yale Child Study Center with Dr. James McPartland. Dr. Stavropoulos’ doctoral dissertation explored neural correlates of reward anticipation to social versus nonsocial stimuli in children with and without autism spectrum disorders (ASD). She has been a faculty member at the University of California, Riverside in the School of Education since 2016. Her research focuses on translational studies to explore the reward system in ASD, as well as how anxiety contributes to social challenges in ASD. She also investigates how behavioral interventions affect neural activity, behavior, and school performance in children with ASD. She is also involved in the diagnosis of children with ASD and is a licensed clinical psychologist in California. She is the Assistant Director of the SEARCH Center at UCR and is a faculty member in the Graduate Program in Neuroscience.",institutionString:null,institution:{name:"University of California, Riverside",institutionURL:null,country:{name:"United States of America"}}},editorTwo:null,editorThree:null},subseries:{paginationCount:2,paginationItems:[{id:"89",title:"Education",coverUrl:"https://cdn.intechopen.com/series_topics/covers/89.jpg",isOpenForSubmission:!1,editor:{id:"260066",title:"Associate Prof.",name:"Michail",middleName:null,surname:"Kalogiannakis",slug:"michail-kalogiannakis",fullName:"Michail Kalogiannakis",profilePictureURL:"https://mts.intechopen.com/storage/users/260066/images/system/260066.jpg",biography:"Michail Kalogiannakis is an Associate Professor of the Department of Preschool Education, University of Crete, and an Associate Tutor at School of Humanities at the Hellenic Open University. He graduated from the Physics Department of the University of Crete and continued his post-graduate studies at the University Paris 7-Denis Diderot (D.E.A. in Didactic of Physics), University Paris 5-René Descartes-Sorbonne (D.E.A. in Science Education) and received his Ph.D. degree at the University Paris 5-René Descartes-Sorbonne (PhD in Science Education). His research interests include science education in early childhood, science teaching and learning, e-learning, the use of ICT in science education, games simulations, and mobile learning. He has published over 120 articles in international conferences and journals and has served on the program committees of numerous international conferences.",institutionString:"University of Crete",institution:{name:"University of Crete",institutionURL:null,country:{name:"Greece"}}},editorTwo:{id:"422488",title:"Dr.",name:"Maria",middleName:null,surname:"Ampartzaki",slug:"maria-ampartzaki",fullName:"Maria Ampartzaki",profilePictureURL:"https://mts.intechopen.com/storage/users/422488/images/system/422488.jpg",biography:"Dr Maria Ampartzaki is an Assistant Professor in Early Childhood Education in the Department of Preschool Education at the University of Crete. Her research interests include ICT in education, science education in the early years, inquiry-based and art-based learning, teachers’ professional development, action research, and the Pedagogy of Multiliteracies, among others. She has run and participated in several funded and non-funded projects on the teaching of Science, Social Sciences, and ICT in education. She also has the experience of participating in five Erasmus+ projects.",institutionString:"University of Crete",institution:{name:"University of Crete",institutionURL:null,country:{name:"Greece"}}},editorThree:null},{id:"90",title:"Human Development",coverUrl:"https://cdn.intechopen.com/series_topics/covers/90.jpg",isOpenForSubmission:!0,editor:{id:"191040",title:"Dr.",name:"Tal",middleName:null,surname:"Dotan Ben-Soussan",slug:"tal-dotan-ben-soussan",fullName:"Tal Dotan Ben-Soussan",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bSBf1QAG/Profile_Picture_2022-03-18T07:56:11.jpg",biography:"Tal Dotan Ben-Soussan, Ph.D., is the director of the Research Institute for Neuroscience, Education and Didactics (RINED) – Paoletti Foundation. 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