Role of echocardiography in screening and evaluation of athletes

Heart ◽  
2020 ◽  
pp. heartjnl-2020-317996 ◽  
Author(s):  
David Niederseer ◽  
Valentina Alice Rossi ◽  
Christine Kissel ◽  
Johannes Scherr ◽  
Stefano Caselli ◽  
...  

The term athlete’s heart describes structural, functional and electrical adaptations of the cardiovascular system due to repetitive intense exercise. Physiological cardiac adaptations in athletes, however, may mimic features of cardiac diseases and therefore make it difficult to distinguish physiological adaptions from disease. Furthermore, regular exercise may also lead to pathological adaptions that can promote or worsen cardiac disease (eg, atrial dilation/atrial fibrillation, aortic dilation/aortic dissection and rhythm disorders). Sudden cardiac death (SCD) is a major concern in sports cardiology, and preparticipation screening (PPS) has demonstrated to be effective in identifying athletes at risk for SCD. In Europe, PPS is advocated to include personal and family history, physical examination and ECG, with further workup including echocardiography only if the initial screening investigations show abnormal findings. We review the current available evidence for echocardiography as a screening tool for conditions associated with SCD in recreational and professional athletes and advocate to include screening echocardiography to be performed at least twice in an athlete’s career. We recommend that the first echocardiography is performed during adolescence to rule out structural heart conditions associated with SCD that cannot be detected by ECG, especially mitral valve prolapse, coronary artery anomalies, bicuspid aortic valve and dilatation of the aorta. A second echocardiography could be performed from the age of 30–35 years, when athletes age and become master athletes, to especially evaluate pathological cardiac remodelling to exercise (eg, atrial and/or right ventricular dilation), late onset cardiomyopathies and wall motion abnormalities due to myocarditis or coronary artery disease.

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
E Gherbesi ◽  
G Chiarello ◽  
V L Paiocchi ◽  
L A Leo ◽  
S A Schlossbauer ◽  
...  

Abstract Background In non-ST-segment elevation acute coronary syndromes (NSTE-ACS) patients, several studies demonstrated that 2D speckle tracking echocardiography (STE) is able to predict the presence of coronary artery disease (CAD). Conversely, the role of STE for the localization of significant CAD is less well established. Purpose To investigate the role of territorial longitudinal (TLS) and circumferential strain (TCS) assessed with STE as a non-invasive predictor of localization of significant CAD in patients with NSTE-ACS. Methods We retrospectively enrolled NSTE-ACS patients with significant stenosis (≥70%) at least in one major epicardial coronary artery and without previous cardiovascular events over two years of time. Echocardiography was recorded before coronary angiography and myocardial strain was evaluated offline by an operator blinded to clinical data. Territorial strain was calculated grouping and averaging the strain values of the segments perfused by the 3 major coronary arteries. Results 150 patients were included (age 66.3±11.8 years, 71% male; 90.7% NSTEMI and 9.3% unstable angina). ROC curve analysis demonstrated the ability of TLS and TCS to identify the presence of coronary stenosis of LAD, LCX or RCA (AUC for TLS-LAD 0.74 [0.66–0.82] p=0.0001; LCX 0.73 [0.65–0.81] p=0.0001; RCA 0.69 [0.60–0.77] p=0.0001-AUC for TCS-LAD 0.80 [0.70–0.90] p=0.0001; LCX 0.76 [0.67–0.85] p=0.0001; RCA 0.65 [0.55–0.75] p=0.0001), superior to territorial wall motion score index (Figure 1). The diagnostic value was confirmed in the subgroup of patients without wall motion abnormalities for TLS and for TCS, except for RCA. Conclusion Territorial strain assessed with STE might be a non-invasive tool to localize coronary artery stenosis in patients with NSTE-ACS, even without wall motion abnormalities. FUNDunding Acknowledgement Type of funding sources: None. Figure 1. ROC curve analyses


2006 ◽  
Vol 3 (2) ◽  
pp. 68-72
Author(s):  
Jennifer Mieres ◽  
Leslee J Shaw ◽  
Robert C Hendel ◽  
D Douglas Miller ◽  
Robert Bonow ◽  
...  


Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 469-P
Author(s):  
MILOS MRAZ ◽  
ANNA CINKAJZLOVA ◽  
ZDENA LACINOVÁ ◽  
JANA KLOUCKOVA ◽  
HELENA KRATOCHVILOVA ◽  
...  

Author(s):  
Г.А. Березовская ◽  
Е.С. Клокова ◽  
Н.Н. Петрищев

Гены тромбообразования и фолатного обмена играют важную роль в развитии и прогрессии ишемической болезни сердца (ИБС). Однако о возможной роли полиморфных маркеров в рецидиве ИБС после чрескожного коронарного вмешательства (ЧКВ) известно недостаточно. Цель исследования: Оценить роль генетических факторов системы тромбообразования и фолатного обмена (полиморфных маркеров генов F5, F2, F13A1, PAI1, HPA1, MTHFR, FGB ), в возобновление клиники ИБС после ЧКВ. Методика: Исследование проводили с использованием выборки из 90 больных ИБС в возрасте от 40 до 75 лет: 75 пациентов после планового ЧКВ (60 мужчин и 15 женщин) и 15 лиц после экстренного ЧКВ (12 мужчин и 3 женщины). Молекулярно-генетическое исследование было выполнено с помощью комплекта реагентов «Сердечно-сосудистые заболевания СтрипМетод»® (ViennaLab Diagnostics GmbH, Австрия), выявляющие следующие варианты: F5, F2, F13A1, PAI1, HPA1, MTHFR, FGB . Результаты: В результате исследования была показана ассоциация полиморфного маркера G103T ( Val34Leu ) гена F13A1 (фактор свертываемости крови 13, субъединица A1) с развитием рецидивирующего состояния ИБС после ЧКВ. Выявлены статистически значимые различия в распределении частот генотипов полиморфного маркера Val34Leu гена F13A1 . Показано, что частота генотипа Val/Val у пациентов с осложнениями была выше, чем у пациентов без таковых: 0,700 и 0,400 соответственно (c = 7,78; p = 0,020), при этом генотип Val/Val проявил себя как фактор риска развития осложнений: ОШ = 3,50 (95%ДИ 1,37-8,93). При сравнении аллелей выявили, что частота аллеля L у больных с осложнениями была ниже, чем у лиц без таковых: 0,167 и 0,375 соответственно (p = 0,004), и носительство аллеля L уменьшало вероятность развития осложнений: ОШ = 0,33 (95%ДИ 0,15-0,72). Заключение: Носительство варианта 34V гена F13A1 , кодирующего A-субъединицу фактора свёртывания 13, предрасполагает к возобновлению клинических проявлений ИБС после ЧКВ. Genes of thrombosis and folate metabolism play an important role in development and progression of coronary artery disease (CAD). However, a possible role of polymorphic markers in CAD relapse following percutaneous coronary intervention (PCI) is not sufficiently understood. Background. Reports have indicated an association of genetic factors generally related with thrombophilia and recurrence of symptoms for coronary artery disease (CAD) following a percutaneous coronary intervention (PCI) due to restenosis and in-stent thrombosis. However, the relapse can also be caused by progression of atherosclerosis and endothelial dysfunction in unoperated blood vessels. Aim: To assess the role of genetic risk factors involved in thrombosis and folate metabolism (polymorphic markers of F5, F2, F13A1, PAI1, HPA1, MTHFR, and FGB genes) in recurrence of CAD symptoms after PCI. Methods: The study included 90 patients with CAD aged 40-75; 75 of these patients had undergone elective PCI (60 men and 15 women) and 15 patients - emergency PCI (12 men and 3 women). Molecular genetic tests were performed using a CVD StripAssays® reagent kit (ViennaLab Diagnostics GmbH, Austria) to identify the following genetic variations: F5, F2, F13A1, PAI1, HPA1, MTHFR, and FGB . Results: The study results showed a significant association of the G103T ( Val34Leu ) polymorphism in the F13A1 gene with relapses of IHD after PCI. Significant differences were found in genotype distribution frequencies of the Val34Leu polymorphism in the F13A1 gene. The frequency of Val / Val genotype was higher in patients with complications than without complications, 0.700 and 0.400, respectively (c = 7.78, p = 0.020). Furthermore, the Val/Val genotype can be classified as a risk factor for complications (OR = 3.50; 95% CI, 1.37-8.93). The L allele frequency was lower in patients with complications than in those without complications (0.167 and 0.375, respectively, p = 0.004), and carriage of the L allele reduced the likelihood of complications (OR = 0.33; 95% CI 0.15-0.72). Conclusion: Carriage of the 34V variant in the F13A1 gene that encodes the coagulation factor XIII A subunit predisposes to a relapse of CAD symptoms after PCI.


Author(s):  
Ishita Sharma ◽  
Tapan Behl ◽  
Simona Bungau ◽  
Monika Sachdeva ◽  
Arun Kumar ◽  
...  

Abstract:: Angina pectoris, associated with coronary artery disease, a cardiovascular disease where, pain is caused by adverse oxygen supply in myocardium, resulting in contractility and discomfort in chest. Inflammasomes, triggered by stimuli due to infection and cellular stress have identified to play a vital role in the progression of cardiovascular disorders and thus, causing various symptoms like angina pectoris. Nlrp3 inflammasome, a key contributor in the pathogenesis of angina pectoris, requires activation and primary signaling for the commencement of inflammation. Nlrp3 inflammasome elicit out an inflammatory response by emission of pro inflammatory cytokines by ROS (reactive oxygen species) production, mobilization of K+ efflux and Ca2+ and by activation of lysosome destabilization that eventually causes pyroptosis, a programmed cell death process. Thus, inflammasome are considered to be one of the factors involved in the progression of coronary artery diseases and have an intricate role in development of angina pectoris.


Life ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 737
Author(s):  
Marko Kumric ◽  
Josip A. Borovac ◽  
Tina Ticinovic Kurir ◽  
Dinko Martinovic ◽  
Ivan Frka Separovic ◽  
...  

Coronary artery disease (CAD) is widely recognized as one of the most important clinical entities. In recent years, a large body of accumulated data suggest that coronary artery calcification, a process highly prevalent in patients with CAD, occurs via well-organized biologic processes, rather than passively, as previously regarded. Matrix Gla protein (MGP), a vitamin K-dependent protein, emerged as an important inhibitor of both intimal and medial vascular calcification. The functionality of MGP hinges on two post-translational modifications: phosphorylation and carboxylation. Depending on the above-noted modifications, various species of MGP may exist in circulation, each with their respective level of functionality. Emerging data suggest that dysfunctional species of MGP, markedly, dephosphorylated-uncarboxylated MGP, might find its application as biomarkers of microvascular health, and assist in clinical decision making with regard to initiation of vitamin K supplementation. Hence, in this review we summarized the current knowledge with respect to the role of MGP in the complex network of vascular calcification with concurrent inferences to CAD. In addition, we discussed the effects of warfarin use on MGP functionality, with concomitant implications to coronary plaque stability.


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