Echocardiography as a Screening Test for Myocardial Scarring in Children with Hypertrophic Cardiomyopathy

Abstract

Introduction. Hypertrophic cardiomyopathy (HCM) is burdened with morbidity and mortality including tachyarrhythmias and sudden cardiac death. These complications are attributed in part to the formation of proarrhythmic scars in the myocardium. The presence of extensive LGE is a risk factor for adverse outcomes in HCM. Late gadolinium enhancement (LGE) cardiac magnetic resonance imaging (cMRI) is the standard for the noninvasive evaluation of myocardial scars. However, echocardiography represents an attractive screening tool for myocardial scarring. The aim of this study was to compare the suitability of echocardiography to detect myocardial scars to the standard of cMRI-LGE. Methods. The cMRI studies and echocardiograms from 56 consecutive children with HCM were independently evaluated for the presence of cMRI-LGE and echocardiographic evidence of scarring by expert readers. Results. Echocardiography had a high sensitivity (93%) and negative predictive value (94%) in comparison to LGE. The false positive rate was high, leading to a low specificity (37%) and a low positive predictive value (35%). Conclusions. Given the poor specificity and positive predictive value, echocardiography is not a suitable screening test for the presence of myocardial scarring in children with HCM. However, children without echocardiographic evidence of myocardial scarring may not need to undergo cardiac magnetic resonance imaging to “rule in” LGE.

The value of fragmented QRS in predicting the prognosis of chronic total occlusion patients with myocardial infarction history undergoing percutaneous coronary intervention: A 24‐months follow‐up study

“…After opening the CTO vessels in patients with fQRS on ECG, the ischemic and dormant myocardium are supplied with blood again. This part of the myocardium will recover its function, which can increase the myocardial blood supply and oxygen supply, thus improving the cardiac function and the quality of life of these patients 44‐46 . Also, with the extension of follow‐up time, the improvement in cardiac function may further increase, which shows that the blood supply of those ischemic myocardium becomes more and more sufficient with time.…”

“…This may be because, when the coronary artery is in progressive stenosis or even complete occlusion, the mechanism of myocardial ischemia protection promotes the formation of CCC, 43 mainly through the mechanism of myocardial ischemia/reperfusion injury, the mechanism of myocardial cell protection, the mechanism of myocardial ischemic pretreatment and the mechanism of increasing the secretion of various growth factors 26,27,40,44 . FQRS complex has been explained by inhomogeneous activation of the myocardium due to myocardial scar or ischemia 28,32,45 . Infarct size is inversely related to collateral circulation and directly related to the occlusion time.…”

“…Infarct size is inversely related to collateral circulation and directly related to the occlusion time. There may be no infracted myocardium within the occluded artery territory in about half of patients with chronic total occlusion 40,41,45 . These patients may remain completely asymptomatic.…”

Reducing Cardiac Fibrosis: Na/K-ATPase Signaling Complex as a Novel Target

“…Serum levels of procollagen type I C-terminal peptide (PCIP) and procollagen type III N-terminal peptide (PIIINP) were often used as secondary surrogates for assessment of tissue fibrosis [52], but their correlation to cardiac fibrosis and cardiac function has not been validated in the clinical studies. Echocardiography has also been used for assessment of cardiac fibrosis with diastolic dysfunction [53–55]. More accurate methods using cardiac resonance imaging (CMR) and T1 mapping have been recently used clinically to evaluate cardiac fibrosis [56,57].…”

Hypertrophic Cardiomyopathy: The Molecular Genetics

“…HCM is primarily a cardiac disease that is one of the most common forms of heritable cardiac diseases [3][4] . HCM is the most common monogenetic disorder with a prevalence of 0.2% irrespective of gender, race or ethnicity [5][6][7] . HCM results in thickening of the myocardial wall and is almost always inherited as an autosomal dominant trait caused by point mutations in structural proteins within the contractile apparatus of cardiac myocytes 8 .…”