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Annals of Noninvasive Electrocardiology... Nov 2014Conventional assessment of left ventricular hypertrophy (LVH) using the electrocardiogram (ECG), for example, by the Sokolow-Lyon, Romhilt-Estes or Cornell criteria,... (Review)
Review
Conventional assessment of left ventricular hypertrophy (LVH) using the electrocardiogram (ECG), for example, by the Sokolow-Lyon, Romhilt-Estes or Cornell criteria, have relied on assessing changes in the amplitude and/or duration of the QRS complex of the ECG to quantify LV mass. ECG measures of LV mass have typically been validated by imaging with echocardiography or cardiovascular magnetic resonance imaging (CMR). However, LVH can be the result of diverse etiologies, and LVH is also characterized by pathological changes in myocardial tissue characteristics on the genetic, molecular, cellular, and tissue level beyond a pure increase in the number of otherwise normal cardiomyocytes. For example, slowed conduction velocity through the myocardium, which can be due to diffuse myocardial fibrosis, has been shown to be an important determinant of conventional ECG LVH criteria regardless of LV mass. Myocardial tissue characterization by CMR has emerged to not only quantify LV mass, but also detect and quantify the extent and severity of focal or diffuse myocardial fibrosis, edema, inflammation, myocarditis, fatty replacement, myocardial disarray, and myocardial deposition of amyloid proteins (amyloidosis), glycolipids (Fabry disease), or iron (siderosis). This can be undertaken using CMR techniques including late gadolinium enhancement (LGE), T1 mapping, T2 mapping, T2* mapping, extracellular volume fraction (ECV) mapping, fat/water-weighted imaging, and diffusion tensor CMR. This review presents an overview of current and emerging concepts regarding the diagnostic possibilities of both ECG and CMR for LVH in an attempt to narrow gaps in our knowledge regarding the ECG diagnosis of LVH.
Topics: Electrocardiography; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Magnetic Resonance Imaging; Reproducibility of Results
PubMed: 25367364
DOI: 10.1111/anec.12223 -
The Journal of the Royal College of... Mar 2017Cardiovascular disease is common in patients with chronic kidney disease. The increased risk of cardiovascular disease seen in this population is attributable to both... (Review)
Review
Cardiovascular disease is common in patients with chronic kidney disease. The increased risk of cardiovascular disease seen in this population is attributable to both traditional and novel vascular risk factors. Risk of sudden cardiac or arrhythmogenic death is greatly exaggerated in chronic kidney disease, particularly in patients with end stage renal disease where the risk is roughly 20 times that of the general population. The reasons for this increased risk are not entirely understood and while atherosclerosis is accelerated in the presence of chronic kidney disease, premature myocardial infarction does not solely account for the excess risk. Recent work demonstrates that the structure and function of the heart starts to alter early in chronic kidney disease, independent of other risk factors. The implications of cardiac remodelling and hypertrophy may predispose chronic kidney disease patients to heart failure, arrhythmia and myocardial ischaemia. Further research is needed to minimise cardiovascular risk associated with structural and functional heart disease associated with chronic kidney disease.
Topics: Cardiovascular Diseases; Dyslipidemias; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Organ Size; Renal Insufficiency, Chronic; Renin-Angiotensin System
PubMed: 28569289
DOI: 10.4997/JRCPE.2017.117 -
European Heart Journal. Cardiovascular... Jan 2022To investigate differences in the prevalence of left ventricular (LV) and left atrial (LA) remodelling in hypertensive patients using various thresholds defined by...
AIMS
To investigate differences in the prevalence of left ventricular (LV) and left atrial (LA) remodelling in hypertensive patients using various thresholds defined by international guidelines and data from the Echocardiographic Measurements in Normal Chinese Adults (EMINCA) study and different indexation methods.
METHODS AND RESULTS
LV mass (LVM), relative ventricular wall thickness, and LA volume (LAV) were measured using 2D echocardiography in 612 healthy volunteers selected from the EMINCA study population and 306 adult Chinese patients with hypertension who were age- and gender-matched using propensity score-matched analysis. LVM and LAV values were indexed to body surface area (BSA), height2.7, height1.7, and height2 recommended by guidelines or investigators. Using a previously reported method, LV geometry was divided into normal geometry, concentric remodelling, eccentric hypertrophy, and concentric hypertrophy. The prevalence of LV hypertrophy (LVH) and LV geometric patterns in hypertensive patients were compared using different thresholds and indexation methods. Echocardiographic thresholds from guidelines and healthy volunteers exhibited notable differences, particularly for LAV indexed to height2 and for LVM indexed to height1.7, which resulted in a significantly lower prevalence of LA dilatation and LVH in healthy volunteers. The total proportion of abnormal LV geometric patterns was significantly lower with thresholds from healthy volunteers than from guidelines when LVM was indexed to BSA, height1.7, and height2,7.
CONCLUSION
Using current echocardiographic thresholds and indexing methods recommended by guidelines may lead to significant misdiagnosis of LA dilatation, and abnormal LV geometry in Chinese patients with hypertension, and thresholds based on ethnic-specific normal echocardiographic reference values and an accurate indexing algorithm are warranted.
Topics: Adult; Atrial Remodeling; Echocardiography; Heart Ventricles; Humans; Hypertension; Hypertrophy, Left Ventricular
PubMed: 34718487
DOI: 10.1093/ehjci/jeab216 -
Echocardiography (Mount Kisco, N.Y.) Feb 2019The myocardial structure differs between secondary left ventricular hypertrophy (LVH) and hypertrophic cardiomyopathy (HCM). We investigated left ventricular function of...
BACKGROUND
The myocardial structure differs between secondary left ventricular hypertrophy (LVH) and hypertrophic cardiomyopathy (HCM). We investigated left ventricular function of these two types of hypertrophy using multilayer strain analysis with two-dimensional echocardiography.
METHODS
Transthoracic echocardiography (Vivid-E9) was performed in 240 patients with preserved left ventricular ejection fraction (LVEF ≥50%) and with either HCM (n = 80, 63 men, age 49.8 ± 14.1 years), hypertensive LVH (n = 80, 63 men, age 51.4 ± 13.3 years) or normal blood pressure and left ventricular structure (n = 80, 63 men, 50.8 ± 12.4 years). Quantitative multilayer longitudinal strain (LS), circumferential strain (CS), and radial strain (RS) were analyzed. The ratio of endo-/epi-myocardial strain was calculated.
RESULTS
Longitudinal strain was significantly (P < 0.001) lower in HCM patients than normal controls (15.2 ± 4.2% vs 23.1 ± 2.7%), especially in hypertrophic segments (14.5 ± 4.4% vs 17.2 ± 3.2% in nonhypertrophic segments, P < 0.01). LS was lower in patients with hypertensive LVH, similarly in all left ventricular segments (20.7 ± 3.7%, P < 0.001 vs controls). CS was lower in the mid- and epicardium (P < 0.01), but not endocardium in HCM (P = 0.4), and preserved in all myocardial layers in hypertensive LVH. The endo-/epi-myocardial ratios of both LS and CS were higher in HCM than hypertensive LVH (P < 0.01). RS was higher (P < 0.01) in HCM than hypertensive LVH and controls. Endocardial CS and global RS were correlated with LVEF (r ≥ 0.32, P < 0.01).
CONCLUSIONS
Hypertrophic cardiomyopathy patients had marked reductions in LS and CS, whereas patients with hypertensive LVH had less reduction in LS and preserved CS. The increased endo-/epi-myocardial ratios of LS and CS may be useful in differentiating HCM from hypertensive LVH.
Topics: Cardiomyopathy, Hypertrophic; Echocardiography; Female; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Male; Middle Aged
PubMed: 30561121
DOI: 10.1111/echo.14222 -
Archives of Cardiovascular Diseases Jan 2020Pulmonary arterial hypertension is a progressive and lethal cardiopulmonary disease. The rise in right ventricular afterload leads to right ventricular hypertrophy and... (Review)
Review
Pulmonary arterial hypertension is a progressive and lethal cardiopulmonary disease. The rise in right ventricular afterload leads to right ventricular hypertrophy and failure. Right ventricular failure is the most important prognostic factor for morbidity and mortality in pulmonary arterial hypertension or pulmonary hypertension caused by left heart diseases. Surprisingly, the right ventricle is not targeted by pulmonary arterial hypertension-specific therapies. The current profound lack of basic understanding of pulmonary arterial hypertension-related right ventricular remodelling can explain, at least in part, this paradox. The physiology and haemodynamic function of the right ventricle in the normal state differ considerably from those of the left ventricle, and the known mechanisms of left ventricular dysfunction cannot be generalized to right ventricular dysfunction. Ion channel activities and calcium homeostasis tightly regulate cardiac function, and their dysfunction contributes to the pathogenesis of cardiac diseases. This review focuses on the ion channels (potassium, calcium) and intracellular calcium handling remodelling involved in right ventricular hypertrophy and dysfunction caused by pulmonary arterial hypertension.
Topics: Action Potentials; Animals; Arterial Pressure; Calcium; Disease Models, Animal; Excitation Contraction Coupling; Heart Failure; Heart Rate; Heart Ventricles; Humans; Hypertrophy, Right Ventricular; Myocardial Contraction; Potassium; Prognosis; Pulmonary Arterial Hypertension; Pulmonary Artery; Risk Factors; Translational Research, Biomedical; Ventricular Dysfunction, Right; Ventricular Function, Right; Ventricular Remodeling
PubMed: 31924541
DOI: 10.1016/j.acvd.2019.10.009 -
Heart (British Cardiac Society) Oct 2017Diastolic dysfunction in aortic stenosis results primarily from left ventricular hypertrophy and myocardial fibrosis due to chronically elevated left ventricular... (Review)
Review
Diastolic dysfunction in aortic stenosis results primarily from left ventricular hypertrophy and myocardial fibrosis due to chronically elevated left ventricular systolic pressure. Currently, diastolic dysfunction does not have an explicit clinical role in management of patients with aortic stenosis. Studies have shown that improvement in diastolic dysfunction follows left ventricular remodelling after aortic valve replacement and that it occurs gradually or incompletely. Retrospective studies suggest that advanced grades of diastolic dysfunction at baseline are associated with increased mortality and adverse events even after aortic valve replacement. Recent studies have also associated myocardial fibrosis, a hallmark of diastolic dysfunction, with worse outcomes. In addition, these results were independent of the degree of aortic stenosis or valve replacement. Indirect evidence of the role of diastolic dysfunction in aortic stenosis also comes from paradoxical low-flow, low-gradient aortic stenosis, where disproportionate left ventricular hypertrophy leads to underfilling of the left ventricle, low-flow state and is associated with worse prognosis. Lastly, a limited number of studies suggest that worse diastolic dysfunction at baseline is detrimental in patients who develop aortic regurgitation after transcatheteraortic valve replacement, due to superimposition of volume overload on a stiff left ventricle. Current major limitations in our understanding of the prognostic role of diastolic dysfunction are the lack of universally accepted classification schemes, its dependence on dynamic loading conditions and the lack of larger prospective studies.
Topics: Aortic Valve Stenosis; Diastole; Echocardiography; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Prognosis; Ventricular Dysfunction, Left; Ventricular Function, Left; Ventricular Remodeling
PubMed: 28684437
DOI: 10.1136/heartjnl-2017-311506 -
Computers in Biology and Medicine Sep 2023Left ventricular hypertrophy (LVH) is a life-threatening condition in which the muscle of the left ventricle thickens and enlarges. Echocardiography is a test performed...
Left ventricular hypertrophy (LVH) is a life-threatening condition in which the muscle of the left ventricle thickens and enlarges. Echocardiography is a test performed by cardiologists and echocardiographers to diagnose this condition. The manual interpretation of echocardiography tests is time-consuming and prone to errors. To address this issue, we have developed an automated LVH diagnosis technique using deep learning. However, the availability of medical data is a significant challenge due to varying industry standards, privacy laws, and legal constraints. To overcome this challenge, we have proposed a data-efficient technique for automated LVH classification using echocardiography. Firstly, we collected our own dataset of normal and LVH echocardiograms from 70 patients in collaboration with a clinical facility. Secondly, we introduced novel zero-shot and few-shot algorithms based on a modified Siamese network to classify LVH and normal images. Unlike traditional zero-shot learning approaches, our proposed method does not require text vectors, and classification is based on a cutoff distance. Our model demonstrates superior performance compared to state-of-the-art techniques, achieving up to 8% precision improvement for zero-shot learning and up to 11% precision improvement for few-shot learning approaches. Additionally, we assessed the inter-observer and intra-observer reliability scores of our proposed approach against two expert echocardiographers. The results revealed that our approach achieved better inter-observer and intra-observer reliability scores compared to the experts.
Topics: Humans; Hypertrophy, Left Ventricular; Reproducibility of Results; Echocardiography; Electrocardiography; Heart Ventricles
PubMed: 37343469
DOI: 10.1016/j.compbiomed.2023.107129 -
Pediatric Cardiology Oct 2018Left ventricular hypertrophy (LVH) is a common finding on pediatric electrocardiography (ECG) leading to many referrals for echocardiography (echo). This study utilizes... (Comparative Study)
Comparative Study
Left ventricular hypertrophy (LVH) is a common finding on pediatric electrocardiography (ECG) leading to many referrals for echocardiography (echo). This study utilizes a novel analytics tool that combines ECG and echo databases to evaluate ECG as a screening tool for LVH. SQL Server 2012 data warehouse incorporated ECG and echo databases for all patients from a single institution from 2006 to 2016. Customized queries identified patients 0-18 years old with LVH on ECG and an echo performed within 24 h. Using data visualization (Tableau) and analytic (Stata 14) software, ECG and echo findings were compared. Of 437,699 encounters, 4637 met inclusion criteria. ECG had high sensitivity (≥ 90%) but poor specificity (43%), and low positive predictive value (< 20%) for echo abnormalities. ECG performed only 11-22% better than chance (AROC = 0.50). 83% of subjects with LVH on ECG had normal left ventricle (LV) structure and size on echo. African-Americans with LVH were least likely to have an abnormal echo. There was a low correlation between VR on ECG and echo-derived Z score of left ventricle diastolic diameter (r = 0.14) and LV mass index (r = 0.24). The data analytics client was able to mine a database of ECG and echo reports, comparing LVH by ECG and LV measurements and qualitative findings by echo, identifying an abnormal LV by echo in only 17% of cases with LVH on ECG. This novel tool is useful for rapid data mining for both clinical and research endeavors.
Topics: Adolescent; Child; Child, Preschool; Cross-Sectional Studies; Databases, Factual; Echocardiography; Electrocardiography; Female; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Infant; Infant, Newborn; Male; Mass Screening; Sensitivity and Specificity
PubMed: 29774391
DOI: 10.1007/s00246-018-1907-7 -
The International Journal of... Apr 2018There are a number of diseases which can increase left ventricular myocardial wall thickness through a number of different mechanisms. Multi-parametric mapping... (Review)
Review
There are a number of diseases which can increase left ventricular myocardial wall thickness through a number of different mechanisms. Multi-parametric mapping techniques are a new addition to the cardiovascular magnetic resonance (CMR) armoury with a number of potential clinical roles. In this review article, we will explore the role of imaging in left ventricular hypertrophy, and particularly developments in CMR. We focus on ability of CMR to characterize myocardial tissue using multiparametric mapping (native T1, T2 and extracellular volume mapping), to bridge from the microscopic histological domain and into the clinical domain of non-invasive imaging.
Topics: Cardiomyopathies; Contrast Media; Fibrosis; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Image Interpretation, Computer-Assisted; Magnetic Resonance Imaging; Predictive Value of Tests; Prognosis; Ventricular Function, Left; Ventricular Remodeling
PubMed: 29500729
DOI: 10.1007/s10554-018-1320-6 -
Journal of Hypertension Sep 2020We investigated the association between obstructive sleep apnoea (OSA) and subclinical cardiac organ damage through a meta-analysis of echocardiographic studies that... (Meta-Analysis)
Meta-Analysis
AIM
We investigated the association between obstructive sleep apnoea (OSA) and subclinical cardiac organ damage through a meta-analysis of echocardiographic studies that provided data on left ventricular hypertrophy (LVH), assessed as a categorical or continuous variable.
DESIGN
The PubMed, OVID-MEDLINE, and Cochrane library databases were systematically analyzed to search English-language articles published from 1 January 2000 to 15 August 2019. Studies were detected by using the following terms: 'obstructive sleep apnea', 'sleep quality', 'sleep disordered breathing', 'cardiac damage', 'left ventricular mass', 'left ventricular hypertrophy', and 'echocardiography'.
RESULTS
Meta-analysis included 5550 patients with OSA and 2329 non-OSA controls from 39 studies. The prevalence of LVH in the pooled OSA population was 45% (CI 35--55%). Meta-analysis of studies comparing the prevalence of LVH in participants with OSA and controls showed that OSA was associated with an increased risk of LVH (OR = 1.70, CI 1.44-2.00, P < 0.001). LV mass was significantly increased in patients with severe OSA as compared with controls (SMD 0.46 ± 0.08, CI 0.29-0.62, P < 0.001) or with mild OSA. This was not the case for studies comparing patients with unselected or predominantly mild OSA and controls (0.33 ± 0.17, CI -0.01 to 0.67, P = 0.057).
CONCLUSION
The present meta-analysis expands previous information on the relationship between OSA and echocardiographic LVH, so far based on individual studies. The overall evidence strongly suggests that the likelihood of LVH increases with the severity of OSA, thus exhibiting a continuous relationship.
Topics: Adult; Aged; Echocardiography; Female; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Male; Middle Aged; Sleep Apnea, Obstructive
PubMed: 32371766
DOI: 10.1097/HJH.0000000000002435