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Journal of Atherosclerosis and... Sep 2023Patients with end-stage kidney disease (ESKD) have an unparalleled risk of left ventricular hypertrophy (LVH) and vascular calcification (VC), both of which introduce...
Left Ventricular Hypertrophy Geometry and Vascular Calcification Co-Modify the Risk of Cardiovascular Mortality in Patients with End-Stage Kidney Disease: A Retrospective Cohort Study.
AIM
Patients with end-stage kidney disease (ESKD) have an unparalleled risk of left ventricular hypertrophy (LVH) and vascular calcification (VC), both of which introduce excessive cardiovascular risk. However, it remains unclear whether LVH geometry co-modulates cardiovascular outcomes with VC in this population.
METHODS
A retrospective cohort study was conducted. Patients with ESKD requiring chronic hemodialysis were identified from Shin Kong Wu Ho-Su Memorial Hospital between October and December 2018, with echocardiographic LVH geometry and aortic arch calcification (AoAC) determined. They were divided into four groups according to AoAC severity and eccentric or concentric LVH. We used Kaplan-Meier analysis and Cox proportional hazard regression to analyze their cardiovascular and all-cause mortality after multivariate adjustment.
RESULTS
Overall, 223 patients with ESKD with LVH were analyzed, among whom 29.1%, 23.3%, 25.1%, and 22.4% had non-to-mild AoAC with eccentric and concentric LVH and moderate-to-severe AoAC with eccentric and concentric LVH, respectively. After 3.5 years of follow-up, patients with ESKD with moderate-to-severe AoAC and concentric LVH had a significantly higher risk of cardiovascular mortality than those with non-to-mild AoAC and eccentric LVH (hazard ratio 3.35, p=0.002). However, those with moderate-to-severe AoAC but eccentric LVH did not have higher cardiovascular mortality. Similarly, patients with ESKD with moderate-to-severe AoAC and concentric LVH had a significantly higher all-cause mortality than those with non-to-mild AoAC and eccentric LVH, whereas the other two groups did not have higher risk.
CONCLUSION
LVH geometry could help stratify the risk of patients with ESKD when they had severe VC, and co-existing severe VC and concentric LVH aggravated cardiovascular risk.
Topics: Humans; Hypertrophy, Left Ventricular; Retrospective Studies; Kidney Failure, Chronic; Heart Ventricles; Vascular Calcification; Ventricular Remodeling
PubMed: 36567124
DOI: 10.5551/jat.63870 -
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 -
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 -
Physiological Reports May 2023Autophagy is important for protein and organelle quality control. Growing evidence demonstrates that autophagy is tightly controlled by transcriptional mechanisms,...
Autophagy is important for protein and organelle quality control. Growing evidence demonstrates that autophagy is tightly controlled by transcriptional mechanisms, including repression by zinc finger containing KRAB and SCAN domains 3 (ZKSCAN3). We hypothesize that cardiomyocyte-specific ZKSCAN3 knockout (Z3K) disrupts autophagy activation and repression balance and exacerbates cardiac pressure-overload-induced remodeling following transverse aortic constriction (TAC). Indeed, Z3K mice had an enhanced mortality compared to control (Con) mice following TAC. Z3K-TAC mice that survived exhibited a lower body weight compared to Z3K-Sham. Although both Con and Z3K mice exhibited cardiac hypertrophy after TAC, Z3K mice exhibited TAC-induced increase of left ventricular posterior wall thickness at end diastole (LVPWd). Conversely, Con-TAC mice exhibited decreases in PWT%, fractional shortening (FS%), and ejection fraction (EF%). Autophagy genes (Tfeb, Lc3b, and Ctsd) were decreased by the loss of ZKSCAN3. TAC suppressed Zkscan3, Tfeb, Lc3b, and Ctsd in Con mice, but not in Z3K. The Myh6/Myh7 ratio, which is related to cardiac remodeling, was decreased by the loss of ZKSCAN3. Although Ppargc1a mRNA and citrate synthase activities were decreased by TAC in both genotypes, mitochondrial electron transport chain activity did not change. Bi-variant analyses show that while in Con-Sham, the levels of autophagy and cardiac remodeling mRNAs form a strong correlation network, such was disrupted in Con-TAC, Z3K-Sham, and Z3K-TAC. Ppargc1a also forms different links in Con-sham, Con-TAC, Z3K-Sham, and Z3K-TAC. We conclude that ZKSCAN3 in cardiomyocytes reprograms autophagy and cardiac remodeling gene transcription, and their relationships with mitochondrial activities in response to TAC-induced pressure overload.
Topics: Mice; Animals; Myocytes, Cardiac; Ventricular Remodeling; Cardiomegaly; Heart Ventricles; Proteins; Mice, Knockout; Aortic Valve Stenosis; Mice, Inbred C57BL; Transcription Factors
PubMed: 37144628
DOI: 10.14814/phy2.15686 -
Circulation. Heart Failure Jul 2021Purkinje fibers (PFs) control timing of ventricular conduction and play a key role in arrhythmogenesis in heart failure (HF) patients. We investigated the effects of HF...
BACKGROUND
Purkinje fibers (PFs) control timing of ventricular conduction and play a key role in arrhythmogenesis in heart failure (HF) patients. We investigated the effects of HF on PFs.
METHODS
Echocardiography, electrocardiography, micro-computed tomography, quantitative polymerase chain reaction, immunohistochemistry, volume electron microscopy, and sharp microelectrode electrophysiology were used.
RESULTS
Congestive HF was induced in rabbits by left ventricular volume- and pressure-overload producing left ventricular hypertrophy, diminished fractional shortening and ejection fraction, and increased left ventricular dimensions. HF baseline QRS and corrected QT interval were prolonged by 17% and 21% (mean±SEMs: 303±6 ms HF, 249±11 ms control; n=8/7; =0.0002), suggesting PF dysfunction and impaired ventricular repolarization. Micro-computed tomography imaging showed increased free-running left PF network volume and length in HF. mRNA levels for 40 ion channels, Ca-handling proteins, connexins, and proinflammatory and fibrosis markers were assessed: 50% and 35% were dysregulated in left and right PFs respectively, whereas only 12.5% and 7.5% changed in left and right ventricular muscle. Funny channels, Ca-channels, and K-channels were significantly reduced in left PFs. Microelectrode recordings from left PFs revealed more negative resting membrane potential, reduced action potential upstroke velocity, prolonged duration (action potential duration at 90% repolarization: 378±24 ms HF, 249±5 ms control; n=23/38; <0.0001), and arrhythmic events in HF. Similar electrical remodeling was seen at the left PF-ventricular junction. In the failing left ventricle, upstroke velocity and amplitude were increased, but action potential duration at 90% repolarization was unaffected.
CONCLUSIONS
Severe volume- followed by pressure-overload causes rapidly progressing HF with extensive remodeling of PFs. The PF network is central to both arrhythmogenesis and contractile dysfunction and the pathological remodeling may increase the risk of fatal arrhythmias in HF patients.
Topics: Action Potentials; Animals; Cardiac Pacing, Artificial; Electrocardiography; Heart Failure; Heart Rate; Heart Ventricles; Male; Models, Animal; Rabbits; Ventricular Remodeling; X-Ray Microtomography
PubMed: 34190577
DOI: 10.1161/CIRCHEARTFAILURE.120.007505 -
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 -
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 -
JACC. Heart Failure Nov 2022
Topics: Humans; Heart Failure; Cardiomyopathy, Hypertrophic; Heart Ventricles; Treatment Outcome
PubMed: 36328652
DOI: 10.1016/j.jchf.2022.07.010 -
Journal of the American Heart... Aug 2021Background Impaired myocardial blood flow (MBF) in the absence of epicardial coronary disease is a feature of hypertrophic cardiomyopathy (HCM). Although most evident in...
Background Impaired myocardial blood flow (MBF) in the absence of epicardial coronary disease is a feature of hypertrophic cardiomyopathy (HCM). Although most evident in hypertrophied or scarred segments, reduced MBF can occur in apparently normal segments. We hypothesized that impaired MBF and myocardial perfusion reserve, quantified using perfusion mapping cardiac magnetic resonance, might occur in the absence of overt left ventricular hypertrophy (LVH) and late gadolinium enhancement, in mutation carriers without LVH criteria for HCM (genotype-positive, left ventricular hypertrophy-negative). Methods and Results A single center, case-control study investigated MBF and myocardial perfusion reserve (the ratio of MBF at stress:rest), along with other pre-phenotypic features of HCM. Individuals with genotype-positive, left ventricular hypertrophy-negative (n=50) with likely pathogenic/pathogenic variants and no evidence of LVH, and matched controls (n=28) underwent cardiac magnetic resonance. Cardiac magnetic resonance identified LVH-fulfilling criteria for HCM in 5 patients who were excluded. Individuals with genotype-positive, left ventricular hypertrophy-negative had longer indexed anterior mitral valve leaflet length (12.52±2.1 versus 11.55±1.6 mm/m, =0.03), lower left ventricular end-systolic volume (21.0±6.9 versus 26.7±6.2 mm/m, ≤0.005) and higher left ventricular ejection fraction (71.9±5.5 versus 65.8±4.4%, 0.005). Maximum wall thickness was not significantly different (9.03±1.95 versus 8.37±1.2 mm, =0.075), and no subject had significant late gadolinium enhancement (minor right ventricle‒insertion point late gadolinium enhancement only). Perfusion mapping demonstrated visual perfusion defects in 9 (20%) carriers versus 0 controls (=0.011). These were almost all septal or near right ventricle insertion points. Globally, myocardial perfusion reserve was lower in carriers (2.77±0.83 versus 3.24±0.63, =0.009), with a subendocardial:subepicardial myocardial perfusion reserve gradient (2.55±0.75 versus 3.2±0.65, =<0.005; 3.01±0.96 versus 3.47±0.75, =0.026) but equivalent MBF (2.75±0.82 versus 2.65±0.69 mL/g per min, =0.826). Conclusions Regional and global impaired myocardial perfusion can occur in HCM mutation carriers, in the absence of significant hypertrophy or scarring.
Topics: Adult; Cardiac Myosins; Cardiomyopathy, Hypertrophic, Familial; Coronary Circulation; Electrocardiography; Female; Genetic Testing; Heart Ventricles; Heterozygote; Humans; Hypertrophy, Left Ventricular; Magnetic Resonance Angiography; Magnetic Resonance Imaging, Cine; Male; Microcirculation; Mutation; Myocardial Perfusion Imaging; Sarcomeres
PubMed: 34310159
DOI: 10.1161/JAHA.120.020227 -
Ultraschall in Der Medizin (Stuttgart,... Aug 2023Aorto-left ventricular tunnel (ALVT) is an extremely rare, albeit prenatally detectable, extracardiac channel that connects the ascending aorta to the cavity of the...
PURPOSE
Aorto-left ventricular tunnel (ALVT) is an extremely rare, albeit prenatally detectable, extracardiac channel that connects the ascending aorta to the cavity of the left ventricle.
MATERIALS AND METHODS
All ALVTs diagnosed prenatally (2006-2020) in five tertiary referral centers were retrospectively assessed for prenatal ultrasound findings, intrauterine course, postnatal outcome, and surgical treatment. We focused on the size of the tunnel and alterations of perfusion of the left ventricular outflow tract and aortic arch.
RESULTS
11 fetuses were diagnosed with ALVT at a mean gestational age of 24.8 weeks. All cases were associated with severe dilatation of the left ventricle and a to-and-fro flow in the left outflow tract. Signs of congestive heart failure were present in five fetuses, four of which were terminated and one of which died in the neonatal period. One fetus died in utero at 34 weeks without prior signs of cardiac failure. Of the five survivors, two underwent the Ross procedure. In both cases the prenatal left ventricular outflow was exclusively via a large tunnel. The remaining three neonates underwent patch closure of the tunnel. In these cases, the prenatal outflow of the left ventricle was via the aortic valve and simultaneously over the tunnel.
CONCLUSION
Prenatal diagnosis of ALVT should be considered in the presence of left ventricular hypertrophy, dilatation of the aortic root, and to-and-fro flow in the aortic outflow tract. Signs of heart failure are associated with an unfavorable outcome. Large tunnels, particularly in combination with the absence of flow over the aortic valve, may be an unfavorable predictor of surgical repair.
Topics: Infant, Newborn; Pregnancy; Female; Humans; Infant; Aortic Valve Insufficiency; Aortico-Ventricular Tunnel; Retrospective Studies; Aorta; Prenatal Diagnosis; Heart Ventricles
PubMed: 35512837
DOI: 10.1055/a-1823-0821