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Progress in Cardiovascular Diseases 2014Abnormal left ventricular (LV) geometry, including LV hypertrophy (LVH), is associated with increased risk of major cardiovascular (CV) events and all-cause mortality... (Review)
Review
Abnormal left ventricular (LV) geometry, including LV hypertrophy (LVH), is associated with increased risk of major cardiovascular (CV) events and all-cause mortality and may be an independent predictor of morbid CV events. Patients with LVH have increased risk of congestive heart failure, coronary heart disease, sudden cardiac death and stroke. We review the risk factors for LVH and its consequences, as well as the risk imposed by concentric remodeling (CR). We also examine evidence supporting the benefits of LVH regression, as well as evidence regarding the risk of CR progressing to LVH, as opposed to normalization of CR. We also briefly review the association of abnormal LV geometry with left atrial enlargement and the combined effects of these structural cardiac abnormalities.
Topics: Echocardiography; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Prognosis; Ventricular Remodeling
PubMed: 25081397
DOI: 10.1016/j.pcad.2014.05.003 -
European Journal of Sport Science Jun 2023Purpose: The aim of the present study was to assess left ventricular (LV) morphological and regional functional adaptations in backs and forwards elite rugby union (RU)...
UNLABELLED
Purpose: The aim of the present study was to assess left ventricular (LV) morphological and regional functional adaptations in backs and forwards elite rugby union (RU) players.
METHODS
Thirty-nine elite male RU players and twenty sedentary controls have been examined using resting echocardiography. RU players were divided into two groups, forwards ( = 22) and backs ( = 17). Evaluations included tissue Doppler and 2D speckle-tracking analysis to assess LV strains and twisting mechanics.
RESULTS
The elite RU players exhibited an LV remodelling characterized by an increase in LV mass indexed to body surface area (82.2 ± 13.2 . 99.9 ± 16.1 and 119.7 ± 13.4 g.m, in controls, backs and forwards; < .001). Compared to backs, forwards exhibited lower global longitudinal strain (19.9 ± 2.5 18.0 ± 1.6%; < .05), lower early diastolic velocity (16.5 ± 1.8 15.0 ± 2.3 cm.s; < .05) and lower diastolic longitudinal strain rate (1.80 ± 0.34 1.54 ± 0.26 s; < .01), especially at the apex. LV twist and untwisting velocities were similar in RU players compared to controls, but with lower apical (-46.2 ± 22.1 -28.2 ± 21.7 deg.s; < .01) and higher basal rotational velocities (33.9 ± 20.9 48.4 ± 20.7 deg.s; < .05).
CONCLUSION
RU players exhibited an increase in LV mass which was more pronounced in forwards. In forwards, LV global longitudinal strain was depressed, LV filling pressures were decreased, and LV relaxation depressed at the apex. Elite RU players exhibited LV hypertrophy, especially in forwards players.LV regional function suggested a drop in LV relaxation and an increase in LV filling pressures in RU players, with higher alterations in forwards.LV remodelling was associated with regional alterations in torsional mechanics: higher rotations and rotational diastolic velocities at the basal level of LV but lower rotation and rotational diastolic velocities at the apex were observed in RU players.
Topics: Humans; Male; Ventricular Function, Left; Rugby; Heart Ventricles; Echocardiography; Hypertrophy, Left Ventricular; Ventricular Remodeling
PubMed: 35734942
DOI: 10.1080/17461391.2022.2092778 -
Cardiovascular Journal of Africa Mar 2012We assessed left ventricular structural alterations associated with chronic kidney disease (CKD) in Congolese patients with type 2 diabetes.
OBJECTIVE
We assessed left ventricular structural alterations associated with chronic kidney disease (CKD) in Congolese patients with type 2 diabetes.
METHODS
This was a cross-sectional study of a case series. We obtained anthropometric, clinical, biological and echocardiographic measurements in 60 consecutive type 2 diabetes patients (37 females, 62% ) aged 20 years or older from the diabetes outpatient clinic, University of Kinshasa Hospital, DRC. We computed creatinine clearance rate according to the MDRD equation and categorised patients into mild (CrCl > 60 ml/min per 1.73 m(2)), moderate (CrCl 30-60 ml/min per 1.73 m(2)) and severe CKD (< 30 ml/min per 1.73 m(2)). Left ventricular hypertrophy (LVH) was indicated by a LV mass index (LVMI) > 51 g/m(2.7) and LV geometry was defined as normal, or with concentric remodelling, eccentric or concentric hypertrophy, using relative wall thickness (RWT) and LVMI.
RESULTS
Compared to patients with normal kidney function, CKD patients had higher uric acid levels (450 ± 166 vs 306 ± 107 µmol/l; p ≤ 0.001), a greater proportion of LVH (37 vs 14%; p ≤ 0.05) and longstanding diabetes (13 ± 8 vs 8 ± 6 years; p ≤ 0.001). Their left ventricular internal diameter, diastolic (LVIDD) was (47.00 ± 6.00 vs 43.00 ± 7.00 mm; p ≤ 0.001), LVMI was (47 ± 19 vs 36.00 ± 15 g/m2.7; p ≤ 0.05) and proportions of concentric (22 vs 11%; p ≤ 0.05) or eccentric (15 vs 3%; p ≤ 0.05) LVH were also greater. Severe CKD was associated with increased interventricular septum, diastolic (IVSD) (12.30 ± 3.08 vs 9.45 ± 1.94 mm; p ≤ 0.05), posterior wall thickness, diastolic (PWTD) (11.61 ± 2.78 vs 9.52 ± 1.77 mm; p ≤ 0.01), relative wall thickness (RWT) (0.52 ± 0.17 vs 0.40 ± 0.07; p ≤ 0.01) rate of LVH (50 vs 30%; p ≤ 0.05), and elevated proportions of concentric remodelling (25 vs 15%; p ≤ 0.05) and concentric LVH (42 vs 10%; p ≤ 0.05) in comparison with patients with moderate CKD. In multivariable adjusted analysis, hyperuricaemia emerged as the only predictor of the presence of LVH in patients with CKD (adjusted OR 9.10; 95% CI: 2.40-33.73).
CONCLUSION
In keeping with a higher rate of cardiovascular events usually reported in patients with impaired renal function, CKD patients exhibited LVH and abnormal LV geometry.
Topics: Aged; Cross-Sectional Studies; Democratic Republic of the Congo; Diabetes Mellitus, Type 2; Disease Progression; Echocardiography; Female; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Male; Middle Aged; Prevalence; Renal Insufficiency, Chronic; Ventricular Remodeling
PubMed: 22447475
DOI: 10.5830/CVJA-2011-028 -
Current Hypertension Reports May 2014Hypertension is a powerful risk factor for cardiovascular mortality and morbidity, including heart failure with both preserved and reduced ejection fraction.... (Review)
Review
Hypertension is a powerful risk factor for cardiovascular mortality and morbidity, including heart failure with both preserved and reduced ejection fraction. Hypertensive heart disease (HHD) defines the complex and diverse perturbations of cardiac structure and function occurring secondary to hypertension. Left ventricular hypertrophy (LVH) is one of the most recognized features of HHD and is an established risk factor for adverse cardiovascular (CV) outcomes in hypertension. Beyond LVH, LV geometry provides additional information regarding the cardiac response to hypertension. Imaging studies from larger cohorts of hypertensive patients reveal wide variability in the prevalence of LVH and LV geometric patterns, with the prevalence of concentric LVH similar to that of eccentric LVH. Hypertension is also associated with concomitant impairments in LV diastolic and systolic function. It remains uncertain why patients develop different patterns of LVH, although demographics and clinical comorbidities appear to influence that response.
Topics: Animals; Echocardiography; Heart Failure; Heart Ventricles; Humans; Hypertension; Hypertrophy, Left Ventricular; Ventricular Remodeling
PubMed: 24639061
DOI: 10.1007/s11906-014-0428-x -
American Journal of Physiology. Heart... Aug 2021Pulmonary hypertension (PH) is associated with structural remodeling of pulmonary arteries (PAs) because of excessive proliferation of fibroblasts, endothelial cells,...
Pulmonary hypertension (PH) is associated with structural remodeling of pulmonary arteries (PAs) because of excessive proliferation of fibroblasts, endothelial cells, and smooth muscle cells (SMCs). The peptide hormone angiotensin II (ANG II) contributes to pulmonary vascular remodeling, in part, through its ability to trigger extracellular signal-regulated kinase (ERK1/2) activation. Here, we demonstrate that the ERK1/2 phosphatase, dual-specificity phosphatase 5 (DUSP5), functions as a negative regulator of ANG II-mediated SMC proliferation and PH. In contrast to wild-type controls, Dusp5 null mice infused with ANG II developed PH and right ventricular (RV) hypertrophy. PH in Dusp5 null mice was associated with thickening of the medial layer of small PAs, suggesting an in vivo role for DUSP5 as a negative regulator of ANG II-dependent SMC proliferation. Consistent with this, overexpression of DUSP5 blocked ANG II-mediated proliferation of cultured human pulmonary artery SMCs (hPASMCs) derived from patients with idiopathic PH or from failed donor controls. Collectively, the data support a role for DUSP5 as a feedback inhibitor of ANG II-mediated ERK signaling and PASMC proliferation and suggest that disruption of this circuit leads to adverse cardiopulmonary remodeling. Dual-specificity phosphatases (DUSPs) serve critical roles in the regulation of mitogen-activated protein kinases, but their functions in the cardiovascular system remain poorly defined. Here, we provide evidence that DUSP5, which resides in the nucleus and specifically dephosphorylates extracellular signal-regulated kinase (ERK1/2), blocks pulmonary vascular smooth muscle cell proliferation. In response to angiotensin II infusion, mice lacking DUSP5 develop pulmonary hypertension and right ventricular cardiac hypertrophy. These findings illustrate DUSP5-mediated suppression of ERK signaling in the lungs as a protective mechanism.
Topics: Angiotensin II; Animals; Case-Control Studies; Cell Proliferation; Cells, Cultured; Dual-Specificity Phosphatases; Heart Ventricles; Humans; Hypertension, Pulmonary; Hypertrophy, Right Ventricular; MAP Kinase Signaling System; Mice; Mice, Knockout; Muscle, Smooth, Vascular; Myocytes, Smooth Muscle; Pulmonary Artery; Vascular Remodeling; Vasoconstrictor Agents
PubMed: 34142888
DOI: 10.1152/ajpheart.00115.2021 -
JACC. Cardiovascular Imaging Apr 2017
Topics: Arrhythmogenic Right Ventricular Dysplasia; Athletes; Cardiomegaly; Heart Ventricles; Humans
PubMed: 27544897
DOI: 10.1016/j.jcmg.2016.05.011 -
Turk Kardiyoloji Dernegi Arsivi : Turk... Apr 2023Down syndrome is a genetic syndrome characterized with various dysmorphisms and congenital malformations such as congenital heart diseases. We aimed to evaluate the...
OBJECTIVE
Down syndrome is a genetic syndrome characterized with various dysmorphisms and congenital malformations such as congenital heart diseases. We aimed to evaluate the relationship between Down syndrome, hypothyroidism, and cardiac ���ndings.
METHODS
Thyroid hormone pro���les and echocardiographic ���ndings were evaluated. Patients with hypothyroidism and Down syndrome were named group 1; patients with hypothyroidism without Down syndrome group 2 and group 3 was control. The echocardiographic parameters (interventricular septum and left ventricular systolic, diastolic posterior wall thickness, left ventricular end-diastolic diameter, ejection fraction) were indexed to body surface area. Left ventricular mass index and relative wall thickness were calculated. Patients with relative wall thickness equal to or below 0.42 were classi���ed as eccentric hypertrophy or normal geometry, while those over 0.42 as concentric remodeling or concentric hypertrophy.
RESULTS
Thyroid stimulating hormone values of groups 1 and 2 were signi���cantly higher than those of group 3. There were no signi���cant di���erences for fT4 between the groups. Interventricular septum and left ventricular posterior wall end-diastolic and end-systolic thickness were signi���cantly higher in group 1 than groups 2 and 3. There was no statistically signi���cant di���erence in left ventricular mass index between groups 1 and 2. In terms of relative wall thickness, 16 out of 29 patients in group 1 were revealed as concentric remodeling, 12 as normal geometry, 1 patient as eccentric hypertrophy. In group 2, 6 patients were revealed as concentric remodeling, 14 as normal geometry. There was no statistically signi���cant di���erence of left ventricular end-diastolic thickness between 3 groups.
CONCLUSION
Cardiac morphology and functions were signi���cantly a���ected by hypothyroidism in patients with Down syndrome. Hypertrophy in Down syndrome may be caused by the cellular changes in myocardium.
Topics: Humans; Child; Down Syndrome; Heart; Echocardiography; Heart Ventricles; Hypertrophy; Hypothyroidism; Hypertrophy, Left Ventricular; Hypertension
PubMed: 36999332
DOI: 10.5543/tkda.2023.70337 -
Annals of Noninvasive Electrocardiology... May 2017Although left ventricular hypertrophy (LVH) detected by electrocardiography (ECG-LVH) and echocardiography (echo-LVH) independently predict cardiovascular disease...
BACKGROUND
Although left ventricular hypertrophy (LVH) detected by electrocardiography (ECG-LVH) and echocardiography (echo-LVH) independently predict cardiovascular disease events, it is unclear if ECG-LVH and echo-LVH independently predict atrial fibrillation (AF).
METHODS
This analysis included 4,904 participants (40% male; 85% white) from the Cardiovascular Health Study who were free of baseline AF and major intraventricular conduction delays. ECG-LVH was defined by Minnesota Code Classification from baseline ECG data. Echo-LVH was defined by sex-specific left ventricular mass values >95th sex-specific percentiles. Incident AF events were identified during the annual study ECGs and from hospitalization discharge data. Cox regression was used to compute hazard ratios (HR) and 95% confidence intervals (CI) for the association of ECG-LVH and echo-LVH with incident AF, separately.
RESULTS
ECG-LVH was detected in 224 (4.6%) participants and echo-LVH was present in 231 (4.7%) participants. Over a median follow-up of 11.9 years, a total of 1,430 AF events were detected. In a multivariable Cox model adjusted for age, sex, race, education, income, smoking, systolic blood pressure, diabetes, body mass index, total cholesterol, high-density lipoprotein cholesterol, aspirin, antihypertensive medications, and cardiovascular disease, ECG-LVH (HR = 1.50; 95% CI = 1.18, 1.90) and echo-LVH (HR = 1.39; 95% CI = 1.09, 1.78) were independently associated with AF. When ECG-LVH (HR = 1.47, 95% CI = 1.16, 1.87) and echo-LVH (HR = 1.36, 1.07, 1.75) were included in the same model, both were predictive of incident AF.
CONCLUSION
The association of ECG-LVH with AF is not dependent on left ventricular mass detected by echocardiography, suggesting that abnormalities in cardiac electrophysiology provide a distinct profile in the prediction of AF.
Topics: Aged; Aged, 80 and over; Atrial Fibrillation; Cohort Studies; Electrocardiography; Female; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Male; Organ Size; Predictive Value of Tests; Prospective Studies; Reproducibility of Results; Risk Factors
PubMed: 28019050
DOI: 10.1111/anec.12419 -
Increased left ventricular mass and hypertrophy are associated with increased risk for sudden death.Journal of the American College of... Nov 1998This study examined the relations of echocardiographically determined left ventricular (LV) mass and hypertrophy to the risk of sudden death. (Comparative Study)
Comparative Study
OBJECTIVES
This study examined the relations of echocardiographically determined left ventricular (LV) mass and hypertrophy to the risk of sudden death.
BACKGROUND
Echocardiographic LV hypertrophy is associated with increased risk for all-cause mortality and cardiovascular disease morbidity and mortality. However, little is known about the association of echocardiographic LV hypertrophy with sudden death.
METHODS
We examined the relations of LV mass and hypertrophy to the incidence of sudden death in 3,661 subjects enrolled in the Framingham Heart Study who were > or =40 years of age. The baseline examination was performed from 1979 to 1983 and LV hypertrophy was defined as LV mass (adjusted for height) > 143 g/m in men and > 102 g/m in women. During up to 14 years of follow-up there were 60 sudden deaths. Cox models examined the relations of LV mass and LV hypertrophy to sudden death risk after adjusting for known risk factors.
RESULTS
The prevalence of LV hypertrophy was 21.5%. The risk factor-adjusted hazard ratio (HR) for sudden death was 1.45 (95% confidence interval [CI] 1.10 to 1.92, p=0.008) for each 50-g/m increment in LV mass. For LV hypertrophy, the risk factor-adjusted HR for sudden death was 2.16 (95% CI 1.22 to 3.81, p=0.008). After excluding the first 4 years of follow-up, both increased LV mass and LV hypertrophy conferred long-term risk of sudden death (HR 1.53, 95% CI 1.01 to 2.28, p=0.047 and HR 3.28, 95% CI 1.58 to 6.83, p=0.002, respectively).
CONCLUSIONS
Increased LV mass and hypertrophy are associated with increased risk for sudden death after accounting for known risk factors.
Topics: Adult; Aged; Aged, 80 and over; Death, Sudden; Disease Progression; Echocardiography; Electrocardiography; Female; Follow-Up Studies; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Incidence; Male; Middle Aged; Prospective Studies; Risk Factors; Survival Rate
PubMed: 9809962
DOI: 10.1016/s0735-1097(98)00407-0 -
JACC. Cardiovascular Imaging Aug 2012The authors investigated 3 important areas related to the clinical use of left ventricular mass (LVM): accuracy of assessments by echocardiography and cardiac magnetic... (Review)
Review
The authors investigated 3 important areas related to the clinical use of left ventricular mass (LVM): accuracy of assessments by echocardiography and cardiac magnetic resonance (CMR), the ability to predict cardiovascular outcomes, and the comparative value of different indexing methods. The recommended formula for echocardiographic estimation of LVM uses linear measurements and is based on the assumption of the left ventricle (LV) as a prolate ellipsoid of revolution. CMR permits a modeling of the LV free of cardiac geometric assumptions or acoustic window dependency, showing better accuracy and reproducibility. However, echocardiography has lower cost, easier availability, and better tolerability. From the MEDLINE database, 26 longitudinal echocardiographic studies and 5 CMR studies investigating LVM or LV hypertrophy as predictors of death or major cardiovascular outcomes were identified. LVM and LV hypertrophy were reliable cardiovascular risk predictors using both modalities. However, no study directly compared the methods for the ability to predict events, agreement in hypertrophy classification, or performance in cardiovascular risk reclassification. Indexing LVM to body surface area was the earliest normalization process used, but it seems to underestimate the prevalence of hypertrophy in obese and overweight subjects. Dividing LVM by height to the allometric power of 1.7 or 2.7 is the most promising normalization method in terms of practicality and usefulness from a clinical and scientific standpoint for scaling myocardial mass to body size. The measurement of LVM, calculation of LVM index, and classification for LV hypertrophy should be standardized by scientific societies across measurement techniques and adopted by clinicians in risk stratification and therapeutic decision making.
Topics: Chagas Cardiomyopathy; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Imaging, Three-Dimensional; Magnetic Resonance Imaging, Cine; Risk Assessment; Ultrasonography
PubMed: 22897998
DOI: 10.1016/j.jcmg.2012.06.003