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British Heart Journal Jul 1984In order to determine the relation between three manifestations of left ventricular hypertrophy--ST-T wave changes on the electrocardiogram, diastolic disturbances, and...
In order to determine the relation between three manifestations of left ventricular hypertrophy--ST-T wave changes on the electrocardiogram, diastolic disturbances, and increased myocardial echo intensity--M mode and cross sectional echocardiograms were recorded in 12 normal subjects, 15 athletes, 16 patients with hypertrophic cardiomyopathy, and 42 patients with secondary left ventricular hypertrophy due to aortic stenosis (20), severe essential hypertension (8), coarctation (7), or subaortic stenosis (7). M mode echocardiograms were digitised and cross sectional echocardiograms were analysed for regional echo intensity. In patients with hypertrophy regional echo amplitude was significantly increased in mid and basal septum and posterior left ventricular wall. Patients with increased echo amplitude in any region showed a higher incidence of ST-T wave abnormalities than those without and of diastolic abnormalities--including prolongation of isovolumic relaxation time, delay in mitral valve opening with respect to minimum cavity dimension, and a reduction in peak rate of posterior wall thinning and dimension increase. There was a significant rank order correlation between median pixel count and these diastolic abnormalities. No significant differences were demonstrable in these relations between the diagnostic groups. By contrast, electrocardiographic findings, diastolic function, and pixel count were uniformly normal in athletes, although the increase in left ventricular mass was similar to that in the patients. Thus an increase in left ventricular mass alone is not responsible for repolarisation or wall motion abnormalities occurring in pathological left ventricular hypertrophy. These latter changes are, however, strongly associated with the change in myocardial properties detected as an increase in echo intensity and may be due to increased interstitial fibrosis.
Topics: Adult; Cardiomegaly; Cardiomyopathy, Hypertrophic; Echocardiography; Electrocardiography; Female; Heart Function Tests; Heart Ventricles; Humans; Male; Middle Aged; Sports
PubMed: 6234908
DOI: 10.1136/hrt.52.1.99 -
Journal of Nuclear Medicine Technology Dec 2010The utility of (99m)Tc-tetrofosmin myocardial SPECT for assessment of pulmonary hypertension and right ventricular thickness has not been well studied. We hypothesized...
UNLABELLED
The utility of (99m)Tc-tetrofosmin myocardial SPECT for assessment of pulmonary hypertension and right ventricular thickness has not been well studied. We hypothesized that a ratio of right ventricular activity to left ventricular activity (RV/LV uptake ratio) from SPECT myocardial perfusion images could identify the presence of increased right ventricular wall thickness and elevated systolic pulmonary artery pressure with or without the use of attenuation correction.
METHODS
We identified 33 patients with normal findings on stress (99m)Tc-tetrofosmin left ventricular myocardial perfusion imaging who had a complete 2-dimensional echocardiographic study within 3 wk of the SPECT study. Two 6 × 6 pixel regions of interest were placed in the right and left ventricular free walls of both non-attenuation-corrected and attenuation-corrected SPECT images. We examined the correlation of RV/LV uptake ratio with echocardiographic right ventricular free-wall thickness and with pulmonary artery systolic pressure.
RESULTS
RV/LV uptake ratio, measured on non-attenuation-corrected images, correlated significantly with both pulmonary artery systolic pressure (r = 0.63 and P < 0.001) and right ventricular wall thickness (r = 0.6 and P < 0.001). Receiver-operating-characteristic analysis of the use of RV/LV uptake ratio to detect significant pulmonary hypertension showed that the area under the curve was 0.78 (95% confidence interval, 0.62-0.95). However, no significant correlation of RV/LV uptake ratio with pulmonary artery systolic pressure or right ventricular wall thickness was found on attenuation-corrected images.
CONCLUSION
RV/LV uptake ratio measured on SPECT images can be used to identify patients with high pulmonary artery pressure or right ventricular hypertrophy.
Topics: Biological Transport; Heart Ventricles; Humans; Hypertension, Pulmonary; Hypertrophy, Right Ventricular; Image Processing, Computer-Assisted; Myocardial Perfusion Imaging; Retrospective Studies; Stress, Physiological; Tomography, Emission-Computed, Single-Photon
PubMed: 21078778
DOI: 10.2967/jnmt.110.080200 -
The American Journal of Cardiology Oct 2013Although concentric remodeling (CR) and concentric hypertrophy (CH) are common forms of left ventricular (LV) remodeling in heart failure with preserved ejection... (Comparative Study)
Comparative Study
Prevalence, clinical characteristics, and outcomes associated with eccentric versus concentric left ventricular hypertrophy in heart failure with preserved ejection fraction.
Although concentric remodeling (CR) and concentric hypertrophy (CH) are common forms of left ventricular (LV) remodeling in heart failure with preserved ejection fraction (HFpEF), eccentric hypertrophy (EH) can also occur in these patients. However, clinical characteristics and outcomes of EH have not been well described in HFpEF. We prospectively studied 402 patients with HFpEF, divided into 4 groups based on LV structure: normal geometry (no LV hypertrophy [LVH] and relative wall thickness [RWT] ≤0.42); CR (no LVH and RWT >0.42); CH (LVH and RWT >0.42); and EH (LVH and RWT ≤0.42). We compared clinical, laboratory, echocardiographic, invasive hemodynamic, and outcome data among groups. Of 402 patients, 48 (12%) had EH. Compared with CH, patients with EH had lower systolic blood pressure and less renal impairment despite similar rates of hypertension. After adjustment for covariates, EH was associated with reduced LV contractility compared with CH: lower LVEF (β coefficient = -3.2; 95% confidence interval [CI] -5.4 to -1.1%) and ratio of systolic blood pressure to end-systolic volume (β coefficient = -1.0; 95% CI -1.5 to -0.5 mm Hg/ml). EH was also associated with increased LV compliance compared with CH (LV end-diastolic volume at an idealized LV end-diastolic pressure of 20 mm Hg β coefficient = 14.2; 95% CI 9.4 to 19.1 ml). Despite these differences, EH and CH had similarly elevated cardiac filling pressures and equivalent adverse outcomes. In conclusion, the presence of EH denotes a distinct subset of HFpEF that is pathophysiologically similar to HF with reduced EF (HFrEF) and may benefit from HFrEF therapy.
Topics: Aged; Disease Progression; Echocardiography; Female; Follow-Up Studies; Heart Failure; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Illinois; Male; Middle Aged; Prevalence; Prognosis; Prospective Studies; Stroke Volume; Ventricular Remodeling
PubMed: 23810323
DOI: 10.1016/j.amjcard.2013.05.061 -
Journal of Molecular and Cellular... Aug 2019The mammalian heart undergoes complex structural and functional remodeling to compensate for stresses such as pressure overload. While studies suggest that, at best, the...
The mammalian heart undergoes complex structural and functional remodeling to compensate for stresses such as pressure overload. While studies suggest that, at best, the adult mammalian heart is capable of very limited regeneration arising from the proliferation of existing cardiomyocytes, how myocardial stress affects endogenous cardiac regeneration or repair is unknown. To define the relationship between left ventricular afterload and cardiac repair, we induced left ventricle pressure overload in adult mice by constriction of the ascending aorta (AAC). One week following AAC, we normalized ventricular afterload in a subset of animals through removal of the aortic constriction (de-AAC). Subsequent monitoring of cardiomyocyte cell cycle activity via thymidine analog labeling revealed that an acute increase in ventricular afterload induced cardiomyocyte proliferation. Intriguingly, a release in ventricular overload (de-AAC) further increases cardiomyocyte proliferation. Following both AAC and de-AAC, thymidine analog-positive cardiomyocytes exhibited characteristics of newly generated cardiomyocytes, including single diploid nuclei and reduced cell size as compared to age-matched, sham-operated adult mouse myocytes. Notably, those smaller cardiomyocytes frequently resided alongside one another, consistent with local stimulation of cellular proliferation. Collectively, our data demonstrate that adult cardiomyocyte proliferation can be locally stimulated by an acute increase or decrease of ventricular pressure, and this mode of stimulation can be harnessed to promote cardiac repair.
Topics: Animals; Biomarkers; Cardiomegaly; Cell Proliferation; Disease Models, Animal; Echocardiography; Fluorescent Antibody Technique; Gene Expression; Heart Ventricles; Hypertrophy, Left Ventricular; Mice; Myocytes, Cardiac; Oxidative Stress; Ventricular Pressure; Ventricular Remodeling
PubMed: 31220468
DOI: 10.1016/j.yjmcc.2019.06.006 -
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 -
International Journal of Molecular... Sep 2019Patients with chronic kidney disease (CKD) are prone to developing cardiac hypertrophy and fibrosis, which is associated with increased fibroblast growth factor 23...
Patients with chronic kidney disease (CKD) are prone to developing cardiac hypertrophy and fibrosis, which is associated with increased fibroblast growth factor 23 (FGF23) serum levels. Elevated circulating FGF23 was shown to induce left ventricular hypertrophy (LVH) via the calcineurin/NFAT pathway and contributed to cardiac fibrosis by stimulation of profibrotic factors. We hypothesized that FGF23 may also stimulate the local renin-angiotensin-aldosterone system (RAAS) in the heart, thereby further promoting the progression of FGF23-mediated cardiac pathologies. We evaluated LVH and fibrosis in association with cardiac FGF23 and activation of RAAS in heart tissue of 5/6 nephrectomized (5/6Nx) rats compared to sham-operated animals followed by in vitro studies with isolated neonatal rat ventricular myocytes and fibroblast (NRVM, NRCF), respectively. Uremic rats showed enhanced cardiomyocyte size and cardiac fibrosis compared with sham. The cardiac expression of and RAAS genes were increased in 5/6Nx rats and correlated with the degree of cardiac fibrosis. In NRVM and NRCF, FGF23 stimulated the expression of RAAS genes and induced indicating mineralocorticoid receptor activation. The FGF23-mediated hypertrophic growth of NRVM and induction of NFAT target genes were attenuated by cyclosporine A, losartan and spironolactone. In NRCF, FGF23 induced and , which were suppressed by losartan and spironolactone, only. Our data suggest that FGF23-mediated activation of local RAAS in the heart promotes cardiac hypertrophy and fibrosis.
Topics: Animals; Fibroblast Growth Factor-23; Fibroblast Growth Factors; Fibroblasts; Fibrosis; Heart Ventricles; Hypertrophy, Left Ventricular; Male; Myocytes, Cardiac; Rats, Sprague-Dawley; Renal Insufficiency, Chronic; Renin-Angiotensin System
PubMed: 31540546
DOI: 10.3390/ijms20184634 -
The Journal of Thoracic and... May 2022
Topics: Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Ventricular Function, Left; Ventricular Remodeling
PubMed: 32981706
DOI: 10.1016/j.jtcvs.2020.09.002 -
PloS One 2020To assess left ventricular hypertrophy, actual left ventricular mass (LVM) normalized for body size has to be compared to the LVM normative data. However, only some...
BACKGROUND
To assess left ventricular hypertrophy, actual left ventricular mass (LVM) normalized for body size has to be compared to the LVM normative data. However, only some published normative echocardiographic data have been produced separately for girls and boys; numerous normative data for the pediatric population are not sex-specific. Thus, this study aimed to assess whether the LVM normative data should be developed separately for girls and boys practicing sports.
METHODS
Left ventricular mass was computed for 331 girls and 490 boys, 5-19 years old, based on echocardiography. The effect of sex on the relationship between LVM and body size was evaluated using a linear regression model. Seven sets of the LVM normative data were developed, using different methodologies, to test concordance between sex-specific and non-specific normative data. Every set consisted of normative data that was sex-specific and non-specific. Upon these normative data, for every study participant, seven pairs of LVM z-scores were calculated based on her/his actual LVM. Each pair consisted of z-scores computed based on sex-specific and non-specific normative data from the same set.
RESULTS
The regression lines fitted to the data points corresponding to LVM of boys had a higher slope than of girls, indicating that sex affects the relationship between LVM and body size. The mean differences between the paired LVM z-scores differed significantly from 0. The percentage of discordant indications, depending on the normalization method, ranged from 66.7% to 100% in girls and from 35.4% to 50% in boys. Application of the LVM normative data that were not sex-specific made relative LVM underestimated in girls and overestimated in boys.
CONCLUSION
The LVM normative data should be developed separately for girls and boys practicing sports. Application of normative data that are not sex-specific results in an underestimation of relative LVM in girls and overestimation in boys.
Topics: Adolescent; Athletes; Body Size; Child; Child, Preschool; Echocardiography; Female; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Linear Models; Male; Retrospective Studies; Sex Characteristics; Young Adult
PubMed: 32716972
DOI: 10.1371/journal.pone.0236632 -
Clinical Cardiology Feb 2006This editorial reviews the clinical presentation, electrocardiographic manifestations, appearance of the left ventricle by imaging techniques, and the state of the... (Review)
Review
This editorial reviews the clinical presentation, electrocardiographic manifestations, appearance of the left ventricle by imaging techniques, and the state of the coronary arteries in four left ventricular apical abnormalities (Table I). Three of these conditions, namely, noncompaction, apical hypertrophy, and left ventricle aneurysm, can be somewhat malignant. The fourth condition--tako-tsubo--is generally benign. Treatment depends on the clinical condition of the patient.
Topics: Cardiomegaly; Electrocardiography; Heart Aneurysm; Heart Ventricles; Humans; Myocardial Stunning; Ventricular Dysfunction, Left
PubMed: 16506637
DOI: 10.1002/clc.4960290202 -
Biomedicine & Pharmacotherapy =... Jan 2021Maternal obesity induces adverse cardiac programming in offspring, and effective interventions are needed to prevent cardiovascular ill-health. Herein we hypothesized...
BACKGROUND
Maternal obesity induces adverse cardiac programming in offspring, and effective interventions are needed to prevent cardiovascular ill-health. Herein we hypothesized that exposure to maternal obesogenic diet-induced obesity in mice results in left ventricular remodelling and hypertrophy in early childhood, and that maternal N-acetylcysteine (NAC) treatment alleviates these effects in a sex-dependent manner.
METHODS AND RESULTS
The maternal obesity was induced in mice by the consumption of a Western diet accompanied by a 20 % sucrose solution. To determine the effect of NAC on the cardiac outcomes induced by maternal obesity, obese dams were continuously exposed to the obesogenic diet, with or without the oral NAC treatment during pregnancy. Left ventricular remodelling and hypertrophy occurred as early as 7 days after birth in the male offspring of obese dams (O-OB) compared with controls (O-CO). An over-expression of key genes and markers related to cardiac fibrosis accompanied by more disorganized myofibrils was observed in the hearts of neonatal male O-OB mice. When we next evaluated the level of oxidative stress in the hearts of neonatal mice, the activity of enzymatic antioxidants declined and expression of NOX enzyme complex was up-regulated in O-OB offspring hearts, but was normal in the offspring of NAC treated mice (O-OB/NAC). Maternal obesity also activated cardiac Akt and mammalian target of rapamycin (mTOR) signalling in offspring, and NAC treatment restored offspring cardiac Akt-mTOR signalling to normal irrespective of sex. NAC treatment did not prevent cardiomyocyte hypertrophy but did alleviate increased heart weight, interventricular septal thickness, and collagen content in male O-OB/NAC pups.
CONCLUSIONS
Collectively, our results indicated that NAC blunted cardiac fibrosis and related ventricular hypertrophy of male neonatal offspring in the setting of maternal obesity, potentially acting by reducing oxidative stress. The present study provides a basis for investigating the role of NAC in nutrition-related cardiac programming.
Topics: Acetylcysteine; Animal Nutritional Physiological Phenomena; Animals; Animals, Newborn; Antioxidants; Disease Models, Animal; Female; Fibrosis; Heart Ventricles; Hypertrophy, Left Ventricular; Male; Maternal Nutritional Physiological Phenomena; Mice, Inbred C57BL; Obesity, Maternal; Oxidative Stress; Pregnancy; Prenatal Exposure Delayed Effects; Sex Factors; Ventricular Function, Left; Ventricular Remodeling; Mice
PubMed: 33378994
DOI: 10.1016/j.biopha.2020.110989