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Circulation. Cardiovascular Imaging Aug 2020
Mediation Effect of Left Ventricular Geometric Adaptation to Lifetime Blood Pressure on Cognitive Function in Middle-Age: The Heart-Brain Connection (Partially) Explained.
Topics: Blood Pressure; Brain; Cognition; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Middle Aged
PubMed: 32772574
DOI: 10.1161/CIRCIMAGING.120.011325 -
Indian Heart Journal 2017We compared electrocardiographic and echocardiographic right ventricular hypertrophy (RVH) in 264 military members in Taiwan. The correlations of the Myers et al. and...
We compared electrocardiographic and echocardiographic right ventricular hypertrophy (RVH) in 264 military members in Taiwan. The correlations of the Myers et al. and Sokolow-Lyon criteria with RV wall thickness were low (r<0.1). Our data supported the American guidance that RVH voltage criteria violations should not receive further echocardiographic investigation.
Topics: Adult; Cohort Studies; Echocardiography; Electrocardiography; Female; Heart Ventricles; Humans; Hypertrophy, Right Ventricular; Incidence; Male; Military Personnel; Prevalence; Taiwan; Ventricular Function, Right
PubMed: 28648425
DOI: 10.1016/j.ihj.2017.04.016 -
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 -
Journal of Hypertension Mar 2020Left ventricular (LV) hypertrophy is the most common cardiac alteration in patients with chronic kidney disease (CKD). Normalization of hypertension in CKD patients...
OBJECTIVE
Left ventricular (LV) hypertrophy is the most common cardiac alteration in patients with chronic kidney disease (CKD). Normalization of hypertension in CKD patients receiving a healthy kidney allograft often reverses LV hypertrophy, but effects on LV fibrosis remain unclear. To study causal interactions between graft and environment on LV hypertrophy, fibrosis and inflammation, we applied cross-kidney transplantation METHODS:: Orthotopic transplantation was performed after inducing CKD in rats by two-third bilateral ablation of kidney mass: Healthy kidney (K) donor to healthy heart (H) recipient (healthy-K→healthy-H); CKD-K→healthy-H; healthy-K→CKD-H; CKD-K→CKD-H; N= 6 per group.
RESULTS
At week 6 after transplantation, mean arterial pressure (MAP) and LV mass index (LVMI) increased in CKD-K versus healthy-K irrespective of recipient. Contrarily, LV fibrosis was more severe in CKD-H versus healthy-H recipients irrespective of graft. Indeed, MAP and plasma creatinine correlated with LVMI but not with LV fibrosis. Increased LVMI in CKD-K→CKD-H not accompanied by cardiomyocyte cross-sectional area gain is consistent with eccentric remodelling. Cardiac RNA sequencing found a strong transcriptional response associated with LV fibrosis but only sparse changes associated with LV hypertrophy. This response was, among others, characterized by changes in extracellular matrix (ECM) and inflammatory gene expression.
CONCLUSION
LVMI reversed and MAP and renal function were normalized early after transplantation of a healthy kidney. However, LV fibrosis persisted, dissociating LV hypertrophy from LV fibrosis within 6 weeks. Elucidating cardiac ECM dynamics in CKD patients, although challenging, appears promising.
Topics: Animals; Disease Models, Animal; Fibrosis; Heart Ventricles; Hypertrophy, Left Ventricular; Kidney Transplantation; Rats; Renal Insufficiency, Chronic
PubMed: 31652182
DOI: 10.1097/HJH.0000000000002285 -
Current Heart Failure Reports Dec 2010There now is strong evidence to recognize the pivotal role of the right ventricle (RV) in heart disease and to establish it as a unique and separate entity than the left... (Review)
Review
There now is strong evidence to recognize the pivotal role of the right ventricle (RV) in heart disease and to establish it as a unique and separate entity than the left ventricle (LV). Here, we summarize the differences between the two ventricles, the diagnosis of RV failure, and the management of acute and chronic RV failure. We review the indices derived by echocardiography used to measure RV function, and novel biomarkers that may play a role diagnosing and prognosticating in RV-specific disease. There are new novel therapies that specifically target the RV in disease. For example, phosphodiesterase type 5 inhibitors improve contractility of the hypertrophied RV while sparing the normal LV in pulmonary arterial hypertension. The metabolism of the hypertrophied RV is another area for therapeutic exploitation by metabolic modulation. We also suggest future potential molecular targets that may be unique to the RV because they are upregulated in RV hypertrophy greater than in LV hypertrophy.
Topics: Biomarkers; Cardiovascular Agents; Case Management; Chronic Disease; Diagnosis, Differential; Heart Ventricles; Humans; Hypertrophy, Right Ventricular; Molecular Targeted Therapy; Phosphodiesterase 5 Inhibitors; Ultrasonography; Ventricular Dysfunction, Right; Ventricular Function, Right
PubMed: 20890792
DOI: 10.1007/s11897-010-0031-7 -
Journal of Cardiovascular Pharmacology 1994The left ventricle can change its size and shape as a result of external load and/or loss of viable myocytes. This process, defined as remodeling, can be adaptive, as in... (Clinical Trial)
Clinical Trial Randomized Controlled Trial Review
The left ventricle can change its size and shape as a result of external load and/or loss of viable myocytes. This process, defined as remodeling, can be adaptive, as in compensatory hypertrophy and dilation secondary to myocardial infarction, or maladaptive in response to long-standing systemic hypertension. In addition to ventricular enlargement and cellular hypertrophy, extensive interstitial collagen deposition also occurs during this remodeling process. The increased fibrous tissue and hypertrophied myocytes can also lead to inappropriate energy production and utilization. Angiotensin-converting enzyme (ACE) inhibitors have the ability to modulate both cellular hypertrophy and collagen deposition. These effects represent, in part, the mechanism by which ACE inhibitors modify ventricular remodeling, the subsequent development and clinical expression of heart failure, and finally, the improvement in the mortality of patients with heart failure.
Topics: Angiotensin-Converting Enzyme Inhibitors; Animals; Follow-Up Studies; Heart Failure; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Myocardial Infarction; Myocardium; Survival Rate; Vascular Resistance
PubMed: 7700061
DOI: No ID Found -
Journal of Computer Assisted Tomography 2009Apical thinning of the left ventricular myocardium has been described by anatomists as a normal feature. Nonetheless, it does not appear in most anatomic atlases. We...
OBJECTIVE
Apical thinning of the left ventricular myocardium has been described by anatomists as a normal feature. Nonetheless, it does not appear in most anatomic atlases. We investigated its presence in healthy patients and patients with left ventricular hypertrophy using coronary computed tomographic arteriography (CCTA).
METHODS
Sixty-four patients without a history of cardiac disease and 8 patients with left ventricular hypertrophy were imaged using coronary computed tomographic arteriography.
RESULTS
All 64 patients had a focus of myocardial thinning at the left ventricular apex (mean, 1.2 mm [SD, 1.1 mm]). Its average span in the oblique coronal plane was 4.4 mm (2.9 mm), corresponding to a median area of 14.3 mm2 with an interquartile range of 3.9 to 31.6. The focus faced 4.8 degrees (5.9 degrees) toward the diaphragmatic side of the apex. The 8 hypertrophied hearts also had a zone of apical thinning. In a subset of 12 patients in whom functional data were analyzed, this focus did not thicken or move over the cardiac cycle.
CONCLUSIONS
A zone of substantial thinning of the left ventricular apex is a normal anatomic feature.
Topics: Coronary Angiography; Female; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Male; Middle Aged; Models, Anatomic; Reference Values; Reproducibility of Results; Sensitivity and Specificity; Tomography, X-Ray Computed
PubMed: 19478623
DOI: 10.1097/RCT.0b013e3181870356 -
European Journal of Pharmacology Jun 2012Cardiac hypertrophy is an important compensatory mechanism in response to a pressure overload, but a sustained excessive cardiac workload may deteriorate to maladaptive...
Cardiac hypertrophy is an important compensatory mechanism in response to a pressure overload, but a sustained excessive cardiac workload may deteriorate to maladaptive hypertrophy and to increased risk of heart failure. In this study, we evaluated the effects of KS370G on left ventricular hypertrophy and function. Abdominal aortic banding was performed by constricting the abdominal aorta. Hypertrophied heart was studied at 8 weeks after the operation. After the operation, KS370G 1mg/kg (K1 group) was administered by oral gavage once a day. Left ventricular function was measured by a 1.2F pressure-volume catheter (Scisense, Canada). The levels of protein for α-SMA (smooth muscle actin), p-AKT (protein kinase B), p-GSK3β (glycogen synthase kinase 3β) and p-ERKs (extracellular signal-regulated kinases) in myocardium were analyzed by Western blot. Plasma levels of angiotensin II, atrial natriuretic peptide and lactate dehydrogenase were analyzed by commercial kits. H.E. staining and M.T. staining methods were also used to observe diameter of cardiomyocytes and collagen accumulation. Chronic oral treatment with 1mg/kg KS370G inhibited cardiac hypertrophy and improved cardiac function induced by pressure overload. KS370G also decreased the plasma levels of atrial natriuretic peptide and lactate dehydrogenase. Besides, pressure overload-induced increase of α-SMA and phosphorylation of ERK, AKT and GSK3β were significantly reduced by chronic oral treatment with KS370G. We also found that chronic oral treatment with KS370G reduced cardiac collagen accumulation. KS370G improved left ventricular function and inhibited cardiac hypertrophy through the decrease of the phosphorylation of ERK, AKT and GSK3β in pressure-overload mice heart.
Topics: Actins; Angiotensin II; Animals; Aorta; Atrial Natriuretic Factor; Caffeic Acids; Cardiotonic Agents; Collagen; Constriction; Extracellular Signal-Regulated MAP Kinases; Glycogen Synthase Kinase 3; Glycogen Synthase Kinase 3 beta; Heart Ventricles; Hypertrophy; L-Lactate Dehydrogenase; Male; Mice; Mice, Inbred ICR; Myocytes, Cardiac; Phosphoproteins; Pressure; Proto-Oncogene Proteins c-akt; Time Factors
PubMed: 22484506
DOI: 10.1016/j.ejphar.2012.03.029 -
Medicine Jan 2019This study aimed to evaluate left ventricular deformation in relation to the geometric pattern in hypertensive patients with normal left ventricular ejection fraction...
This study aimed to evaluate left ventricular deformation in relation to the geometric pattern in hypertensive patients with normal left ventricular ejection fraction using speckle tracking echocardiography (STE).Transthoracic echocardiography was performed in 80 hypertensive patients and 50 age- and gender-matched normotensive subjects. Left ventricular geometric pattern was defined according to left ventricular mass index and relative wall thickness as normal geometry, concentric remodeling, concentric hypertrophy, and eccentric hypertrophy, respectively. Quantitative measurements of longitudinal, circumferential, and radial strain were performed for endocardial, middle, and epicardial layers of the left ventricular wall at each segment.The longitudinal strain in hypertension was lower for all 3 layers in concentric (n = 20) and eccentric hypertrophy (n = 20) than normotensive subjects (n = 50, P < .01). It was also significantly lower for the endocardial layer in concentric remodeling (n = 20, P = .04 vs normotensive subjects). The circumferential strain in hypertension was higher in normal geometry or concentric remodeling, lower in concentric hypertrophy, and at similar level in eccentric hypertrophy, in comparison with normotensive subjects. The difference from normotensive subjects was statistically significant for the endocardial and middle layers in normal geometry (P < .03), for the endocardial layer in concentric remodeling (P < .02), and for the middle and epicardial layers in concentric hypertrophy (P≤.001). The radial strain and twist did not differ between normotensive and hypertensive subjects (P > .08).Left ventricular deformation in hypertension occurs with various geometric patterns disproportionately in the endocardial, middle and epicardial layers and differently in the longitudinal and circumferential orientations.
Topics: Adult; Case-Control Studies; Echocardiography; Endocardium; Female; Heart Ventricles; Humans; Hypertension; Hypertrophy, Left Ventricular; Male; Middle Aged; Stroke Volume; Ventricular Function, Left
PubMed: 30681621
DOI: 10.1097/MD.0000000000014257 -
The Journal of Pediatrics Mar 2016
Topics: Female; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Male; Models, Cardiovascular; Ultrasonography
PubMed: 26746118
DOI: 10.1016/j.jpeds.2015.12.042