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Cells Oct 2022Right ventricular failure (RVF) is the most important prognostic factor for morbidity and mortality in pulmonary arterial hypertension (PAH) or pulmonary hypertension... (Review)
Review
Right ventricular failure (RVF) is the most important prognostic factor for morbidity and mortality in pulmonary arterial hypertension (PAH) or pulmonary hypertension (PH) caused by left heart diseases. However, right ventricle (RV) remodeling is understudied and not targeted by specific therapies. This can be partly explained by the lack of basic knowledge of RV remodeling. Since the physiology and hemodynamic function of the RV differ from those of the left ventricle (LV), the mechanisms of LV dysfunction cannot be generalized to that of the RV, albeit a knowledge of these being helpful to understanding RV remodeling and dysfunction. Store-operated Ca entry (SOCE) has recently emerged to participate in the LV cardiomyocyte Ca homeostasis and as a critical player in Ca mishandling in a pathological context. In this paper, we highlight the current knowledge on the SOCE contribution to the LV and RV dysfunctions, as SOCE molecules are present in both compartments. he relative lack of studies on RV dysfunction indicates the necessity of further investigations, a significant challenge over the coming years.
Topics: Male; Humans; Heart Ventricles; Ventricular Dysfunction, Right; Ventricular Remodeling; Hypertension, Pulmonary; Myocytes, Cardiac
PubMed: 36291148
DOI: 10.3390/cells11203282 -
Georgian Medical News Sep 2023Right ventricular (RV) morphologic and functional changes still remain a mystery in patients with AH. The aim of this study was to evaluate the influence of essential...
Right ventricular (RV) morphologic and functional changes still remain a mystery in patients with AH. The aim of this study was to evaluate the influence of essential hypertension on RV function and morphology. 75 nonsmoker hypertensive male patients (mean age 57.13±7.27) and 25 normotensive control subjects (mean age 57.56±7.55) were recruited in a study. All participants underwent 24-hour ambulatory blood pressure monitoring. Heart ultrasonography was performed to assess RV morphology and its systolic and diastolic function. In comparison with normotensive subjects, hypertensive patients had significantly higher RV wall thickness and significantly lower TAPSE (5.36±0.98 and 19.86±2.68 vs 4.11±0.50 mm and 22.52±2.02, P<0.0001). RV hypertrophy was found in 38.66% of hypertensive subjects. EF of RV in normotensive subjects was significantly higher than in hypertensives (62.73±12.81 vs 57.58±7.53%, respectively). RV mean E/A was significantly lower in hypertensive group (1.41±0.13 vs 0.89±0.15, P<0.001). RV diastolic dysfunction was found in 54.6% and systolic dysfunction in 7% of hypertensive subjects. The RV E/e' ratio was increased in hypertensives (4.84±0.97 vs. 3.88±0.32 in the control group, P<0.05). Tricuspid and mitral E'/A' ratio was decreased in hypertensive group (0.79±0.13 and 0.90±0.19 in hypertensive vs. 1.21±0.15 and 1.29±0.15 in the control groups, respectively, P<0.001 for both). According to study data, AH affects both ventricles simultaneously and causes concentric remodeling, hypertrophy, and functional disturbances in both ventricles; hence, in comparison with systolic dysfunction, existence of diastolic dysfunction was more prevalent in hypertensive population.
Topics: Humans; Male; Middle Aged; Aged; Blood Pressure Monitoring, Ambulatory; Hypertension; Heart Ventricles; Essential Hypertension; Hypertrophy
PubMed: 37991973
DOI: No ID Found -
The Journal of Pharmacy and Pharmacology Dec 2021Investigate if azilsartan protects against myocardial hypertrophy by upregulating nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated pathways.
OBJECTIVES
Investigate if azilsartan protects against myocardial hypertrophy by upregulating nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated pathways.
METHODS
Abdominal aortic constriction (AAC)-induced cardiac hypertrophy in rats was applied. Azilsartan or vehicle was administered daily for 6 weeks in sham or AAC rats. Cardiac morphology and ventricular function were determined. Azilsartan effects upon neonatal rat cardiomyocyte (NRCM) hypertrophy and molecular mechanisms were studied in angiotensin (Ang) II-stimulated NRCMs in vitro. Nrf2-small interfering RNA (siRNA) was used to knockdown Nrf2 expression. Messenger RNA (mRNA)/protein expression of Kelch-like erythroid cell-derived protein (Keap)1 and Nrf2 and its downstream antioxidant enzymes was determined by real-time reverse transcription-quantitative polymerase chain reaction and western blotting, respectively.
KEY FINDINGS
Azilsartan treatment ameliorated cardiac hypertrophy/fibrosis significantly in AAC rats. Azilsartan increased expression of Nrf2 protein but decreased expression of Keap1 protein. Upregulation of protein expression of Nrf2's downstream antioxidant enzymes by azilsartan treatment was observed. Azilsartan inhibited Ang II-induced NRCM hypertrophy significantly and similar effects on the Keap1-Nrf2 pathway were observed in vivo. Nrf2 knockdown markedly counteracted the beneficial effects of azilsartan on NRCM hypertrophy and the Keap1-Nrf2 pathway.
CONCLUSIONS
Azilsartan restrained pressure overload-induced cardiac remodelling by activating the Keap1-Nrf2 pathway and increasing expression of downstream antioxidant enzymes to alleviate oxidative stress.
Topics: Angiotensin II; Angiotensin Receptor Antagonists; Animals; Antioxidants; Benzimidazoles; Cardiomegaly; Female; Heart Ventricles; Kelch-Like ECH-Associated Protein 1; Male; Myocardium; Myocytes, Cardiac; NF-E2-Related Factor 2; Oxadiazoles; Oxidative Stress; RNA, Messenger; Rats, Sprague-Dawley; Signal Transduction; Up-Regulation; Rats
PubMed: 34343333
DOI: 10.1093/jpp/rgab097 -
International Journal of Environmental... Jul 2022The long-term practice of judo can lead to various changes in the heart including increased dimensions of the left ventricle in diastole and thickening of the...
The long-term practice of judo can lead to various changes in the heart including increased dimensions of the left ventricle in diastole and thickening of the interventricular septum and the posterior wall of the left ventricle. This study aimed to assess left ventricular morphology and function in elite male judokas. A comparative cross-sectional study was conducted that included a total of 20 subjects, 10 judokas, and 10 healthy non-athletes aged 24 ± 2.85 years. Demographic and anthropometric data were analyzed. All subjects underwent a medical examination and a two-dimensional transthoracic echocardiogram. Different parameters of left ventricular morphology and function were measured and compared between athletes and non-athletes. Left ventricle mass and LV mass index were higher in judokas than in non-athletes (p < 0.05), as well as PW thickness (9.78 ± 0.89 mm vs. 8.95 ± 0.76 mm). A total of six (n = 6) of athletes had eccentric hypertrophy, while others had normal heart geometry. LVEDd, LVEDs, LVEDd/BSA, and LVEDs/BSA were significantly higher in judokas (p < 0.05). LVEDd in athletes ranged from 48 to 62 mm. These values, combined with normal diastolic function, ejection fraction, and shortening fraction, indicate that the judokas’ cardiac adaptation was physiological rather than pathological.
Topics: Athletes; Cross-Sectional Studies; Echocardiography; Heart; Heart Ventricles; Humans; Male; Martial Arts; Ventricular Function, Left
PubMed: 35886693
DOI: 10.3390/ijerph19148842 -
Journal of the American Heart... Apr 2021Background In patients undergoing transcatheter aortic valve replacement (TAVR), those with small left ventricle (LV) may have an increased risk of poor outcomes,...
Background In patients undergoing transcatheter aortic valve replacement (TAVR), those with small left ventricle (LV) may have an increased risk of poor outcomes, because small LV is associated with low-flow (LF), left ventricular hypertrophy. However, the impact of small LV on patients undergoing TAVR remains unknown. Methods and Results We examined 2584 patients who underwent TAVR between October 2013 and May 2017 using data from the Japanese multicenter registry. On the basis of the American Society of Echocardiography guidelines, small LV was defined as left ventricular end-diastolic dimension <42.0 mm for men or <37.8 mm for women. The 2-year clinical outcomes were compared between patients with and without small LV using multivariable Cox regression analyses and propensity score matching. Subgroup analyses by LF, left ventricular hypertrophy were performed. Of 2584 patients who underwent TAVR, 466 (18.0%) had small LV. Patients with small LV had smaller body size and less comorbidity, and were more likely to have LF status compared with those without. Small LV was associated with a higher 2-year all-cause (20.8% versus 14.3%; adjusted hazard ratio [HR],1.58 [95% CI, 1.20-2.09]; =0.0013) and cardiovascular mortality (8.8% versus 5.5%; adjusted HR, 1.93 [95% CI, 1.25-2.98]; =0.0028). Propensity score matching analysis showed consistent findings. In subgroup analyses, LF, left ventricular hypertrophy did not interact with small LV. Conclusions Small LV, determined by a simple echocardiographic parameter, was associated with poorer clinical outcomes after TAVR regardless of LF, left ventricular hypertrophy. LV size may be useful for assessing clinical outcomes after TAVR. Registration URL: https://www.umin.ac.jp/ctr/index.htm; Unique identifier: UMIN000020423.
Topics: Aged, 80 and over; Aortic Valve; Aortic Valve Stenosis; Diastole; Echocardiography; Female; Follow-Up Studies; Heart Ventricles; Humans; Male; Organ Size; Propensity Score; Registries; Retrospective Studies; Risk Factors; Severity of Illness Index; Stroke Volume; Transcatheter Aortic Valve Replacement; Ventricular Function, Left
PubMed: 33749309
DOI: 10.1161/JAHA.120.019543 -
Biomolecules & Biomedicine Nov 2023Pressure overload-induced pathological cardiac hypertrophy (CH) is a complexed and adaptive remodeling of the heart, predominantly involving an increase in cardiomyocyte...
Pressure overload-induced pathological cardiac hypertrophy (CH) is a complexed and adaptive remodeling of the heart, predominantly involving an increase in cardiomyocyte size and thickening of ventricular walls. Over time, these changes can lead to heart failure (HF). However, the individual and shared biological mechanisms of both processes remain poorly understood. This study aimed to identify key genes and signaling pathways associated with CH and HF following aortic arch constriction (TAC) at four weeks and six weeks, respectively, and to investigate potential underlying molecular mechanisms in this dynamic transition from CH to HF at the whole cardiac transcriptome level. Initially, a total of 363, 482, and 264 differentially expressed genes (DEGs) for CH, and 317, 305, and 416 DEGs for HF were identified in the left atrium (LA), left ventricle (LV), and right ventricle (RV), respectively. These identified DEGs could serve as biomarkers for the two conditions in different heart chambers. Additionaly, two communal DEGs, elastin (ELN) and hemoglobin beta chain-beta S variant (HBB-BS), were found in all chambers, with 35 communal DEGs in the LA and LV and 15 communal DEGs in the LV and RV in both CH and HF. Functional enrichment analysis of these genes emphasized the crucial roles of the extracellular matrix and sarcolemma in CH and HF. Lastly, three groups of hub genes, including the lysyl oxidase (LOX) family, fibroblast growth factors (FGF) family, and NADH-ubiquinone oxidoreductase (NDUF) family, were determined to be essential genes of dynamic changes from CH to HF.
Topics: Humans; Cardiomegaly; Heart Failure; Myocytes, Cardiac; Heart Ventricles; Heart Atria; Aortic Valve Stenosis
PubMed: 37334749
DOI: 10.17305/bb.2023.8997 -
American Journal of Physiology. Heart... Oct 2021Although pulmonary arterial hypertension (PAH) leads to right ventricle (RV) hypertrophy and structural remodeling, the relative contributions of changes in myocardial...
Although pulmonary arterial hypertension (PAH) leads to right ventricle (RV) hypertrophy and structural remodeling, the relative contributions of changes in myocardial geometric and mechanical properties to systolic and diastolic chamber dysfunction and their time courses remain unknown. Using measurements of RV hemodynamic and morphological changes over 10 wk in a male rat model of PAH and a mathematical model of RV mechanics, we discriminated the contributions of RV geometric remodeling and alterations of myocardial material properties to changes in systolic and diastolic chamber function. Significant and rapid RV hypertrophic wall thickening was sufficient to stabilize ejection fraction in response to increased pulmonary arterial pressure by without significant changes in systolic myofilament activation. After , RV end-diastolic pressure increased significantly with no corresponding changes in end-diastolic volume. Significant RV diastolic chamber stiffening by was not explained by RV hypertrophy. Instead, model analysis showed that the increases in RV end-diastolic chamber stiffness were entirely attributable to increased resting myocardial material stiffness that was not associated with significant myocardial fibrosis or changes in myocardial collagen content or type. These findings suggest that whereas systolic volume in this model of RV pressure overload is stabilized by early RV hypertrophy, diastolic dilation is prevented by subsequent resting myocardial stiffening. Using a novel combination of hemodynamic and morphological measurements over 10 wk in a male rat model of PAH and a mathematical model of RV mechanics, we found that compensated systolic function was almost entirely explained by RV hypertrophy, but subsequently altered RV end-diastolic mechanics were primarily explained by passive myocardial stiffening that was not associated with significant collagen extracellular matrix accumulation.
Topics: Animals; Biomechanical Phenomena; Diastole; Disease Models, Animal; Fibrosis; Heart Ventricles; Hypertrophy, Right Ventricular; Male; Models, Cardiovascular; Myocardium; Pulmonary Arterial Hypertension; Rats, Sprague-Dawley; Systole; Time Factors; Ventricular Dysfunction, Right; Ventricular Function, Right; Ventricular Remodeling; Rats
PubMed: 34448637
DOI: 10.1152/ajpheart.00046.2021 -
Nutrients Jul 2022Osteoprotegerin (OPG) is a molecule which belongs to the tumor necrosis factor receptor superfamily. OPG concentration is elevated in patients with left ventricle...
Serum Osteoprotegerin Is an Independent Marker of Left Ventricular Hypertrophy, Systolic and Diastolic Dysfunction of the Left Ventricle and the Presence of Pericardial Fluid in Chronic Kidney Disease Patients.
BACKGROUND
Osteoprotegerin (OPG) is a molecule which belongs to the tumor necrosis factor receptor superfamily. OPG concentration is elevated in patients with left ventricle hypertrophy, heart failure and acute myocardial infarction. OPG concentrations rise in chronic kidney disease (CKD). The aim of this study was to investigate the association between OPG concentrations and cardiovascular complications, such as left ventricle hypertrophy, systolic and diastolic dysfunction of left ventricle and dysfunction of right ventricle in chronic kidney disease patients not treated with dialysis. The relation between OPG and the amount of pericardial fluid was also examined.
METHODS
One hundred and one men with CKD stage 3-5 not treated with dialysis were included in the study. Overhydration, body fat mass and lean body mass were measured using bioimpedance spectroscopy (BIS). Echocardiography was performed to evaluate the amount of pericardial fluid and to measure the thickness of the interventricular septum (IVS), systolic and diastolic function of left ventricle, as well as systolic function of right ventricle.
RESULTS
We observed a significant positive association between OPG and the thickness of the interventricular septum, the size of the left atrium (LA) and the presence of pericardial fluid. A negative relationship was observed between OPG and ejection fraction (EF).
CONCLUSIONS
Our results suggest that OPG can be an independent marker of left ventricular hypertrophy, systolic and diastolic dysfunction of left ventricle and the presence of pericardial fluid in chronic kidney disease patients.
Topics: Heart Failure; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Male; Osteoprotegerin; Pericardial Fluid; Renal Dialysis; Renal Insufficiency, Chronic; Ventricular Dysfunction, Left
PubMed: 35889849
DOI: 10.3390/nu14142893 -
Nutrients Oct 2021Although insulin-induced cardiac hypertrophy is reported, very little information is available on the hypertrophic effect of insulin on ventricular cardiomyocytes and...
Although insulin-induced cardiac hypertrophy is reported, very little information is available on the hypertrophic effect of insulin on ventricular cardiomyocytes and the regulation of sodium and calcium homeostasis. Taurine is a non-essential amino acid synthesized by cardiomyocytes and the brain and is present in low quantities in many foods, particularly seafood. The purpose of this study was to investigate whether chronic exposure to insulin induces hypertrophy of ventricular cardiomyocytes that are associated with changes in Na and Ca homeostasis and whether taurine pre-treatment prevents these effects. Our results showed that chronic treatment with insulin leads to cardiomyocyte hypertrophy that is associated with an increase in basal intracellular Na and Ca levels. Furthermore, long-term taurine treatment prevents morphological and ionic remodeling induced by insulin. In addition, blocking the Na-taurine co-transporter prevented the taurine antihypertrophic effect. Finally, the insulin-induced remodeling of cardiomyocytes was associated with a decrease in the ratio of phospho-CREB (pCREB) to total cAMP response element binding protein (CREB); taurine prevented this effect. In conclusion, our results show that insulin induces ventricular cardiomyocyte hypertrophy via downregulation of the pCREB/tCREB level and that chronic taurine treatment prevents this effect.
Topics: Animals; Calcium; Cardiomegaly; Cells, Cultured; Cyclic AMP Response Element-Binding Protein; Down-Regulation; Heart Ventricles; Homeostasis; Insulin; Male; Myocytes, Cardiac; Rats; Sodium; Symporters; Taurine; Ventricular Remodeling; beta-Alanine
PubMed: 34835942
DOI: 10.3390/nu13113686 -
Journal of the American Heart... Aug 2019Background Left ventricular hypertrophy (LVH) is associated with an increased risk for cardiovascular disease (CVD) events and all-cause mortality. Many individuals...
Background Left ventricular hypertrophy (LVH) is associated with an increased risk for cardiovascular disease (CVD) events and all-cause mortality. Many individuals without LVH have a left ventricular mass that exceeds the level predicted by their sex, body size, and cardiac workload, a condition called inappropriate left ventricular mass (iLVM). We investigated the association of iLVM with CVD events and all-cause mortality among blacks. Methods and Results We analyzed data from the Jackson Heart Study, a community-based cohort of blacks. The current analysis included 4424 participants without CVD and with an echocardiogram at baseline. Among this cohort, the prevalence of iLVM was 13.8%. There were 262 CVD events and 419 deaths over a median follow-up of 9.7 years (maximum, 12 years). Compared with participants without iLVM, participants with iLVM had a higher rate of CVD events and all-cause mortality. After multivariable adjustment, including for the presence of LVH, iLVM was associated with an increased risk of CVD events (hazard ratio, 1.87; 95% CI, 1.33-2.62). The multivariable-adjusted hazard ratio for all-cause mortality was 1.29 (95% CI, 0.98-1.70). Among participants without and with LVH, the multivariable-adjusted hazard ratios of iLVM for CVD events were 2.53 (95% CI, 1.68-3.81) and 1.21 (95% CI, 0.74-2.00), respectively (P=0.029); and for all-cause mortality, the hazard ratios were 1.24 (95% CI, 0.81-1.89) and 1.26 (95% CI, 0.86-1.85), respectively (P=0.664). Conclusions iLVM is associated with an increased risk for CVD events among blacks without LVH.
Topics: Adult; Black or African American; Aged; Antihypertensive Agents; Cardiovascular Diseases; Cause of Death; Cohort Studies; Echocardiography; Female; Heart Ventricles; Humans; Hypertension; Hypertrophy, Left Ventricular; Longitudinal Studies; Male; Middle Aged; Mortality; Multivariate Analysis; Organ Size; Proportional Hazards Models; Stroke Volume; United States
PubMed: 31407619
DOI: 10.1161/JAHA.118.011897