Thickness Of Right Ventricle Research Articles

Fatty infiltration and ventricular premature beats originating from right ventricular outflow tract: association or causality?

Anatomical evidence reveals heterogeneous fat distribution in both atrial and ventricular myocardium that are considered normal, but at the same time arrhythmogenic, and numerous cardiac pathophysiological conditions are associated with myocardial fat deposits. The relationship between fatty infiltration, especially in the epicardial layer and its pathophysiological implication is not completely understood. The aim of this study was to establish a positive or negative relationship between the ventricular burden and several parameters related to right ventricle (RV) adipose tissue - the RV thickness, RV indexed mass, body mass index (BMI), age, gender. Twenty-three patients with documented premature ventricular contractions (PVCs) originating from right ventricular outflow tract based on electrocardiography (ECG) evaluation were hospitalized between January 2018-November 2022 for electrophysiological study and PVCs ablation. Data obtained after collecting the clinical characteristics, ECG, RV measurements from transthoracic echocardiography (TTE), cardiac computed tomography (CT) and magnetic resonance imaging (MRI) were analyzed. A weak positive relationship between the ventricular burden and BMI (r=0.14, p=0.49), tricuspid annular plane systolic excursion (TAPSE) (r=0.07, p=0.7), the RV thickness (r=0.03, p=0.8), epicardial adipose tissue (r=0.13, p=0.55), RV mass indexed (r=0.05, p=0.82) was observed. No clear cut-off of the PVCs burden could be established in terms related to the increase in BMI, RV thickness, epicardial adipose tissue, RV mass indexed. No significant positive or negative relationship between the ventricular burden and the RV thickness, RV indexed mass were found in individuals with a high PVCs originating from right ventricular outflow tract (RVOT) burden.

Transthyretin amyloid cardiomyopathy in patients with unexplained increased left ventricular wall thickness

Amyloid cardiomyopathy (CA) was previously considered a rare disease; however, rapid advancements in imaging modalities have led to an increased frequency of its diagnosis. The aim of this prospective study was to assess the prevalence and clinical phenotype of transthyretin amyloidosis (ATTR) cardiomyopathy in patients exhibiting unexplained increased left ventricular (LV) wall thickness. From 2020 to 2022, we enrolled 100 consecutive adults with unexplained increased LV wall thickness in the study. The analysis included clinical data, electrocardiography, transthoracic echocardiography, single-photon emission computed tomography/computed tomography with 3,3-disphono-1,2-propanodicarboxylic acid, genetic testing. Overall, 18% of patients were diagnosed with CA, comprising 5% with light-chain amyloidosis, and 12% with ATTR. To evaluate associations with the ATTR diagnosis, a LOGIT model and multivariate analysis were applied. Notably, age, polyneuropathy, gastropathy, carpal tunnel syndrome, lumbar spine stenosis, low voltage, ventricular arrhythmia, LV mass, LV ejection fraction, global longitudinal strain (GLS), E/A, E/E′, right ventricle (RV) thickness, right atrium area, RV VTI, TAPSE, apical sparing, ground glass appearance of myocardium, thickening of interatrial septum, thickening of valves, and the “5–5–5” sign were found to be significantly associated with ATTR (p < 0.05). The best predictive model for ATTR diagnoses exhibited an area under the curve of 0.99, including LV mass, GLS and RV thickness. This study, conducted at a cardiology referral center, revealed that a very considerable proportion of patients with unexplained increased LV wall thickness may suffer from underlying CA. Moreover, the presence of ATTR should be considered in patients with increased LV mass accompanied by reduced GLS and RV thickening.

Heat stress‐induced changes in the myocardium

Prolonged exposure to heat can lead to environment‐induced heat stress (EIHS), which may be a threat to human health. How EIHS affects cardiac morphology and the myocardium are unknown. We hypothesized that EIHS would alter cardiac morphology and cause cellular dysfunction. To test this hypothesis, crossbred female pigs were exposed to thermoneutral (TN; 20.6 ± 0.2 ºC; n=8) or EIHS (37.4 ± 0.2 ºC; n=8) conditions for 24 h. Rectal temperature (RT), skin temperature (ST), and respiratory rate (RR) were recorded every 4 h during the environmental challenge. Pigs were euthanized following the environmental challenge and hearts were collected. Hearts were weighed and heart length (apex to base), width (left/right dimension), and left ventricle (LV) and right ventricle (RV) wall thickness were measured with calipers. Portions of LV and RV were lyophilized to measure tissue water content or homogenized for protein extraction and western blotting. Environment‐induced heat stress increased RT by 1.3 ºC (p&lt;0.01), ST by 11 °C (p&lt;0.01) and RR by 72 breaths per minute (p&lt;0.01) compared to TN. Heart weight tended to be decreased (7.6%; p=0.07) and heart length was decreased (8.5%; p=0.01) by EIHS, but heart width was similar between groups. Left ventricle wall thickness was increased (22%; p=0.02) and RV thickness was decreased (26%; p=0.04) in EIHS compared to TN. Water content in the RV was similar between groups, however, in LV it was increased (8.6%; p&lt;0.01) in EIHS compared to TN, suggesting edema contributed to increased LV thickness. Lastly, using a western blot approach we discovered that pathways regulating energy homeostasis were impacted by EIHS and sometimes differed between RV and LV. In RV and LV, phosphorylation (p) of AMP‐activated protein kinase (AMPK) was decreased by EIHS (RV – 73%, p&lt;0.02; LV – 54%, p=0.04), and in the RV was accompanied by increased protein phosphate type 2A (PP2A; 15.5%, p&lt;0.01), which regulates pAMPK, and decreased p‐Acetyl‐CoA carboxylase (ACC; 40%, p&lt;0.01), a client protein of pAMPK, whereas these were similar in LV. In RV, mTOR signaling appeared to be blunted, mitochondrial content increased, and markers of mitophagy increased by EIHS compared to TN, however, LV was resistant to these changes. In total, these data demonstrate that a single bout of EIHS caused cardiac morphological changes and biochemical changes in the myocardium and that EIHS affects the LV and RV differently.

The role of echocadiography in the differential diagnosis between PRKAG2 syndrome and Fabry disease

Abstract Funding Acknowledgements Type of funding sources: None. Background Storage of glycogen and glycosphingolipids occurs in the heart with PRKAG2 Syndrome and Fabry Disease (FD), respectively. Identification of specific echocardiographic parameters could contribute to early diagnosis, which is fundamental to initiate appropriate treatment and improve prognosis. Material and methods: Prospective, transversal, observational study involving 45 patients, 30 genetically identified with the PRKAG2 gene mutation and 15 with FD. Conventional transthoracic, bi-, and tridimensional echocardiography as well as strain/strain rate speckle tracking were measured during one examination. Specific echocardiographic measurements were obtained and the data exported to a workstation for subsequent evaluation. Analyses were performed with 5% significance using the R program, version 3.1.3. Results: Compared to FD patients, PRKAG2 patients presented increased left atrium volume index, mean LV septum, posterior wall thickness, right ventricle (RV) dimensional values, and RV thickness in diastole. LV hypertrophy was found in varying degrees in 25 (86%) of PRKAG2 and 8 (53%) of FD Pts. We detected a binary appearance of LV endocardial border ("binary sign") and hypertrophy of the anterolateral papilary muscle in 60% of FD Pts. PRKAG2 Pts showed reduced global longitudinal strain (2DGLS), 4D GLS, 4D global radial strain (GRS), and aortic diameter compared to FD patients. In PRKAG2 Pts the bull’s-eye plot showed a stripe-like pattern. In FD Pts, however, it showed a peak systolic strain reduction in basal and mid- anterolateral segments. Conclusion: Echocardiography is an important technique in differentiating both diseases to determine adequate treatment and prognosis. We have demonstrated that PRKAG2 Pts present moderately greater cardiac involvement than FD Pts.

Difference in Thickness Between Right Ventricle and Left Ventricle of Adult Human Heart: A Cadaveric Study

Background: The left ventricle is longer and narrower than the right ventricle, extending from its base in the plane of the atrioventricular groove to the cardiac apex. The wall of the left ventricle is three times thicker (8-12 mm) than those of right ventricle. The wall of the right ventricle is relatively thin (3–5 mm), the ratio of the thickness of the two ventricular walls usually being 1:3. Hypertrophic cardiomyopathy is characterized by myocardial wall thickening, particularly a disproportionate thickening of the interventricular septum in comparison with the posterior wall. An athlete’s heart may physiologically hypertrophy but in a uniform fashion. The objective of the study is to determine the thickness of wall of right and left ventricle of adult human heart and ratio of thickness of right and left ventricle. Materials and Methods: Adult human hearts were procured from the specimens preserved in Anatomy Department of Jawaharlal Nehru Institute of Medical Sciences. A cross-sectional study was conducted on forty- four specimen of adult heart. The measurement of the right and left ventricular wall was done with digital vernier caliper. The measurements were done at three levels in both right and left ventricle: upper, middle and lower part. Result and Conclusion: The ratio of the thickness of the wall of right and left ventricle is well known as 1:3. However, in our study we found the ratio as 1:1.4. We found the thickness of the right ventricle thicker than the normal thickness reported in previous studies. We wish to continue the study with a larger sample size. KEY WORDS: Heart, Right ventricle, left ventricle, Thickness Ratio, Myocardium.

Anti-inflammatory nutrition with high protein attenuates cardiac and skeletal muscle alterations in a pulmonary arterial hypertension model

Pulmonary arterial hypertension (PAH) is characterized by remodelling of the pulmonary arteries and right ventricle (RV), which leads to functional decline of cardiac and skeletal muscle. This study investigated the effects of a multi-targeted nutritional intervention with extra protein, leucine, fish oil and oligosaccharides on cardiac and skeletal muscle in PAH. PAH was induced in female C57BL/6 mice by weekly injections of monocrotaline (MCT) for 8 weeks. Control diet (sham and MCT group) and isocaloric nutritional intervention (MCT + NI) were administered. Compared to sham, MCT mice increased heart weight by 7%, RV thickness by 13% and fibrosis by 60% (all p < 0.05) and these were attenuated in MCT + NI mice. Microarray and qRT-PCR analysis of RV confirmed effects on fibrotic pathways. Skeletal muscle fiber atrophy was induced (P < 0.05) by 22% in MCT compared to sham mice, but prevented in MCT + NI group. Our findings show that a multi-targeted nutritional intervention attenuated detrimental alterations to both cardiac and skeletal muscle in a mouse model of PAH, which provides directions for future therapeutic strategies targeting functional decline of both tissues.

МОРФОМЕТРИЧНІ ОСОБЛИВОСТІ СТІНОК ШЛУНОЧКІВ ТА МІЖШЛУНОЧКОВОЇ ПЕРЕГОРОДКИ СЕРЦЯ ЩУРІВ У НОРМІ ТА ПІСЛЯ ВНУТРІШНЬОПЛІДНОЇ ДІЇ АНТИГЕНУ

Recently diseases of cardiovascular system in children take one of the first places in Ukraine.The aim of the study – studying the morphometric features of walls and interventricular septum thickness of rat’s heart in normal conditions and after antenatal antigen impact.Materials and Methods. 144 hearts of laboratory rats were investigated. They were divided into 3 groups: I group – intact rats, ІІ – control group, that get intrauterine injection of Sodium Chloride solution 0.9 % 0.05 ml on the 18th day of antenatal development. III – the experimental group of rats, who were injected by 0.05 ml of anatoxin in a similar method. Serial sections were stained with hematoxylin and eosin.Results and Discussion. In the experimental group in newborn animals the indices of the thickness of right ventricle, left ventricle and interventricular septum are much lower than in the control. This tendency is observed until the 21st day, and on the 45th day all thickness indicators were significantly higher in experimental animals. Obtained results can be related with changes in the ratio of muscle and connective tissues by reducing of the first and increasing of the second. Wall’s thickening in experimental animals on the 45th day can be considered as a development of hypertrophic cardiomyopathy, which is one of the manifestations of UCTD in the heart.Conclusions. Intrauterine antenatal administration of the antigen may cause a disturbance in the formation of the connective tissue of the heart, which in the future may lead to decreasing of the adaptive capacity of the myocardium.

Establishment of modified right ventricular outflow tract obstruction animal model in rats

Objective To modify the model of right ventricular outflow tract obstruction (RVOTO) in rats, and to search for the optimal method for the model establishment. Methods Thirty male SD rats were randomly divided to three groups: RVOTO group, sham group and control group. There were 10 rats in each group. The animals in RVOTO group were given pulmonary arterial constriction (PAC), those in sham group thoracotomy without PAC, and those in control group no surgical operation. The heart specimens were harvested after 4 weeks. The thickness of right ventricle, the hyperplastic state of myocardiac cells and the fiber volume ratio of myocardiac cells were analyzed by the t test. Results The modified RVOTO model was established in 4 weeks. The thickness of right ventricle in RVOTO group was greater than that in sham group and control group [RVOTO group: (0.938±0.054) mm; sham group: (0.260±0.436) mm; control group: (0.249±0.587) mm, P=0.000]. The thickness of right ventricular outflow tract was significantly increased as compared with the free wall of right ventricle. The fiber volume ratio of myocardiac cells in RVOTO group was significantly higher than in sham group and control group [RVOTO group: (20.17±5.87)%; sham group: (8.35±4.23)%; control group: (7.57±2.31)%, P=0.000]. Conclusion The modified model of RVOTO in rats is significantly cheaper, easier, safer and more consistent with the clinical features than the traditional one. Key words: Right ventricular outflow tract obstruction; Right ventricular hypertrophys; U-shaped clamp; Models, animal

Abstract 68: p38 MAP Kinase Regulates Chamber Specific Postnatal Remodelling of Cardiac Ventricles

Background: Left ventricle (LV) and right ventricle (RV) in mouse heart undergo dramatically different chamber-specific remodeling after birth, leading to rapid increase in LV vs. RV chamber size. However, the underlying regulatory mechanism mediating chamber specific remodeling process remains enigmatic. Results and Methods: In neonatal mouse heart, p38 MAP kinase activity is dynamically activated in a chamber specific manner. p38 activity is specifically elevated in RV comparing to LV at E18.5, postnatal day 3 (P3) and P7 stages whereas p38 activity is lower in both ventricles at P0 and P1. In mouse heart with cardiomyocyte specific-knockout of p38α and β (p38ab-cdKO), total p38 activity was diminished in both chambers. The p38ab-cdKO mice had significant neonatal lethality associated with RV specific chamber enlargement and significant increase in both RV wall thickness (RVW) and inner diameter of RV (RVID) as early as P3. Interestingly, p38 inactivation suppressed myocyte apoptotic activity specifically in RV while increased RV myocyte proliferation and hypertrophy during neonatal period. Unexpectedly, RNA-seq results implicated Xbp1 mediated transcriptional regulation significantly contributing to p38 dependent transcriptome reprogramming in RV. Indeed, IRE1α expression in neonatal cardiomyocyte is sufficient to induce proliferation in vitro. Furthermore, knockdown of Xbp1 blunted p38 inhibition-induced myocyte proliferation, suggesting that IRE1a/Xbp1 mediate p38 signaling in neonatal myocyte proliferation. Conclusion: Chamber-specific remodeling in neonatal heart involves temporally regulated and RV specific p38 MAP kinase activity. RV specific myocyte proliferation and hypertrophy concurrent with RV specific programmed myocyte death is orchestrated by two innate stress-response pathways, p38 and Xbp1.

The sexual dimorphism associated with pulmonary hypertension corresponds to a fibrotic phenotype.

Although female predominance in the development of all types of pulmonary hypertension (PH) is well established, many clinical studies have confirmed that females have better prognosis and higher survival rate than males. There is no clear explanation of why sex influences the pathogenesis and progression of PH. Using a rat angioproliferative model of PH, which closely resembles the primary pathological changes observed in humans, we evaluated the role of sex in the development and progression of PH. Female rats had a more pronounced increase in medial thickness in the small pulmonary arteries. However, the infiltration of small pulmonary arteries by inflammatory cells was found only in male rats, and this corresponded to increased myeloperoxidase activity and abundant adventitial and medial fibrosis that were not present in female rats. Although the level of right ventricle (RV) peak systolic pressure was similar in both groups, the survival rate in male rats was significantly lower. Moreover, male rats presented with a more pronounced increase in RV thickness that correlated with diffuse RV fibrosis and significantly impaired right cardiac function. The reduction in fibrosis in female rats correlated with increased expression of caveolin-1 and reduced endothelial nitric oxide synthase-derived superoxide. We conclude that, in the pathogenesis of PH, female sex is associated with greater remodeling of the pulmonary arteries but greater survival. Conversely, in males, the development of pulmonary and cardiac fibrosis leads to early and severe RV failure, and this may be an important reason for the lower survival rate among males.

Oxidative status and chymotrypsin-like activity in right and left ventricle hypertrophy in an experimental model of emphysema

Although cardiac muscle hypertrophy has been studied in association with several diseases, its mechanism in patients with emphysema, in particular in relation to oxidative stress and proteolysis, remains unknown. The role of oxidative stress and proteolysis in right and left ventricle hypertrophy was investigated in hamsters with emphysema induced by 2 different doses of papain (20mg/mL, E20 and 40mg/mL, E40). The thickness of the ventricles, total and cardiac weight, lipid peroxidation, carbonyl proteins, total antioxidant capacity (TAC), and proteasomal proteolytic activity were evaluated in the right ventricle (RV) and the left ventricle (LV) of control and emphysema hamsters. RV thickness was increased by 12% in the E20 group and by 29% in the E40 group. Lipid peroxidation measured by chemiluminescence was increased in the E40 group (from 3350.68±392.44URL/g tissue to 4696.63±1076.70URL/g tissue, p<0.05). TAC also increased only in the E40 group. In the LV, chemiluminescence values increased from 4044.77±503.39 to 5517.10±388.27 in the E20 group and to 8169.14±1748.77URL/g tissue in the E40 group (p<0.05, both). TAC significantly increased in the E20 and E40 groups. No differences were detected in substances reactive to thiobarbituric acid or carbonyl proteins when comparing ventricles or doses. Chymotrypsin-like proteolytic activity significantly decreased in both groups and ventricles. Emphysema can induce right and left ventricle lipid peroxidation and result in antioxidant mobilization. These data together support the idea that cardiac hypertrophy in response to emphysema is mediated in part by proteolytic pathways with involvement of reactive species.

Effects of obstructive sleep apnea-hypopnea syndrome upon cardiac structure and function

To investigate the effects of obstructive sleep apnea-hypopnea syndrome (OSAHS) upon cardiac structure and function of patients. According to apnea hypopnea index, 75 OSAHS patients were divided into three groups: mild (n = 25), moderate (n = 25) and serious (n = 25); according to the course of disease, < 5 years (n = 22), 5-10 years (n = 26) and > 10 years (n = 27). The control group included 25 healthy adults. All subjects received polysomnogram and echocardiography. The following parameters were recorded: aortic dimension, pulmonary artery inner diameter, chambers heart size, interventricular septal thickness, anterior wall thickness and movement extent of end-diastole right ventricle, left ventricular ejection fraction (LVEF), shortening fraction (FS) and E/A ratio, etc. Pulmonary artery inner diameter of mild, moderate, serious and control groups were (21.4 +/- 2.5), (24.7 +/- 2.0), (26.7 +/- 2.1), (21.2 +/- 2.7) mm, right ventricle internal diameter (19.0 +/- 1.8), (22.0 +/- 2.1), (23.9 +/- 2.1), (18.9 +/- 1.8) mm, and anterior wall thickness of right ventricle (4.7 +/- 1.2), (6.5 +/- 1.3), (7.5 +/- 1.4), (4.1 +/- 1.0) mm. The moderate and serious groups were all higher than control and mild groups obviously (P < 0.01). The serious group was higher than the moderate group (P < 0.01). LVEF of four groups: (63.1 +/- 8.1)%, (60.0 +/- 10.2)%, (54.5 +/- 9.1)%, (63.6 +/- 7.7)%, FS: (38.1 +/- 4.3)%, (37.0 +/- 6.4)%, (33.6 +/- 5.4)%, (39.5 +/- 4.9)%, and E/A: (1.13 +/- 0.13), (0.96 +/- 0.16), (0.85 +/- 0.12), (1.28 +/- 0.15). LVEF and FS of the serious group were lower than those of the control, mild and moderate groups (P < 0.05). E/A ratio of the mild, moderate and serious groups were lower than the control group (P < 0.01). The interclass comparison of mild, moderate and serious groups had significant differences (P < 0.01). Right ventricle internal diameter, pulmonary artery inner diameter, anterior wall thickness of right ventricle of > 10 years group were higher than 5-10 years group obviously (P < 0.05, P < 0.01). The 5-10 years group was higher than the < 5 years and control groups obviously (P < 0.05, P < 0.01). LVEF, FS, and E/A ratio of > 10 years group were lower than 5-10 years, < 5 years and control groups obviously (P < 0.05, P < 0.01). OSAHS causes structural and functional cardiac changes worsening with disease aggravation and course extension.

Modelo experimental de bandagem ajustável do tronco pulmonar para preparo rápido do ventrículo

OBJETIVO: Um dispositivo de bandagem do tronco pulmonar (TP) com ajuste percutâneo foi desenvolvido com o objetivo de induzir a hipertrofia rápida do ventrículo subpulmonar. MATERIAL E MÉTODOS: Consiste de um manguito de silicone insuflável percutaneamente, através de um botão de silicone auto-selante. Os corações de 7 cabritos jovens (peso médio: 8,7 kg) foram submetidos à sobrecarga sistólica imposta pelo dispositivo e avaliados sob os aspectos hemodinâmicos, ecocardiográficos e morfológicos. Foram extraídas biópsias basais do miocárdio do ventrículo direito (VD) para análise microscópica (perímetro e área do miócito). O dispositivo foi implantado no TP. As pressões do VD, TP e aorta foram monitorizadas. Após convalescença, foi iniciado o protocolo de insuflação do dispositivo de bandagem do TP. Foi injetada água destilada no botão auto-selante (via percutânea), até que a pressão sistólica do VD atingisse 70% da pressão sistólica do VE. As avaliações ecocardiográfica e hemodinâmica foram realizadas a cada 24 horas. A sobrecarga sistólica do VD foi mantida por um período de 96 horas, com insuflações progressivas no limite máximo tolerado, a cada 24 horas. Após esse período, os animais foram sacrificados para análise morfológica dos corações. Outros 9 cabritos (peso médio: 7,7 kg) foram utilizados como grupo controle, para análise do peso do VD. RESULTADOS: Após 96 horas de sobrecarga sistólica do VD, foi observado um aumento do gradiente sistólico VD/TP de 10,1±4,3 mmHg para 60,0±11,0 mmHg e da pressão sistólica no VD de 22,4±4,1 mmHg para 71,0±10,0 mmHg (p<0,0001). O ecocardiograma revelou aumento da espessura muscular do VD, de 4,4±0,5 mm para 7,3±1,7 mm (p=0,001). Quando comparado ao grupo controle, houve um ganho de peso de 74% do VD submetido à sobrecarga sistólica (p<0,0001). À microscopia óptica, foi observado aumento de 27% no perímetro e de 69% na área dos miócitos (p=0,0001). CONCLUSÕES: O dispositivo proposto neste trabalho é efetivo e facilmente ajustável por via percutânea, possibilitando a hipertrofia do ventrículo subpulmonar em 96 horas de sobrecarga sistólica. A melhora na ajustabilidade da bandagem do TP poderá permitir melhores resultados da operação de Jatene em dois estágios, nos pacientes com transposição das grandes artérias.

Cardiac compliance and dimensions in carbon monoxide-induced cardiomegaly

Adult male rats inhaled 500 ppm CO continuously for 38 to 47 days to produce significant cardiomegaly. In a first experiment in which heart wall stiffness was examined, haematocrit rose 45.1% and the ratio of the sum of right ventricle (RV) and left ventricle (LV) to body weight (mg X g-1) increased from 2.69 to 3.34. Compliance (ml X mmHg-1) of CO LV's and RV's studied from 0 to 25 mmHg intraluminal pressure, was generally greater than that of LV's and RV's from controls at the same pressure. These differences were greater for RV's. There was no difference between control RV's and LV's at the same distending pressure. The differences between treated and control groups disappeared when compliance was normalised per g heart weight. In a second experiment in which heart dimensions were examined, haematocrit ratio increased 48.6% and 2V (RV + LV) to body weight ratio (mg X g-1) increased from 2.77 to 3.45. Atrial weight was also greater. LV apex to base length increased 6.4% and LV outside diameter increased 7.3. No significant differences in LV, RV or interventricular septum (S) thickness resulted from CO exposure, as measured at three sites in each, in four cross-sections of the heart between the apex and base. In general, LV wall was slightly thicker than S, while RV was about 35% that of LV. The findings suggest that chronic carboxyhaemoglobinaemia produces largely eccentric cardiomegaly, and that there is no intrinsic change in wall stiffness.