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It has been raised that marathon running may significantly impair cardiac performance. However, the post-race diastolic function has not been extensively analyzed. We aimed to assess whether the marathon run causes impairment of the cardiac diastole, which ventricle is mostly affected and whether the septal (IVS) function is altered. The study included 34 male amateur runners, in whom echocardiography was performed two weeks before, at the finish line and two weeks after the marathon. Biventricular diastolic function was assessed not only with conventional Doppler indices but also using the heart rate-adjusted isovolumetric relaxation time (IVRTc). After the run, IVRTc elongated dramatically at the right ventricular (RV) free wall, to a lesser extent at the IVS and remained unchanged at the left ventricular lateral wall. The post-run IVRTc_IVS correlated with IVRTc_RV (r = 0.38, p < 0.05), and IVRTc_RV was longer in subjects with IVS hypertrophy (88 vs. 51 ms; p < 0.05). Participants with measurable IVRT_RV at baseline (38% of runners) had longer post-race IVRTc_IVS (102 vs. 83 ms; p < 0.05). Marathon running influenced predominantly the RV diastolic function, and subjects with measurable IVRT_RV at baseline or those with IVS hypertrophy can experience greater post-race diastolic fatigue.
Right ventricular (RV) dysfunction is the main cause of death in pulmonary arterial hypertension (PAH). Our understanding of the pathophysiology of RV dysfunction is limited but improving. Methods to better diagnose RV dysfunction earlier and treatments specifically designed to minimize or reverse the remodeling process are likely to improve outcomes. We review the current understanding of RV dysfunction in chronic pressure overload and introduce some novel insights based on recent investigations into pathophysiology, diagnosis, and treatment.
The objective of this study was to investigate the prognostic importance of right ventricular dysfunction (RVD) and tricuspid regurgitation (TR) in patients with moderate-severe functional mitral regurgitation (FMR) receiving MitraClip procedure. RVD and TR grade are associated with cardiovascular mortality in the general population and other cardiovascular diseases. However, there are limited data from observational studies on the prognostic significance of RVD and TR in FMR receiving MitraClip procedure.
The muscle-specific protein NRAP is concentrated at cardiac intercalated disks, plays a role in myofibril assembly, and is upregulated early in mouse models of dilated cardiomyopathy. Using a tet-off system, we developed novel transgenic lines exhibiting cardiac-specific NRAP overexpression ~2.5 times greater than normal. At 40-50 weeks, NRAP overexpression resulted in dilation and decreased ejection fraction in the right ventricle, with little effect on the left ventricle. Expression of transcripts encoding brain natriuretic peptide and skeletal α-actin was increased by cardiac-specific NRAP overexpression, indicative of a cardiomyopathic response. NRAP overexpression did not alter the levels or organization of N-cadherin and connexin-43. The results show that chronic NRAP overexpression in the mouse leads to right ventricular cardiomyopathy by 10 months, but that the early NRAP upregulation previously observed in some mouse models of dilated cardiomyopathy is unlikely to account for the remodeling of intercalated disks and left ventricular dysfunction observed in those cases.
Diastolic dysfunction, a leading cause of heart failure in the US, is a complex pathology which manifests morphological and hemodynamic changes in the heart and circulatory system. Recent advances in time-resolved phase-contrast cardiac magnetic resonance imaging (4D Flow) have allowed for characterization of blood flow in the right ventricle (RV) and right atrium (RA), including calculation of vorticity and qualitative visual assessment of coherent flow patterns. We hypothesize that right ventricular diastolic dysfunction (RVDD) is associated with changes in vorticity and right heart blood flow. This paper presents background on RVDD, and 4D Flow tools and techniques used for quantitative and qualitative analysis of cardiac flows in the normal and disease states. In this study, 20 patients with RVDD and 14 controls underwent cardiac 4D Flow and echocardiography. A method for determining the time-step for peak early diastole using 4D Flow data is described. Spatially integrated early diastolic vorticity was extracted from the RV, RA, and combined RV/RA regions of each subject using a range of vorticity thresholding and scaling methods. Statistically significant differences in vorticity were found in the RA and combined RA/RV in RVDD subjects compared to controls when vorticity vectors were both thresholded and scaled by cardiac index.
The right and left ventricles have traditionally been studied as individual entities. Furthermore, modifications found in diseased left ventricles are assumed to influence on right ventricle alterations, but the connection is poorly understood. In this review, we describe the differences between ventricles under physiological and pathological conditions. Understanding the mechanisms that differentiate both ventricles would facilitate a more effective use of therapeutics and broaden our knowledge of right ventricle (RV) dysfunction. RV failure is the strongest predictor of mortality in pulmonary arterial hypertension, but at present, there are no definitive therapies directly targeting RV failure. We further explore the current state of drugs and molecules that improve RV failure in experimental therapeutics and clinical trials to treat pulmonary arterial hypertension and provide evidence of their potential benefits in heart failure.
Coronavirus disease 2019 (COVID-19) frequently involves cardiovascular manifestations such as right ventricular (RV) dysfunction and alterations in pulmonary hemodynamics. We evaluated the application of the critical care ultrasonography ORACLE protocol to identify the most frequent alterations and their influence on adverse outcomes, especially those involving the RV (dilatation and dysfunction).
Background Left ventricular (LV) involvement is common in arrhythmogenic right ventricular cardiomyopathy (ARVC). We aim to evaluate LV involvement in ARVC patients by cardiovascular magnetic resonance feature tracking. Methods and Results Sixty-eight patients with ARVC and 30 controls were prospectively enrolled. ARVC patients were divided into 2 subgroups: the preserved LV ejection fraction (LVEF) group (LVEF ≥55%, n=27) and the reduced LVEF group (LVEF <55%, n=41). Cardiovascular magnetic resonance with late gadolinium enhancement (LGE) and cardiovascular magnetic resonance feature tracking were performed in all subjects. LV global and regional (basal, mid, apical) peak strain (PS) in radial, circumferential and longitudinal directions were assessed, respectively. Right ventricular global PS in three directions were also analyzed. Compared with the controls, LV global and regional PS were all significantly impaired in the reduced LVEF group (all P<0.05). However, only LV global longitudinal PS as well as mid and apical longitudinal PS were impaired in the preserved LVEF group (all P<0.05), and all these parameters were significantly associated with right ventricular global radial PS (r=-0.47, -0.47, and -0.49, respectively, all P<0.001). The reduced LVEF group showed significantly higher prevalence of LGE (95.10% versus 63.00%, P=0.002) than the preserved LVEF group. Moreover, LV radial PS was significantly reduced in LV segments with LGE (33.15±20.42%, n=46) than those without LGE (41.25±15.98%, n=386) in the preserved LVEF group (P=0.016). Conclusions In patients with ARVC, cardiovascular magnetic resonance feature tracking could detect early LV dysfunction, which was associated with LV myocardial LGE and right ventricular dysfunction.
Background. Right ventricular (RV) dysfunction during cancer therapy related cardiotoxicity and its prognostic implications have not been examined. Aim. We sought to determine the incidence and prognostic value of RV dysfunction at time of LV defined cardiotoxicity. Methods. We retrospectively identified 30 HER2+ female patients with breast cancer treated with trastuzumab (± anthracycline) who developed cardiotoxicity and had a diagnostic quality transthoracic echocardiography. LV ejection fraction (LVEF), RV fractional area change (RV FAC), and peak systolic longitudinal strain (for both LV and RV) were measured on echocardiograms at the time of cardiotoxicity and during follow-up. Thirty age balanced precancer therapy and HER2+ breast cancer patients were used as controls. Results. In the 30 patients with cardiotoxicity (mean ± SD age 54 ± 12 years) RV FAC was significantly lower (42 ± 7 versus 47 ± 6%, P = 0.01) compared to controls. RV dysfunction defined by global longitudinal strain (GLS < -20.3%) was seen in 40% (n = 12). During follow-up in 16 out of 30 patients (23 ± 15 months), there was persistent LV dysfunction (EF < 55%) in 69% (n = 11). Concomitant RV dysfunction at the time of LV cardiotoxicity was associated with reduced recovery of LVEF during follow-up although this was not statistically significant. Conclusion. RV dysfunction at the time of LV cardiotoxicity is frequent in patients with breast cancer receiving trastuzumab therapy. Despite appropriate management, LV dysfunction persisted in the majority at follow-up. The prognostic value of RV dysfunction at the time of cardiotoxicity warrants further investigation.
Right ventricular (RV) dysfunction induced type II cardiorenal syndrome (CRS) has a high mortality rate, but little attention has been paid to this disease, and its unique molecular characteristics remain unclear. This study aims to investigate the transcriptomic expression profile in this disease and identify key RNA pairs that regulate related molecular signaling networks. We established an RV dysfunction-induced type II CRS mouse model by pulmonary artery constriction (PAC). PAC mice developed severe RV hypertrophy and fibrosis; renal atrophy and dysfunction with elevated creatinine were subsequently observed. Expression profiles in RV and kidney tissues were obtained by whole transcriptome sequencing, revealing a total of 741 and 86 differentially expressed (DE) mRNAs, 159 and 29 DEmiRNAs and 233 and 104 DEcircRNAs between RV and kidney tissue, respectively. Competing endogenous RNA (ceRNA) networks were established. A significant alteration in proliferative, fibrotic and metabolic pathways was found based on GO and KEGG analyses, and the network revealed key ceRNA pairs, such as novel_circ_002631/miR-181a-5p/Creb1 and novel_circ_002631/miR-33-y/Kpan6. These findings indicate that significantly dysregulated pathways in RV dysfunction induced type II CRS include Ras, PI3K/Akt, cGMP-PKG pathways, and thyroid metabolic pathways. These ceRNA pairs can be considered potential targets for the treatment of type II CRS.
Chronic pulmonary hypertension in infancy and childhood frequently culminates in right-ventricular (RV) failure and early death. Current management may include prolonged treatment with inhaled nitric oxide (iNO). Our objective was to examine the effects of iNO on established chronic hypoxic pulmonary hypertension in juvenile rats, a model of chronic neonatal pulmonary hypertension characterized by increased pulmonary vascular resistance, vascular remodeling (RV hypertrophy and arterial medial wall thickening), and significant RV dysfunction. Pups were exposed to air or hypoxia (13% O(2)) from postnatal day 1 to 21 while receiving iNO (20 ppm) from day 14 to 21. In hypoxia-exposed animals, treatment with iNO decreased pulmonary vascular resistance, but did not augment RV output or reverse vascular remodeling. In addition, RV output was significantly reduced in air-exposed iNO-treated pups. Nitrotyrosine (a marker of peroxynitrite-mediated reactions), apoptosis, and expression of nitric oxide synthases 1 and 2 were increased in RV (but not left-ventricular) tissue from both air- and hypoxia-exposed pups treated with iNO. Concurrent treatment with a peroxynitrite decomposition catalyst (FeTPPS, 30 mg/kg/day, ip) prevented apoptosis and completely normalized RV output in iNO-exposed animals. Our results provide the first evidence that iNO may adversely impact the right ventricle through increased local generation of peroxynitrite.
Left ventricular (LV) involvement in diabetic cardiomyopathy has been reported; however, only limited data exist on right ventricular (RV) involvement. Therefore, our purpose was to investigate RV systolic dysfunction and its association with LV longitudinal myocardial dysfunction in patients with type 2 diabetes mellitus (T2DM) and preserved LV ejection fraction (LVEF).
Lung hyperinflation and systemic inflammation are currently believed to be the most important causes of right heart alterations in chronic obstructive pulmonary disease (COPD) patients. A multicentre observational study was performed to assess the morphological and functional parameters of right ventricle (RV) in COPD subjects, as well as to evaluate the potential prognostic impact on the development of major cardiovascular adverse events (MACEs).
We retrospectively analyzed data from the Medical Information Mart for Intensive Care-III critical care database to determine whether visually-assessed right ventricular (RV) dysfunction was associated with clinical outcomes in septic shock patients. Associations between visually-assessed RV dysfunction by echocardiography and in-hospital mortality, lethal arrhythmia, and hemodynamic indicators to determine the prognostic value of RV dysfunction in patients with septic shock were analyzed. Propensity score analysis showed RV dysfunction was associated with increased risk of in-hospital death in patients with septic shock (adjusted odds ratio [OR] 2.15; 95% confidence interval [CI] 1.99-2.32; P < 0.001). In multivariate logistic regression analysis, RV dysfunction was associated with in-hospital death (OR 2.19; 95% CI 1.91-2.53; P < 0.001), lethal arrhythmia (OR 2.19; 95% CI 1.34-3.57; P < 0.001), and tendency for increased blood lactate levels (OR 1.31; 95% CI 1.14-1.50; P < 0.001) independent of left ventricular (LV) dysfunction. RV dysfunction was associated with lower cardiac output, pulmonary artery pressure index, and RV stroke work index. In patients with septic shock, visually-assessed RV dysfunction was associated with in-hospital mortality, lethal arrhythmia, and circulatory insufficiency independent of LV dysfunction. Visual assessment of RV dysfunction using echocardiography might help to identify the short-term prognosis of patients with septic shock by reflecting hemodynamic status.
The Wingless (Wnt) pathway has been implicated in the pathogenesis of dilated cardiomyopathy (DCM). To explore the role of Wnt modulators Wnt5a and sFRP3 in DCM patients we analyzed the expression of Wnt5a and sFRP3 in plasma and myocardium of DCM patients and evaluated their effects on NFAT luciferase activity in neonatal mouse cardiomyocytes. Elevated circulating Wnt5a (n = 102) was associated with increased pulmonary artery pressures, decreased right ventricular function and adverse outcome, with a stronger association in more severely affected patients. A higher Wnt5a/sFRP3 ratio (n = 25) was found in the right ventricle vs. the left ventricle and was correlated with NFAT activation as well as pulmonary artery pressures. Wnt5a induced NFAT activation and sFRP3 release in cardiomyocytes in vitro, while sFRP3 antagonized Wnt5a. Wnt5a is associated with right ventricular dysfunction and adverse outcome in DCM patients and may promote the progression of DCM through NFAT signaling.
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