Adaptive capacity of the right ventricle: why does it fail?

Poels, Ella; Martins, Paula; Empel, Vanessa van

doi:10.1152/ajpheart.00573.2014

Cited by 21 publications

(20 citation statements)

References 142 publications

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“…The failing RV undergoes a variety of changes that differ from those of the adapted RV (Figure 4). 1,5,7,8,25,70 Some of these changes may have already begun in the adaptive phase and some may be the “byproducts” of maladaptation, with little relation to RVF. The following sections focus on several studied mechanisms that underlie transition to RVF when the adaptive processes fail.…”

Section: Right Ventricular Failurementioning

confidence: 99%

Right heart in pulmonary hypertension: from adaptation to failure

Ren¹,

Johns

Gao

2019

Pulm. circ.

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Right ventricular (RV) failure (RVF) has garnered significant attention in recent years because of its negative impact on clinical outcomes in patients with pulmonary hypertension (PH). PH triggers a series of events, including activation of several signaling pathways that regulate cell growth, metabolism, extracellular matrix remodeling, and energy production. These processes render the RV adaptive to PH. However, RVF develops when PH persists, accompanied by RV ischemia, alterations in substrate and mitochondrial energy metabolism, increased free oxygen radicals, increased cell loss, downregulation of adrenergic receptors, increased inflammation and fibrosis, and pathologic microRNAs. Diastolic dysfunction is also an integral part of RVF. Emerging non-invasive technologies such as molecular or metallic imaging, cardiac MRI, and ultrafast Doppler coronary flow mapping will be valuable tools to monitor RVF, especially the transition to RVF. Most PH therapies cannot treat RVF once it has occurred. A variety of therapies are available to treat acute and chronic RVF, but they are mainly supportive, and no effective therapy directly targets the failing RV. Therapies that target cell growth, cellular metabolism, oxidative stress, and myocyte regeneration are being tested preclinically. Future research should include establishing novel RVF models based on existing models, increasing use of human samples, creating human stem cell-based in vitro models, and characterizing alterations in cardiac excitation–contraction coupling during transition from adaptive RV to RVF. More successful strategies to manage RVF will likely be developed as we learn more about the transition from adaptive remodeling to maladaptive RVF in the future.

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Section: Right Ventricular Failurementioning

confidence: 99%

Right heart in pulmonary hypertension: from adaptation to failure

Ren¹,

Johns

Gao

2019

Pulm. circ.

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“…65 In contrast, chronic RV volume overload is characterized by limited contractile reserve. 63,65 The successful implementation of an adaptive response depends on switching to the "fetal RV phenotype", 64 where chronic hypoxia promotes (1) metabolism switch to predominant aerobic glycolysis and glutaminolysis, (2) capillary dysplasia and upregulated angiogenesis, (3) autonomic dysregulation, and (4) altered alpha, beta, and dopaminergic receptors sensitivity. The ultimate result is RV hypertrophy with chronic ischemia.…”

Section: Other Factors Affecting Rv Function In MV Disease: Beyond Pumentioning

confidence: 99%

“…65 There is also some evidence suggesting there are likely separate molecular signaling pathways mediating RV pressure overload and RV volume overload. [62][63][64] Therefore, it is possible that the adaptive RV phenotype characteristic of MS and MR are fundamentally different. 63 In general, there are alterations a different levels, including (1) altered myosin and actin gene expression, (2) alteration in extracellular matrix protein expression in cellular mechanoreceptor systems, (3) neurohormonal activation of renin-angiotensinaldosterone system, and (4) inflammatory response with elevated pro-inflammatory cytokines and cellular proliferation (ie, neutrophils and monocytes/macrophages infiltration).…”

Section: Other Factors Affecting Rv Function In MV Disease: Beyond Pumentioning

confidence: 99%

Right Ventricular Function in Left Heart Disease

Rio

Grecu

Nicoara

2018

Semin Cardiothorac Vasc Anesth

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Right ventricular (RV) function is an independent prognostic factor for short- and long-term outcomes in cardiac surgical patients. Patients with mitral valve (MV) disease are at increased risk of RV dysfunction before and after MV operations. Yet RV function is not part of criteria for decision making or risk stratification in this setting. The role of MV disease in the development of pulmonary hypertension (PHTN) and the ultimate impact of PHTN on RV function have been well described. Nonetheless, there are other mechanisms by which MV disease and MV surgery affect RV performance. Research suggests that PHTN may not be the most important determinant of RV dysfunction. Both RV dysfunction and PHTN have independent prognostic significance. This review explores the unique anatomic and functional features of the RV and the pathophysiologic and prognostic implications of RV dysfunction in patients with MV disease in the perioperative period.

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“…In contrast, the decrease in RV function occurs much more slowly in patients with ASD-associated PH. 14,15 This study has several limitations, i.e. the subjects sample size is small and the parameter of RV systolic dysfunction is only one parameter i.e.…”

Section: Discussionmentioning

confidence: 99%

Association between serum soluble ST2 level and right ventricle systolic function on pulmonary hypertension due to atrial septal defect

et al. 2020

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Pulmonary hypertension (PH) due to atrial septal defect (ASD) may cause a decline in right ventricle (RV) function. Soluble ST2 isa prognostic biomarker for left ventricle dysfunction. However, its role in RV function has not been investigated. This study aimed to investigate the association between serum soluble ST2 with RV systolic function in patients with ASD-associated PH. This was a cross sectional study. Subjects were patients participated in the COHARD-PH registry performed in Dr. Sardjito General Hospital, Yogyakarta Indonesia. The patients with ASD and PH confirmed by right heart catheterization (RHC) were enrolled in this study. The soluble ST2 level was measured in the serum collected from pulmonary artery during RHC. Right ventricle systolic function was determined by transthoracic echocardiography using peak systolic velocity of tricuspid annulus (S') parameter. This study was performed in 32 adults with uncorrected ASD. They predominantly females [n=29 (90.6%)] with median age of 31(22.5-44.0) years old. Mean ASD diameter was 2.69±0.53 cm. Median mean pulmonary artery pressure (mPAP) 45.0 (36.25-70.0) mmHg. Median soluble ST2 level was 23.28 ng/mL. There were no significant correlations between soluble ST2 level with S'value (r=0.071; p=0.35), with mPAP (r=0.043; p=0.815), with pulmonary vasculer resistance (PVR) (r=0.025; p=0.893) and with right ventricle (RV) diameter (r=0.200; p=0.273). Soluble ST2 level was found higher in subject with RV dysfunction but not statistically significant. In conclusion, serum soluble ST2 level did not associate with RV systolic function, measured by S', in adult ASD-associated PH.

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Adaptive capacity of the right ventricle: why does it fail?

Cited by 21 publications

References 142 publications

Right heart in pulmonary hypertension: from adaptation to failure

Right heart in pulmonary hypertension: from adaptation to failure

Right Ventricular Function in Left Heart Disease

Association between serum soluble ST2 level and right ventricle systolic function on pulmonary hypertension due to atrial septal defect

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