Table of Contents Author Guidelines Submit a Manuscript
BioMed Research International
Volume 2018, Article ID 2868437, 3 pages

The Right Ventricle: From Bench to Bedside

1Institute of Emergency for Cardiovascular Diseases “Prof. Dr. C.C. Iliescu”, University of Medicine and Pharmacy “Carol Davila”, Bucharest, Romania
2Oslo University Hospital, Center for Cardiological Innovation, Department of Cardiology, Unit for Cardiac Genetic Diseases, Oslo, Norway
3University of Oslo, Oslo, Norway
4Clinical Research Department, Baker Heart and Diabetes Institute, Melbourne, VIC, Australia

Correspondence should be addressed to Ruxandra Jurcut; moc.liamg@tucrujr

Received 11 March 2018; Accepted 18 March 2018; Published 14 May 2018

Copyright © 2018 Ruxandra Jurcut et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

1. Introduction

The right ventricle (RV) remains the cardiac chamber for which scientific data regarding structure, function, adaptation to load, or arrhythmogenic potential is still behind what we know for the left ventricle, despite more recent efforts in this field. RV function is critical in numerous pathologies, related to pressure overload (like pulmonary hypertension but also arterial hypertension), volume overload (left-to-right shunts, tricuspid regurgitation), and myocardial diseases (which can be global, left ventricular, or right ventricular, more specific cardiomyopathies) as well as right ventricular ischemia or infarction. Moreover, the adaptation of the RV to more extreme physiologic situations (e.g., hypoxia at high altitude, high-level exercise) opens windows for understanding its physiology.

Despite data on the prognostic value of RV function, there is still debate on the best parameters that describe it and their clinical relevance. Important developments in right ventricular imaging have occurred during the last years, from myocardial deformation imaging to 3D-echocardiography and from cardiac MRI to right ventriculoarterial coupling studies, which have all contributed to a better understanding of right ventricular pathophysiology.

2. Anatomy and Physiology of the Right Ventricle

The RV is the most anterior cardiac chamber and is situated immediately behind the sternum. With a triangular shape, it has three components: inlet (sinus) portion, apical trabecular section, and outlet (conus) section. The muscular wall of the RV is normally very thin (3–5 mm), adequately serving the ejection of blood in a low impedance pulmonary circulation [1]. The RV free wall has subepicardial myofibers with transverse orientation and longitudinally arranged apex to base subendocardial myofibers [2, 3]. The middle layer of circumferential fibers seen in the left ventricle (LV) is absent in RV [4].

The shape, architecture, and structure of the RV facilitate the understanding of its physiology. Owing to the curvature of the interventricular septum (IVS) in the normal heart, the RV is described as wrapping around the LV. This particular shape, as well as the connection of the two ventricles through the IVS, constitute the interventricular dependence. In consequence, in cross section, the RV has a crescent shape which is formed because of its lower pressures, thinner walls, and greater compliance compared to the LV [5].

RV contraction has a longitudinal “peristaltic” pattern, with a 30–40 ms delay from the onset of contraction of the RV free wall from apex to the outflow tract [6], facilitating the ejection of blood to the outflow tract in the crescent shaped cavity. Under normal loading conditions, there are little short axis thickening, rotation, and twisting [7, 8].

Several studies have tried to understand the mechanisms of adaptation and maladaptation of the RV to volume and pressure overload, respectively. A few years ago, we demonstrated that at similar levels of pressure overload the RV is less dilated and performs better in patients with pulmonary stenosis as compared with those with pulmonary arterial hypertension (PAH) [9], which was in line with experimental observations. These data suggested that beyond pressure overload effects on the sarcomeric function other pathogenic factors should be taken into account. In the present issue, S. Guimaron et al. discuss the current knowledge and recent advances of RV molecular biology and metabolism from congenital heart disease to chronic PAH, with a common pathway during RV failure of metabolic glycolytic shift and altered angiogenesis.

Moreover, acute RV failure is increasingly seen in the intensive care unit and can cause or aggravate many common critical diseases. It can be due to either acute pressure or volume overload or other aggravating factors leading to a reduction of myocardial contractility owing to ischemia, cardiomyopathy, or arrhythmia [10]. J. C. Grignola and E. Domingo discuss in their paper from the present issue the mechanisms and management of acute RV dysfunction in the intensive care unit.

3. Pulmonary Hypertension and RV Changes

It has been demonstrated that, beyond etiology, a key element for establishing prognosis in patients with PAH is RV function [11]. The RV is especially challenged when it has to adapt to markedly (up to four- to fivefold) increased chronic afterload. According to the law of Laplace, myocardial hypertrophy allows normal wall stress, while initially preserving RV function. Over time, however, this adaptive mechanism is overrun, and contractile dysfunction and RV dilation occur, with subsequent increase in wall stress which stimulates further hypertrophy, leading to a vicious circle of declining RV performance, with ensuing RV failure and eventually death [7]. The evolution of RV failure in this setting is highly variable. Especially in the setting of congenital heart disease, as in Eisenmenger syndrome or pulmonary stenosis, RV performance may only decline slowly, showing that increased afterload is not the only determinant of RV failure [12, 13].

While pulmonary vasodilators appear to have impacted on the natural history of PAH, there have been few investigations assessing the impact of these drugs on RV remodeling. In the study of N. Rai et al. from the present issue, both sildenafil and riociguat prevented the deterioration of RV function, as determined by a decrease in RV dilation and restoration of the RV ejection fraction, while riociguat also prevented RV fibrosis induced by pulmonary artery banding (a model of fixed RV pressure overload). These experimental data need further investigation in the clinical setting.

4. Right Ventricular Dysfunction Secondary to Left Heart Disease

It is well known that the most frequent cause of RV failure in clinical practice is related to pulmonary hypertension due to left heart disease (e.g., systolic and diastolic LV dysfunction or left side valvular diseases) [14]. The prognostic importance of RV failure in this setting has been well demonstrated [15, 16], and data has emerged on the prognostic significance of exercise induced RV dysfunction in valvular heart disease [17]. Moreover, the association of RV dysfunction to left valvulopathies, even if not included in surgical risk scores, is often perceived as a limitation for surgery in these patients [18]. New less aggressive techniques for valvular repair, as the Mitral Clip, can surpass this barrier, and M. Hünlich et al. showed in their paper that Mitral Clip implantation improved pulmonary artery pressure, tricuspid regurgitation, and TAPSE after 12 months, while there was also a decrease in the RVOT diameter.

5. Right Ventricular Myocardial Changes in Specific Diseases

Various systemic or cardiac diseases can directly affect the RV. This has been described for genetic and nonhereditary cardiomyopathies. For example, diseases like hypertrophic cardiomyopathy, amyloidosis, Fabry’s cardiomyopathy, and dilated cardiomyopathy can have biventricular involvement which occurs most often late during the disease evolution.

Not only cardiomyopathies but also immune and inflammatory diseases with cardiac tropism can affect the RV as well. Chagas disease is a tropical disease caused by T. cruzi protozoan infection, which can be at the root of more than 10% of heart failure cases in endemic regions (like Brazil). As it is often associated with systemic congestion, studies of RV involvement were started years ago, and the review of M. M. D. Romano et al. in this issue has discussed the role of imaging in the diagnosis of RV involvement in Chagas cardiomyopathy. While no specific cardiovascular imaging tools appear to assess myocardial involvement in this infectious disease, there is a place for speckle tracking imaging and cardiac MRI to identify early functional changes during the course of disease.

Systemic sclerosis (SSc) is a disease which can involve the RV in various ways. Being the leading cause of pulmonary arterial hypertension (PAH) among connective tissue diseases, it has been reported to result in increased pressure afterload of the RV in up to 12% of cases, which can subsequently result in right ventricular failure. Moreover, a direct effect of scleroderma on the myocardium consists of increased fibrosis and inflammatory lesions, and autopsy studies identified significant cardiac fibrotic changes in 70–80% of the examined patients [19]. Moreover, Hachulla et al. found that decreased left ventricular (LV) ejection fraction could be demonstrated on cardiac MRI in almost one-quarter of SSc patients. Mid-myocardial LV delayed contrast enhancement in a noncoronary distribution was also observed suggesting fibrosis mediated by an inflammatory process [20]. The paper of R. Cucuruzac et al. in the present issue provides an in-depth discussion of the current knowledge on RV remodeling and function in scleroderma patients.

6. Future Directions

More studies investigating the normal right ventricle structure and function and especially its adaptation to physiological states (e.g., exercise, pregnancy) and disease are warranted. While its relation to prognosis in PAH was demonstrated, quantitative parameters of RV dysfunction are not yet considered a part of risk stratification for these patients, proving insufficient knowledge of the best parameter to follow.

Ruxandra Jurcut
Kristina Haugaa
Andre La Gerche


  1. S. Giusca, R. Jurcut, C. Ginghina, and J.-U. Voigt, “The right ventricle: Anatomy, physiology and functional assessment,” Acta Cardiologica, vol. 65, no. 1, pp. 67–77, 2010. View at Publisher · View at Google Scholar · View at Scopus
  2. S. Y. Ho and P. Nihoyannopoulos, “Anatomy, echocardiography, and normal right ventricular dimensions,” Heart, vol. 92, supplement 1, pp. i2–i13, 2006. View at Publisher · View at Google Scholar · View at Scopus
  3. F. Torrent-Guasp, G. D. Buckberg, C. Clemente, J. L. Cox, H. C. Coghlan, and M. Gharib, “The structure and function of the helical heart and its buttress wrapping. I. The normal macroscopic structure of the heart,” Seminars in Thoracic and Cardiovascular Surgery, vol. 13, no. 4, pp. 301–319, 2001. View at Publisher · View at Google Scholar · View at Scopus
  4. R. H. Anderson, M. Smerup, D. Sanchez-Quintana, M. Loukas, and P. P. Lunkenheimer, “The three-dimensional arrangement of the myocytes in the ventricular walls,” Clinical Anatomy, vol. 22, no. 1, pp. 64–76, 2009. View at Publisher · View at Google Scholar · View at Scopus
  5. K. M. Chin and G. Coghlan, “Characterizing the right ventricle: Advancing our knowledge,” American Journal of Cardiology, vol. 110, no. 6, 2012. View at Publisher · View at Google Scholar · View at Scopus
  6. G. D. Meier, A. A. Bove, W. P. Santamore, and P. R. Lynch, “Contractile function in canine right ventricle,” American Journal of Physiology-Heart and Circulatory Physiology, vol. 239, no. 6, pp. H794–H804, 1980. View at Publisher · View at Google Scholar
  7. N. F. Voelkel, R. A. Quaife, L. A. Leinwand et al., “Right ventricular function and failure: report of a National Heart, Lung, and Blood Institute working group on cellular and molecular mechanisms of right heart failure,” Circulation, vol. 114, no. 17, pp. 1883–1891, 2006. View at Publisher · View at Google Scholar · View at Scopus
  8. H. A. Leather, R. Ama', C. Missant, S. Rex, F. E. Rademakers, and P. F. Wouters, “Longitudinal but not circumferential deformation reflects global contractile function in the right ventricle with open pericardium,” American Journal of Physiology-Heart and Circulatory Physiology, vol. 290, no. 6, pp. H2369–H2375, 2006. View at Publisher · View at Google Scholar · View at Scopus
  9. R. Jurcut, S. Giusca, R. Ticulescu et al., “Different patterns of adaptation of the right ventricle to pressure overload: A comparison between pulmonary hypertension and pulmonary stenosis,” Journal of the American Society of Echocardiography, vol. 24, no. 10, pp. 1109–1117, 2011. View at Publisher · View at Google Scholar · View at Scopus
  10. V.-P. Harjola, A. Mebazaa, and J. Čelutkiene, “Contemporary management of acute right ventricular failure: a statement from the Heart failure association and the Working Group on pulmonary circulation and right ventricular function of the European Society of Cardiology,” European Journal of Heart Failure, vol. 18, no. 3, pp. 226–241, 2016. View at Publisher · View at Google Scholar · View at Scopus
  11. S. Giusca, R. Jurcut, I. M. Coman et al., “Right ventricular function predicts clinical response to specific vasodilator therapy in patients with pulmonary hypertension,” Journal of Echocardiography, vol. 30, no. 1, pp. 17–26, 2013. View at Publisher · View at Google Scholar · View at Scopus
  12. W. E. Hopkins, “The remarkable right ventricle of patients with Eisenmenger syndrome,” Coronary Artery Disease, vol. 16, no. 1, pp. 19–25, 2005. View at Publisher · View at Google Scholar · View at Scopus
  13. S. Giusca, E. Popa, M. S. Amzulescu et al., “Is Right Ventricular Remodeling in Pulmonary Hypertension Dependent on Etiology? An Echocardiographic Study,” Echocardiography (Mount Kisco, N.Y.), vol. 33, no. 4, pp. 546–554, 2016. View at Publisher · View at Google Scholar · View at Scopus
  14. J. Magne, P. Pibarot, P. P. Sengupta, E. Donal, R. Rosenhek, and P. Lancellotti, “Pulmonary hypertension in valvular disease: A comprehensive review on pathophysiology to therapy from the HAVEC group,” JACC: Cardiovascular Imaging, vol. 8, no. 1, pp. 83–99, 2015. View at Publisher · View at Google Scholar · View at Scopus
  15. Y. Juilliere, G. Barbier, L. Feldmann, A. Grentzinger, N. Danchin, and F. Cherrier, “Additional predictive value of both left and right ventricular ejection tractions on long-term survival in idiopathic dilated cardiomyopathy,” European Heart Journal, vol. 18, no. 2, pp. 276–280, 1997. View at Publisher · View at Google Scholar · View at Scopus
  16. F. L. Dini, U. Conti, P. Fontanive et al., “Right ventricular dysfunction is a major predictor of outcome in patients with moderate to severe mitral regurgitation and left ventricular dysfunction,” American Heart Journal, vol. 154, no. 1, pp. 172–179, 2007. View at Publisher · View at Google Scholar · View at Scopus
  17. K. Kusunose, Z. B. Popović, H. Motoki, and T. H. Marwick, “Prognostic significance of exercise-induced right ventricular dysfunction in asymptomatic degenerative mitral regurgitation,” Circulation: Cardiovascular Imaging, vol. 6, no. 2, pp. 167–176, 2013. View at Publisher · View at Google Scholar · View at Scopus
  18. R. Rosenhek, B. Iung, P. Tornos et al., “ESC working group on valvular heart disease position paper: Assessing the risk of interventions in patients with valvular heart disease,” European Heart Journal, vol. 33, no. 7, pp. 822–828, 2012. View at Publisher · View at Google Scholar · View at Scopus
  19. W. P. Follansbee, T. R. Miller, and E. I. Curtiss, “A controlled clinicopathologic study of myocardial fibrosis in systemic sclerosis (scleroderma),” The Journal of Rheumatology, vol. 17, no. 5, pp. 656–662, 1990. View at Google Scholar
  20. A.-L. Hachulla, D. Launay, V. Gaxotte et al., “Cardiac magnetic resonance imaging in systemic sclerosis: A cross-sectional observational study of 52 patients,” Annals of the Rheumatic Diseases, vol. 68, no. 12, pp. 1878–1884, 2009. View at Publisher · View at Google Scholar · View at Scopus