Taking the Good With the Bad – Assigning Value and Blame to the Right Heart in Cardiovascular Disease

For many years the right ventricle (RV) was considered a nominal participant in the narrative of normal cardiac physiology – its value depreciated, in particular, by several early canine experiments that intimated a marginal role for right ventricular function in systemic venous and pulmonary arterial pressure regulation.^1-3 A maturing evidence base, however, has more recently affirmed the significance of right ventricular performance. It is now well recognized that the right heart is vitally important following cardiac surgery,⁴ during periods of myocardial ischemia, after mechanical circulatory support,⁵ and among growing populations of patients with congenital and pulmonary vascular disease.

While no longer overshadowed by its left-sided counterpart, it is still important to point out that the right heart is unique in many ways. Its distinctive embryologic, anatomic, and physiologic traits make it at the same time both resilient and quite fragile. The right ventricle is indeed a fickle chamber, the study and management of which has been confounded for decades by diagnostic uncertainty, therapeutic controversy, and even inconsistent nomenclature

Though the contemporary management of right heart failure has been the subject of prior consensus documents,⁶ the American Heart Association (AHA) Scientific Statement submitted by Konstam and colleagues is additive and complementary, impressively comprehensive, yet practical in its delivery.⁷ The writing committee consists of multiple stakeholders with a vested interest in understanding and managing this complex syndrome, and their manuscript should serve as a valuable reference for students, seasoned physicians, and investigators, alike.

Right ventricular dysfunction is a known harbinger of poor clinical outcomes. Though usually requiring considerably less energy expenditure than the left ventricle (LV) for normal output, and tolerant to even large shifts in blood volume, pressure (or more specifically, afterload) is its Achilles heel. The implications of RV congestion are numerous, as it can lead to impaired coronary blood flow, myocardial ischemia, and hypo-perfusion to many of the body’s other vital organs. The presence of RV dysfunction is also associated with increased morbidity, mortality, and diminished functional capacity in patients with left heart failure, regardless of whether or not LV contractile function is preserved.^8,9

The authors dedicate ample attention towards discussing the unique pathophysiology underscoring right heart failure following cardiac surgery, a particularly prudent topic given the increasingly acknowledged impact of RV dysfunction after mechanical circulatory support.5 Similarly, the authors carefully describe the importance of the right heart among aging adults with congenital heart abnormalities – an exponentially growing collection of patients.¹⁰

Perhaps the greatest triumph of this paper, however, is in the abundance of pragmatic guidance it delivers focusing particularly on diagnostic and therapeutic priorities for the treating clinician. Supported by an admittedly limited evidence, the authors nonetheless go to great lengths to provide practical recommendations for the use of imaging, invasive hemodynamic, and ancillary studies, along with pharmacologic and mechanical technologies, for managing both acute and chronic right heart failure syndromes. The included illustrations and algorithms successfully complement these discussions.

Though our understanding of the RV has grown considerably, there is still very much to learn. As the authors point out, the pathophysiology of right heart failure remains immensely misunderstood.⁷ The impact of this knowledge deficit threatens our ability to care for a growing group of patients with, and at risk for, its major complications and associated conditions. Education and investigation will, no doubt, be vital components of our future efforts to tackle this complex syndrome.