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Percutaneous repair or replacement techniques for the aortic and mitral valves have widespread acceptance as effective alternatives for patients who are not surgical candidates. Similar techniques for the tricuspid valve are now on the rise. Tricuspid valve disease is prevalent in a diverse population of patients ranging from 8 to almost 80 years of age. Currently there is a substantial division between the treated and diseased population, with the latter increasing in number. Experience and studies have shown that surgery for moderate or severe tricuspid regurgitation (TR) has a significant negative impact on morbidity and mortality. Progressive TR in itself has been shown to be a risk factor for decreased survival. Percutaneous techniques for management of TR offer these patients an attractive and efficient option. Novel devices have been constructed with the intent to restore the anatomy and physiology of the tricuspid valve complex. TR is most commonly due to secondary causes like left heart failure. Results so far are promising for most devices, and some human trials are underway. In coming years, feasibility and safety data along with experience with these devices will grow. It is possible that percutaneous tricuspid repair may become an alternative for some patients with TR.

In this chapter we describe the role of the right ventricle in structural and functional left ventricular failure in children. The ventriculo-ventricular interaction of the sub-pulmonary and sub-aortic ventricle is discussed in the context of (1) the right ventricle in left heart failure with decreased ejection fraction, (2) the right ventricle in restrictive cardiomyopathy or a borderline left ventricle and heart failure with preserved ejection fraction.

The right ventricle (RV) because of its low pressure working conditions and its complex geometry stands in stark contrast to the left ventricle (LV). Thus, under normal baseline conditions the RV’s unique anatomy, myocardial ultrastructure, and coronary physiology reflect a high volume low pressure pump. Early work by Starr et al. (Am Heart J 26:291–301, 1943), Bakos (Circulation 1:724–731, 1950), Kagan (Circulation 5:816–823, 1952), Donald and Essex (Am J Physiol 176:155–161, 1954) described the RV as a passive conduit with minimal pumping capability. Despite the marked differences in loading conditions and geometry in the normal state, RV myocardial and chamber dynamics respond in a manner similar to the LV pump mechanics. Over the years with improved functional imaging capabilities, it is now well appreciated that through its own unique properties and a mechanism of ventricular interdependence, RV systolic function and diastolic load are extremely important in the prognosis and treatment of congestive heart failure.

“Heart failure may be defined as the pathophysiologic state in which an abnormality of cardiac function is responsible for failure of the heart to pump blood at a rate commensurate with the requirements of the metabolizing tissues. Heart failure occurs as the consequence of many forms of heart disease afflicting at least 4 million Americans of all ages.”1 Heart failure also occurs with the failure of compensatory mechanisms such as myocardial hypertrophy, which may accompany dilatation of the ventricular chambers. Heart failure can be divided into left and right heart failure, although if the heart failure becomes chronic then left heart failure can result in right heart failure, so that both can occur concomitantly. Heart failure may be due to failure of myocardial contraction or it may be due to an excessive hemodynamic burden. The heart will compensate for this physiologically, but also pathologically with myocyte hypertrophy with or without ventricular dilatation. The rate of onset of heart failure also will in fluence the clinical and pathological manifestations.