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Large ventricular septal defect and coexisting chronic constrictive pericarditis: “reversible Eisenmenger syndrome”—5 years after corrective surgery

We previously reported a child with large ventricular septal defect (VSD) and pulmonary hypertension with chronic constrictive pericarditis (CCP) masquerading as Eisenmenger syndrome [1]. Despite elevated pulmonary vascular resistance (PVR) and resting cyanosis, pericardiectomy followed by VSD closure resulted in substantial reduction in pulmonary artery (PA) pressure. We hereby present long-term follow-up data of this unusual association. At 5 years follow-up, this 13-yearold boy is in NYHA functional class I with good effort tolerance. Echocardiogram showed tiny muscular VSD shunting left-to-right with a gradient of 70 mm Hg. Hemodynamic data confirmed mild pulmonary artery hypertension (PAH) and ratio of pulmonary to systemic blood flow (Qp/Qs) 1.2 (Table I) validating our claims of “reversible Eisenmenger syndrome.” Late risk of progressive pulmonary vascular disease in patients with large VSD and elevated PVR warrants careful followup [2, 3]. With no similar prior reports, it is important to document this follow-up data in such a case. Cyanosis in a patient with large VSD, in the absence of pulmonary stenosis and lung parenchymal disease, almost always indicate Eisenmenger syndrome. It is vitally important to identify any factor/s that could be reversible. CCP and resultant elevated pulmonary wedge pressure were reversible factors in our patient. Similarly, post capillary PAH from mitral valve disease could have protective hemodynamic effect and a favorable clinical course in patients with VSD and severe PAH [4, 5]. It is imperative to recognize these factors causing “reversible Eisenmenger syndrome” to avoid missing an operable lesion.