ABSTRACT
BACKGROUND: Heart transplantation (HTx) is increasingly utilized as therapy for end-stage cyanotic congenital heart disease. This study investigates the presence and impact of aortopulmonary collaterals (APCs) associated with cyanotic heart disease on the early post-operative course of patients undergoing transplantation. High output cardiac failure due to residual aortopulmonary collaterals can affect outcome following heart transplantation. METHODS: Seven patients with hemodynamically significant APCs post-transplant were identified among 40 patients with cyanotic congenital heart disease undergoing HTx. The peri- and intra-operative courses of these patients were reviewed. All 7 patients required prolonged inotropic support despite normal ventricular function and no allograft rejection; 5 were ventilator-dependent due to significant pulmonary vascular congestion. Selective angiography demonstrated the presence of significant aortopulmonary collaterals at 7 to 19 days post-transplant. Coil embolization of aortopulmonary collaterals was performed in all patients; a mean of 6 (2 to 16) vessels/patient were embolized. RESULTS: After embolization, pulmonary edema resolved and heart size normalized in all patients; inotropic support was weaned within 2 to 10 days in 5 patients. One patient developed transient renal failure secondary to excessive contrast load and another had enterococcal sepsis within 24 hours after the procedure. All patients were asymptomatic from 4 to 10 years of follow-up post-HTx. CONCLUSIONS: Aortopulmonary collaterals should be considered a cause of early donor heart failure in children following HTx for cyanotic congenital heart disease. Early detection and treatment of aortopulmonary collaterals by coil embolization is necessary to improve the post-transplant course in these complex patients.
Subject(s)
Collateral Circulation , Coronary Circulation/physiology , Heart Defects, Congenital/surgery , Heart Transplantation , Pulmonary Circulation/physiology , Adolescent , Adult , Child , Child, Preschool , Embolization, Therapeutic , Humans , Infant , Infant, NewbornABSTRACT
BACKGROUND: The exact role of adrenoceptors in norepinephrine (NE)-mediated regulation of the human coronary circulation has yet to be elucidated. Thus, the goals of this study were to characterize the adrenoceptors involved in the responses to NE in isolated human coronary arterioles and small arteries. METHODS AND RESULTS: Arterioles (n=39) and small arteries from the left ventricle of explanted human hearts were isolated and cannulated. Vessels from the hearts of 21 patients were studied: 15 males and 6 females, aged 0.5 to 63 years. Nineteen patients were considered to be New York Heart Association class 4. All hearts exhibited hypertrophy (190+/-20%). The passive diameter of arterioles was 167+/-8 microm (range 97 to 323 microm). NE (10(-7) to 3x10(- 7) mol/L) elicited concentration-dependent dilations (47+/-4 microm) that were unaffected by endothelium removal, N(omega)-nitro-L-arginine (10(- 4) mol/L, an NO synthase inhibitor), or practolol (10(-6) mol/L, a beta1-receptor blocker). However, administration of propranolol (10(-5) mol/L, a combined beta1- and beta2-blocker) or butoxamine (10(-6) mol/L, a beta2-receptor blocker) completely eliminated the NE-induced dilation. Constrictions to NE (2 of 39 vessels) were inhibited by prazosin (10(-6) mol/L, an alpha1-receptor blocker). Methoxamine (10(-9) to 10(-5) mol/L, an alpha1-agonist) had no effect, whereas U44619, a thromboxane mimetic, elicited dose-dependent constriction of vessels. CONCLUSIONS: Our data indicate that isolated human coronary arterioles and small arteries dilate to NE via beta2-receptors on smooth muscle. These findings are important to our understanding of the mechanisms action of NE in the human coronary circulation.