Acquired heart block: A possible complication of patent ductus arteriosus in a preterm infant

A large patent ductus arteriosus (PDA) is a frequently encountered clinical problem in extremely low birth weight (ELBW) infants. It leads to an increased pulmonary blood flow and in a decreased or reversed diastolic flow in the systemic circulation, resulting in complications. Here we report a possible complication of PDA not previously published. On day 8 of life, a male ELBW infant (birth weight 650 g) born at a gestational age of 23 weeks and 3 days developed an atrioventricular block (AV block). The heart rate dropped from 168/min to 90/min, and the ECG showed a Wenckebach second-degree AV block and intraventricular conduction disturbances. Echocardiography demonstrated a PDA with a large left-to-right shunt and large left atrium and left ventricle with high contractility. Within several minutes after surgical closure of the PDA, the heart rate increased, and after 30 min the AV block had improved to a 1: 1 conduction ratio. Echocardiography after 2 h revealed a significant decrease of the left ventricular and atrial dimensions. Within 12 h, the AV block completely reversed together with the intraventricular conduction disturbances. We suggest that PDA with a large left-to-right shunt and left ventricular volume overload may lead to an AV block in an ELBW infant. Surgical closure of the PDA may be indicated. Copyright (C) 2007 S. Karger AG, Basel

Surgical management of coronary insufficiency in a child with Kawasaki\u27s disease: use of bilateral internal mammary arteries.

Coronary insufficiency is an important sequela of Kawasaki\u27s disease. Successful myocardial revascularization with saphenous vein grafts and, more recently, with internal mammary artery grafts has been performed. We report a case of Kawasaki\u27s disease with chronic coronary insufficiency in which complete myocardial revascularization was accomplished using bilateral internal mammary arteries, and we present a review of the literature

Developmental differences in cardiac myocyte calcium homeostasis after steady-state potassium depolarization: mechanisms and implications for cardioplegia.

We previously reported developmental differences in the response of cytosolic free calcium ([Cai]) to extracellular potassium ([Kex]) depolarization (cardioplegia) in juvenile (4 weeks post partum) and mature (12 to 18 months post partum) cardiac myocytes (rabbit). Our present study explored the physiologic basis for these observations. Single calcium-tolerant cardiac myocytes were isolated by sequential exposure to proteolytic agents, loaded with a fluorescent probe for calcium (fura-2) and [Cai] measured by standard fluorescence techniques. The response of [Cai] to [Kex] depolarization (30 mmol/L) was determined in the presence of varying levels of extracellular calcium [Caex], verapamil, ouabain, and amiloride. At nominal levels of [Caex] (0 mmol/L), no significant increases in [Cai] from the juvenile (2.1% +/- 3.3%) or mature (8.5% +/- 3.1%) myocytes were seen. At increasing [Caex], there was a progressive increase in the response of [Cai] to [Kex] depolarization in mature animals\u27 cells (191.8% +/- 40.7%) but not in the juveniles\u27 cells (28.0% +/- 11.5%). Exposure to verapamil resulted in an approximate 80% reduction in relative increase in [Cai] in the mature compared with 60% in the juvenile myocytes. Finally, ouabain exposure resulted in a significant increase in the relative change of [Cai] in juvenile cells (30% to 126.4% +/- 39.4%) but not in the adults\u27 cells. This increase in the juvenile myocytes was blocked by amiloride. We conclude that increases in cardiac myocyte [Cai] after [Kex] depolarization occur predominantly through the calcium channel in the mature animal and through sodium-calcium exchange in the juvenile

Developmental differences in the response of cytosolic free calcium to potassium depolarization and cardioplegia in cardiac myocytes.

Several biochemical and functional characteristics of immature myocardium suggest a diminished capacity to regulate intracellular Ca2+ during stress. In particular, cellular calcium overload has been postulated as an important pathogenetic mechanism accounting for suboptimal functional recovery following cardioplegia in immature myocardium. Using intracellular Fura-2 fluorescence as Ca2+ indicator, we measured cytosolic free calcium ([Cai]) in single myocytes and cell suspensions derived from both juvenile (4 weeks post-partum) and mature (6-12 months post-partum) New Zealand white rabbits. Resting [Cai] in juvenile heart cells (26 +/- 3 nM) were approximately 50% of that found in adult myocytes (55 +/- 5 nM). In addition, on exposure to increasing concentrations of extracellular potassium ([Kex]), adult but not juvenile myocytes exhibited increases in [Cai]. These two observations underscore developmental differences in intracellular Ca2+ homeostasis. Of particular clinical relevance is the [Cai] response to cardioplegia containing 16 mM [Kex]: neither group demonstrated the expected [Cai] increase in response to potassium depolarization. The lack of [Cai] response to cardioplegia was most likely due to the high levels of Mg2+ (32 mM) contained in cardioplegic solutions. We conclude that cellular calcium overload does not occur following exposure to cardioplegia alone. Accordingly, these findings do not account for recognized developmental differences in functional recovery from myocardial protection

Transcatheter vascular occlusion of the small patent ductus arteriosus: an alternative method.

The current strategies concerning a small