Previous studies suggesting that norepinephrine is directly trophic for the vascular wall have been confounded by concomitant hemodynamic disturbances. Herein, a microcatheter connected to an osmotic minipump was implanted adjacent to the rat carotid for 2-wk perivascular suffusion of agents at systemic levels ϳ1,000 times below the threshold for altering arterial pressure. Norepinephrine decreased lumen and adventitial areas and circumference by 10, 14, and 5%, respectively (all P Ͻ 0.05); a nonsubtype-specific ␣ 1-adrenoceptor (AR) antagonist had no effect. When begun at the time of balloon injury, 2-wk norepinephrine increased lumen loss by 45%, increased neointimal area by 64% and collagen content by 33%, and reduced vessel circumference by 5% (all P Ͻ 0.05). ␣ 1-AR antagonists decreased neointimal area by 33% (all P Ͻ 0.05). ␣ 1A-AR antagonist reduced lumen loss by 70%, neointimal area by 54%, circumference decline by 84%, and adventitial thickening by 87% (all P Ͻ 0.05), whereas ␣ 1B-, ␣1D-, ␣2-and ␤-AR antagonists were without effect. These are the first in vivo studies demonstrating that norepinephrine is directly trophic for the vascular wall and augments injury-induced intimal lesion growth. artery; smooth muscle; adventitia; injury; adrenergic VASCULAR HYPERTROPHY and remodeling are adaptive structural changes in response to sustained increases in arterial pressure or altered shear stress that favor restoration of normal physiological regulation. On the other hand, excessive wall growth, fibrosis, and inward or inadequate outward remodeling cause failure of surgical procedures (e.g., restenosis after angioplasty/ stent, atherectomy, and bypass grafting) and underlie diseases such as atherosclerosis, pulmonary hypertension, and accelerated arteriosclerosis (31,35). Thus the mechanisms regulating growth of vascular wall cells are under intense investigation. Besides the vasoactive actions of norepinephrine (NE), there is growing evidence that NE may be a trophic mediator for vascular smooth muscle cells (SMCs) and adventitial fibroblasts (AFBs). In vivo studies using surgical or systemic sympathetic denervation (16), systemic infusion of catecholamines (7, 21), or ␣-adrenoceptor (AR) antagonists (20), as well as positive correlation of plasma catecholamines with wall hypertrophy and stiffness (8) and severity of atherosclerosis (22) in humans, suggest that NE may have direct trophic effects on the normal and diseased vascular wall. Moreover, in the ballooninjured rat and rabbit carotid, chronic systemic ␣ 1 -AR antagonists reduced cell proliferation, neointimal growth, and restenosis by at least 50% (14,18,30,34). ␣ 1 -AR antagonists also attenuated angiotensin II-induced DNA synthesis (33) and atherogenesis (26,29). However, interpretation of these past in vivo studies is complicated by concomitant hemodynamic disturbances that, themselves, have trophic effects. For example, chemical or immunological systemic denervation and systemic ␣-AR antagonists cause significant hypotension and humoral changes. A...

To our knowledge, this is the first systematic evaluation of the cardiac effects of aripiprazole in children and adolescents. The results are consistent with previously published literature in adults that aripiprazole has no significant cardiac effects and can be deemed a low risk for causing sudden death. It will be important to confirm these findings in a randomized controlled trial.

In conclusion, transthoracic echocardiography underestimated right ventricular ejection fraction compared to cardiac magnetic resonance imaging. Cardiac magnetic resonance imaging had consistently higher image quality and better visualization of the baffles. Cost differences are minimal. We propose that cardiac magnetic resonance imaging be considered first line for imaging in certain patients' status post atrial switch procedure.

Patients may develop hemodynamic abnormalities after right ventricular outflow tract (RVOT) repair. Re-intervention timing remains a dilemma. This study evaluates exercise capacity and RV function before and after intervention using age-related comparisons. Twenty-six patients with severe pulmonary regurgitation (PR) after initial repair scheduled for pulmonary valve replacement (PVR) were enrolled. Metabolic treadmill testing (EST) and MRI were obtained before and after surgery. EST results were compared with matched controls. Preoperative exercise time and peak oxygen consumption (VO2 max) were significantly diminished compared with controls but were not significantly different postoperatively. The patients were then split into age-related cohorts. When comparing pre-PVR and post-PVR exercise time and VO2 max among themselves, neither cohort showed significant differences. However, patients younger than 25 years had better postoperative results, an age-related difference not seen in the controls. Preoperative MRI showed significantly dilated RV, PR, and low normal function. After PVR, the right to left ventricular end-diastolic volume ratio (RVEDV:LVEDV) and pulmonary artery regurgitant fraction (RF) significantly decreased. There was no change in ventricular ejection fractions (EF). Severe PR, decreased RVEF, and RV dilation can significantly diminish exercise capacity. PVR improves RVEDV:LVEDV and RF, but not EF. Younger patients had better exercise capacity that was maintained postoperatively. This age-related difference was not seen in the controls, indicating that earlier intervention may preserve exercise capacity. Serial ESTs in patients with severe PR following RVOT repair may identify deteriorating exercise capacity as an early indicator for the need for PVR.