Keith DesRochers

Accuracy of Doppler methods for estimating peak-to-peak and peak instantaneous gradients across coarctation of the aorta: An In vitro study.

Although data exist that address the attempt to correlate noninvasive Doppler-derived pressure gradients with invasive catheter pressure gradients in patients with coarctation of the aorta, few data exist about stiffness of the proximal descending aorta (precoarctation) and its relation to these pressure measurements. In this study, an in vitro flow model of a simulated neonatal aorta with a coarctation was developed. Three proximal descending aortas of different stiffnesses were used. The stiffness index of the proximal descending aorta was calculated as beta = ln [systolic pressure/diastolic pressure/(systolic diameter - diastolic diameter)]. We evaluated pressure gradients obtained by continuous wave Doppler and standard catheter methods and looked at acceleration of flow velocity determined by pulsed wave Doppler in the 3 precoarctation segments of differing stiffnesses. Pressures in the proximal descending aorta (precoarctation) increased with increasing stiffness, ranging from 105 mm Hg (soft) to greater than 300 mm Hg (stiff). Continuous wave Doppler instantaneous pressure gradients overestimated the catheter instantaneous pressure gradients substantially (mean 41% +/- 19%). The stiffer the precoarctation segment, the more the degree of overestimation: soft, 0% to 63% (= 3.47); medium, 13% to 54% (beta = 4.42); and stiff, 43% to 66% (beta = 5.91). Inclusion of the precoarctation velocity [V1] component in the Bernoulli equation did not significantly improve the correlation or the agreement. An additional observation was that pullback catheter peak-to-peak gradients were higher than simultaneous peak-to-peak gradients. In the stiff aorta, this difference could be greater than 22 mm Hg (>19%). Acceleration of flow velocity toward the coarctation was evident by pulsed wave Doppler interrogation. Increasing the stiffness of the precoarctation segment also increased the degree of acceleration within this proximal segment: soft, 0.4 to 0.8 m/s; medium, 0.5 to 1. 4 m/s; and stiff, 0.7 to 1.5 m/s. These data suggest that increasing stiffness of the proximal descending aorta can alter the continuous wave detected Doppler gradient and although the gradient itself has increased, it may not predict accurately the true severity of the localized, most severely obstructed segment.

The dorsomedial hypothalamus mediates stress-induced hyperalgesia and is the source of the pronociceptive peptide cholecystokinin in the rostral ventromedial medulla

While intense or highly arousing stressors have long been known to suppress pain, relatively mild or chronic stress can enhance pain. The mechanisms underlying stress-induced hyperalgesia (SIH) are only now being defined. The physiological and neuroendocrine effects of mild stress are mediated by the dorsomedial hypothalamus (DMH), which has documented connections with the rostral ventromedial medulla (RVM), a brainstem region capable of facilitating nociception. We hypothesized that stress engages both the DMH and the RVM to produce hyperalgesia. Direct pharmacological activation of the DMH increased sensitivity to mechanical stimulation in awake animals, confirming that the DMH can mediate behavioral hyperalgesia. A behavioral model of mild stress also produced mechanical hyperalgesia, which was blocked by inactivation of either the DMH or the RVM. The neuropeptide cholecystokinin (CCK) acts in the RVM to enhance nociception and is abundant in the DMH. Using a retrograde tracer and immunohistochemical labeling, we determined that CCK-expressing neurons in the DMH are the only significant supraspinal source of CCK in the RVM. However, not all neurons projecting from the DMH to the RVM contained CCK, and microinjection of the CCK2 receptor antagonist YM022 in the RVM did not interfere with SIH, suggesting that transmitters in addition to CCK play a significant role in this connection during acute stress. While the RVM has a well-established role in facilitation of nociception, the DMH, with its well-documented role in stress, may also be engaged in a number of chronic or abnormal pain states. Taken as a whole, these findings establish an anatomical and functional connection between the DMH and RVM by which stress can facilitate pain.

Echocardiography in Pediatric and Adult Congenital Heart Disease

Benjamin W. Eidem, MD, FACC, FASE; Frank Cetta, MD, FACC, FASE; and Patrick W. O’Leary, MD, FACC, FASE, eds. 500 pages. Philadelphia, USA: Lippincott Williams and Wilkins, 2010.

A NEW 3D STRAIN METHOD FOR PROCESSING OF 4D ECHO IMAGES CAN DELINEATE REGIONAL MYOCARDIAL DYSFUNCTION: VALIDATION AGAINST SONOMICROMETRY

229.00 ISBN 0-7817-8136-1 It has been nearly 8 years since a textbook on echocardiography specifically for pediatric congenital heart disease (CHD) has been published. A specific work on both pediatric and adult CHD emphasizing imaging is a new endeavor. Three expert senior clinicians from the Mayo Clinic are the editors and primary authors of this multiauthor textbook, which includes young investigators, midcareer investigators, and senior experts in pediatric and congenital heart echocardiography and imaging from around the United States and Canada. In their Introduction, the editors, citing the evolution of echocardiography, remind us of the major contributions of Drs James Seward and Jamil Tajik and Drs William Edwards and Donald Hagler to the field of 2-dimensional echocardiography and CHD in 1987, after the original investigations of M-mode echocardiography and 2-dimensional echocardiography by this reviewer (D.J.S.). Richard Meyer and Nils Lundstrom, the editors of this new text, also, in their Introduction, give special attention to Dr. Edwards, the renowned cardiac pathologist and a major resource. This textbook is well organized. The first chapter relates to principles of cardiovascular ultrasound, followed by practical issues, anatomic orientation, and segmental cardiovascular analysis; quantitative methods for echocardiography, basic and advanced; and then lesion-oriented chapters, including pulmonary venous abnormalities and abnormalities of the atrial septum, atrial ventricular septal defects, Ebstein malformation, mitral valve abnormalities, congenitally corrected transposition, ventricular septal defects, univentricular connections, …