Category: RespirAct

Assessment of Myocardial Reactivity to Controlled Hypercapnia with Free-breathing T2-prepared Cardiac Blood Oxygen Level–Dependent MR Imaging

Hsin-Jung Yang, Roya Yumul, Richard Tang, Ivan Cokic, Michael Klein, Avinash Kali, Olivia Sobczyk, Behzad Sharif, Jun Tang, Xiaoming Bi, Sotirios A. Tsaftaris, Debiao Li, Antonio Hernandez Conte, Joseph A. Fisher, Rohan Dharmakumar.
 
Cardiac stress testing is the standard of care for diagnosing ischemic heart disease (1). It is performed in nearly 10 million patients each year in the United States alone. It is conventionally initiated with exercise to induce hyperemia, and it is coupled with imaging to identify stress-induced failure to increase perfusion, or frank hypoperfusion in myocardial territories.

Measuring Cerebrovascular Reactivity: the Dynamic Response to a Step Hypercapnic Stimulus

Julien Poublanc, Adrian P Crawley, Olivia Sobczyk, Gaspard Montandon, Kevin Sam, Daniel M Mandell, Paul Dufort, Lashmikumar Venkatraghavan, James Duffin, David J Mikulis, Joseph A Fisher. J Cereb Blood Flow Metab. 2015 Nov;35(11):1746-56. doi: 10.1038/jcbfm.2015.114. Epub 2015 Jul 1.
 
We define cerebral vascular reactivity (CVR) as the ratio of the change in blood oxygen level-dependent (BOLD) magnetic resonance imaging (MRI) signal (S) to an increase in blood partial pressure of CO2 (PCO2): % Δ S/Δ PCO2 mm Hg. Our aim was to further characterize CVR into dynamic and static components and then study 46 healthy subjects collated into a reference atlas and 20 patients with unilateral carotid artery stenosis. We applied an abrupt boxcar change in PCO2 and monitored S.

A Conceptual Model for CO2-induced Redistribution of Cerebral Blood Flow with Experimental Confirmation using BOLD MRI

O Sobczyk, A Battisti-Charbonney, J Fierstra, D M Mandell, J Poublanc, A P Crawley, D J Mikulis, J Duffin, J A Fisher. Neuroimage. 2014 May 15;92:56-68. doi: 10.1016/j.neuroimage.2014.01.051. Epub 2014 Feb 5.
 
Cerebrovascular reactivity (CVR) is the change in cerebral blood flow (CBF) in response to a change in a vasoactive stimulus. Paradoxical reductions in CBF in response to vasodilatory stimulation (‘steal’) are associated with vascular pathology. However, a pathophysiological interpretation of ‘steal’ requires a comprehensive conceptual model linking pathology and changes in blood flow. Herein, we extend a simple model explaining steal published in the late 1960s by incorporating concepts of CBF regulation from more recent studies to generate a comprehensive dynamic model.