Impact of Intermittent Apnea on Myocardial Tissue Oxygenation—A Study Using Oxygenation-Sensitive Cardiovascular Magnetic Resonance

Abstract

BackgroundCarbon dioxide (CO2) is a recognized vasodilator of myocardial blood vessels that leads to changes in myocardial oxygenation through the recruitment of the coronary flow reserve. Yet, it is unknown whether changes of carbon dioxide induced by breathing maneuvers can be used to modify coronary blood flow and thus myocardial oxygenation. Oxygenation-sensitive cardiovascular magnetic resonance (CMR) using the blood oxygen level-dependent (BOLD) effect allows for non-invasive monitoring of changes of myocardial tissue oxygenation. We hypothesized that mild hypercapnia induced by long breath-holds leads to changes in myocardial oxygenation that can be detected by oxygenation-sensitive CMR.Methods and ResultsIn nine anaesthetized and ventilated pigs, 60s breath-holds were induced. Left ventricular myocardial and blood pool oxygenation changes, as monitored by oxygenation-sensitive CMR using a T2*-weighted steady-state-free-precession (SSFP) sequence at 1.5T, were compared to changes of blood gas levels obtained immediately prior to and after the breath-hold. Long breath-holds resulted in an increase of paCO2, accompanied by a decrease of paO2 and pH. There was a significant decrease of blood pressure, while heart rate did not change. A decrease in the left ventricular blood pool oxygenation was observed, which was similar to drop in SaO2. Oxygenation in the myocardial tissue however, was maintained throughout the period. Changes in myocardial oxygenation were strongly correlated with the change in paCO2 during the breath-hold (r = 0.90, p = 0.010).ConclusionDespite a drop in blood oxygen levels, myocardial oxygenation is maintained throughout long breath-holds and is linearly correlated with the parallel increase of arterial CO2, a known coronary vasodilator. Breathing maneuvers in combination with oxygenation-sensitive CMR may be useful as a diagnostic test for coronary artery function.

Hyperoxia Exacerbates Myocardial Ischemia in the Presence of Acute Coronary Artery Stenosis in Swine

“…Several recent studies have used OS-CMR to monitor changes of myocardial oxygenation after changing blood gas levels, especially O 2 and CO 2 . 3,10,11,30 Those studies showed that OS-CMR is a reliable tool to assess the impact of hyperoxia on myocardial oxygenation. 31 Coronary artery stenosis in our animals was verified by an FFR of <0.75.…”

“…1 Importantly, oxygen and carbon dioxide both have vasoactive properties. Although increased CO 2 levels have vasodilative properties in cerebral and coronary arteries, 2,3 high oxygen tension may have vasoconstricting effects on coronary arteries. 4 If such vasoconstriction would result in a net reduction of blood flow in the territory of a severely stenotic coronary artery, tissue oxygenation may drop.…”

Myocardial T2* Mapping with Ultrahigh Field Magnetic Resonance: Physics and Frontier Applications

“…By exploiting the blood oxygenation level-dependent (BOLD) effect [3], T 2 * sensitized CMR has been proposed as a means of assessing myocardial tissue oxygenation and perfusion. T 2 * mapping has been shown to be capable of detecting myocardial ischemia caused by coronary artery stenosis [4], to reveal myocardial perfusion deficits under pharmacological stress [5][6][7][8][9][10], to study endothelial function [11] or to assess breathing maneuver-dependent oxygenation changes in the myocardium [12][13][14][15]. Preclinical studies have also demonstrated the potential of T 2 * mapping to detect structural changes in the infarcted heart muscle and even to distinguish between focal and diffuse fibrosis [16][17][18].…”

Impact of hyperventilation and apnea on myocardial oxygenation in patients with obstructive sleep apnea – An oxygenation-sensitive CMR study

“…Breathing maneuvers have been proposed as a physiological vasoactive stimulus leading to consistent myocardial signal intensity changes in oxygenation-sensitive MR images [8,[20][21][22][23].…”

“…Mostly related to changes in blood carbon dioxide (CO 2 ), a breath-hold (leading to hypercapnia with a net increase of blood CO 2 ) is an effective vasodilator, whereas hyperventilation with hypocapnia causes vasoconstriction [8,[20][21][22]. By combining these maneuvers, the achievable changes in pCO 2 are increased, resulting in a more extended range in vascular resistance with greater changes in OS signal intensity Because of an abnormal coronary vascular response in patients with OSAS, we hypothesized that the coronary vascular response to hyperventilation and long breath-hold is diminished in patients with OSAS when compared to healthy volunteers, as reflected by changes in myocardial oxygenation during voluntary apnea following hyperventilation.…”