Effect of Hyperoxia on Myocardial Oxygenation and Function in Patients With Stable Multivessel Coronary Artery Disease

Abstract

Background The impact of hyperoxia, that is, supraphysiological arterial partial pressure of O2, on myocardial oxygen balance and function in stable multivessel coronary artery disease (CAD) is poorly understood. In this observational study, we assessed myocardial effects of inhalational hyperoxia in patients with CAD using a comprehensive cardiovascular magnetic resonance exam. Methods and Results Twenty-five patients with stable CAD underwent a contrast-free cardiovascular magnetic resonance exam in the interval between their index coronary angiography and subsequent revascularization. The cardiovascular magnetic resonance exam involved T1 and T2 mapping for tissue characterization (fibrosis, edema) as well as function imaging, from which strain analysis was derived, and oxygenation-sensitive cardiovascular magnetic resonance imaging. The latter modalities were both acquired at room air and after breathing pure O2 by face mask at 10 L/min for 5 minutes. In 14 of the 25 CAD patients (56%), hyperoxia induced poststenotic myocardial deoxygenation with a subsequent oxygenation discordance across the myocardium. Extent of deoxygenation was correlated to degree of stenosis (r=-0.434, P=0.033). Hyperoxia-associated poststenotic deoxygenation was accompanied by ipsiregional reduction of diastolic strain rate (1.39±0.57 versus 1.18±0.65; P=0.045) and systolic radial velocity (37.40±17.22 versus 32.88±13.58; P=0.038). Increased T2, as well as lower cardiac index, and defined abnormal strain parameters on room air were predictive for hyperoxia-induced abnormalities (P<0.05). Furthermore, in patients with prolonged native T1 (>1220 ms), hyperoxia reduced ejection fraction and peak strain. Conclusions Patients with CAD and pre-existent myocardial injury who respond to hyperoxic challenge with strain abnormalities appear susceptible for hyperoxia-induced regional deoxygenation and deterioration of myocardial function. Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT02233634.

Keywords: blood‐oxygen level dependence; coronary artery disease; hyperoxia; oxygen; oxygenation‐sensitive cardiovascular magnetic resonance.

Figures

Figure 1

Exemplary coronary artery disease patient with hyperoxia‐induced decrease of global systolic and diastolic function. This patient had a maximal left anterior descending coronary artery (LAD) diameter stenosis of 61% (A) at CMR (cardiovascular magnetic resonance). The left circumflex coronary artery with a left‐dominant pattern was reperfused (stented) after presenting with a non–ST‐segment–elevation myocardial infarction 44 days before the staged percutaneous coronary intervention and CMR. Left ventricular ejection fraction decreased below 50% and cardiac index below 2.5 L/min/m2 during hyperoxia (B). The T1 mapping image (C, top) shows myocardial injury in the subendocardial layer of the anteroseptal segment (orange). This matches a hyperoxia‐induced oxygenation deficit (blue; C, bottom) observed in the LAD territory. This further corresponded to a regional decrease in early diastolic circumferential peak strain rate (D). Diastolic SR indicates diastolic strain rate; OS (%), % change in oxygenation‐sensitive signal intensity.

Figure 2

Exemplary patient with systolic dysfunction. Findings in an 80‐year‐old male patient with serial left anterior descending artery stenoses (C, maximal degree: 63% diameter stenosis). This patient had a previous percutaneous coronary intervention of serial right coronary artery stenoses following presentation with typical stable angina and inconclusive ergometry. In this patient, left ventricular ejection fraction dropped from 64% to 57% and cardiac index from 2.77 to 2.37 L/min/m2 after breathing oxygen, respectively. The T1 mapping image (A, top) shows myocardial injury in the septum and inferior wall, which is colocalized with both the oxygenation deficit (A, bottom) and circumferential strain (PSC) abnormalities induced with hyperoxia. At rest, the septum exhibits subnormal peak circumferential strain at end‐systole (B), which is exacerbated further at hyperoxia (yellow region). The graph shows that peak circumferential strain in poststenotic segments is attenuated across the entire cardiac cycle at hyperoxia (green) in comparison with normoxemia at room air (black). OS (%) indicates % change in oxygenation‐sensitive signal intensity.

Figure 3

Association between parameters of myocardial injury and hyperoxic ventricular function. Patients with indicators of myocardial injury (T1 ≥1220 ms, purple) demonstrate reduced ejection fraction (EF) and peak strain in both circumferential (PSC) and radial (PSR) orientation, all of which significantly differ from those in patients with T1 <1220 ms (orange, P=0.017, 0.025, and 0.047, respectively). Shaded green areas represent reference ranges, with the darker shade indicating mean±1 SD of healthy control measurements at normoxemia (room air) and the lighter shade representing the ±2 SD cutoff.

Figure 4

Indicators of regional myocardial oxygenation discordance. The plot shows the correlation coefficient (r) with 95% CI demonstrating the association between measurements obtained at normoxemia and hyperoxia‐induced myocardial oxygenation discordance (56% of patients). Green indicates P<0.05. Increasingly positive values are considered abnormal for circumferential peak strain and systolic strain rate, as well as for radial diastolic velocity and strain rate. FT‐CMR indicates feature tracking cardiovascular magnetic resonance; LV, left ventricular.