Abstract
Aims: Microvascular alterations occurring after myocardial infarction (MI) may represent a risk factor for multi-organ failure. Here we used in vivo photoacoustic (PA) imaging to track and define the changes in vascular oxygen saturation (sO2) occurring over time after experimental MI in multiple peripheral organs and in the brain.Methods and Results: Experimental MI was obtained in BALB/c mice by permanent ligation of the left anterior descending artery. PA imaging (Vevo LAZR-X) allowed tracking mouse-specific sO2 kinetics in the cardiac left ventricular (LV) anterior wall, brain, kidney, and liver at 4 h, 1 day, and 7 days post-MI. Here we reported a correlation between LV sO2 and longitudinal anterior myocardial strain after MI (r = −0.44, p < 0.0001, n = 96). Acute LV dysfunction was associated with global hypoxia, specifically a decrease in sO2 level in the brain (−5.9%), kidney (−6.4%), and liver (−7.3%) at 4 and 24 h post-MI. Concomitantly, a preliminary examination of capillary NG2DsRed pericytes indicated cell rarefication in the heart and kidney. While the cardiac tissue was persistently impacted, sO2 levels returned to pre-MI levels in the brain and in peripheral organs 7 days after MI.Conclusions: Collectively, our data indicate that experimental MI elicits precise trajectories of vascular hypoxia in peripheral organs and in the brain. PA imaging enabled the synchronous tracking of oxygenation in multiple organs and occurring post-MI, potentially enabling a translational diagnostic modality for the identification of vascular modifications in this disease setting.
Highlights
Tissular hypoxia following end-organ hypoperfusion after myocardial infarction (MI) is associated with cardiogenic shock incidence and elevated mortality [1]
We tested the ability of photoacoustic imaging (PAI) to detect sO2 changes in the anterior wall after left anterior descending coronary artery (LAD) occlusion (Figures 2C,D)
A decrease in sO2 level occurred in the left ventricular (LV) anterior wall t 4 h, 1 day, and 7 days after LAD ligation (Figure 2C)
Summary
Tissular hypoxia following end-organ hypoperfusion after myocardial infarction (MI) is associated with cardiogenic shock incidence and elevated mortality [1]. Despite the use of early coronary revascularization and the advances in cardiogenic shock treatment, the inability to rapidly restore regional tissular normoxia represents a critical factor impacting MI prognosis [2]. Monitoring, as early as possible, organ-specific dynamics of hypoxia represents a candidate strategy to guide treatments and to timely identify high-risk patients [3]. Lactate is not specific to an organ, whereas microvascular perfusion is naturally heterogeneous [4]. Continuous real-time monitoring of specific organ oxygenation is clinically relevant, and using near infrared spectroscopy (NIRS) was proposed to monitor hypoxia and to enable a guided therapy in shock patients [6]. Our understanding of the patterns of multi-organ hypoxia elicited in response to MI remains incomplete
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