Imaging Inflammation in the Cardio-Renal Axis After Acute Myocardial Infarction

Ziel/Aim Cardiorenal syndrome is characterized by bidirectional interaction between the failing heart and the kidneys. We speculated that inflammation contributes to this crosstalk and sought to obtain further mechanistic insights into this interaction by retrospective analysis of CXCR4-targeted images in myocardial infarction (MI).

Methodik/Methods Serial CXCR4-targeted ⁶⁸Ga-pentixafor PET images were previously acquired in mice (n = 65) after MI or sham surgery at 1d, 3d, 7d, and 6 wks. Cardiac function was assessed by magnetic resonance. Additionally, CXCR4-directed PET datasets of 96 acute MI patients were evaluated for infarct and kidney tracer retention.

Ergebnisse/Results In mice, CXCR4 upregulation was significantly elevated in the infarct region at 1d and unchanged at 7d after MI compared to sham (%ID/g, 1.12±0.20* vs 0.59 ±0.12, *P < 0.0001 vs. sham). Renal CXCR4 signal was unchanged at 1d but reduced at 7d compared to sham (%ID/g, 1.23±0.17 vs 1.07±0.2*, *P < 0.05 vs. sham). Tracer uptake in heart and kidneys were directly correlated (r = 0.62, p < 0.0001). Histopathology confirmed the presence of CD68+ macrophages in the kidney after acute MI. CXCR4 signal intensity in kidney at 7d was inversely proportional to cardiac function at 6 weeks after MI, particularly among animals with more severe contractile impairment (ejection fraction <30 %, R=−0.79, p < 0.05). Among patients, renal CXCR4 signal was independent of glomerular filtration rate (GFR) early after MI, but tended to correlate with the infarct signal (R = 0.19, P=0.05). After median follow-up of 8 months, 32/96 (33.3 %) of the MI patients developed impaired renal function (GFR: 70±15 vs 100±6 mL/min/1.73m², p<0.0001). These patients exhibited higher renal CXCR4 signal on initial assessment (SUV, 4.52±1.59 vs 3.63±0.62, P<0.05), suggesting that early renal inflammation post-MI may predict subsequent renal impairment.

Schlussfolgerungen/Conclusions Taken together, these findings suggest inflammatory crosstalk between the injured heart and kidneys early after MI, which may contribute to adverse outcome for both organs.