Abstract 198 Increased aortic stiffness and vascular inflammation in myocardial dysfunction in Long COVID-19 disease.

Background: Long COVID is an increasingly recognized late complication of COVID-19 infection and inflammatory cardiovascular involvement has also been implicated. Increased aortic stiffness is an independent predictor of cardiovascular risk and is associated with systemic inflammation.

Methods: Prospective observational cohort study of patients recently recovered from COVID-19 illness and no previously known cardiovascular disease included between April 2020 and April 2021. Demographic characteristics, cardiac blood markers, and cardiovascular magnetic resonance (CMR) imaging a minimum of 4 weeks from the diagnosis were obtained.

Results: 153 included COVID-19 patients (males n=79, 52%, mean age 46 (±13) years) in comparison to healthy subjects (n=55) and risk factor (RF) matched controls (n=83) had significantly higher pulse wave velocity (PWV, m/s: 7.2±2.1 vs. 5.6±1.7 vs. 6.4±1.8, p<0.01), native T1 (ms: 1124±38 vs. 1076±25 vs. 1114±36, p<0.01), native T2 (ms: 38.1±1.8 vs. 35±1.5 vs. 37 ±2.2, p<0.01 hs-TropT (pg/ml: 8.6±2 vs. 3.5±1.3 vs. 5.1±8, p=0.017), NT-proBNP(pg/ml, 67(55) vs 44.4(32) vs. 59(48), p=0.23), hsCRP (pg/ml, 0.20(0.12) vs. 0.13(0.10) vs. 0.16(0.12), p=0.049) and reduced circumferential strain (%, 18±3.4 vs. 22±6.1 vs. 18±33.5) and LVEF (%, 56±5.3 vs 60±4.8 vs. 59±12.1, p<0.001). In COVID-19 patients, PWV was significantly associated with native T1 (r=0.51, p<0.001), native T2 (r=0.24, p=0.003), hsTropT (r=0.24, p=0.003) and NT-proBNP (r=0.34, p<0.001), longitudinal (r=0.18, p=0.03) and circumferential strain (r=0.17, p=0.04), whereas in healthy subjects and RF matched controls PWV only correlated with strains (r~0.28, p<0.05) and NT-proBNP (r=0.36, p=0.008), respectively.

Conclusion: In this cohort of patients recently recovered from COVID-19 infection, we demonstrate a significant increase in aortic stiffness, which is associated with serological markers of cardiac injury as well as interstitial inflammatory remodelling by myocardial native T1 and T2, strain and LVEF. These findings suggest that ongoing symptoms relate to an increased cardiovascular stiffness due to ongoing inflammation in the aftermath of COVID-19 infection.

Clin Res Cardiol (2022). https://doi.org/10.1007/s00392-022-02002-5
Increased aortic stiffness and vascular inflammation in myocardial dysfunction in Long COVID-19 disease.
E. Giokoglu¹, S. Martin², B. Vanchin², N. Holm², C. Arendt², A. Karyou², A. M. Zeiher¹, E. Nagel², V. Puntmann³
¹Med. Klinik III - Kardiologie Zentrum der Inneren Medizin, Universitätsklinikum Frankfurt, Frankfurt am Main; ²Kardiovaskuläre Bildgebung, Universitätsklinikum Frankfurt, Frankfurt am Main; ³Goethe CVI, Universitätsklinikum Frankfurt, Frankfurt am Main;
Background: Long COVID is an increasingly recognized late complication of COVID-19 infection and inflammatory cardiovascular involvement has also been implicated. Increased aortic stiffness is an independent predictor of cardiovascular risk and is associated with systemic inflammation. Methods: Prospective observational cohort study of patients recently recovered from COVID-19 illness and no previously known cardiovascular disease included between April 2020 and April 2021. Demographic characteristics, cardiac blood markers, and cardiovascular magnetic resonance (CMR) imaging a minimum of 4 weeks from the diagnosis were obtained. Results: 153 included COVID-19 patients (males n=79, 52%, mean age 46 (±13) years) in comparison to healthy subjects (n=55) and risk factor (RF) matched controls (n=83) had significantly higher pulse wave velocity (PWV, m/s: 7.2±2.1 vs. 5.6±1.7 vs. 6.4±1.8, p<0.01), native T1 (ms: 1124±38 vs. 1076±25 vs. 1114±36, p<0.01), native T2 (ms: 38.1±1.8 vs. 35±1.5 vs. 37 ±2.2, p<0.01 hs-TropT (pg/ml: 8.6±2 vs. 3.5±1.3 vs. 5.1±8, p=0.017), NT-proBNP(pg/ml, 67(55) vs 44.4(32) vs. 59(48), p=0.23), hsCRP (pg/ml, 0.20(0.12) vs. 0.13(0.10) vs. 0.16(0.12), p=0.049) and reduced circumferential strain (%, 18±3.4 vs. 22±6.1 vs. 18±33.5) and LVEF (%, 56±5.3 vs 60±4.8 vs. 59±12.1, p<0.001). In COVID-19 patients, PWV was significantly associated with native T1 (r=0.51, p<0.001), native T2 (r=0.24, p=0.003), hsTropT (r=0.24, p=0.003) and NT-proBNP (r=0.34, p<0.001), longitudinal (r=0.18, p=0.03) and circumferential strain (r=0.17, p=0.04), whereas in healthy subjects and RF matched controls PWV only correlated with strains (r~0.28, p<0.05) and NT-proBNP (r=0.36, p=0.008), respectively. Conclusion: In this cohort of patients recently recovered from COVID-19 infection, we demonstrate a significant increase in aortic stiffness, which is associated with serological markers of cardiac injury as well as interstitial inflammatory remodelling by myocardial native T1 and T2, strain and LVEF. These findings suggest that ongoing symptoms relate to an increased cardiovascular stiffness due to ongoing inflammation in the aftermath of COVID-19 infection.
https://dgk.org/kongress_programme/jt2022/aP1223.html