Brief Research Report: Quantitative Analysis of Potential Coronary Microvascular Disease in Suspected Long-COVID Syndrome.

Background: Case series have reported persistent cardiopulmonary symptoms, often termed long-COVID or post-COVID syndrome, in more than half of patients recovering from Coronavirus Disease 19 (COVID-19). Recently, alterations in microvascular perfusion have been proposed as a possible pathomechanism in long-COVID syndrome. We examined whether microvascular perfusion, measured by quantitative stress perfusion cardiac magnetic resonance (CMR), is impaired in patients with persistent cardiac symptoms post-COVID-19.
Methods: Our population consisted of 33 patients post-COVID-19 examined in Berlin and London, 11 (33%) of which complained of persistent chest pain and 13 (39%) of dyspnea. The scan protocol included standard cardiac imaging and dual-sequence quantitative stress perfusion. Standard parameters were compared to 17 healthy controls from our institution. Quantitative perfusion was compared to published values of healthy controls.
Results: The stress myocardial blood flow (MBF) was significantly lower [31.8 ± 5.1 vs. 37.8 ± 6.0 (μl/g/beat), P < 0.001] and the T2 relaxation time was significantly higher (46.2 ± 3.6 vs. 42.7 ± 2.8 ms, P = 0.002) post-COVID-19 compared to healthy controls. Stress MBF and T1 and T2 relaxation times were not correlated to the COVID-19 severity (Spearman r = -0.302, -0.070, and -0.297, respectively) or the presence of symptoms. The stress MBF showed a U-shaped relation to time from PCR to CMR, no correlation to T1 relaxation time, and a negative correlation to T2 relaxation time (Pearson r = -0.446, P = 0.029).
Conclusion: While we found a significantly reduced microvascular perfusion post-COVID-19 compared to healthy controls, this reduction was not related to symptoms or COVID-19 severity.
Competing Interests: PD owns stock of Siemens and Bayer. AF was a shareholder of BOCAhealthcare GmbH. CS was an employer of Philips Healthcare. BP reported receiving personal fees from Bayer, Bristol Myers Squib, Daiichi Sankyo, Medscape, MSD, Novartis, Stealth Peptides, and Vifor Pharma, and grants and personal fees from Astra-Zeneca. CS and JS-G were employees of Philips Healthcare. CT, BP, and SK received funding from the DZHK (German Centre for Cardiovascular Research) and by the BMBF (German Ministry of Education and Research) and personal fees from Servier, outside of the current work. SK received an unrestricted research grant from Philips Healthcare and received lecture honoraria from Medis, NL. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
(Copyright © 2022 Doeblin, Steinbeis, Scannell, Goetze, Al-Tabatabaee, Erley, Faragli, Pröpper, Witzenrath, Zoller, Stehning, Gerhardt, Sánchez-González, Alskaf, Kühne, Pieske, Tschöpe, Chiribiri and Kelle.)