Cardiovascular magnetic resonance imaging revealed that global myocardial perfusion reserve was significantly reduced in post-COVID-19 patients compared to healthy controls (2.73 vs 4.82, p=0.005).
Cross-Sectional (n=55)
No
Does vasodilator-stress CMR detect reduced myocardial perfusion reserve indicative of coronary microvascular disease in post-COVID-19 patients with persistent dyspnoea compared to healthy controls?
Post-COVID-19 patients with persistent dyspnoea and fatigue exhibit reduced myocardial perfusion reserve on CMR, suggesting coronary microvascular disease as a potential mechanism for their ongoing symptoms.
Absolute Event Rate: 2.73% vs 4.82%
p-value: p=0.005
Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and is primarily characterised by a respiratory disease. However, SARS-CoV-2 can directly infect vascular endothelium and subsequently cause vascular inflammation, atherosclerotic plaque instability and thereby result in both endothelial dysfunction and myocardial inflammation/infarction. Interestingly, up to 50% of patients suffer from persistent exercise dyspnoea and a post-viral fatigue syndrome (PVFS) after having overcome an acute COVID-19 infection. In the present study, we assessed the presence of coronary microvascular disease (CMD) by cardiovascular magnetic resonance (CMR) in post-COVID-19 patients still suffering from exercise dyspnoea and PVFS. N = 22 patients who recently recovered from COVID-19, N = 16 patients with classic hypertrophic cardiomyopathy (HCM) and N = 17 healthy control patients without relevant cardiac disease underwent dedicated vasodilator-stress CMR studies on a 1.5-T MR scanner. The CMR protocol comprised cine and late-gadolinium-enhancement (LGE) imaging as well as velocity-encoded (VENC) phase-contrast imaging of the coronary sinus flow (CSF) at rest and during pharmacological stress (maximal vasodilation induced by 400 µg IV regadenoson). Using CSF measurements at rest and during stress, global myocardial perfusion reserve (MPR) was calculated. There was no difference in left ventricular ejection-fraction (LV-EF) between COVID-19 patients and controls (60% 57-63% vs. 63% 60-66%, p = NS). There were only N = 4 COVID-19 patients (18%) showing a non-ischemic pattern of LGE. VENC-based flow measurements showed that CSF at rest was higher in COVID-19 patients compared to controls (1.78 ml/min 1.19-2.23 ml/min vs. 1.14 ml/min 0.91-1.32 ml/min, p = 0.048). In contrast, CSF during stress was lower in COVID-19 patients compared to controls (3.33 ml/min 2.76-4.20 ml/min vs. 5.32 ml/min 3.66-5.52 ml/min, p = 0.05). A significantly reduced MPR was calculated in COVID-19 patients compared to healthy controls (2.73 2.10-4.15-11 vs. 4.82 3.70-6.68, p = 0.005). No significant differences regarding MPR were detected between COVID-19 patients and HCM patients. In post-COVID-19 patients with persistent exertional dyspnoea and PVFS, a significantly reduced MPR suggestive of CMD-similar to HCM patients-was observed in the present study. A reduction in MPR can be caused by preceding SARS-CoV-2-associated direct as well as secondary triggered mechanisms leading to diffuse CMD, and may explain ongoing symptoms of exercise dyspnoea and PVFS in some patients after COVID-19 infection.
Drakos et al. (2021) conducted a cross-sectional in COVID-19 (post-viral fatigue syndrome and exertional dyspnoea) (n=55). Cardiovascular magnetic resonance (CMR) imaging vs. Healthy controls and hypertrophic cardiomyopathy (HCM) patients was evaluated on Global myocardial perfusion reserve (MPR) per minute (p=0.005). Cardiovascular magnetic resonance imaging revealed that global myocardial perfusion reserve was significantly reduced in post-COVID-19 patients compared to healthy controls (2.73 vs 4.82, p=0.005).