Many possible biological factors related to the COVID-19 infection could be involved in the physiopathological cascade that could precipitate cardiovascular complications [2]:

• High levels of systemic proinflammatory cytokine and mediators of atherosclerosis may determine the plaque rupture through local inflammation.
• Procoagulant effects of systemic inflammation may cause coronary thrombosis: plaque thrombosis, stent thrombosis, and spontaneous thrombosis.
• Oxygen imbalance caused by pneumonia, with an infection-induced increase in metabolic demand and reduced cardiac reserve.
• Direct viral infection of myocardial and vascular cells.

In a observational study of 46 asymptomatic covid-19 patients, and 130 symptomatic covid-19 patients admitted with confirmed STEMI treated with primary percutaneous coronary intervention and thrombus aspiration, all patients had a nasopharyngeal PCR test as well as PCR in coronary thrombus obtained after thromboaspiration. This analysis demonstrates increased thrombus dimension in asymptomatic covid-19 STEMI patients compared with STEMI patients who are not infected. Interestingly, 39 (84.9%) of asymptomatic patients with SARS-COV-2 positive respiratory specimens also had coronary thrombus specimens positive for SARS-COV-2 [3].

Coronary aneurysm ectasia is defined as localized or diffuse dilatation of the coronary arteries more than 1.5 times the diameter of and adjacent healthy reference segment on coronary angiography [4].

Ectasias and coronary aneurysms are uncommon coronary artery diseases, can coexist and are poorly known. Their principal etiology in adults is coronary atherosclerosis. It has been suggested that these abnormalities would have poor prognosis and that slow flow could lead to in situ thrombosis and distal embolisation. However, ectasias and aneurysms are most often associated with coronary stenosis [5].

A Turkish study of 4,119 patients undergoing elective coronary angiography between 2003 and 2005, 173 patients (139 males, 34 females; mean age 61+/-11 years) had CAE, with a prevalence of 4.2%. Distribution of CAE was made according to the classification of Markis et al. The results were compared with those of 145 control patients (115 males, 30 males; mean age 61+/-10 years) who had CAD but not CAE. Following coronary angiography, treatment was designed as aortocoronary bypass (n=3), percutaneous coronary intervention (n=36), and medical therapy (n=98). The mean follow-up was 34.2+/-2.5 months [6].

Our case associated two throbogenic factors (Covid-19, and Ectasias)

Optical coherence tomography (OCT) has emerged as the most accurate method for intracoronary evaluation. Owing to a resolution of 10 to 20 μm, OCT is more accurate than intravascular ultrasound (IVUS) and is useful for the evaluation and characterization of plaque features, both in stable and acute coronary artery disease [7]. Unfortunately, due to the large size of the affected vessel, OCT was not feasible.

When treated by primary percutaneous coronary intervention, the existence of a massive intracoronary thrombus may lead to increased incidence of adverse outcomes. During balloon dilatation or stent implantation, the thrombus was crushed. This procedure could have subsequently caused the thrombus to embolize distally. The dislodged thrombus further activated platelets and this resulted in no reflow in the infarct-related artery [8]. In our case, we did not perform a balloon dilatation because of the absence of flow reduction and because of the risk of no-reflow.

We don’t make thrombectomy because of the massive thrombosis and the risk of the distal embolization and stroke and because of the conserved flow in the artery.

The effective anticoagulation was not prolonged due to the total regression of the thrombus and the conclusion that it was a complication of atherosclerotic plaque, which remains the primary etiology of coronary aneurysms.