DISCUSSION
The patient was an old woman with multi risk factors suffering from acute coronary syndrome, COVID 19, PTE and acute CVA. Recent reports indicated that older patients with cardiovascular disease constitute the highest-risk group. This high-risk group is likely to have coagulopathy; hence, an interim guideline was issued by the International Society on Thrombosis and Hemostasis, suggesting low-dose prophylactic heparin for the management of coagulopathy[5]. Venous thromboembolism threatens patients with COVID-19 and adds the risk of acute respiratory distress syndrome. Venous thromboembolism seems to remain underdiagnosed in COVID-19 patients. These patients have pulmonary hypertension and right ventricular dysfunction and small acute PTE may deteriorate the condition.
Pulmonary thromboembolism occurred in 20% of COVID-19 ICU patients during 1 month descriptive study by Poissy J et al ; twice the number in the same duration in 2019. Of note, the proportion of PTE in COVID-19 was estimated to be twice the number in influenza outbreak[6].
Large vessel stroke has also been discussed in association with COVID-19 in another study by Oxley et al[7]. In the recent study by Yanan Liet al , a single center observational study was performed on 221 COVID-19 patients. In their registry, 11% developed acute ischemic stroke. Old patients with COVID-19 were more prone to acute CVA[8].
With respect to our 70-year-old female patient infected with COVID-19, the deterioration in her clinical status with a baseline acute cardiac condition may have been due to a combination of lung injury and cardiac damage. We repeatedly performed echocardiography and detected RV dysfunction and exacerbated tricuspid regurgitation (by comparison with the previous echocardiography findings). Indeed the patient’s dependence on inotropes made us suspicious of acute PTE. What further obfuscates the picture in patients with COVID-19 is the presence of tachypnea, tachycardia, hypoxia, and high D-dimer levels, rendering the differentiation between this infection and PTE challenging. High D-dimer is associated with a poor prognosis among patients with COVID-19 whether or not there is concomitant PTE.
We cannot be certain about the exact time of the occurrence of PTE in our patient. It is likely that PTE occurred in the hospital following PCI and her unwanted immobility due to hypoxia and femoral puncture. She was on therapeutic doses of heparin before PCI and prophylactic doses afterward. Another theory may be the coincidence of acute coronary syndrome, COVID-19, and PTE, which prompted the patient to refer to our emergency department, albeit with a 4-day delay.
Since COVID-19 patients are predisposed to thromboembolism, early diagnosis and treatment of such concomitant problems will improve their condition. We should be cautious to ascribe every sign and symptoms during hospitalization to just COVID-19.
Alongside coagulopathy, COVID-19 causes significant hypoxia along with an inflammatory milieu, which may lead to secondary myocardial infarction and also atherosclerotic plaque rupture. Hence, patients with COVID-19 are predisposed to both embolic and atherosclerotic events due to baseline inflammation[9].