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].