Discussion
It was noticed recently, that COVID-19 causes significant alterations in
blood cells, including morphological and mechanical abnormalities like
enlarged sizes, sometimes lasting for months after hospital
discharge.[9] Through a variety of mechanisms, including tissue
factor release, endothelial damage brought on by inflammation and
hypoxia, and platelet activation, COVID-19 has a major impact on the
etiology of coagulopathy.[10] Endothelial protein C receptor and
thrombomodulin levels are elevated along with procoagulates such as
factor VIII, P-selectin, and von Willebrand factor and downregulated
along with thrombomodulin as a result of the cytokine storm released by
endothelial and immune cells.[11]
It is also known that patients with left ventricular assist devices
(LVAD) are at a greater risk of pump thrombosis if having any concurrent
infections.[12]
One of the key problems that can lead to life-threatening low-flow or
pump malfunction is LVAD thrombus development in the inflow cannula,
device body, or outflow graft, implicating hemodynamic instability,
hemolysis, renal or hepatic failure, or cerebral or peripheral
thromboembolism.[13] LVAD thrombosis has been found to occur in
2–13% of adult LVAD patients who use current continuous-flow
devices.[14]
The clinical picture of pump thrombosis shows a wide range of
variability.[15, 16]
Our patient had pump thrombosis three years after HMIII insertion which
was considered the longest period compared to other case reports which
presented mostly during the first 2 years in COVID and none COVID
patients (Tables 2, 3). symptoms like other COVID reported cases ( Table
3 ) . Reviewing the literature regarding to LVAD thrombosis, indicated
that patient had COVID-19 had higher morbidity and mortality as
indicated in table 2 no-COVID and table 3 COVID patients.
CTA showed complete outflow graft thrombosis with low flow of 0.5 L/M.
Our patient had supratherapeutic INR measuring 6.1, and 9.0 on 0 at day
2 and day 3, respectively. Following that tPA was stopped. That
signifies the importance of anticoagulation balance in VAD patients with
COVID infection.
LVAD thrombosis has very high mortality and the pathophysiology of LVAD
thrombosis is complicated, and it is mainly due to emboli secondary to
sluggish blood flow in the left ventricle’s endocardium, clots formed in
the left atrial appendage, or in ventricular debris from prior surgery,
inadequate anticoagulation, and inflow cannula malposition.[17]
In the clinical situation of advancing heart failure symptoms, LVAD
low-flow alert, abnormal test results for hemoglobin, free-hemoglobin,
and LDH, and symptoms refractory to fluid infusion, making LVAD
thrombosis highly suspicious..[16] TTE and CTA are helpful
diagnostic methods for LVAD thrombus detection, and a positive thrombus
diagnosis may lead to timely alterations in patient management.[18]
The most conclusive forms of treatment for suspected thrombosis are
immediate heart transplantation or surgical device exchange.[19]
Initiating medical management to deal with pump thrombosis is crucial
for transplant candidates or individuals who cannot endure surgery.
Heparin monotherapy is the first instituted along with
inotropic/diuretic depending on heart failure symptoms.[20]
Additional medications including direct thrombin inhibitors,
thrombolytics, and glycoprotein IIb/IIIa inhibitors may be used in the
dissolution of pump thrombosis.[14] t-PA can be administered along
with heparin to accelerate the dissolution of the LVAD thrombus and
successful outcomes have been reported in some cases.[21, 22]
Furthermore, there are no specific guidelines available for the dose and
treatment of t-PA administration in patients with LVAD thrombosis. As a
result, since there is no acknowledged method for addressing t-PA,
administration depends on personal experience and the favored tactic in
each facility.[16] A substantial risk of hemorrhage does exist with
t-PA therapy which was also seen in our patient as bleeding from CVC and
melena.[14] Although transplant and LVAD exchange are definitive
forms of treatment, our patient’s persistent multiorgan failure
prohibited him from being a good surgical candidate.