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.