Spontaneous Thrombolysis in Left Ventricular Thrombosis Post Dengue Myocarditis
Author : H. Lim, I.B. Wibhuti, K.B. Nadha
Upload Date : 19-04-2018
Background: Dengue fever majority are asymptomatic or relatively mild manifestation, with estimated 1% - 5% patients admitted with several complications, including multiple organ failure, bleeding, and capillary plasma leakage. Various cardiac manifestation can occur after dengue infection, including rare case of fulminant myocarditis to more common of myocardial dysfunction and arrhythmia. Cardiac manifestation already included in criteria of severe dengue (WHO 2009 revised classification). Myocarditis mostly caused by viral infection can manifest as dilated cardiomyopathy and associated with increase in platelet activation. Several cases reported, an increased incidence of fibrin deposition and thrombus formation during acute myocarditis. We reported a case of
Case Illustration: Patient female 43 years old, admitted to intensive care unit with dengue shock syndrome. During admission, bedside echocardiography demonstrated reduced global left ventricular contractility (LVEF 29%) with moderate mitral regurgitation. Patient responded well to intensive therapy and regained normal perfusion also cardiac function. During follow-up, echocardiography full study showed normal cardiac function (LVEF 71%, TAPSE 2.8cm) and visible mobile mass during systolic and diastolic phase attached to left ventricular apical. Patient advised to take anticoagulant therapy and routin check-up, but patient did not comply. Another echocardiography follow-up 1 month later, no intracardiac mass visible with normal cardiac function and moderate mitral regurgitation.
Discussion: According to Virchow’s triad, endocardial injury, hypercoagulability, and blood flow stasis caused by myocardial dysfunction are responsible for thrombus formation. Dengue infection triggers fibrinolysis activation resulting in decrease of fibrinogen which secondary activated procoagulant homeostatic mechanism. Combination of this mechanism and decreased of myocardial contractility during acute myocarditis resulting in fibrin deposition in ventricular. Thrombosis and platelet activation trigger activity of endogenous thrombolysis, including release of tissue plasminogen activator (t-PA) and urokinase plasminogen activator (u-PA) from plasma and blood vessel to prevent thrombus formation, and also release of elastase and cathepsin from neutrophils and monocytes to break down fibrin. In this case, possibility spontaneous thrombolysis caused by combination of healthy endogenous thrombolysis system and recovery of cardiac function.
KEYWORDS : thrombolysis, myocarditis, dengue fever.