Discussion
Venous thromboembolism has a broad spectrum of clinical syndromes associated with varying clinical outcomes [1-2]. Right heart thrombi (RHT) are uncommon but probably underdiagnosed in patients with pulmonary embolism [1]. Mobile right-heart thrombi are detected in range from 2.6% to 18% [5].
RHT had a higher prevalence in patients with a history of chronic heart failure, cancer, immobilization, or recent major bleeding compared with those without RHT [2]. Three RHTs (A, B, and C) are described, suggesting specific etiologies [3]. Type A describes a highly mobile serpiginous thrombus, often trapped in right heart cavities, representing the result of a migration of thrombi [3]. Hence, type A thrombi are associated with DVT and PE. Type B thrombi are fixed, formed in situ, and associated with cardiac abnormalities [3]. Type C assumes intermediate characteristics [3]. Stasis in the dilated right heart due either to acute severe pulmonary embolism, pre-existing congestive heart failure, or both seems to enhance the risk of RHT, regardless of whether it is due to in situ thrombosis or to entrapment of transiting thrombi [2].
There is a lack of comprehensive data on the prevalence, predictors, and prognostic significance of RHT in pulmonary embolism [2]. When compared to patients without RHT, patients with RHT are more hemodynamically compromised, with lower systolic blood pressure, higher heart rate, and more frequent hypoxemia and syncope [2]. A patent foramen ovale also increases the risk of ischemic stroke due to paradoxical embolism [4]. The literature review suggests that patients with acute pulmonary embolism and RHT had a significantly higher cumulative mortality than patients with acute pulmonary embolism without RHT [2]. Among low-risk PE patients with RHT, the risk of death was about seven times higher than in patients without RHT [2]. Among patients with low and intermediate risk of pulmonary embolism (i.e., right ventricular dysfunction), those with RHT had an increased mortality compared with those without RHT [2]. Our patient was thus considered to have having higher mortality risk.
Primary treatment includes optimizing oxygenation and ventilation status, volume optimization, and vasopressors and inotropes as needed [4]. Further therapeutic options in these patients consist of anticoagulation, thrombolysis, or surgical embolectomy [2]. However, the optimal treatment of right heart thrombi remains unclear, as no randomized studies exist. Current available data show that in patients who received anticoagulation alone, the risk of death was about three times higher in those with RHT than in those without RHT [2]. Data also suggested that normotensive patients with PE and coexisting RHT had a threefold increased risk of short-term death compared with patients without RHT [5]. It was thus concluded that anticoagulation is not enough as the sole treatment of pulmonary embolism with RHT [1], and the feasibility of thrombolysis was considered in our patient.
In normotensive patients with intermediate-risk PE, defined as the presence of RV dysfunction and elevated troponin levels, the impact of thrombolytic treatment was investigated in the Pulmonary Embolism Thrombolysis (PEITHO) trial, which showed a significant reduction in the risk of hemodynamic decompensation or collapse. Still, an increased risk of severe extracranial and intracranial bleeding parallelled this [4]. The efficacy of ”half-dose” or ”safe dose” thrombolytic therapy in the resolution of five cases of FRHT was presented in a case series [6]. Here, half-dose thrombolytic therapy (50 mg of alteplase) was administered to the patients and followed up with an echocardiogram that revealed complete resolution of the FRHT and considerable improvement in the right heart function with no bleeding events [6-7]. Hence, in our case, we perform thrombolysis with half dose to further reduce the risk of bleeding.