Both of our patients died; however, our first patient died due to infectious complications and not due to obstructive shock itself. As appropriately described in literature, our first patient had surgical embolectomy and survived from acute problem of right heart thrombus (RHT), while in the second case, there was not enough time before patient deteriorated and died. This feature describes the importance of early diagnosis and aggressive treatment of RHT. In current era, many bedside echocardiographs are performed not only by cardiology team but also by emergency and internal medicine house staff; recognition of RHT and its aggressive treatment is crucial.
Right heart thrombi occur in about 4% of pulmonary embolism (PE) [1]. They result either from dislodging clot from deep venous thrombosis, or form in situ mostly due to atrial fibrillation. They can also be associated with intracardiac foreign bodies such as pacemakers and prosthetic valves.
Mortality rate in patients with RHT is about 28%, with mortality rates in untreated patients of 80–100%. In contrast, the in-hospital mortality rate for acute pulmonary embolism (PE) is about 2.5% [1]. Patients with RHT have shorter duration of symptoms, lower systolic blood pressure, more frequent right ventricular hypokinesis and congestive heart failure [2].
Three major types of right heart thrombus can be distinguished on echocardiography [2]: type A is most common, is usually the result of deep venous thrombosis and has the highest risk of embolization. It is elongated, with a worm-like appearance and is freely mobile within the heart chambers. Type B thrombus is thought to originate within the atrium or ventricle, and is firmly attached to the chamber wall and ovoid shape. Type C thrombi are rare, highly mobile and resembling cardiac myxomas. Transesophageal echocardiography (TEE) provides better visualization of the thrombus and should be considered when TTE is suboptimal or non-diagnostic [3]; it can localize thrombus in pulmonary artery or lodged in patent foramen ovale.
Both of our patients had type A thrombus. In addition, both of our patients had signs of severe right ventricular pressure overload. Akinesis of mid-free wall of the right ventricle and normal motion of apex such as in our second patient (McConnell’s sign) is particularly suggestive of PE [4].
Treatment modalities for RHT include anticoagulation therapy, systemic thrombolysis and surgical embolectomy. Optimal therapeutic approach is still subject of discussion as no randomized controlled trials have directly compared the treatment methods. In a meta-analysis of 119 patients by Kinney from 1989, there was a small survival benefit with anticoagulation (70%) when compared to surgical embolectomy or thrombolysis (62%) [5]. However, not all patients had a pulmonary embolism in the study. A multicenter observational European study from the same year reported a markedly lower mortality with surgical embolectomy (27%) as compared to anticoagulation (>60%) [2]. A meta-analysis by Rose from 2002 of 177 patients with RHT demonstrated a superiority of thrombolytic therapy over surgical embolectomy (OR for mortality: 2.83, 95% CI 1.04–7.69) and anticoagulation (OR for mortality: 3.03, 95% CI 1.02–3.125) [6]. These results were confirmed by the largest meta-analysis to date by Ganesh et al. from 2015 that evaluated total 328 patients. In this meta-analysis, 70 patients received anticoagulation, 122 patients received thrombolysis and 120 patients had surgical embolectomy. Mortality rates were 37.1, 18.3 and 13.9%, respectively. After adjusting for age and hemodynamic status, the OR for survival was 4.83 (95% CI 1.51–15.36) with thrombolysis and 2.61 (95% CI 0.90–7.58) with surgical embolectomy [7]. Data on catheter-based interventions are scarce.