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Heart 78:515-516 doi:10.1136/hrt.78.5.515
  • Short cases in cardiology

Successful thrombolysis of right atrial and ventricle thrombi in a patient with peripartum cardiomyopathy and extensive thromboembolism

  1. Uwe Janssens,
  2. Heinrich G Klues,
  3. Peter Hanrath
  1. Medical Clinic I, University of Aachen, Pauwelsstraβe 30, D-52057 Aachen, Germany
  1. Dr.med. Janssens.
  • Accepted 24 June 1997

Right sided heart thrombi may develop within the right heart chambers or they may be peripheral venous clots that, on their way to the lungs, accidentally lodge in a patent foramen ovale, tricuspid chordae or Chiari’s network. Type A thrombi have a worm-like shape and are extremely mobile.1 These pleomorphic thrombi are mainly localised to the right atrium, frequently move back and forth through the tricuspid orifice, and may cause cardiovascular collapse when entrapment occurs.2 Type B thrombi attach to the atrial or ventricle wall indicating that they are probably of local origin.

Case report

Right sided deep vein thrombosis evolved three days after left heart catheterisation in a 27 year old woman with severe peripartum cardiomyopathy (ejection fraction < 30%). Acute orthopnoea four days later with severe hypotension (80/40 mm Hg) and tachycardia (132 beats/min) necessitating mechanical ventilation was highly suggestive of massive pulmonary embolism. Abdominal ultrasonography revealed a nearly complete occlusion of the inferior vena cava. Transoesophageal echocardiography (TOE) showed a great floating thrombus in the right atrium and thrombotic material obliterating the dilated right ventricle. The central pulmonary artery was distended without detection of further thrombi. Thrombolysis was started with 100 mg recombinant tissue plasminogen activator (rtPA) every two hours on day 8 followed by 40 mg rtPA every 12 hours on days 9–14 (fig 1). Serial TOE studies demonstrated complete dissolution of the right sided heart thrombi (fig2).

Figure 1

Clinical course of patient with peripartum cardiomyopathy and severe thromboembolism. DVT, deep vein thrombosis; rtPA, recombinant tissue plasminogen activator; TOE, transoesophageal echocardiography; PE, pulmonary embolism; RA, right atrium; RV, right ventricle; IVC, inferior vena cava; iv, intravenous; A-D, TOE studies.

Figure 2

Transoesophageal echocardiography in patient with right sided heart thrombus. (A) Transgastral short axis view with extensive wall adherent thrombus of the right ventricle (RV) before thrombolysis. (B) Transgastral short axis view on day 2 of thrombolysis. (C) Transgastral short axis view on day 3 of thrombolysis. (D) Transoesophageal four chamber view on day 7 of thrombolysis without any further thrombus formation in the right atrium (RA) and right ventricle.

There were no signs of recurrent pulmonary embolism during treatment. Haemodynamics greatly improved and extubation was performed on day 15. Vena caval interruption with a Greenfield umbrella was performed because of a persisting thrombus in the inferior vena cava 4 cm distal the renal veins. Antithrombin-III, protein C and protein S deficiency, and heparin induced thrombocytopenia and thrombosis were excluded as well as anticardiolipin antibodies.

Discussion

This case illustrates the association of pulmonary embolism with right sided heart thrombi. Patients with type A thrombi have a very poor short term prognosis with high early mortality of 44% with severe and often fatal pulmonary embolism mainly because these highly mobile, poorly fixed clots are at high risk for embolisation.1Patients with type B thrombi seem to be a low risk group with a thrombus related mortality of 4%.1 There is no consensus regarding the optimal treatment for patients with right sided heart thrombi. In a meta-analysis of these thromboembolic complications estimated probability of survival in patients receiving heparin, thrombolytic agents, embolectomy, or none of the above was 0.70, 0.62, 0.62, and 0.19, respectively.3 The present patient’s underlying cardiac disease was considered too risky for surgical removal but the nearly complete thrombotic obliteration of the right ventricle with impairment of blood flow necessitated clot removal. Thrombolysis is first line treatment in patients with massive pulmonary embolism. Several reports describe successful thrombolysis in right sided heart thrombi.4 5 To the best of our knowledge this is the first report of successful thrombolysis with rtPA over several days in a patient with right sided heart thrombi. There are no data to support the daily administration of thrombolytics as superior to standard lytic treatment given over a short time frame with conversion to heparin and warfarin for this condition. TOE was extremely helpful in diagnosing right sided heart thrombi and monitoring the efficacy of thrombolysis in this patient. We strongly recommend echocardiography studies for all patients with suspected pulmonary embolism to avoid missing right sided heart thrombi. This finding not only supports the diagnosis of pulmonary embolism but also creates an acute emergency situation precluding further diagnostic procedures such as right heart catheterisation with the potential risk for dislodging the thrombi in the pulmonary arteries. Further prospective studies are needed to elucidate the role of thrombolysis in management of patients with pulmonary embolism and right sided heart thrombi.

References