Cardiac thrombi in different clinical scenarios.

Intracardiac thrombi are commonly found in patients with ischemic stroke. The echocardiographic identification of thrombi is important in decision-making since it represents an indication to long-term anticoagulation, in order to reduce the risk of new stroke. Intracardiac thrombi can develop during the time course of several cardiac pathologies that favor blood stasis and/or predispose to the aggregation of thrombotic material. Examples of cardiac pathologies that favor the formation of thrombus are illustrated and discussed.

INTRODUCTION

Intracardiac thrombi are frequent findings that cardiologists encounter in their practice. It is one of the three common differential diagnoses of intracardiac masses besides vegetation and tumors. Intracardiac thrombi are common findings in patients with ischemic stroke (up to 26% of patients with cerebrovascular events).1 It is important to recognize the appearance and features of a thrombus so that anticoagulant therapy can be instituted promptly.

Echocardiography plays a major role in detecting intracardiac masses; however, distinguishing the nature of such masses can be difficult. Careful attention to the clinical presentation of the patient as well as knowledge of echocardiographic features of the mass can lead to correct diagnosis and appropriate management.

The following six cases illustrate examples of the wide spectrum of clinical scenarios that the patients with cardiac thrombus might present.

Case no. 1

A 27-year-old Indian man presented with four months history of fatigue and exertional dyspnea. Clinical examination revealed atrial fibrillation with mid-diastolic murmur heard best at the apex. Transthoracic echo revealed severe mitral stenosis and marked dilatation of the left atrium (LA) with “smoke-like” echo in the LA cavity suggesting high possibility of LA thrombus. Transesophageal echocardiolgraphy (TEE) [Figure 1a–c] showed a large thrombus in the LA and left appendage.

Figure 1a

TEE image: Severe rheumatic mitral stenosis with significant dilatation of left atrium

Figure 1c

TEE image:Jelly-like appearance of a big thrombus attached to upper part of left atrium

TEE image: Smoke-like echo in left atrium and big thrombus occupying the left atrial appendage

Comment

LA thrombi classically reside in the atrial appendage, but can also form in the body of the LA. The presence of an enlarged chamber, atrial fibrillation, a stenotic mitral valve, low cardiac output state, and spontaneous contrast echoes, all favor blood stasis and thrombus formation.

Case no. 2

A 54-year-old woman with breast cancer and on chemotherapy through an-indwelling catheter was referred for echocardiography [Figure 2].

Figure 2a

TEE image: Bicaval view showing homogeneous mass attached to the right atrium opposite to the tip of the catheter seen in superior vena cava used for administration of chemotherapy

TEE image: Thrombus (T) in the right atrium

TEE image: Disappearance of the size of the thrombus after treatment with anticoagulation

Central venous catheters (CVC) are commonly used in clinical practice. One of foremost complications associated with their use is the potential for symptomatic or asymptomatic thrombosis. Catheter-related right atrial thrombosis (CRAT) is a rare as well as underreported but potentially life-threatening complication of CVC. Limit use of CVC for a short period, and if CVC is to be used for a longer time, keep a high index of suspicion for CRAT.[2]

In-dwelling catheter thrombus is most commonly attached to the catheter but thrombus could occur away from the catheter, on the wall of the cardiac cavity. Intracavitary right atrial thrombosis is most often considered to result from line-tip thrombosis extension. However, there are other mechanisms of thrombus formation in the setting of an in-dwelling catheter. The to and fro motion of the catheter within the right atrial cavity may produce endocardial injury, and thus predispose to thrombus formation.[3] Another hypothesis is that delivery of chemotherapeutic agent may cause “jet lesion” injury, thus setting the stage for thrombogenesis. (3).

Certain materials such as teflon or polyurethane have been reported to be particularly thrombogenic, whereas silicone catheters are biologically inert and more resistance to thrombosis. Polyurethane, a commonly used material for catheter construction, includes a broad class of thermoplastic polymers that have an intermediate level of thrombogenicity.[4]

Case no. 3

A middle-aged man presented with difficulty in breathing, chest pain and tachycardia. Blood investigation was positive for anticardiolipin antibody (ACLA) suggestive of antiphospholipid syndrome. Transthoracic echo as shown in [Figure 3].

Figure 3a

TTE image: Parasternal long axis view showing dilatation of the right ventricle

TTE image: Modified four-chamber view demonstrating multiple thrombi seen in the right ventricular cavity

TTE image: Short axis of great vessels showing occlusion of left pulmonary artery with thrombus that embolized from Right ventricle

Antiphospholipid antibodies such as ACLA that are strongly associated with thrombosis appear to be the most common of the acquired blood protein defect causing thrombosis. The precise mechanisms whereby antiphospholipid antibodies alter hemostasis to induce a hypercoagulable state remain unclear.

In patients with phospholipid syndrome, thrombus formation in the cardiac cavities and the aorta can be observed due to thrombophilia. The most common thrombotic events associated are deep vein thrombosis and pulmonary embolus, coronary or peripheral artery thrombosis, and cerebrovascular/retinal vessel thrombosis.[5] Thrombus formation in the cardiac cavities and the aorta can be observed due to thrombophilia. Thrombophilic complications originating from venous system often induce chronic pulmonary hypertension due to chronic pulmonary embolism.[6]

Most patients with antiphospholipid thrombosis syndrome will fail warfarin therapy and, except for retinal vascular thrombosis, most will fail anti-platelet therapy. Thus, it is of major importance to make this diagnosis so that patients can be treated with the most effective therapy for secondary prevention: Low-molecular weight heparin (LMWH) or unfractionated heparin (UHF).[5]

Case no. 4

A 50-year-old man with two weeks history of massive anterolateral myocardial infarction (MI), admitted with ischemic stroke. Transthoracic echo revealed big thrombus in the LV [Figure 4].

Figure 4

TTE four chamber apical view showing dilated left ventricle with aneurysmal apex and a large well-defined thrombus attached to it

Ventricular thrombi formation usually occurs in the early phase of anterior myocardial infarction or poorly contracting ventricles. They are most often located in the LV apex in association with anterior and large infarcts, with reported incidence of 10-40%. Several echo features of LV thrombus must be evaluated including the shape (mural or protruding) within the cavity, the the motion, which may be fixed or mobile, and size. A higher risk of embolization is attributable to larger thrombus size and/or thrombi, which are mobile and protrude into LV chamber. After diagnosis, echocardiographic follow-up is needed until thrombus eradication is obtained using anticoagulants.

Apical abnormalities can be difficult to visualize because native tissue harmonic echocardiography is weak at near field. Contrast opacification facilitates the identification of apical abnormalities; hence, contrast echocardiography is now recognized as the technique of choice for establishing or excluding the presence of LV apical thrombus, and assists in the differential diagnosis with other apical abnormalities such as apical hypertrophic cardiomyopathy, LV non-compaction, and ventricular pseudoaneurysm.[7]

Case no. 5

A 22-year-old man with prosthetic mitral valve (MV) replacement secondary to rheumatic heart disease presented with picture of acute heart failure after two weeks from stopping his warfarin treatment [Figure 5].

Figure 5

TEE images. Restricted motions of both leaflets with two echogenic masses attached to the medial and lateral part of the sewing ring of the mitral valve prosthesis indicative of thrombi (arrows). Spontaneous contrast on the significantly dilated left atrium with color Doppler showing obstruction of mitral prosthesis

The incidence of prosthetic valve obstruction has been estimated at 0.1 to 0.4% per year, depending on valve size, type, location, and adequacy of anticoagulation. Obstruction of a mitral mechanical prosthesis is caused more frequently by thrombus whereas obstruction of an aortic mechanical prosthesis is caused more frequently by pannus formation. When a prosthetic valve becomes obstructed, it is difficult to quantify the restriction of excursion with surface 2D echocardiography. TEE may be able to visualize normal and abnormal motion of a prosthetic valve. The most accurate method for detecting and quantifying the degree of prosthetic obstruction is Doppler echocardiography.[8]

Case no. 6

A 50-year-old man, smoker, was admitted with stroke. MRI showed occluded distal vertebral artery. Transthoracic echo showed no abnormality, however, TEE showed thrombus in the aortic arch [Figure 6a], which resolved with anticoagulation.

Figure 6a

TEE image: Two thrombi seen in the aortic arch

TEE image: Complete disappearance of the two thrombi after two weeks of anticoagulation treatment. Thrombophilia screen was found to be positive in this patient

Atheroma prevalence increases with age, smoking and hypertension. Atherosclerotic plaques and debris are common findings in elderly patients. Aortic atheromas are characterized by irregular intimal thickening of at least 2 mm, with increased echogenicity. Aortic plaques usually are irregularly shaped and frequently mobile. They often have superimposed mobile components, chiefly thrombi. Atheromatous plaques of 4 mm or more in thickness are more likely to cause an embolic event. TEE is the imaging modality of choice for diagnosing aortic atheromas.[9]

The risk of stroke has been shown to be significantly higher in patients with atherosclerotic disease of the aorta. Warfarin is effective in preventing stroke in this population.[10]

CONCLUSIONS

Some cardiac masses are suspected from the clinical presentation of the patient and others are incidental findings. Cardiac masses can be classified as a cardiac tumor, thrombus, vegetation, iatrogenic material, normal variant or extracardiac structure. These masses can usually be differentiated by their size, shape, location, mobility, and attachment site as well as by their clinical presentation. Accurate diagnosis is crucial because misinterpretation may lead to an incorrect management strategy, including an unnecessary surgical procedure.[8]

Intracardiac sources of cerebrovascular ischemic events are increasingly being recognized. Echocardiography is the ideal tool for diagnosis and assessment of cardiac thrombi. TEE has been shown to be a superior method for the identification of most cardiac sources of emboli.[11]

A thrombus is identified as a discrete echo-dense mass with well-defined borders that are distinct from the endocardium and seen throughout systole and diastole. The morphology and structure of thrombi have been assessed carefully, since dimensions, shape, regularity or irregularity and homogeneity are all characteristics features that define the embolic risk and therapeutic management.