The Role of Echocardiography in the Management of the Sources of Embolism

Roberta Esposito; Rosa Raia; Daniela De Palma; Ciro Santoro; Maurizio Galderisi


Future Cardiol. 2012;8(1):101-114. 

In This Article

Conditions Predisposing to Embolism

Patent Foramen Ovale

PFO – the congenital persistence of a slit-like communication between left atrium and right atrium in the cranial portion of the fossa ovalis – is present in 25–50% of the overall adult population.[5] This communication is virtual because two membranes, septum secundum (on the right side) and septum primum (on the left side of the fossa ovalis) remain attached one another by normal positive left-to-right atrial pressure gradient. However, if right atrial pressure exceeds LA pressure – as happens in the presence of chronic or acute pulmonary arterial hypertension or even in healthy subjects during the strain phase of Valsalva maneuver – a right to left shunt occurs generating a true small atrial septal defects. In some patients this abnormality is associated with an atrial septal aneurysm (ASA), echocardiographically corresponding to a fixed or mobile displacement of the fossa ovalis region of atrial septum towards the left atrium, right atrium or both, exceeding 10 mm from the mid-line (a line from the basal interventricular septum to the insertion of the septum secundum to atrial wall) (Figure 8).[41] ASA may act as a 'net', capturing thrombi and conveying them to the PFO when it is present (ASA may be present even without PFO). Although the demonstration that the PFO is the origin of unexplained stroke remains challenging and the PFO closure has been questioned recently, a statistical association of cryptogenic stroke (especially in young patients) with PFO[42–44] – and also with an additional ASA[45] – has been documented. In addition, large provokable right-to-LA shunts have a stronger association with neurological events than small shunts.[46] These findings can be explained on the basis of a paradoxical embolism of venous thrombi through the PFO. For these reasons, in relatively young patients (<55 years) with ischemic neurological events, a search for the presence of PFO is required and if PFO is found, the therapeutic options are either anticoagulation or PFO device closure. A well-defined diagnostic journey of PFO should include the following sequential steps:

Figure 8.

Representation of five different types of atrial septum aneurysm.
The classification is based on septal bulging modality. Type 1R: the aneurysm bulges into the right atrium; Type 2L: the aneurysm bulges into the left atrium; Types 3RL and 4LR: bilateral excursions are present, but the maximal bulging occurs into the right atrium or left atrium, respectively; Type 5: bilateral excursions with equal bulging into the right and left atrium occur.
Modified from [41].

  • Preliminary transcranial Doppler, which provides the first clue of a right to left shunt by detecting intravenous microbubbles (agitated solution) in the midcerebral artery after intravenous fluid injection. The sensitivity of this technique is >90% but its specificity is variable (65–90%);[47–50]

  • Direct color Doppler detection of passage between the two atria in the fosse ovalis by TTE or TEE;

  • If color Doppler is not diagnostic, detection of intravenous microbubbles (agitated solution, saline–blood mixture or contrast agents) passage from the right atrium to left atrium, either spontaneously or after a Valsalva maneuver.[51] The number of bubbles crossing the atrial septum could be indicative of the shunt magnitude. Limitations of this method include however the fact that the number of bubbles injected is influenced by the pressure difference between right and left atrium and the lack of standardization for Valsalva maneuver.

TEE is the gold standard for PFO detection (sensitivity: 89%; specificity: 100%)[52] but TTE with harmonic imaging may have similar diagnostic accuracy (sensitivity: 90.5%; specificity: 96.5% if TEE is considered to be the gold standard) when the imaging quality is adequate.[53,54] Recent studies have demonstrated that real time 3D echocardiography (RT3DE) can avoid the underestimation of area of complex-shaped atrial septal defects own of TEE[55] and is a clinically useful, complementary option to 2D TEE for interventional guidance.[56]

Aortic Atherosclerosis

Despite some controversies,[57] aortic atherosclerosis has been demonstrated to be an important risk factor for the development of embolic events.[57–60] Aortic atheromas are characterized by echo-derived irregular intimal thickening ≥2 mm. Morphologically atheromas can be classified as either simple or complex plaques, the latter ulcerating and disrupting the elastic internal lamina and burrowing into and beyond the aortic media. Although TTE is diagnostic in 84% of aortic arch atherosclerosis,[60] TEE remains the best imaging modality since it characterizes the plaque by measuring plaque thickness (≥4 mm is associated with a high embolic risk)[58] and identifies ulceration, calcification and superimposed mobile thrombi (i.e., the embolic potential of each plaque). A grading system is used to classify aortic atherosclerosis:

  • Grade I: intimal thickening <4 mm

  • Grade II: diffuse intimal thickening ≥4 mm

  • Grade III: atheromas <5 mm

  • Grade IV: atheromas >5 mm

  • Grade V: any mobile atheromas [61]

TEE identification of large mobile thrombi is important, since they can lead to systemic emboli.[62] The optimal management of this complication remains, however, undefined: anticoagulants and statins can be useful but surgical removal could be taken in consideration if embolic events are recurrent.

Mitral Valve Prolapse

Mitral valve prolapse (2% of the general population, more frequent in women) is evident in a third of patients <35 years with cerebral ischemia and myxomatous degeneration of the mitral valve itself can be considered as a risk factor for stroke.[5] Mechanisms predisposing to stroke in mitral prolapse include possible formation of platelet-fibrin thrombi on the surface of redundant mitral leaflets and embolization.

Mitral Valve Calcification

Although the Framingham Heart Study demonstrated a twofold increase of stroke in this clinical setting,[63] mitral valve calcification has to be taken into account as a generic cause of stroke. Mobile plaques, clearly identifiable by both TTE and TEE, represent truly embolic sources.

Calcified Aortic Stenosis

Embolic complications are very uncommon in patients with calcified aortic valve but TTE or TEE may rarely identify mobile plaques on the surface of the aortic cusps and/or at the annular level which can represent potential sources of embolism.[5]


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