Presentation on theme: "Echocardiography in the Evaluation of Intracardiac Sources of Embolism"— Presentation transcript:
1 Echocardiography in the Evaluation of Intracardiac Sources of Embolism Airley E. Fish, MDImaging ConferenceWednesday May 13, 2009
2 Introduction Intracardiac sources of CVA TEE Account for k of 500k strokes/year in U.S.TEESearch for source of cardiac emboli is the leading clinical indication for TEEMore cost effective than TTESuperior to TTE for most cardiac sources of emboliExceptionsAssessment of LV systolic functionIdentification of LV apical thrombi
3 Superiority of TEE vs TTE Pearson et al 1991 in JACC79 patients with cryptogenic strokeTEE ID’ed source in 57%TTE ID’ed source in only 15%Rauh et al 1996 in Stroke30 patients with CVA and low-risk for embolismSinus rhythmNo cardiac disease related to embolismMinimal carotid artery stenosisTTE showed no embolic sourcesTEE showedAortic plaques in 19PFO in 7LAA thrombus in 3Atrial septal aneurysm in 2
4 Major Sources of Emboli MassesLA/LV ThrombiAtherosclerotic plaquesVegetationsTumorsPropensity for Thrombus FormationLA spontaneous echo contrastMACPassageways for Paradoxical EmbolismPFO/ASD
5 Major Cardioembolic Sources Aortic Atherosclerotic PlaquesAtrial myxomaLA Thrombus-Atrial fibrillation-Sustained atrial flutterPFO/ASDRheumatic Mitral (MAC) or Aortic Valve DiseaseLA SpontaneousEcho ContrastLV Thrombus-Recent AMI-EF < 30%Mechanical or Bioprosthetic ValveVegetationsTumors
6 Most Common Sources of Emboli LA ThrombiLA Spontaneous Echo ContrastAortic AtherosclerosisLV ThrombiProsthetic Valve ThrombiAbnormalities of the Interatrial Septum
7 LA Thrombi Account for 45% of cardiogenic thromboemboli Manning et al 1995, Annals of Internal MedicineIntraoperative visualization vs TEE LA/LAASensitivity and specificity TEE 100%, 99%TTE LA/LAASensitivity and specificity TTE 39%, 65%Most often associated withAtrial fibrillation and/orRheumatic mitral stenosis
8 LA Thrombi – AF vs NSR Leung et al 1997, Am Journal of Cardiology 2894 patients underwent TEE for various indications94/2894 patients with LA thrombus83/94 in AFStoddard et al 1995, J American College of CardiologyTEE looking for LA thrombus in patients with AFAcute AF - 14% with thrombusChronic AF – 27% with thrombusAF and clinical thrombus - 43% with thrombus (?up to 57% with migration)Omran et al 2000, American Heart Journal869 patients with embolic CVA or TIAIf NSR, no MV disease, and normal LA functionOnly 1% with LA thrombusTherefore, routine TEE in sub-population not recommended
10 LA ThrombiFIGURE In a patient with untreated rheumatic heart disease, a very large LA thrombus (arrows) is seen. The RA is also severely dilated.
11 LAA ThrombiFIGURE TEE image of the left atrial appendage (LAA) in a patient with rheumatic MS and a LAA thrombus. Irregular echo density mass filling the LAA (thin arrows). Boundary of the wall of the LAA is as noted by the heavier arrows.
12 LA ThrombiFIGURE A, B: Thrombus straddling the interatrial septum through a PFO and extending into the LA (small arrows). Thrombus was highly mobile & likely originated in the lower extremities. Increased mobility of atrial septal tissue indicated by large arrow.
14 LA Spontaneous Echo Contrast (SEC) “Smoke-like” echoes seen within LA during TEEMost common TEE finding in work up of thrombus sourceEspecially if AF or LAEMay also be seen in NSR26/1288 with SEC3/26 with LA thrombus (LAE, decreased LAA emptying velocity)2º RBC aggregation in low shear rate conditionsRBC aggregation mediated by plasma proteinsParticularly fibrinogenPromote RBC rouleaux formation (via elimination of normal negative electrostatic forces of RBC’s aggregation)Increased plasma fibrinogen levelsHypercoagulable state – Mitral stenosis>2/3 patients with MS have TEE e/o SECAtrial blood stasisIncreased LA levels of prothrombin 1 and 2 (procoagulants)MR may spontaneous echo contrast frequency
15 LA Spontaneous Echo Contrast FIGURE TEE in a patient with rheumatic MS, LAE, and marked stasis of the blood within the LA and LAA. In the real-time image, the stasis of the blood appears as a dense swirling cloud of “smoke'' filling the LA and LAA.
16 LA Spontaneous Echo Contrast FIGURE Expanded view of the LAA in a patient with AF. No distinct thrombus but vague swirling smoke-like echoes suggesting stagnant blood in the body of the LAA.
17 LA Spontaneous Echo Contrast FIGURE Small thrombus within the LAA
18 Aortic Atherosclerosis TEE sensitive for visualization of aortic intimaCT/MRI experience limited, cannot characterize plaque mobilityAortic atherosclerotic plaques source ofThromboemboli (relatively common)Unstable atherosclerotic plaque, superimposed thrombi embolizeTend to be single, lodge in small or medium arteriesOften resulting in CVA/TIACan also result in limb and organ (kidney, GI, etc.) ischemiaAtheroemboli/Cholesterol Emboli (fairly rare)Arterio-arterial embolism of small pieces of atheromatous materialMultiple small artery occlusions tissue/organ damageIschemic digits, retinal ischemia, intestinal infarction, etc.Patients withUnexplained CVATIAArterial embolization
20 Aortic Atherosclerosis: Thromboembolism Postmortem specimen of a terminal aorta with a thromboembolus from a cat with HCM and an acute onset of caudal limb pain and paresis. Thromboembolus lodged at the terminal aorta ("saddle" thromboembolus), with portions extending into the external iliac arteries
24 Aortic Atherosclerosis: Thromboembolism FIGURE Suprasternal notch TTE in a patient with atheromatous involvement of the proximal descending thoracic aorta. Notice the relatively normal aortic arch (Ao) and the distinct echo density protruding into the lumen of the proximal descending thoracic aorta that represents focal pedunculated atheroma.
25 Aortic Atherosclerosis: Thromboembolism FIGURE 20.51A. TEE in short-axis view of the descending thoracic aorta. Note the relatively circular aorta into which there is marked protrusion by pedunculated atheroma
26 Aortic Atherosclerosis: Thromboembolism FIGURE TEE recorded in the longitudinal plane of a descending thoracic aorta with aneurysm. The arrows outline the external boundary of the aorta with all space in between representing an aneurysm with complex atheroma. Note the markedly complex atheroma with multiple pedunculated and mobile components filling the dilated lumen.
27 Aortic Atherosclerosis: Thromboembolism Treat for 2º prevention of CVD ifComplex aortic plaque (regardless of CVA/peripheral embolism)or Simple aortic plaque and unexplained CVA/peripheral embolism2º Prevention of CVDAspirin (or other antiplatelet agents) – ARCH trial underway in EuropeIf CVA and plaque > 4 mm and/or mobile?Warfarin with goal INR statin?Aspirin 325 mg PO q day + statinIf no CVA and plaque mobileIf no CVA and plaque > 4 mmStatins (recommend same goal as for known CAD, no RCT’s to date)Blood pressure controlSmoking cessationIf diabetic, glycemic control
28 Aortic Atherosclerosis: Thromboembolism Possible benefit of aortic arch replacementProphylactic atherectomy ? ‘ed CVA riskUndergoing cardiac surgery considerIntraoperative U/S to guide aortic manipulation sitesUse of off-pump CABG may be beneficialCross-clamping & performance of proximal anastamosis may risk of embolization 2º mechanical disruption
31 Aortic Atherosclerosis: Cholesterol Emboli Light micrograph of an atheroembolus in a muscular renal artery showing cleft-like spaces (arrow) due to washout of the cholesterol crystals during histologic processing
32 Aortic Atherosclerosis: Cholesterol Emboli TEE descending thoracic aortaMassive atherosclerotic plaqueImages on the right (1A, 2A, 3A) taken 1-2 seconds after their respective pictures on the leftArrows point to small particles of embolic material moving intransit in the aortic lumenPatient died fromIntestinal infarctionRenal failure
33 Aortic Atherosclerosis: Cholesterol Emboli Risk factors for atheroembolic diseaseAgeSmokingHypercholesterolemiaHypertensionAgmon et al 2000, in CirculationPopulation-based study of those with aortic plaqueOdds of complex plaque increased as ambulatory SBP increasedOR 1.43 for each 10 mmHg increaseObesityDiabetesCRP
34 Aortic Atherosclerosis: Cholesterol Emboli Often blamed on Rx with anticoagulant drugs?plaque hemorrhage as precipitantTunick et al 2002, in Am J Cardiology519 with severe aortic plaqueCholesterol emboli in only 5/519 over > 3 yearsNo difference between anticoagulation and events2/206 on warfarin3/313 off warfarin
35 Aortic Atherosclerosis: Cholesterol Emboli 2º Prevention of CVDAspirin (or other antiplatelet agents)Statins (same goal as for 2º CAD, no RCT’s to date)?Lower LDL?Pleotrophic effects of plaque stabilizationIn above retrospective trial of 519 patients, statins associated with a significantly lower rate of recurrent CVA & thromboembolismBlood pressure controlSmoking cessationIf diabetic, glycemic control
36 LV Thrombi – Background & Incidence Among most common complications of STEMIDependent upon infarct location and sizeLarge, anterior STEMI’sAneurysm formation and akinesis or dyskinesisReduced LVEFIncreased WMA’sDevelop early (within 2 weeks, median 5 days), embolization within 1st 4 monthsIncidence in reperfusion era – (predominantly thrombolytic therapy)8326 patients GISSI-3 databaseLV thrombus 5.1%, overallAnterior infarct 11.5% with LV thrombusOther infarcts 2.3% with LV thrombusMay be underestimate (excluded severe CHF and SBP < 100 mmHg)Incidence in reperfusion era – (primary PCI)163 patientsLV thrombus 4.3%, overallAnterior infarct 10.4% with LV thrombusOther infarcts 0% with LV thrombus
37 LV Thrombi – Incidence and Risk Factors In reperfusion era (incidence decreasing)LV aneurysm 8-15% of Q wave infarctionsMural thrombus ID’ed in >50% of these casesTwo factors contribute to clot formationStasis of flow in aneurysm cavityContact of blood with fibrous tissue in aneurysm (rather than normal endocardium)
38 LV Thrombi - DiagnosisTTE is a Class I indication for assessment of mural thrombus after acute STEMIPresence of thrombusRisk factors for embolization
39 LV Thrombi - Appearance Thrombus appearanceVery fresh/redProtrude into cavity centerHighly mobileDifficult to differentiate from effect of slowly moving cavitary blood seen within LV aneurysms (highly reflective, luminescent)OlderSmooth cavitary surface (resemble liver tissue)Less likely to change or embolize
40 LV Thrombi – Risk for Embolization High risk for embolizationMobile thrombiEmbolization in 26/119 with LV thrombus s/p STEMIFree mobility in 58% of patients with embolization15/18 patients with free mobility (83% vs 11%) embolizedFree mobility in 3% of patients without embolizationProtruding thrombi (into LV cavity)Protrusion in 88% of patients with emboli23/40 patients with protruding thrombi embolized (58% vs 4%)Protrusion in 18% of patients without emboli
41 LV Thrombi - Prevention ACE-I thought to result in fewer LV thrombi via preservation of LVEF and wall motionNo difference in patients on/off lisinopril in GISSI-3Short-term (10 days)Unfractionated Heparin vs Heparin SQOut of 221 patients, LV thrombus in 11% vs 32%2004 ACC/AHA STEMI guidelinesWarfarin reasonable with severe LV dysfxn/WMA’s for the prevention of LV thrombus formation
42 LV Thrombi – Embolization Prevention No RCT’sWarfarin reduces risk of embolizationMay prevent thrombus extensionMay prevent thrombus endothelializationMay not promote thrombus resolution2004 ACC/AHA STEMI guidelines - LV thrombusWarfarin 3-6 monthsIndefinitely, if no increased risk of bleeding2006 AHA/ASA – prevention of ischemic CVAWarfarin 3 months – 1 yearGoal INR 2-3Also recommend concurrent ASA Rx for 2º preventionConsider increased risk of bleeding in PCI (triple Rx)
43 LV ThrombiFIGURE Apical view in a patient with a vague echo density on noncontrast imaging. After IV injection of a perfluorocarbon-based agent, a distinct spherical filling defect is noted in the apex, consistent with a pedunculated apical thrombus
44 LV ThrombiFIGURE Apical four-chamber view recorded in a patient with an acute anterior apical MI and early thrombus formation. Note the regional dilation of the LV at the apex and the pedunculated, multilobulated mass protruding into the cavity of the LV.
45 LV ThrombiFIGURE Apical four-chamber view recorded in a patient with an acute anteroapical MI and a pedunculated, slightly mobile apical thrombus
46 LV ThrombiFIGURE Apical two-chamber view recorded in a patient with an anteroapical MI & multiple large pedunculated & mobile thrombi. Note multiple masses protruding into the cavity of the LV apex & the mobile nature of these thrombi in the real-time image.
47 Prosthetic Valve Thrombi Common in patients with mechanical valvesEspecially if mitral/tricuspid valves (“low-flow”)Especially if suboptimal anticoagulationGoal INRBest evaluated by TEEAlthough often assumed clinicallyNo other obvious causeSub-therapeutic INRConfirmatory, but doesn’t change RxUnless valvular dysfunction 2º to a massive thrombus
48 Prosthetic Valve Thrombus – Aorta FIGURE 14.39A. Even a small thrombus, if properly located, can result in obstruction. A: A St. Jude aortic prosthesis is shown. A thrombus was not visualized. B: Color Doppler imaging demonstrates increased turbulence and significant aortic regurgitation (arrow). C: From the transthoracic study, a peak pressure gradient of 95 mm Hg confirms the presence of significant obstruction.
49 Prosthetic Valve Thrombus – Mitral FIGURE 14.37A. In this example, a large thrombus was visualized on transthoracic (A) imaging. The thrombus can be seen on the LA aspect of the mitral prosthesis.
50 Abnormalities of the Interatrial Septum Thromboemboli via 2 mechanismsR L shunting via PFO/ASDInteratrial septal aneurysm
51 PFO/ASD Echocardiography with contrast (IV saline) RestCoughValsalvaAlternatively, transmitral Doppler with contrast
52 PFOFIGURE Contrast injection demonstrates a PFO on TEE. In this case, increased mobility of the atrial septum is present. The tunnel-like gap within the interatrial septum is evident, and bubbles can be seen traversing the PFO from right to left.
53 PFOFIGURE A TEE of the interatrial septum demonstrates a small PFO using color Doppler imaging.
54 PFOFIGURE 21.42A. A large, tubular-shaped thrombus demonstrated as it crosses a PFO. The shape of the thrombus suggests that it was formed within the veins of the lower extremities. Its presence within the left heart greatly increases the likelihood of systemic embolization.
55 ASDFIGURE Contrast echocardiography can be used to demonstrate intracardiac shunting through an ASD. In this example, sequential images after IV contrast injection demonstrate the appearance of bubbles in the right heart.
56 ASDFIGURE 18.52A&B. A secundum ASD is detected during TEE. A: The location and size of the defect are evident. B: Color Doppler imaging reveals flow predominantly from the LA to the RA
57 ASDFIGURE TEE recorded after placement of an atrial septal closure device. IV contrast has been injected to confirm the lack of persistent shunting.
58 Atrial Septal Aneurysm (ASA) Congenital malformation2º redundant atrial septal tissueTypically involving the region of the fossa ovalisPrevalence 0.5% via TTE, up to 5% via TEEEmbolic events viaAssociated PFODirect thrombus formation in the aneurysm’s neck
59 Atrial Septal Aneurysm (ASA) FIGURE 21.53A. An example of an atrial septal aneurysm is shown. A: The aneurysm billows into the LA. B: The redundant tissue billows into the RA. Injection of contrast into the right heart confirms an associated PFO by demonstrating right-to-left shunting.
60 Atrial Septal Aneurysm (ASA) FIGURE A: An apical four-chamber view demonstrates an extreme form of an atrial septal aneurysm with a “windsock'' appearance of the aneurysmal tissue into the right atrium and partially through the tricuspid valve.
61 Atrial Septal Aneurysm (ASA) FIGURE B: After contrast agent injection, the windsock is outlined by the contrast that flows around it from the RA to the RV. In addition, the presence of a PFO allows some contrast agent to cross into the left heart.
62 Atrial Septal Aneurysm (ASA) Retrospective studies in patients with CVAApproximately 10% with atrial septal aneurysmProspective trial in ASA suggests CVA risk low846 patients undergoing TEE during cardiac surgery4.9% with incidental finding of ASA56% with a patent aneurysm67% of those with a patent aneurysm rx’ed with aspirinNo CVA’s or systemic embolization in 70 months
63 PFO/ASD Conflicting Data Association between paradoxical emboli & cryptogenic CVA well established in patients < 55, less so if > 55Meta-analysis of case control studiesPFO (OR 3.1 <55, OR 1.3 >55)ASD (OR 6.1 <55, OR 3.4 >55)Both (OR 15.6 <55, OR 5.1 >55)Population-based studiesNo statistically significant association between risk of 1st CVA & presence of a PFOProspective studiesPresence of a PFO alone is NOT associated with an risk of recurrent CVA in patients with cryptogenic strokePFO + Interatrial septal aneurysm may CVA risk
64 PFO/ASD Rx for 2º Prevention of CVA No RCT’s completedInsufficient evidence for surgical/percutaneous vs medical managementRisk reduction strategiesHTN, hyperlipidemia (statins), antiplatelet RxGeneral measuresAvoid Valsalva (transient R-L shunting)Prevention of DVT (body positions that provoke)
65 PFO/ASD Rx for 2º Prevention of CVA Isolated PFO (? in recurrent CVA)Antiplatelet agent (Aspirin 81 vs 325, no dose RCT’s)Percutaneous closure of PFO in recurrent cryptogenic CVA despite warfarin approved in 2001 under HDE, but > 4000 patients would have qualified so approval withdrawn in 2006PFO+ASA (? in recurrent CVA < 55, Ø death)Conflicting data for antiplatelet/warfarin (? Ø difference)Warfarin if felt to be at high risk for recurrence or if DVTIsolated ASA (10 pts in French study on ASA, no repeat CVA)Warfarin if CVA associated with DVTConsider surgical excision if recurrence on antiplatelet/anticoagulation