Echocardiography in the Evaluation of Intracardiac Sources of Embolism Airley E. Fish, MD Imaging...

Echocardiography in the Echocardiography in the Evaluation of Evaluation of

Intracardiac Sources of Intracardiac Sources of EmbolismEmbolism

Airley E. Fish, MDAirley E. Fish, MD

Imaging ConferenceImaging Conference

Wednesday May 13, 2009Wednesday May 13, 2009

IntroductionIntroduction Intracardiac sources of CVAIntracardiac sources of CVA

– Account for 75-100k of 500k strokes/year in U.S.Account for 75-100k of 500k strokes/year in U.S.

TEETEE– Search for source of cardiac emboli is the Search for source of cardiac emboli is the

leading clinical indication for TEEleading clinical indication for TEE– More cost effective than TTEMore cost effective than TTE– Superior to TTE for Superior to TTE for most most cardiac sources of cardiac sources of

emboliemboli ExceptionsExceptions

– Assessment of LV systolic functionAssessment of LV systolic function– Identification of LV apical thrombiIdentification of LV apical thrombi

Superiority of TEE vs TTESuperiority of TEE vs TTE Pearson et al 1991 in JACCPearson et al 1991 in JACC

– 79 patients with cryptogenic stroke79 patients with cryptogenic stroke TEE ID’ed source in 57%TEE ID’ed source in 57% TTE ID’ed source in only 15%TTE ID’ed source in only 15%

Rauh et al 1996 in StrokeRauh et al 1996 in Stroke– 30 patients with CVA and low-risk for embolism30 patients with CVA and low-risk for embolism

Sinus rhythmSinus rhythm No cardiac disease related to embolismNo cardiac disease related to embolism Minimal carotid artery stenosisMinimal carotid artery stenosis

– TTE showed TTE showed nono embolic sources embolic sources

– TEE showedTEE showed Aortic plaques in 19Aortic plaques in 19 PFO in 7PFO in 7 LAA thrombus in 3LAA thrombus in 3 Atrial septal aneurysm in 2Atrial septal aneurysm in 2

Major Sources of EmboliMajor Sources of Emboli MassesMasses

– LA/LV ThrombiLA/LV Thrombi– Atherosclerotic plaquesAtherosclerotic plaques– VegetationsVegetations– TumorsTumors

Propensity for Thrombus FormationPropensity for Thrombus Formation– LA spontaneous echo contrastLA spontaneous echo contrast– MACMAC

Passageways for Paradoxical EmbolismPassageways for Paradoxical Embolism– PFO/ASDPFO/ASD

Major Cardioembolic SourcesMajor Cardioembolic Sources

LA Thrombus-Atrial fibrillation-Sustained atrial flutter

LV Thrombus-Recent AMI-EF < 30%

Atrial myxoma

Aortic Atherosclerotic Plaques

LA SpontaneousEcho Contrast

PFO/ASD

Mechanical or Bioprosthetic Valve Vegetations

Tumors

Rheumatic Mitral (MAC) or Aortic Valve Disease

Most Common Sources of Most Common Sources of EmboliEmboli

LA ThrombiLA Thrombi

LA Spontaneous Echo ContrastLA Spontaneous Echo Contrast

Aortic AtherosclerosisAortic Atherosclerosis

LV ThrombiLV Thrombi

Prosthetic Valve ThrombiProsthetic Valve Thrombi

Abnormalities of the Interatrial Abnormalities of the Interatrial SeptumSeptum


Account for 45% of cardiogenic Account for 45% of cardiogenic thromboembolithromboemboli

Manning et al 1995, Annals of Internal Manning et al 1995, Annals of Internal MedicineMedicine– Intraoperative visualization vs TEE LA/LAA Intraoperative visualization vs TEE LA/LAA

Sensitivity and specificity TEE 100%, 99%Sensitivity and specificity TEE 100%, 99%

– TTE LA/LAA TTE LA/LAA Sensitivity and specificity TTE 39%, 65%Sensitivity and specificity TTE 39%, 65%

Most often associated withMost often associated with– Atrial fibrillation Atrial fibrillation and/orand/or– Rheumatic mitral stenosis

LA Thrombi – AF vs NSRLA Thrombi – AF vs NSR

Leung et al 1997, Am Journal of CardiologyLeung et al 1997, Am Journal of Cardiology– 2894 patients underwent TEE for various indications2894 patients underwent TEE for various indications– 94/2894 patients with LA thrombus94/2894 patients with LA thrombus– 83/94 in AF83/94 in AF

Stoddard et al 1995, J American College of CardiologyStoddard et al 1995, J American College of Cardiology– TEE looking for LA thrombus in patients with AFTEE looking for LA thrombus in patients with AF

Acute AF - 14% with thrombusAcute AF - 14% with thrombus Chronic AF – 27% with thrombusChronic AF – 27% with thrombus AF and clinical thrombus - 43% with thrombus (?up to 57% with AF and clinical thrombus - 43% with thrombus (?up to 57% with

migration)migration)

Omran et al 2000, American Heart JournalOmran et al 2000, American Heart Journal– 869 patients with embolic CVA or TIA869 patients with embolic CVA or TIA– If NSR, no MV disease, and normal LA functionIf NSR, no MV disease, and normal LA function

Only 1% with LA thrombusOnly 1% with LA thrombus Therefore, routine TEE in sub-population not recommended Therefore, routine TEE in sub-population not recommended


FIGURE 21.34. In a patient with untreated rheumatic heart disease, a very large LA thrombus (arrows) is seen. The RA is also severely dilated.

LAA ThrombiLAA Thrombi

FIGURE 11.32. 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.


FIGURE 21.41. 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.

LA Spontaneous Echo Contrast LA Spontaneous Echo Contrast (SEC)(SEC)

““Smoke-like” echoes seen within LA during TEESmoke-like” echoes seen within LA during TEE– Most common TEE finding in work up of thrombus sourceMost common TEE finding in work up of thrombus source

EspeciallyEspecially if AF or LAE if AF or LAE May also be seen in NSR May also be seen in NSR

– 26/1288 with SEC26/1288 with SEC– 3/26 with LA thrombus (LAE, decreased LAA emptying velocity)3/26 with LA thrombus (LAE, decreased LAA emptying velocity)

– 22º º RBC aggregation in low shear rate conditionsRBC aggregation in low shear rate conditions– RBC aggregation mediated by plasma proteinsRBC aggregation mediated by plasma proteins

Particularly fibrinogen Particularly fibrinogen Promote RBC rouleaux formation (via elimination of normal negative Promote RBC rouleaux formation (via elimination of normal negative

electrostatic forces of RBC’s aggregation)electrostatic forces of RBC’s aggregation)– Increased plasma fibrinogen levelsIncreased plasma fibrinogen levels– Hypercoagulable state – Mitral stenosisHypercoagulable state – Mitral stenosis

>2/3 patients with MS have TEE e/o SEC>2/3 patients with MS have TEE e/o SEC Atrial blood stasisAtrial blood stasis Increased LA levels of prothrombin 1 and 2 (procoagulants)Increased LA levels of prothrombin 1 and 2 (procoagulants)

MR may spontaneous echo contrast frequencyMR may spontaneous echo contrast frequency


FIGURE 11.30. 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.


FIGURE 22.48. 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.


FIGURE 21.39. Small thrombus within the LAA

Aortic AtherosclerosisAortic Atherosclerosis TEE sensitive for visualization of aortic intimaTEE sensitive for visualization of aortic intima

– CT/MRI experience limited, cannot characterize plaque mobilityCT/MRI experience limited, cannot characterize plaque mobility

Aortic atherosclerotic plaques source ofAortic atherosclerotic plaques source of

– Thromboemboli (relatively common)Thromboemboli (relatively common) Unstable atherosclerotic plaque, Unstable atherosclerotic plaque, superimposed thrombi embolizesuperimposed thrombi embolize Tend to be single, lodge in small or medium arteriesTend to be single, lodge in small or medium arteries Often resulting in CVA/TIAOften resulting in CVA/TIA Can also result in limb and organ (kidney, GI, etc.) ischemiaCan also result in limb and organ (kidney, GI, etc.) ischemia

– Atheroemboli/Cholesterol Emboli (fairly rare)Atheroemboli/Cholesterol Emboli (fairly rare) Arterio-arterial Arterio-arterial embolism of small pieces of atheromatous materialembolism of small pieces of atheromatous material Multiple small artery occlusions tissue/organ damageMultiple small artery occlusions tissue/organ damage Ischemic digits, retinal ischemia, intestinal infarction, etc.Ischemic digits, retinal ischemia, intestinal infarction, etc.

Patients withPatients with– Unexplained CVAUnexplained CVA– TIATIA– Arterial embolizationArterial embolization

Aortic Atherosclerosis: Aortic Atherosclerosis: ThromboembolismThromboembolism


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


Thoracic aortic plaque/plaque mobility – Thoracic aortic plaque/plaque mobility – TEETEE

Complex aortic plaqueComplex aortic plaque– >> 4 mm thick (more likely to be lipid-laden) 4 mm thick (more likely to be lipid-laden)– MobileMobile– UlceratedUlcerated– PedunculatedPedunculated


FIGURE 20.49. 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.

Aortic Atherosclerosis: Aortic Atherosclerosis: Thromboembolism 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

Aortic Atherosclerosis: Aortic Atherosclerosis: Thromboembolism Thromboembolism

FIGURE 20.52. 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.


Treat for 2Treat for 2º prevention of CVD if º prevention of CVD if – Complex aortic plaque (regardless of CVA/peripheral embolism)Complex aortic plaque (regardless of CVA/peripheral embolism)– or or Simple aortic plaque Simple aortic plaque andand unexplained CVA/peripheral unexplained CVA/peripheral

embolismembolism

22º Prevention of CVDº Prevention of CVD– Aspirin (or other antiplatelet agents) – ARCH trial underway in Aspirin (or other antiplatelet agents) – ARCH trial underway in

EuropeEurope If CVA and plaque If CVA and plaque >> 4 mm and/or mobile 4 mm and/or mobile

– ?Warfarin with goal INR 2-3 + statin?Warfarin with goal INR 2-3 + statin– ?Aspirin 325 mg PO q day + statin?Aspirin 325 mg PO q day + statin

If no CVA and plaque mobileIf no CVA and plaque mobile– ?Warfarin with goal INR 2-3 + statin?Warfarin with goal INR 2-3 + statin

If no CVA and plaque If no CVA and plaque >> 4 mm 4 mm– ?Aspirin 325 mg PO q day + statin?Aspirin 325 mg PO q day + statin

– Statins (recommend same goal as for known CAD, no RCT’s to Statins (recommend same goal as for known CAD, no RCT’s to date)date)

– Blood pressure controlBlood pressure control– Smoking cessationSmoking cessation– If diabetic, glycemic controlIf diabetic, glycemic control


Possible benefit of aortic arch replacementPossible benefit of aortic arch replacement

Prophylactic atherectomy ? ‘ed CVA riskProphylactic atherectomy ? ‘ed CVA risk

Undergoing cardiac surgery consider Undergoing cardiac surgery consider – Intraoperative U/S to guide aortic manipulation Intraoperative U/S to guide aortic manipulation

sitessites– Use of off-pump CABG may be beneficialUse of off-pump CABG may be beneficial

Cross-clamping & performance of proximal Cross-clamping & performance of proximal anastamosis may risk of embolization 2anastamosis may risk of embolization 2º mechanical º mechanical disruption disruption

Aortic Atherosclerosis: Cholesterol Aortic Atherosclerosis: Cholesterol EmboliEmboli


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


TEE descending thoracic aortaTEE descending thoracic aorta

Massive atherosclerotic plaqueMassive atherosclerotic plaque

Images on the right (1A, 2A, Images on the right (1A, 2A, 3A) taken 1-2 seconds after 3A) taken 1-2 seconds after their respective pictures on the their respective pictures on the leftleft

Arrows point to small particles Arrows point to small particles of embolic material moving inof embolic material moving in

transit in the aortic lumentransit in the aortic lumen

Patient died fromPatient died from– Intestinal infarctionIntestinal infarction– Renal failureRenal failure


Risk factors for atheroembolic diseaseRisk factors for atheroembolic disease– AgeAge– SmokingSmoking– HypercholesterolemiaHypercholesterolemia– HypertensionHypertension

Agmon et al 2000, in CirculationAgmon et al 2000, in Circulation Population-based study of those with aortic plaquePopulation-based study of those with aortic plaque Odds of complex plaque increased as ambulatory SBP Odds of complex plaque increased as ambulatory SBP

increasedincreased– OR 1.43 for each 10 mmHg increaseOR 1.43 for each 10 mmHg increase

– ObesityObesity– DiabetesDiabetes– CRPCRP


Often blamed on Rx with anticoagulant Often blamed on Rx with anticoagulant drugsdrugs– ?plaque hemorrhage as precipitant?plaque hemorrhage as precipitant

Tunick et al 2002, in Am J CardiologyTunick et al 2002, in Am J Cardiology– 519 with severe aortic plaque519 with severe aortic plaque– Cholesterol emboli in only 5/519 over > 3 yearsCholesterol emboli in only 5/519 over > 3 years– No difference between anticoagulation and No difference between anticoagulation and

eventsevents 2/206 on warfarin2/206 on warfarin 3/313 off warfarin3/313 off warfarin


22º Prevention of CVDº Prevention of CVD– Aspirin (or other antiplatelet agents) Aspirin (or other antiplatelet agents) – Statins (same goal as for 2º CAD, no RCT’s to Statins (same goal as for 2º CAD, no RCT’s to

date)date) ?Lower LDL?Lower LDL ?Pleotrophic effects of plaque stabilization?Pleotrophic effects of plaque stabilization

– In above retrospective trial of 519 patients, statins In above retrospective trial of 519 patients, statins associated with a significantly lower rate of recurrent CVA associated with a significantly lower rate of recurrent CVA & thromboembolism& thromboembolism

– Blood pressure controlBlood pressure control– Smoking cessationSmoking cessation– If diabetic, glycemic controlIf diabetic, glycemic control

LV Thrombi – Background & LV Thrombi – Background & IncidenceIncidence

Among most common complications of STEMIAmong most common complications of STEMI

Dependent upon infarct location and sizeDependent upon infarct location and size– Large, anterior STEMI’sLarge, anterior STEMI’s– Aneurysm formation and akinesis or dyskinesisAneurysm formation and akinesis or dyskinesis– Reduced LVEFReduced LVEF– Increased WMA’sIncreased WMA’s

Develop early (within 2 weeks, median 5 days), embolization within 1Develop early (within 2 weeks, median 5 days), embolization within 1stst 4 4 monthsmonths

Incidence in reperfusion era – (predominantly thrombolytic therapy) Incidence in reperfusion era – (predominantly thrombolytic therapy) – 8326 patients GISSI-3 database8326 patients GISSI-3 database– LV thrombus 5.1%, overallLV thrombus 5.1%, overall– Anterior infarct 11.5% with LV thrombusAnterior infarct 11.5% with LV thrombus– Other infarcts 2.3% with LV thrombusOther infarcts 2.3% with LV thrombus– May be May be underestimate underestimate (excluded severe CHF and SBP < 100 mmHg)(excluded severe CHF and SBP < 100 mmHg)

Incidence in reperfusion era – (primary PCI)Incidence in reperfusion era – (primary PCI)– 163 patients163 patients– LV thrombus 4.3%, overallLV thrombus 4.3%, overall– Anterior infarct 10.4% with LV thrombusAnterior infarct 10.4% with LV thrombus– Other infarcts 0% with LV thrombusOther infarcts 0% with LV thrombus

LV Thrombi – Incidence and Risk LV Thrombi – Incidence and Risk FactorsFactors

In reperfusion era (incidence decreasing)In reperfusion era (incidence decreasing)– LV aneurysm 8-15% of Q wave infarctionsLV aneurysm 8-15% of Q wave infarctions– Mural thrombus ID’ed in >50% of these casesMural thrombus ID’ed in >50% of these cases

Two factors contribute to clot formation Two factors contribute to clot formation – Stasis of flow in aneurysm cavityStasis of flow in aneurysm cavity– Contact of blood with fibrous tissue in Contact of blood with fibrous tissue in

aneurysm (rather than normal endocardium)aneurysm (rather than normal endocardium)

LV Thrombi - DiagnosisLV Thrombi - Diagnosis

TTE is a Class I indication for TTE is a Class I indication for assessment of mural thrombus after assessment of mural thrombus after acute STEMIacute STEMI – Presence of thrombusPresence of thrombus– Risk factors for embolizationRisk factors for embolization

LV Thrombi - AppearanceLV Thrombi - Appearance

Thrombus appearanceThrombus appearance– Very fresh/redVery fresh/red

Protrude into cavity centerProtrude into cavity center Highly mobileHighly mobile Difficult to differentiate from effect of slowly Difficult to differentiate from effect of slowly

moving cavitary blood seen within LV aneurysms moving cavitary blood seen within LV aneurysms (highly reflective, luminescent)(highly reflective, luminescent)

– OlderOlder Smooth cavitary surface (resemble liver tissue)Smooth cavitary surface (resemble liver tissue) Less likely to change or embolizeLess likely to change or embolize

LV Thrombi – Risk for LV Thrombi – Risk for EmbolizationEmbolization

High risk for embolizationHigh risk for embolization– Mobile thrombiMobile thrombi

Embolization in 26/119 with LV thrombus s/p STEMIEmbolization in 26/119 with LV thrombus s/p STEMI Free mobility in 58% of patients with embolizationFree mobility in 58% of patients with embolization

– 15/18 patients with free mobility (83% vs 11%) embolized15/18 patients with free mobility (83% vs 11%) embolized

Free mobility in 3% of patients without embolizationFree mobility in 3% of patients without embolization

– Protruding thrombi (into LV cavity)Protruding thrombi (into LV cavity) Protrusion in 88% of patients with emboliProtrusion in 88% of patients with emboli

– 23/40 patients with protruding thrombi embolized (58% vs 23/40 patients with protruding thrombi embolized (58% vs 4%)4%)

Protrusion in 18% of patients without emboliProtrusion in 18% of patients without emboli

LV Thrombi - PreventionLV Thrombi - Prevention

ACE-I thought to result in fewer LV thrombi ACE-I thought to result in fewer LV thrombi via preservation of LVEF and wall motionvia preservation of LVEF and wall motion– No difference in patients on/off lisinopril in GISSI-3No difference in patients on/off lisinopril in GISSI-3

Short-term (10 days)Short-term (10 days)– Unfractionated Heparin vs Heparin SQUnfractionated Heparin vs Heparin SQ– Out of 221 patients, LV thrombus in 11% vs 32%Out of 221 patients, LV thrombus in 11% vs 32%

2004 ACC/AHA STEMI guidelines2004 ACC/AHA STEMI guidelines– Warfarin Warfarin reasonablereasonable with severe LV dysfxn/WMA’s with severe LV dysfxn/WMA’s

for the prevention of LV thrombus formationfor the prevention of LV thrombus formation

LV Thrombi – Embolization LV Thrombi – Embolization PreventionPrevention

No RCT’sNo RCT’s

Warfarin reduces risk of embolizationWarfarin reduces risk of embolization– May prevent thrombus extensionMay prevent thrombus extension– May prevent thrombus endothelializationMay prevent thrombus endothelialization– May May notnot promote thrombus resolution promote thrombus resolution

2004 ACC/AHA STEMI guidelines - LV thrombus2004 ACC/AHA STEMI guidelines - LV thrombus– Warfarin 3-6 monthsWarfarin 3-6 months– Indefinitely, if no increased risk of bleedingIndefinitely, if no increased risk of bleeding

2006 AHA/ASA – prevention of ischemic CVA2006 AHA/ASA – prevention of ischemic CVA– Warfarin 3 months – 1 yearWarfarin 3 months – 1 year– Goal INR 2-3Goal INR 2-3

Also recommend concurrent ASA Rx for 2Also recommend concurrent ASA Rx for 2º preventionº prevention

Consider increased risk of bleeding in PCI (triple Rx)Consider increased risk of bleeding in PCI (triple Rx)


FIGURE 4.24. 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


FIGURE 15.39. 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.


FIGURE 15.64. Apical four-chamber view recorded in a patient with an acute anteroapical MI and a pedunculated, slightly mobile apical thrombus


FIGURE 15.65. 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.

Prosthetic Valve ThrombiProsthetic Valve Thrombi

Common in patients with mechanical valves Common in patients with mechanical valves – Especially if mitral/tricuspid valves (“low-flow”)Especially if mitral/tricuspid valves (“low-flow”)– Especially if suboptimal anticoagulationEspecially if suboptimal anticoagulation

Goal INR 2.5-4.9Goal INR 2.5-4.9

Best evaluated by TEEBest evaluated by TEE– Although often assumed clinicallyAlthough often assumed clinically

No other obvious causeNo other obvious cause Sub-therapeutic INRSub-therapeutic INR

– Confirmatory, but doesn’t change RxConfirmatory, but doesn’t change Rx Unless valvular dysfunction 2Unless valvular dysfunction 2º to a massive º to a massive

thrombusthrombus

Prosthetic Valve Thrombus – Prosthetic Valve Thrombus – AortaAorta

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.

Prosthetic Valve Thrombus – Prosthetic Valve Thrombus – Mitral 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.

Abnormalities of the Interatrial Abnormalities of the Interatrial SeptumSeptum

Thromboemboli via 2 mechanismsThromboemboli via 2 mechanisms– R L shunting via PFO/ASDR L shunting via PFO/ASD– Interatrial septal aneurysmInteratrial septal aneurysm

PFO/ASDPFO/ASD

Echocardiography with contrast (IV Echocardiography with contrast (IV saline)saline)– RestRest– CoughCough– ValsalvaValsalva

Alternatively, transmitral Doppler with Alternatively, transmitral Doppler with contrastcontrast

PFOPFO

FIGURE 7.14. 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.

PFOPFO

FIGURE 7.12. A TEE of the interatrial septum demonstrates a small PFO using color Doppler imaging.

PFOPFO

FIGURE 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.

ASDASD

FIGURE 18.51. 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.

ASDASD

FIGURE 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

ASDASD

FIGURE 19.63. TEE recorded after placement of an atrial septal closure device. IV contrast has been injected to confirm the lack of persistent shunting.

Atrial Septal Aneurysm (ASA)Atrial Septal Aneurysm (ASA)

Congenital malformationCongenital malformation– 22º redundant atrial septal tissueº redundant atrial septal tissue– Typically involving the region of the fossa ovalisTypically involving the region of the fossa ovalis

Prevalence 0.5% via TTE, up to 5% via TEEPrevalence 0.5% via TTE, up to 5% via TEE

Embolic events viaEmbolic events via– Associated PFOAssociated PFO– Direct thrombus formation in the aneurysm’s Direct thrombus formation in the aneurysm’s

neckneck


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.


FIGURE 7.18. 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.


FIGURE 7.18. 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.


Retrospective studies in patients with CVARetrospective studies in patients with CVA– Approximately 10% with atrial septal aneurysmApproximately 10% with atrial septal aneurysm

Prospective trial in ASA suggests CVA risk lowProspective trial in ASA suggests CVA risk low– 846 patients undergoing TEE during cardiac surgery846 patients undergoing TEE during cardiac surgery– 4.9% with incidental finding of ASA4.9% with incidental finding of ASA– 56% with a patent aneurysm56% with a patent aneurysm

67% of those with a patent aneurysm rx’ed with aspirin67% of those with a patent aneurysm rx’ed with aspirin

– No CVA’s or systemic embolization in 70 monthsNo CVA’s or systemic embolization in 70 months

PFO/ASD Conflicting DataPFO/ASD Conflicting Data Association between paradoxical emboli & Association between paradoxical emboli &

cryptogenic CVA well established in patients < 55, cryptogenic CVA well established in patients < 55, less so if > 55less so if > 55– Meta-analysis of case control studiesMeta-analysis of case control studies

PFO (OR 3.1 <55, OR 1.3 >55)PFO (OR 3.1 <55, OR 1.3 >55) ASD (OR 6.1 <55, OR 3.4 >55)ASD (OR 6.1 <55, OR 3.4 >55) Both (OR 15.6 <55, OR 5.1 >55)Both (OR 15.6 <55, OR 5.1 >55)

Population-based studiesPopulation-based studies– No statistically significant association between risk of 1No statistically significant association between risk of 1stst

CVA & presence of a PFOCVA & presence of a PFO Prospective studiesProspective studies

– Presence of a PFO alone is Presence of a PFO alone is NOTNOT associated with an risk associated with an risk of recurrent CVA in patients with cryptogenic strokeof recurrent CVA in patients with cryptogenic stroke

– PFO + Interatrial septal aneurysm PFO + Interatrial septal aneurysm may may CVA riskCVA risk

PFO/ASD Rx for 2PFO/ASD Rx for 2º Prevention of º Prevention of CVA CVA

No RCT’s completedNo RCT’s completed– Insufficient evidence for surgical/percutaneous Insufficient evidence for surgical/percutaneous

vs medical managementvs medical management Risk reduction strategiesRisk reduction strategies

– HTN, hyperlipidemia (statins), antiplatelet RxHTN, hyperlipidemia (statins), antiplatelet Rx General measuresGeneral measures

– Avoid Valsalva (transient R-L shunting)Avoid Valsalva (transient R-L shunting)– Prevention of DVT (body positions that provoke)Prevention of DVT (body positions that provoke)

PFO/ASD Rx for 2PFO/ASD Rx for 2º Prevention of º Prevention of CVACVA

Isolated PFO (? in recurrent CVA)Isolated PFO (? in recurrent CVA)– Antiplatelet agent (Aspirin 81 vs 325, no dose RCT’s)Antiplatelet agent (Aspirin 81 vs 325, no dose RCT’s)– Percutaneous closure of PFO in Percutaneous closure of PFO in recurrentrecurrent cryptogenic CVA cryptogenic CVA

despite warfarin approved in 2001 under HDE, but > 4000 despite warfarin approved in 2001 under HDE, but > 4000 patients would have qualified so approval withdrawn in 2006patients would have qualified so approval withdrawn in 2006

PFO+ASA (? in recurrent CVA < 55, PFO+ASA (? in recurrent CVA < 55, Ø Ø death)death)– Conflicting data for antiplatelet/warfarin (? Conflicting data for antiplatelet/warfarin (? ØØ difference) difference)– Antiplatelet agent (Aspirin 81 vs 325, no dose RCT’s)Antiplatelet agent (Aspirin 81 vs 325, no dose RCT’s)– Warfarin if felt to be at high risk for recurrence or if DVTWarfarin if felt to be at high risk for recurrence or if DVT

Isolated ASA (10 pts in French study on ASA, no repeat Isolated ASA (10 pts in French study on ASA, no repeat CVA)CVA)– Antiplatelet agent (Aspirin 81 vs 325, no dose RCT’s)Antiplatelet agent (Aspirin 81 vs 325, no dose RCT’s)– Warfarin if CVA associated with DVTWarfarin if CVA associated with DVT– Consider surgical excision if recurrence on Consider surgical excision if recurrence on

antiplatelet/anticoagulationantiplatelet/anticoagulation

Echocardiography in the Evaluation of Intracardiac Sources of Embolism Airley E. Fish, MD Imaging...

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