Presentation is loading. Please wait.

Presentation is loading. Please wait.

Echocardiography in the Evaluation of Intracardiac Sources of Embolism Airley E. Fish, MD Imaging Conference Wednesday May 13, 2009.

Similar presentations


Presentation on theme: "Echocardiography in the Evaluation of Intracardiac Sources of Embolism Airley E. Fish, MD Imaging Conference Wednesday May 13, 2009."— Presentation transcript:

1 Echocardiography in the Evaluation of Intracardiac Sources of Embolism Airley E. Fish, MD Imaging Conference Wednesday May 13, 2009

2 Introduction Intracardiac sources of CVA Intracardiac sources of CVA –Account for 75-100k of 500k strokes/year in U.S. TEE TEE –Search for source of cardiac emboli is the leading clinical indication for TEE –More cost effective than TTE –Superior to TTE for most cardiac sources of emboli  Exceptions –Assessment of LV systolic function –Identification of LV apical thrombi

3 Superiority of TEE vs TTE Pearson et al 1991 in JACC Pearson et al 1991 in JACC –79 patients with cryptogenic stroke  TEE ID’ed source in 57%  TTE ID’ed source in only 15% Rauh et al 1996 in Stroke Rauh et al 1996 in Stroke –30 patients with CVA and low-risk for embolism  Sinus rhythm  No cardiac disease related to embolism  Minimal carotid artery stenosis –TTE showed no embolic sources –TEE showed  Aortic plaques in 19  PFO in 7  LAA thrombus in 3  Atrial septal aneurysm in 2

4 Major Sources of Emboli Masses Masses –LA/LV Thrombi –Atherosclerotic plaques –Vegetations –Tumors Propensity for Thrombus Formation Propensity for Thrombus Formation –LA spontaneous echo contrast –MAC Passageways for Paradoxical Embolism Passageways for Paradoxical Embolism –PFO/ASD

5 Major Cardioembolic Sources LA Thrombus -Atrial fibrillation -Sustained atrial flutter LV Thrombus -Recent AMI -EF < 30% Atrial myxoma Aortic Atherosclerotic Plaques LA Spontaneous Echo Contrast PFO/ASD Mechanical or Bioprosthetic Valve Vegetations Tumors Rheumatic Mitral (MAC) or Aortic Valve Disease

6 Most Common Sources of Emboli LA Thrombi LA Thrombi LA Spontaneous Echo Contrast LA Spontaneous Echo Contrast Aortic Atherosclerosis Aortic Atherosclerosis LV Thrombi LV Thrombi Prosthetic Valve Thrombi Prosthetic Valve Thrombi Abnormalities of the Interatrial Septum Abnormalities of the Interatrial Septum

7 LA Thrombi Account for 45% of cardiogenic thromboemboli Account for 45% of cardiogenic thromboemboli Manning et al 1995, Annals of Internal Medicine Manning et al 1995, Annals of Internal Medicine –Intraoperative visualization vs TEE LA/LAA  Sensitivity and specificity TEE 100%, 99% –TTE LA/LAA  Sensitivity and specificity TTE 39%, 65% Most often associated with Most often associated with –Atrial fibrillation and/or – –Rheumatic mitral stenosis

8 LA Thrombi – AF vs NSR Leung et al 1997, Am Journal of Cardiology Leung et al 1997, Am Journal of Cardiology –2894 patients underwent TEE for various indications –94/2894 patients with LA thrombus –83/94 in AF Stoddard et al 1995, J American College of Cardiology Stoddard et al 1995, J American College of Cardiology –TEE looking for LA thrombus in patients with AF  Acute AF - 14% with thrombus  Chronic AF – 27% with thrombus  AF and clinical thrombus - 43% with thrombus (?up to 57% with migration) Omran et al 2000, American Heart Journal Omran et al 2000, American Heart Journal –869 patients with embolic CVA or TIA –If NSR, no MV disease, and normal LA function  Only 1% with LA thrombus  Therefore, routine TEE in sub-population not recommended

9 LA Thrombi

10 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.

11 LAA 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.

12 LA Thrombi 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.

13 LA Thrombi

14 LA Spontaneous Echo Contrast (SEC) “Smoke-like” echoes seen within LA during TEE “Smoke-like” echoes seen within LA during TEE –Most common TEE finding in work up of thrombus source  Especially if AF or LAE  May also be seen in NSR –26/1288 with SEC –3/26 with LA thrombus (LAE, decreased LAA emptying velocity) –2º RBC aggregation in low shear rate conditions –RBC aggregation mediated by plasma proteins  Particularly fibrinogen  Promote RBC rouleaux formation (via elimination of normal negative electrostatic forces of RBC’s aggregation) –Increased plasma fibrinogen levels –Hypercoagulable state – Mitral stenosis  >2/3 patients with MS have TEE e/o SEC  Atrial blood stasis  Increased LA levels of prothrombin 1 and 2 (procoagulants) MR may spontaneous echo contrast frequency MR may spontaneous echo contrast frequency

15 LA Spontaneous Echo Contrast 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.

16 LA Spontaneous Echo Contrast 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.

17 LA Spontaneous Echo Contrast FIGURE 21.39. Small thrombus within the LAA

18 Aortic Atherosclerosis TEE sensitive for visualization of aortic intima TEE sensitive for visualization of aortic intima –CT/MRI experience limited, cannot characterize plaque mobility Aortic atherosclerotic plaques source of Aortic atherosclerotic plaques source of –Thromboemboli (relatively common)  Unstable atherosclerotic plaque, superimposed thrombi embolize  Tend to be single, lodge in small or medium arteries  Often resulting in CVA/TIA  Can also result in limb and organ (kidney, GI, etc.) ischemia –Atheroemboli/Cholesterol Emboli (fairly rare)  Arterio-arterial embolism of small pieces of atheromatous material  Multiple small artery occlusions tissue/organ damage  Ischemic digits, retinal ischemia, intestinal infarction, etc. Patients with Patients with –Unexplained CVA –TIA –Arterial embolization

19 Aortic Atherosclerosis: Thromboembolism

20 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

21 Aortic Atherosclerosis: Thromboembolism

22 Thoracic aortic plaque/plaque mobility – TEE Thoracic aortic plaque/plaque mobility – TEE Complex aortic plaque Complex aortic plaque –> 4 mm thick (more likely to be lipid-laden) –Mobile –Ulcerated –Pedunculated

23 Aortic Atherosclerosis: Thromboembolism

24 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.

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 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.

27 Aortic Atherosclerosis: Thromboembolism Treat for 2º prevention of CVD if Treat for 2º prevention of CVD if –Complex aortic plaque (regardless of CVA/peripheral embolism) –or Simple aortic plaque and unexplained CVA/peripheral embolism 2º Prevention of CVD 2º Prevention of CVD –Aspirin (or other antiplatelet agents) – ARCH trial underway in Europe  If CVA and plaque > 4 mm and/or mobile –?Warfarin with goal INR 2-3 + statin –?Aspirin 325 mg PO q day + statin  If no CVA and plaque mobile –?Warfarin with goal INR 2-3 + statin  If no CVA and plaque > 4 mm –?Aspirin 325 mg PO q day + statin –Statins (recommend same goal as for known CAD, no RCT’s to date) –Blood pressure control –Smoking cessation –If diabetic, glycemic control

28 Aortic Atherosclerosis: Thromboembolism Possible benefit of aortic arch replacement Possible benefit of aortic arch replacement Prophylactic atherectomy ? ‘ed CVA risk Prophylactic atherectomy ? ‘ed CVA risk Undergoing cardiac surgery consider Undergoing cardiac surgery consider –Intraoperative U/S to guide aortic manipulation sites –Use of off-pump CABG may be beneficial  Cross-clamping & performance of proximal anastamosis may risk of embolization 2º mechanical disruption

29 Aortic Atherosclerosis: Cholesterol Emboli

30

31 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 aorta TEE descending thoracic aorta Massive atherosclerotic plaque Massive atherosclerotic plaque Images on the right (1A, 2A, 3A) taken 1-2 seconds after their respective pictures on the left Images on the right (1A, 2A, 3A) taken 1-2 seconds after their respective pictures on the left Arrows point to small particles of embolic material moving in Arrows point to small particles of embolic material moving in transit in the aortic lumen transit in the aortic lumen Patient died from Patient died from –Intestinal infarction –Renal failure

33 Aortic Atherosclerosis: Cholesterol Emboli Risk factors for atheroembolic disease Risk factors for atheroembolic disease –Age –Smoking –Hypercholesterolemia –Hypertension  Agmon et al 2000, in Circulation  Population-based study of those with aortic plaque  Odds of complex plaque increased as ambulatory SBP increased –OR 1.43 for each 10 mmHg increase –Obesity –Diabetes – CRP

34 Aortic Atherosclerosis: Cholesterol Emboli Often blamed on Rx with anticoagulant drugs Often blamed on Rx with anticoagulant drugs –?plaque hemorrhage as precipitant Tunick et al 2002, in Am J Cardiology Tunick et al 2002, in Am J Cardiology –519 with severe aortic plaque –Cholesterol emboli in only 5/519 over > 3 years –No difference between anticoagulation and events  2/206 on warfarin  3/313 off warfarin

35 Aortic Atherosclerosis: Cholesterol Emboli 2º Prevention of CVD 2º Prevention of CVD –Aspirin (or other antiplatelet agents) –Statins (same goal as for 2º CAD, no RCT’s to date)  ?Lower LDL  ?Pleotrophic effects of plaque stabilization –In above retrospective trial of 519 patients, statins associated with a significantly lower rate of recurrent CVA & thromboembolism –Blood pressure control –Smoking cessation –If diabetic, glycemic control

36 LV Thrombi – Background & Incidence Among most common complications of STEMI Among most common complications of STEMI Dependent upon infarct location and size Dependent upon infarct location and size –Large, anterior STEMI’s –Aneurysm formation and akinesis or dyskinesis –Reduced LVEF –Increased WMA’s Develop early (within 2 weeks, median 5 days), embolization within 1 st 4 months Develop early (within 2 weeks, median 5 days), embolization within 1 st 4 months Incidence in reperfusion era – (predominantly thrombolytic therapy) Incidence in reperfusion era – (predominantly thrombolytic therapy) –8326 patients GISSI-3 database –LV thrombus 5.1%, overall –Anterior infarct 11.5% with LV thrombus –Other infarcts 2.3% with LV thrombus –May be underestimate (excluded severe CHF and SBP < 100 mmHg) Incidence in reperfusion era – (primary PCI) Incidence in reperfusion era – (primary PCI) –163 patients –LV thrombus 4.3%, overall –Anterior infarct 10.4% with LV thrombus –Other infarcts 0% with LV thrombus

37 LV Thrombi – Incidence and Risk Factors In reperfusion era (incidence decreasing) In reperfusion era (incidence decreasing) –LV aneurysm 8-15% of Q wave infarctions –Mural 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 cavity –Contact of blood with fibrous tissue in aneurysm (rather than normal endocardium)

38 LV Thrombi - Diagnosis TTE is a Class I indication for assessment of mural thrombus after acute STEMI TTE is a Class I indication for assessment of mural thrombus after acute STEMI –Presence of thrombus –Risk factors for embolization

39 LV Thrombi - Appearance Thrombus appearance Thrombus appearance –Very fresh/red  Protrude into cavity center  Highly mobile  Difficult to differentiate from effect of slowly moving cavitary blood seen within LV aneurysms (highly reflective, luminescent) –Older  Smooth cavitary surface (resemble liver tissue)  Less likely to change or embolize

40 LV Thrombi – Risk for Embolization High risk for embolization High risk for embolization –Mobile thrombi  Embolization in 26/119 with LV thrombus s/p STEMI  Free mobility in 58% of patients with embolization –15/18 patients with free mobility (83% vs 11%) embolized  Free mobility in 3% of patients without embolization –Protruding thrombi (into LV cavity)  Protrusion in 88% of patients with emboli –23/40 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 motion ACE-I thought to result in fewer LV thrombi via preservation of LVEF and wall motion –No difference in patients on/off lisinopril in GISSI-3 Short-term (10 days) Short-term (10 days) –Unfractionated Heparin vs Heparin SQ –Out of 221 patients, LV thrombus in 11% vs 32% 2004 ACC/AHA STEMI guidelines 2004 ACC/AHA STEMI guidelines –Warfarin reasonable with severe LV dysfxn/WMA’s for the prevention of LV thrombus formation

42 LV Thrombi – Embolization Prevention No RCT’s No RCT’s Warfarin reduces risk of embolization Warfarin reduces risk of embolization –May prevent thrombus extension –May prevent thrombus endothelialization –May not promote thrombus resolution 2004 ACC/AHA STEMI guidelines - LV thrombus 2004 ACC/AHA STEMI guidelines - LV thrombus –Warfarin 3-6 months –Indefinitely, if no increased risk of bleeding 2006 AHA/ASA – prevention of ischemic CVA 2006 AHA/ASA – prevention of ischemic CVA –Warfarin 3 months – 1 year –Goal INR 2-3 Also recommend concurrent ASA Rx for 2º prevention Also recommend concurrent ASA Rx for 2º prevention Consider increased risk of bleeding in PCI (triple Rx) Consider increased risk of bleeding in PCI (triple Rx)

43 LV Thrombi 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

44 LV Thrombi 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.

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

46 LV Thrombi 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.

47 Prosthetic Valve Thrombi Common in patients with mechanical valves Common in patients with mechanical valves –Especially if mitral/tricuspid valves (“low-flow”) –Especially if suboptimal anticoagulation  Goal INR 2.5-4.9 Best evaluated by TEE Best evaluated by TEE –Although often assumed clinically  No other obvious cause  Sub-therapeutic INR –Confirmatory, but doesn’t change Rx  Unless 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 mechanisms Thromboemboli via 2 mechanisms –R L shunting via PFO/ASD –Interatrial septal aneurysm

51 PFO/ASD Echocardiography with contrast (IV saline) Echocardiography with contrast (IV saline) –Rest –Cough –Valsalva Alternatively, transmitral Doppler with contrast Alternatively, transmitral Doppler with contrast

52 PFO 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.

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

54 PFO 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.

55 ASD 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.

56 ASD 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

57 ASD 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.

58 Atrial Septal Aneurysm (ASA) Congenital malformation Congenital malformation –2º redundant atrial septal tissue –Typically involving the region of the fossa ovalis Prevalence 0.5% via TTE, up to 5% via TEE Prevalence 0.5% via TTE, up to 5% via TEE Embolic events via Embolic events via –Associated PFO –Direct 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 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.

61 Atrial Septal Aneurysm (ASA) 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.

62 Atrial Septal Aneurysm (ASA) Retrospective studies in patients with CVA Retrospective studies in patients with CVA –Approximately 10% with atrial septal aneurysm Prospective trial in ASA suggests CVA risk low Prospective trial in ASA suggests CVA risk low –846 patients undergoing TEE during cardiac surgery –4.9% with incidental finding of ASA –56% with a patent aneurysm  67% of those with a patent aneurysm rx’ed with aspirin –No CVA’s or systemic embolization in 70 months

63 PFO/ASD Conflicting Data Association between paradoxical emboli & cryptogenic CVA well established in patients 55 Association between paradoxical emboli & cryptogenic CVA well established in patients 55 –Meta-analysis of case control studies  PFO (OR 3.1 55)  ASD (OR 6.1 55)  Both (OR 15.6 55) Population-based studies Population-based studies –No statistically significant association between risk of 1 st CVA & presence of a PFO Prospective studies Prospective studies –Presence of a PFO alone is NOT associated with an risk of recurrent CVA in patients with cryptogenic stroke –PFO + Interatrial septal aneurysm may CVA risk

64 PFO/ASD Rx for 2º Prevention of CVA No RCT’s completed No RCT’s completed –Insufficient evidence for surgical/percutaneous vs medical management Risk reduction strategies Risk reduction strategies –HTN, hyperlipidemia (statins), antiplatelet Rx General measures General measures –Avoid 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) 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 2006 PFO+ASA (? in recurrent CVA < 55, Ø death) PFO+ASA (? in recurrent CVA < 55, Ø death) –Conflicting data for antiplatelet/warfarin (? Ø difference) –Antiplatelet agent (Aspirin 81 vs 325, no dose RCT’s) –Warfarin if felt to be at high risk for recurrence or if DVT Isolated ASA (10 pts in French study on ASA, no repeat CVA) Isolated ASA (10 pts in French study on ASA, no repeat CVA) –Antiplatelet agent (Aspirin 81 vs 325, no dose RCT’s) –Warfarin if CVA associated with DVT –Consider surgical excision if recurrence on antiplatelet/anticoagulation

66


Download ppt "Echocardiography in the Evaluation of Intracardiac Sources of Embolism Airley E. Fish, MD Imaging Conference Wednesday May 13, 2009."

Similar presentations


Ads by Google