Mechanistic Rationale for LAA Closure with AF and Stroke Prevention


Setting

No. of patients

Thrombus location

Reference no.

LA appendage

LA cavity

Operation

581

26

17

[16]

Autopsy

136

12

11

[17]

Operation

818

20

23

[18]

TEE

50

12

4

[19]

Operation

21

6

0

[20]

Operation

293

11

10

[21]

TEE/operation

110

13

8

[22]

TEE/operation

19

5

0

[23]

TEE

20

1

1

[24]

Operation

581

25

16

[25]

Autopsy

26

13

5

[26]

TEE

260

17

16

[27]

Operation

80

33

13

[28]

Autopsy

509

60

68

[29]

Total

3504

254

192
 

LA left atrium, TEE transesophageal echocardiography




Table 3.2
Review of published reports detailing the frequency and site of thrombus location in patients with non-rheumatic atrial fibrillation (after Blackshear [13])














































































Setting

No. of patients

Thrombus location

Reference no.

LA appendage

LA cavity

TEEa

317

66

1

[30]

TEE

233

34

1

[31]

Autopsy

506

35

12

[17]

TEE

52

2

2

[19]

TEE

48

12

1

[32]

TEE and operation

171

8

3

[33]

SPAF III TEE study

359

19

1

[34]

TEE

272

19

0

[35]

TEE

60

6

0

[36]

Total

1288

201

21
 


a5 % of this cohort had mitral stenosis or a prosthetic mitral valve

LA left atrium, SPAF III stroke prevention in atrial fibrillation trial, TEE transesophageal echocardiography




Approaches to Stroke Prevention in AF


Based upon the increased thrombogenicity as previously described and the stasis that is manifest in the localized region on the LA and particularly the LAA, the approach to intervening to prevent stroke in association with AF could be with either of two potential options. The first approach, which is decades old with clear delineation of its benefits and risks, is to counteract the thrombogenicity resulting in the presence of the stasis by treating with anticoagulants. The range of intravenous, subcutaneous, and oral anticoagulants are all potentially successful avenues to assist in counteracting this effect. An alternative would be to eliminate the local environment where that thrombogenicity is most manifest or to prevent the emergence of thrombi from that local environment (LAA).

Although appearing simple, there are multiple limitations associated with long-term anticoagulant therapy [37]. These include:

1.

Increased risk of bleeding

 

2.

Warfarin’s narrow therapeutic window requiring persistent monitoring of coagulation (International Normalized Ratio, INR)

 

3.

Patient noncompliance

 

4.

Physician reluctance to prescribe, especially to elderly patients, associated falls, hypertension, and comorbidities

 

5.

Need for therapy discontinuation for surgery, procedures, and diagnostic tests

 

Increased bleeding, both major and minor, is inherent to all antithrombotic therapy. In a meta-analysis including 50,578 patients from three randomized trials, Capodanno et al. [38] reported major bleeding rates of 5.0 % and 5.4 % for NOAC and warfarin, respectively. Even minor bleeding may lead to discontinuation of antithrombotic therapy and exposure to stroke risk. A local solution that offers the benefit of embolic protection in the absence of the long-term risks associated with systemic anticoagulation would be an attractive solution.

The potential avenues to remove the local environment would be to excise the LAA, to occlude its ostium therefore separating the thrombogenic environment from the left heart circulation, or to place a filter at the ostium that would prevent the emergence of thrombi that may form distally into the systemic circulation. The challenges of such an approach are multiple, with many potential pitfalls depending upon the approach that is adopted. Almost all the approaches must contend with the issue of: where is the ostium of the appendage? This leads to a number of further issues:



  • At what point is the exclusion of the appendage effective at reducing embolic risk?


  • Must it all be removed?


  • Is a remaining cul de sac thrombogenic?


  • Is there a critical size of a residual cul de sac for efficacy?


  • Are there residual leaks?


  • Is there a critical size of residual leak?


  • Does device design play a role in efficacy regarding residual leaks and thrombogenicity?

Based upon the distinct approaches adopted, each will have variable benefits and failures: e.g., surgical excision may leave a cul de sac or miss a proximal lobe, surgical stitching or stapling have the same issues but also residual or recurrent leak [39, 40]. Different devices (e.g., Watchman and ACP) define the ostium differently, which may be distinct to the true anatomical ostium resulting in different depths of deployment [41, 42]. This may result in device-dependent distinctions in depths of residual cul de sac and subsequent efficacy.

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Jul 1, 2017 | Posted by in CARDIOLOGY | Comments Off on Mechanistic Rationale for LAA Closure with AF and Stroke Prevention

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