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Atrial fibrillation: Stroke prevention strategies
Risk of thromboembolism
Atrial fibrillation (AF) is a major risk factor for thromboembolism, causing approximately 15% of the ischemic strokes in the United States, 36% of strokes in patients older than 80 years, and up to 20% of cryptogenic strokes. Moreover, cardioembolic strokes caused by AF are large and multiple, often involve bilateral infarcts, and are associated with the highest rates of mortality and permanent disability. Specifically, patients with AF-related stroke show a 50% likelihood of death within 1 year, compared with 27% for strokes not related to AF. Patients with AF-related stroke have twice the risk of mortality and three times the risk of stroke recurrence within 1 year compared with patients without AF.
In the Framingham Heart Study, patients with rheumatic heart disease and AF had a 17-fold increased risk of stroke compared with age-matched controls. For nonvalvular AF, the risk of stroke is estimated to be two to seven times that of subjects without arrhythmia, thus resulting in an average incidence of stroke of 5% per year. This rate may increase to 7% per year when silent cerebral ischemic events and transient ischemic attacks are taken into account.
Although patients with AF in the setting of rheumatic valvular disease are expected to be at high risk of stroke, the stroke risk in nonvalvular AF is not homogeneous across the various subgroups of patients. The risk ranges from less than 1.5% per year in otherwise healthy AF patients who are less than 59 years old to more than 10% per year in older patients, especially when AF is associated with specific conditions or comorbidities. Prior history of stroke, transient ischemic attack, or thromboembolism, age, gender, ethnicity, hypertension, diabetes, coronary artery disease, peripheral artery disease, cardiomyopathy, and heart failure are important risk factors.
AF-related thromboembolism can also involve peripheral and visceral arteries and is responsible for up to 55% of acute splenic thromboembolic infarctions, 40% to 70% of acute renal thromboembolic infarctions, and 50% of acute mesenteric embolism. Additionally, AF is diagnosed in 6% to 95% of patients with acute limb ischemia.
Stroke risk stratification
Nonvalvular atrial fibrillation
Several prominent risk stratification schemes have been developed to help distinguish patients with AF who are at high risk of ischemic stroke and other systemic thromboembolism from those with a risk sufficiently low that anticoagulation may not be beneficial when considering the associated bleeding risks.
The CHADS 2 index, named for a combination of clinical risk factors ( Table 19.1 ), was the first risk stratification scheme to gain widespread acceptance due to its relative ease of use. The CHADS 2 system stratifies patients into low-risk (CHADS 2 score of 0), moderate-risk (score of 1–2), and high-risk (score of 3–6) categories. The stroke rate per 100 patient-years without antithrombotic therapy increases by a factor of approximately 1.5 for each one-point increase in the CHADS 2 score: from 1.9% for a score of 0 to 18.2% for a score of 6. A major limitation of the CHADS 2 scheme is the inadequate discrimination of risk. In fact, a large proportion (>60%) of patients are classified as having intermediate risk. Furthermore, this risk scheme is not adequately sensitive in identifying AF patients who are truly at low risk; many patients with AF categorized as low risk by the CHADS 2 score still have stroke rates exceeding 1% per year.
TABLE 19.1
CHADS 2 Scoring System for Predicting Stroke and Thromboembolism in Atrial Fibrillation
| LETTER | CLINICAL CHARACTERISTIC | POINTS |
|---|---|---|
| C | Congestive heart failure | 1 |
| H | Hypertension | 1 |
| A | Age ≥ 75 yr | 1 |
| D | Diabetes mellitus | 1 |
| S 2 | Stroke, transient ischemic attack, or thromboembolism | 2 |
| Maximum points | 6 |
Some of the limitations of the CHADS 2 scheme have been addressed by the newer CHA 2 DS 2 -VASc scoring system, which incorporates all components of the CHADS 2 system but with greater emphasis on age and includes two additional factors: female sex and vascular disease ( Table 19.2 ). The CHA 2 DS 2 -VASc score has the major advantage of discriminating risk probability in lower-risk patients and has been shown in multiple cohorts to be the best for identifying truly low-risk patients, even in those with a CHADS 2 score of 0 ( Table 19.3 ). A low-risk score is defined as a CHA 2 DS 2 -VASc score of 0, and an intermediate risk is defined as a score of 1, whereas a high-risk CHA 2 DS 2 -VASc score is defined as a score of 2 or greater. Of note, female sex alone does not appear to convey increased risk in the absence of other factors. While many studies demonstrated that female sex carries a 1.3-fold increased risk of stroke, the excess risk for females was greatest for females ≥75 years of age and was especially evident among those with ≥2 non-sex-related stroke risk factors. Thus, female sex is considered a risk modifier that matters for age >65 years or ≥2 non-sex-related stroke risk factors.
TABLE 19.2
CHA 2 DS 2 -VASc Scoring System for Predicting Stroke and Thromboembolism in Atrial Fibrillation
| LETTER | CLINICAL CHARACTERISTIC | POINTS |
|---|---|---|
| C | Congestive heart failure or left ventricular dysfunction | 1 |
| H | Hypertension | 1 |
| A 2 | Age ≥ 75 yr | 2 |
| D | Diabetes mellitus | 1 |
| S 2 | Stroke, transient ischemic attack, or thromboembolism | 2 |
| V | Vascular disease (prior myocardial infarction, peripheral artery disease, or aortic plaque) | 1 |
| A | Age 65–74 yr | 1 |
| S | Sex category (i.e., female gender) | 1 |
| Maximum points | 9 |
TABLE 19.3
Stroke or Other Thromboembolism Events Based on the CHA 2 DS 2 -VASc Scoring System
| COHORT OF PATIENTS ON ANTICOAGULATION | COHORT OF PATIENTS OFF ANTICOAGULATION | |||
|---|---|---|---|---|
| CHA 2 DS 2 -VASC SCORE | PATIENTS ( N = 7239) | ADJUSTED STROKE RATE * (% PER YR) | PATIENTS ( N = 1084) | ADJUSTED STROKE RATE † (% PER YR) |
| 0 | 1 | 0 | 103 | 0 |
| 1 | 422 | 1.3 | 162 | 0.7 |
| 2 | 1230 | 2.2 | 184 | 1.9 |
| 3 | 1730 | 3.2 | 203 | 4.7 |
| 4 | 1718 | 4.0 | 208 | 2.3 |
| 5 | 1159 | 6.7 | 95 | 3.9 |
| 6 | 679 | 9.8 | 57 | 4.5 |
| 7 | 294 | 9.6 | 25 | 10.1 |
| 8 | 82 | 6.7 | 9 | 14.2 |
| 9 | 14 | 15.2 | 1 | 100 |
CHA 2 DS 2 -VASc , updated version of the CHADS 2 ( c ongestive heart failure, h ypertension, a ge, d iabetes, and s troke [doubled]) system, with additional risk factors.
* Theoretical thromboembolism rates without anticoagulation therapy: assuming that warfarin provides a 64% reduction in thromboembolic risk. (Data from Lip GY, Frison L, Halperin JL, Lane DA. Identifying patients at risk of stroke despite anticoagulation. Stroke. 2010;41:2731–2738.)
† Theoretical thromboembolism rates without antiplatelet therapy: assuming that aspirin provides a 22% reduction in thromboembolic risk. (Data from Lip GY, Nieuwlaat R, Pisters R, et al. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach. Chest. 2010;137:263–272.)
The R 2 CHADS 2 risk model has emerged from an analysis of the ROCKET-AF (Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and Embolism Trial in Atrial Fibrillation) population and was validated in an ATRIA (Anticoagulation and Risk Factors in Atrial Fibrillation) population. In addition to incorporating the same components of the CHADS 2 score, the R 2 CHADS 2 scheme awards 2 points for renal dysfunction.
The ATRIA score contains elements of R 2 CHADS 2 but importantly gives different scores for age ranges that vary according to whether the patient had also suffered a stroke or transient ischemic attack ( Table 19.4 ). In one report, the ATRIA score outperformed CHADS 2 and CHA 2 DS 2 -VASc risk scores largely because its use resulted in an appropriate downward classification (toward no risk).
TABLE 19.4
ATRIA Stroke Risk Score
| RISK FACTOR | POINTS WITHOUT PRIOR STROKE | POINTS WITH PRIOR STROKE |
|---|---|---|
|
|
|
| Female | 1 | 1 |
| Diabetes mellitus | 1 | 1 |
| CHF | 1 | 1 |
| Hypertension | 1 | 1 |
| Proteinuria | 1 | 1 |
| eGFR < 45 or ESRD | 1 | 1 |
The ABC (age, biomarkers, clinical history) stroke risk score incorporates two biomarkers (NT-proBNP and high-sensitivity cardiac troponin) and two clinical risk predictors (age and prior stroke/transient ischemic attack) ( Fig. 19.1 ). In a recent independent external validation study, the ABC-stroke score performed well (and better than the CHA 2 DS 2 -VASc risk score) for stratifying the risk of stroke or systemic embolic events in a well-characterized anticoagulated cohort from a large multinational trial.
It is important to note that all current risk scores for the prediction of ischemic stroke in AF perform modestly. The ACC/AHA/HRS and ESC guidelines recommend the CHA 2 DS 2 -VASc score for stroke risk stratification in AF because of improved stratification of lower-risk patients.
Previous systematic reviews have not identified AF pattern (paroxysmal, persistent, or permanent) as an important prognostic risk factor for thromboembolism. In fact, AF stroke risk prediction models have in general not included AF type, and current clinical guidelines recommend that decisions regarding OAC be made independently of AF pattern. However, recent data suggest that, in nonanticoagulated patients, persistent and permanent AF is associated with an almost twofold higher rate of stroke or systemic embolism than paroxysmal AF after adjustment for other independent predictors. On the other hand, in patients treated with anticoagulants, the risk of stroke appears similar across all AF patterns.
Severe findings on transesophageal echocardiography (TEE) have been identified as independent predictors of stroke and thromboembolism, including the presence of a left atrial (LA) thrombus (relative risk, 2.5), complex aortic plaques (relative risk, 2.1), spontaneous echocardiographic contrast (relative risk, 3.7), and low LA appendage (LAA) peak flow velocities (up to 20 cm/sec; relative risk, 1.7).
The LAA morphology is currently classified into four categories: chicken-wing, windsock, cauliflower, and cactus. Chicken-wing is the most common and appears relatively protective against the formation of LAA thrombus independent of age, gender, left ventricular (LV) ejection fraction, and the use of anticoagulation.
Limited data suggest that large LAA dimensions, extensive LA fibrosis on late-enhancement cardiac magnetic resonance imaging, and abnormal sinus P-wave axis (defined as any value outside 0°–75 ° ) on 12-lead surface ECG may predict a higher risk of thromboembolism.
Atrial fibrillation with valvular heart disease
The designation of “valvular” and “nonvalvular” is mainly used to determine the appropriate type of long-term OAC therapy. Valvular AF generally refers to AF in the setting of moderate-to-severe mitral stenosis (potentially requiring surgical intervention) or in the presence of an artificial (mechanical) heart valve. Valvular AF is considered an indication for long-term anticoagulation with vitamin K antagonists. AF patients with mitral stenosis are at a particularly high risk for systemic thromboembolism and have been excluded from any further trials studying anticoagulation regimens for AF. On the other hand, “nonvalvular” AF does not imply the absence of valvular heart disease; rather, it refers to AF in the absence of moderate-to-severe mitral stenosis or a mechanical heart valve.
To define categories of valvular heart disease, the European Society of Cardiology (ESC) issued a consensus document, Evaluated Heartvalves, Rheumatic or Artificial (EHRA), which classifies valvular heart disease into EHRA type 1 and EHRA type 2. EHRA type 1 valvular heart disease includes greater than moderate-severe mitral stenosis and/or mechanical heart valve where only vitamin K antagonist is the OAC of choice, and further risk stratification with the CHA 2 DS 2 -VASc score is not required. EHRA type 2 valvular heart disease encompasses all other valvular heart diseases, inclusive of mitral regurgitation, aortic, tricuspid or pulmonary regurgitation or stenosis, repaired valve disease, and bioprosthetic/percutaneous valve replacement. According to this consensus document, stroke risk stratification using the above risk schemes (such as the CHA 2 DS 2 -VASc score) appears to be adequate to guide treatment decisions regarding prophylactic OAC (either warfarin or non–vitamin K antagonist oral anticoagulants [NOACs]) in patients with EHRA type 2 valvular heart disease.
It is worth noting that stroke risk assessment schemes have been established for AF patients without severe valvular heart disease or bioprosthetic valves, and very limited published experience exists for their validity for stroke risk stratification in patients with EHRA valvular heart disease type 2. In a recent report, left valvular disease was present in 22% of all nonvalvular AF patients, and although the embolic risk is higher in these patients compared with those without valve disease, neither the valve disease per se nor its severity was clearly associated with this risk, and a higher CHA 2 DS 2 -VASc score in these patients was likely to explain these results. Nonetheless, a recent study of nonanticoagulated AF patients with EHRA type 2 valvular heart disease and low CHA 2 DS 2 -VASc score (0 or 1) found a risk of thromboembolism at 1 year after AF diagnosis of 1.2% to 1.5%. This is relevant because AF patients with a CHA 2 DS 2 -VASc score ≤1 are considered to be at a lower risk of stroke (<1% per year) and not likely to benefit from OAC therapy. Whether the presence of EHRA type 2 valvular heart disease per se (in the absence of traditional stroke risk factors) increases thromboembolic risk to a level that warrants long-term OAC therapy remains to be investigated. Until then, current guidelines do not consider or offer a recommendation other than grouping no valvular heart disease and EHRA type 2 valvular heart disease in a single category of “nonvalvular AF.”
Bleeding risk stratification
It is estimated that up to 44% of patients with AF have one or more absolute or relative contraindications for long-term OAC therapy, most commonly related to increased risk of bleeding. Therefore, an assessment of bleeding risk should be part of the patient assessment before starting anticoagulation. The risk of bleeding should be weighed against the potential benefit of stroke prevention in individual patients considered for OAC therapy.
Several risk models have been proposed to predict bleeding risk on antithrombotic therapy. Only the HAS-BLED ( Table 19.5 ), HEMORR 2 HAGES ( Table 19.6 ), ATRIA ( Table 19.7 ), and ORBIT scores ( Table 19.8 ) have been derived or validated in AF populations.
TABLE 19.5
Clinical Characteristics Comprising the HAS-BLED Bleeding Risk Score
| LETTER | CLINICAL CHARACTERISTICS | POINTS |
|---|---|---|
| H | Hypertension | 1 |
| A | Abnormal liver or renal function | 1 or 2 |
| S | Stroke | 1 |
| B | Bleeding | 1 |
| L | Labile INR * | 1 |
| E | Elderly (age > 65) | 2 |
| D | Drugs or alcohol | 1 or 2 |
| Maximum score | 9 |
INR , International normalized ratio.
* Hypertension is defined as systolic blood pressure higher than 160 mmHg. Abnormal kidney function is defined as the presence of long-term dialysis or renal transplantation or serum creatinine concentration of at least 200 μmol/L. Abnormal liver function is defined as chronic hepatic disease (e.g., cirrhosis) or biochemical evidence of significant hepatic derangement (e.g., bilirubin more than twice the upper limit of normal, in association with aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase more than three times the upper limit of normal). Bleeding refers to previous bleeding history or predisposition to bleeding, or both (e.g., bleeding diathesis, anemia). Labile INR refers to unstable or high INRs or poor time in therapeutic range (e.g., <60%). Drugs or alcohol use refers to concomitant use of drugs (e.g., antiplatelet agents, nonsteroidal antiinflammatory drugs, or alcohol abuse).
TABLE 19.6
HEMORR 2 HAGES Bleeding Risk Score
| LETTER | CLINICAL CHARACTERISTICS | POINTS |
|---|---|---|
| H | Hepatic or renal disease | 1 |
| E | Ethanol abuse | 1 |
| M | Malignancy | 1 |
| O | Older age | 1 |
| R | Reduced platelet count or function | 1 |
| R | Rebleeding risk | 2 |
| H | Hypertension | 1 |
| A | Anemia | 1 |
| G | Genetic factors | 1 |
| E | Excessive fall risk | 1 |
| S | Stroke | 1 |
| Maximum score | 12 |
TABLE 19.7
ATRIA Bleeding Risk Score
| CLINICAL CHARACTERISTICS | POINTS |
|---|---|
| Anemia | 3 |
| Severe renal disease | 3 |
| Age ≥ 75 yr | 2 |
| Prior bleeding | 1 |
| Hypertension | 1 |
| Maximum score | 10 |
TABLE 19.8
ORBIT Bleeding Risk Score
| LETTER | CLINICAL CHARACTERISTIC | POINTS |
|---|---|---|
| O | Older age (≥75 yr old) | 1 |
| R | Reduced hemoglobin, reduced hematocrit, or anemia | 2 |
| B | Bleeding history | 2 |
| I | Insufficient kidney function (eGFR < 60 mg/dL/1.73 m 2 ) | 1 |
| T | Treatment with antiplatelets | 1 |
| Maximum score | 7 |
In a study evaluating three bleeding risk scores (HAS-BLED, HEMORR 2 HAGES, and ATRIA) risk models, all three tested risk schemes demonstrated only modest performance in predicting the outcome of any clinically relevant bleeding, although the HAS-BLED score performed better than the HEMORR 2 HAGES and ATRIA scores; only HAS-BLED demonstrated a significant predictive performance for intracranial hemorrhage. Given its simplicity, the HAS-BLED score may be an attractive method for the estimation of oral anticoagulant–related bleeding risk for use in clinical practice, as recommended by the ESC guidelines. Patients are categorized as low, intermediate, and high bleeding risk according to HAS-BLED scores 0 to 1, 2, and 3 or higher, respectively. A score higher than 2 suggests a risk of major bleeding of 1.9% per year, whereas a score of 5 is associated with a risk of major bleeding of up to 12.5% per year. Nonetheless, depending on the population studied, the HAS-BLED score has modest risk discrimination ability and, because the score incorporates several of the same factors used to calculate ischemic stroke risk (age, hypertension, prior stroke), it lacks the ability to uniquely discriminate bleeding risk from stroke risk.
More recently, the ABC-bleeding score, which incorporates age, history of bleeding, hemoglobin, high sensitivity cardiac troponin, and growth differentiation factor-15 (a marker of tissue hypoxia, inflammation, and oxidative stress), has been validated in an anticoagulated cohort from a large multinational trial and performed better than HAS-BLED score. An advantage of the ABC-bleeding score is that it does not overlap with the ABC-stroke risk factors, other than age. Despite these important confirmatory data, the ABC scores will need to be validated in patients outside of clinical trials.
It is important to note that bleeding risk assessment is not a static phenomenon, and many common clinical factors that increase bleeding risk are potentially reversible. Further, a high bleeding risk score per se is not a reason to withhold OAC therapy as such patients can potentially derive even greater net clinical benefit while on OAC therapy. Instead, a high score should prompt careful review and follow-up as well as aggressive efforts at amelioration of potentially reversible bleeding risk factors (e.g., uncontrolled hypertension, labile INRs, balance problems, concomitant use of antiplatelet agents, alcohol excess, anemia, and renal or hepatic insufficiency).
Increased bleeding risk is a primary barrier to effective utilization of OAC therapy in patients with AF and is the most commonly cited contraindication to OAC. Rates of contraindications to anticoagulation in nonvalvular AF have varied between studies from 20% to 50%. A major reason for such variability is that contraindications to OAC are often relative and subjective. The challenge is to clearly demarcate the relative and absolute contraindications for OACs and identify the patients in whom the associated risk of bleeding with OAC outweighs the benefits of stroke prevention. There are very few absolute contraindications, such as intracranial tumors or intracerebral bleed due to amyloid angiopathy. Although several comorbidities often are perceived to indicate sufficiently high risk of bleeding, mandating indefinite ineligibility for OAC therapy (such as intracranial hemorrhage, blood dyscrasias, and severe gastrointestinal bleeding), many of these conditions are transient or can be treated, and while they may contraindicate immediate anticoagulation, subsequent anticoagulation may be possible after the acute event has resolved or once the bleeding source is fully identified and treated. It is also imperative to investigate the circumstances around the bleeding event (e.g., supratherapeutic INR levels under warfarin; combination with other antithrombotic drugs, transient factors for increased bleeding risk) to identify transient, avoidable, or reversible causes of bleeding.
Additionally, some analyses have demonstrated a net clinical benefit of OAC even among patients with very high bleeding risk based on bleeding scores. A recent study of nonvalvular AF patients with increased stroke risk and a high bleeding risk contraindication to OAC (chronic blood dyscrasias, history of severe gastrointestinal bleeding, intracranial hemorrhage, or end-stage liver disease) found that, although the risk of intracranial bleeding was higher, the rates of death, hospitalization, and all-cause stroke were lower among patients who continued to receive OAC despite the contraindications as compared to those not treated with OAC. Therefore, at the population level, it appears that the higher risk of bleeding events may be outweighed by favorable stroke and mortality risk reduction. Nevertheless, there still can be individual patients for whom the risk of a fatal hemorrhagic complication truly is prohibitively high, and identifying those patients is an important goal.
Prevention of systemic embolization
Antiplatelet therapy
Aspirin is associated with only a modest (22%) reduction in the incidence of stroke, corresponding to an absolute stroke risk reduction of 1.5% per year as compared with placebo. Thus, except in the lowest-risk patients, aspirin alone is not a viable treatment option for stroke prevention. The combination of aspirin plus clopidogrel is superior to aspirin therapy alone (28% relative risk reduction), but it is associated with a significantly increased risk of major bleeding (2.0% versus 1.3% per year) to levels generally similar to those associated with warfarin therapy.
Vitamin K antagonists
Vitamin K antagonists (warfarin) reduce stroke risk by approximately 64%, corresponding to an absolute annual strokes risk reduction of 2.7% as compared with placebo. Warfarin is superior to aspirin, with a relative risk reduction of 39% for stroke and 29% for cardiovascular events. However, warfarin increases the risk of major bleeding by approximately 70% compared with aspirin. Although the risk of intracranial hemorrhage is doubled with adjusted-dose warfarin compared with aspirin, the absolute risk increase appears to be small (0.2% per year). Additionally, randomized clinical trials have shown that warfarin is superior to the combination of aspirin plus clopidogrel for the prevention of vascular events in patients with AF at high risk of stroke (relative risk reduction of 40%), with similar risks for major bleeding events. Combinations of warfarin (INR, 2.0–3.0) with antiplatelet therapy offer no incremental benefit in stroke risk reduction while they increase the risk of bleeding.
The reduction in ischemic stroke with warfarin in patients with paroxysmal AF is probably similar to that in patients with persistent or permanent AF. The benefit of warfarin is greatest for patients at higher risk of stroke, and there appears to be little benefit for those with no risk factors. The true efficacy of warfarin is likely to be even higher than suggested by trial results because many of the strokes in the warfarin-treated groups occurred in patients who were noncompliant at the time of the stroke.
The estimated annual incidence of bleeding associated with warfarin therapy is 0.6% for fatal bleeding, 3.0% for major bleeding, and 9.6% for major or minor bleeding. The risk of bleeding appears to be especially high during the first year of treatment. The addition of aspirin to warfarin further increases the rate of bleeding with a threefold increase in the rates of intracranial hemorrhage. Notably, the risk of major bleeding in older patients (>80 years) receiving warfarin therapy, although higher than in younger patients, is acceptably low (2.5% per year), and these patients can still benefit from warfarin prophylaxis when a good quality of anticoagulation is obtained. The risk of falling and intracranial bleeding should be considered but not overstated.
An INR between 2.0 and 3.0 is recommended for most patients with AF who receive warfarin therapy. The risk of stroke doubles when the INR falls to 1.7, and values up to 3.5 do not confer an increased risk of bleeding complications. A higher goal (INR between 2.5 and 3.5) is reasonable for patients at particularly high risk for embolization (e.g., prior thromboembolism, rheumatic heart disease, prosthetic heart valves). Similarly, in patients who sustain ischemic stroke or systemic embolism during treatment with therapeutic doses of warfarin (INR, 2.0–3.0), raising the intensity of anticoagulation to a higher INR range of 3.0 to 3.5 should be considered. This approach is probably preferable to adding an antiplatelet agent because an appreciable risk of major bleeding is seen with warfarin only when the INR is greater than 3.5 and is likely to be less than that associated with combination therapy.
Warfarin therapy is associated with several limitations that have dampened the enthusiasm of both patients and clinicians: a narrow therapeutic window that requires periodic INR monitoring and frequent dose adjustments, multiple drug and dietary interactions, genetic variability in response (accounting for 39%–56% of the variability in the warfarin dose), long half-life (36–42 hours), and slow onset of action. In several trials, more than one-third of the patients refused warfarin therapy, largely because of the lifestyle changes required, the inconvenience of INR monitoring, and concern about bleeding risk. These issues have contributed to the underutilization of anticoagulation therapy in patients who can stand to derive benefit from it. In fact, it is estimated that less than 50% of eligible patients were treated with warfarin. Of those patients prescribed warfarin, there is ongoing attrition of its use to approximately 40% by 4 years.
Several series have highlighted the difficulties of maintaining the INR in the therapeutic range. More than one-third of patients taking warfarin are not maintained in the therapeutic range, thus exposing them to increased risk of either stroke (with subtherapeutic INRs) or bleeding (with supratherapeutic INRs). It has been found that if a patient’s INR is not maintained in the therapeutic range at least 65% of the time, the advantage of taking warfarin over aspirin is nullified. The use of the SAMe-TT 2 R 2 score ( Table 19.9 ) can potentially identify those patients in whom warfarin therapy is more likely to be associated with labile INRs and, consequently, serious bleeding and thromboembolism (SAMe-TT 2 R 2 score > 2). In those patients, NOACs are expected to offer a particular advantage.
TABLE 19.9
SAMe-TT 2 R 2 Score
| LETTER | CLINICAL CHARACTERISTIC | POINTS |
|---|---|---|
| S | Sex (female) | 1 |
| A | Age (<60 yr) | 1 |
| Me | Medical history * | 1 |
| T | Treatment strategy (rhythm control) † | 1 |
| T | Tobacco use (within 2 yr) | 2 |
| R | Race (nonwhite) | 2 |
| Maximum points | 8 |
† Interacting drugs, e.g., amiodarone for rhythm control.
* Two of the following: hypertension, diabetes mellitus, coronary disease or prior myocardial infarction, peripheral vascular disease, congestive heart disease, previous stroke, pulmonary disease, and hepatic or renal disease.
Non–vitamin K antagonist oral anticoagulants
There are two classes of NOACs: factor Xa inhibitors (such as rivaroxaban, apixaban and edoxaban) and direct thrombin inhibitors (dabigatran). In general, NOACs are at least as effective as, and in some trials superior to, warfarin for the prevention of stroke and systemic thromboembolism in patients with nonvalvular AF and are associated with lower risks of serious bleeding and intracranial hemorrhage and serious bleeding. However, limited data exist concerning the potential advantage of using NOACs in patients taking warfarin with optimal INR control (time in therapeutic range >75%).
NOACs have several potential advantages over warfarin, including their rapid onset of action, predictable therapeutic effect, less complex pharmacodynamics, limited dietary and drug interactions, and stable dose-related coagulation profile allowing for fixed dosing and obviating the need for routine monitoring. These advantages will likely promote greater use of anticoagulants, enhance patients’ compliance, allow for routine therapy without monitoring, and possibly eliminate the need for anticoagulation with parenteral agents such as heparin (“bridge therapy”). However, warfarin will remain the mainstay of treatment for patients with “valvular” AF and those with mechanical heart valves.
In a meta-analysis of trials randomizing NOACs to warfarin, NOACs were associated with: (1) significantly reduced composite stroke or systemic embolic events (19%), primarily driven by a reduction in hemorrhagic stroke; (2) a nonsignificant (14%) reduction in major bleeding, a reflection of decreased intracranial hemorrhage; and (3) a significant reduction in all-cause mortality. Major bleeding rates with these agents exceeded 2% to 3% per year, and minor bleeding rates were over 10% per year. In addition, by 2 years, 21% to 33% of patients discontinued the NOAC.
There are no direct head-to-head trials comparing the NOACs. In a meta-analysis using adjusted indirect comparisons, there was significant heterogeneity in results. Dabigatran lowered the composite of systemic emboli or stroke (versus rivaroxaban), and apixaban lowered the risk of major gastrointestinal bleeding (versus both rivaroxaban and dabigatran). Additionally, some studies suggested that specific NOACs, such as apixaban, may have lower risks of bleeding (including intracranial hemorrhage) and improved efficacy for stroke prevention, whereas the risk of bleeding for rivaroxaban is comparable to that of warfarin. Currently, there is no clear evidence to support a possible class-effect of a direct thrombin inhibitor or factor Xa inhibitors.
In patients with mechanical aortic or mitral valves, the use of dabigatran was associated with unacceptable thromboembolic and bleeding event rates, as compared to warfarin. Data are lacking for the safety and efficacy of other NOACs in this patient population. Therefore, according to current guidelines, all NOACs are contraindicated in patients with mechanical heart valves.
Similarly, NOACs are not approved for patients with moderate to severe mitral stenosis, since data on drug safety and efficacy are lacking in this patient population. The recent trials of NOACs in AF excluded patients with significant mitral stenosis, mainly because of their noninferiority design.
Renal function and hepatic function should be evaluated before initiation of a NOAC and at least annually while on NOACs. The four NOACs approved in the United States (dabigatran, rivaroxaban, apixaban and edoxaban) have dosing defined by renal function (creatinine or creatinine clearance [CrCl] using the Cockcroft-Gault equation). For patients with end-stage chronic kidney disease (CrCl < 15 mL/min), apixaban or warfarin can be used for anticoagulation. On the other hand, dabigatran, rivaroxaban, and edoxaban are not recommended in this patient population because of the lack of data on safety. In addition, for the factor Xa inhibitors, hepatic function should occasionally be monitored. NOACs are not recommended for use in patients with severe hepatic dysfunction.
Although commercial assays to measure NOAC serum levels are now available, the reference ranges that correlate well with safety and efficacy are yet to be defined. Nonetheless, measuring drug serum levels can potentially be of value to assess patient compliance, determine the need for drug reversal in patients undergoing urgent surgical procedures, or guide dose adjustment in patients with chronic kidney disease and severe obesity or patients using other drugs with potential interaction with NOACs.
Nonpharmacological interventions
The LAA has been implicated as the source of emboli in approximately 90% of patients with nonvalvular AF. Therefore, several approaches have targeted exclusion of the LAA from the systemic circulation to prevent systemic thromboembolism and obviate the need for long-term OAC therapy in patients with nonvalvular AF. These approaches can be of value in many AF patients, given the fact that 20% to 50% of patients with AF have one or more absolute or relative contraindications for chronic OAC therapy, most commonly related to increased risk of bleeding. Furthermore, the safety and efficacy of chronic anticoagulation therapy can be limited by medication compliance, costs, and interactions with food and other medications.
Three main techniques are being utilized to accomplish LAA exclusion: percutaneous endocardial, percutaneous epicardial, and surgical approaches. Device-based endocardial left atrial appendage occlusion (LAAO), such as Watchman (Boston Scientific, Minneapolis, MN, USA) and Amulet (Abbott, Chicago, IL, USA), result in mechanical occlusion of the LAA. LAAO with the endoepicardial system (Lariat, SentreHEART, Redwood City, CA, USA) and surgical epicardial ligation result in both mechanical and electrical isolation of the LAA as a result of LAA infarction.
Several studies have demonstrated the safety and efficacy of endocardial device LAAO as an alternative therapeutic approach for stroke reduction in selected patients with nonvalvular AF. Currently, the two approved endocardial LAAO devices (Watchman and Amulet) require postprocedural antithrombotic therapy. Antiplatelet therapy is recommended for at least 3 to 6 months after the Amulet procedure. For the Watchman procedure, current guidelines in the United States require a brief period of postprocedural OAC followed by antiplatelet therapy, whereas in Europe, antiplatelet therapy alone suffices.
On the other hand, epicardial and surgical LAAO techniques do not require postprocedure antithrombotic therapy. However, these approaches are more invasive compared to endocardial device LAAO technologies. Observational data suggest stroke rates are reduced after LAA ligation, although they lack standardization of anticoagulation strategies and ligation techniques.
Percutaneous epicardial LAA ligation using the Lariat device has been performed by a few experienced centers in a substantial number of patients, predominantly in AF patients with increased stroke risk and contraindications to OAC. There are several theoretical advantages of epicardial LAAO. Generally, OAC and antiplatelet therapies are not required preoperatively; thus, this procedure is feasible in patients with absolute contraindications to these medications. Also, Lariat LAAO can be an option in some patients with LAA anatomy that is incompatible with device LAAO. Additionally, unlike endocardial device LAAO, epicardial LAA ligation results in LAA necrosis and, hence, LAA electrical isolation, which can potentially be of value as an adjunctive therapy to pulmonary vein (PV) isolation in patients with persistent AF. Therefore, the Lariat procedure can potentially fill a void of therapeutic options for stroke prevention in AF patients. However, it is important to note that evidence for procedural effectiveness and safety remains limited. While several observational studies and multicenter registries demonstrated high acute procedural success rates with stroke reduction comparable to that achieved with endocardial LAAO, the rate of periprocedural complications remains a concern. Additionally, no direct comparison of endocardial and epicardial LAAO devices in terms of safety and effectiveness in nonvalvular AF patients intolerant to long-term OAC therapy has been published to date. ,
Recommendations for long-term stroke prevention
Pharmacological therapy
The cornerstone of the management of patients with AF is adequate thromboprophylaxis. Essential to this is appropriate risk stratification and the need to balance the benefit of stroke prevention and the risk of bleeding with anticoagulant therapies (see above). Decision making for thromboprophylaxis by OAC therapy must balance the risk of stroke against the risk of major bleeding, especially intracranial hemorrhage, which is associated with a high risk of death and disability.
Patients with “valvular” AF (those with moderate-to-severe mitral stenosis or valvular mechanical prosthesis [i.e., EHRA type 1 valvular heart disease]) should be managed with long-term anticoagulation with vitamin K antagonists and further risk stratification with the CHA 2 DS 2 -VASc score is not required.
For “nonvalvular” AF, the CHA 2 DS 2 -VASc scoring system ( Tables 19.2 ) is currently the most widely used scheme for risk stratification and is advocated by both European and US guidelines. The initial decision step is to identify patients who are truly at low risk for ischemic stroke, in whom OAC therapy can be omitted. These include patients without clinical stroke risk factors (i.e., CHA 2 DS 2 -VASc score of 0 in men or 1 in women). As noted, female sex is considered a risk modifier and it does not appear to increase stroke risk in the absence of other stroke risk factors. On the other hand, OAC therapy is recommended for patients of both sexes with 2 or more non-sex-related stroke risk factors (i.e., CHA 2 DS 2 -VASc score of ≥2 in men or ≥3 in women). Those recommendations apply to all patients with AF irrespective of the type of AF (paroxysmal or nonparoxysmal).
There is uncertainty regarding the optimal antithrombotic therapy in low thromboembolic risk patients (i.e., CHA 2 DS 2 -VASc score of 1 in men or 2 in women). According to the 2019 AHA/ACC/HRS guidelines, OAC therapy may be considered but is not mandated in these patients. On the other hand, recent studies, as well as ESC guidelines, support a positive advantage for stroke prevention with OAC compared with no therapy or with aspirin in these patients. Furthermore, the use of NOACs may lower the threshold for initiating anticoagulation for AF patients, given the positive net clinical benefit of NOACs, even in patients with a CHA 2 DS 2 -VASc score of 1.
Although subclinical device-detected AF is associated with increased stroke risk, the threshold burden of the duration of AF episodes that warrants anticoagulation remains uncertain. The decision to determine whether to initiate long-term OAC should consider the duration of device-detected AF, CHA 2 DS 2 -VASc score, and bleeding risk, as well as patient preferences.
The 2019 AHA/ACC/HRS guidelines recommend NOACs over warfarin in NOAC-eligible AF patients. As noted previously, NOACs may be used for patients with “nonvalvular” AF, including those with EHRA type 2 valvular heart disease, but are not approved for AF patients with “valvular” AF (EHRA type 1 valvular heart disease). However, the choice of anticoagulation therapy (warfarin versus NOACs) often is influenced by patient’s preference, comorbidities, renal function, cost, and drug interactions.
Importantly, treatment decisions should be individualized. Careful assessment of the risk of bleeding and patient preference is crucial. The expected clinical benefit of anticoagulation therapy should be balanced against the bleeding risk and should be thoroughly discussed with the informed patient. For equivocal cases, considering other possible risk predictors and risk models beyond the CHA 2 DS 2 -VASc scheme (e.g., renal function, biomarkers, findings on TEE) can potentially provide additional prognostic information and help identify those patients at a truly low thromboembolic risk.
Although dual-antiplatelet therapy (aspirin plus clopidogrel) has been used in high-risk patients who cannot be treated with OAC, it should be recognized that dual antiplatelet therapy is significantly less effective for stroke prevention and should not be considered an alternative to OAC. Even in patients who are intolerant to OAC because of high bleeding risk, such an approach may not offer a particular advantage since the risk of major bleeding associated with dual antiplatelet therapy is generally similar to that with OAC. In the latter group, aspirin monotherapy is associated with lesser bleeding risk but at the expense of less protection from systemic thromboembolism. Percutaneous LAAO procedures have become an important therapeutic alternative to long-term OAC therapy in these patients.
Nonpharmacological therapy
Nonpharmacological stroke prevention strategies need to be considered in nonvalvular AF patients with high stroke risk (i.e., CHA 2 DS 2 -VASc score of ≥2 in men or ≥3 in women) and relative or absolute contraindication to OAC. The procedure is contraindicated in patients at low stroke risk, those with valvular AF (e.g., mitral stenosis, mechanical cardiac valves), in the presence of other indications for long-term or lifelong OAC therapy (e.g., venous thromboembolism), LAA thrombus, and contraindications for transseptal catheterization ( Table 19.10 ).
TABLE 19.10
Contraindications for Percutaneous LAA Closure in Patients With Nonvalvular AF
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AF , Atrial fibrillation; LAA , left atrial appendage.
In the United States, the Watchman device is approved as an alternative to warfarin for stroke prevention in patients with nonvalvular AF who: (1) are at increased risk of stroke and systemic embolism on the basis of the CHA 2 DS 2 -VASc score; (2) are deemed by their physicians to be suitable for warfarin therapy; and (3) have an appropriate rationale to seek a nonpharmacological alternative to warfarin, taking into account the safety and efficacy of the device compared with warfarin. The safety of the Watchman procedure in patients who are poor candidates for even short-term OAC is currently being investigated. In the United States, patients with an absolute contraindication to oral anticoagulation therapy are presently not considered candidates for the Watchman device. European guidelines do not mandate post-Watchman OAC. The Amulet device is approved as an alternative to OAC for stroke prevention and relative or absolute contraindication to OAC in both the United States and Europe and does not necessitate postprocedural OAC.
It is important to note that LAAO procedures should not be considered universally as a substitute for OAC therapy. Many of the disadvantages of warfarin therapy can be addressed by using NOACs rather than LAAO, especially given that existing evidence for prevention of stroke and systemic embolism in high-risk AF patients is more robust for OAC (especially NOACs) than that for LAAO. Furthermore, prospective randomized studies demonstrated noninferiority of the LAAO against warfarin, and given the efficacy and safety profile of NOACs, one cannot assume noninferiority of LAAO against NOACs. Although a recent trial demonstrated that endovascular LAAO was noninferior to NOACs, that study enrolled only patients with high bleeding risk or intolerance to, or failure of, NOACs. Therefore, current guidelines agree that nonpharmacological stroke prevention strategies should not be offered as an equal alternative to OAC in AF patients who have no significantly increased risk for bleeding.
Noncompliance is a relevant and important aspect of drug treatment in AF treatment. Some patients are unwilling or unable to take OAC (e.g., due to active lifestyle, risky profession, prior unfavorable experience with such medications, memory problems, or financial issues). For patients with documented noncompliance, in whom attempts to resolve the reasons for noncompliance have failed, LAAO can be discussed as a therapeutic alternative.
Limited data suggest the potential value of LAAO in patients with ischemic stroke (with a high likelihood of cardioembolic origin) despite well-controlled OAC therapy. These patients are often treated by intensification of antithrombotic therapy, which is associated with even higher bleeding risk. Some data also suggest percutaneous LAAO for patients who underwent electrical isolation of the LAA as part of a left-sided AF ablation procedure. These patients appear to exhibit an increased risk of stroke despite OAC. Currently, data are scarce and insufficient to make specific recommendations for this patient population.
Additionally, in patients with increased risk of bleeding and stroke who undergo catheter ablation of AF, combining ablation and LAAO in one procedure can potentially be of advantage over consecutive procedures, but outcome data comparing the two approaches are lacking. Importantly, although having access to the LA obtained for AF ablation offers an opportunity to perform LAAO, the indication for LAAO in patients undergoing AF ablation should follow the same risk-benefit analysis as in patients without AF ablation.
For patients in whom both OAC and antiplatelet therapies are totally contraindicated, even for a short interval, and are thus not candidates for endocardial LAAO, epicardial LAAO (the Lariat system) or thoracoscopic LAA exclusion might be options. However, evidence of efficacy and safety remains limited. Additionally, surgical LAAO may be considered in patients with AF undergoing cardiac surgery, as a component of an overall heart team approach to the management of AF. ,
Anticoagulation in the pericardioversion period
Stable patients without a contraindication to OAC who have been in AF for more than 48 hours or for unknown duration should receive 3 to 4 weeks of OAC with warfarin or NOACs (with documented therapeutic INRs for those on warfarin) prior to and after any mode of cardioversion (electrical, pharmacological, or ablation), regardless of the CHA 2 DS 2 -VASc score. This approach is also recommended for AF in patients with high thrombotic risk (e.g., severe valvular or congenital heart disease, LV dysfunction, recent thromboembolism), even when the duration of AF is less than 48 hours.
The rationale for anticoagulation prior to cardioversion is based on observational studies showing that more than 85% of LA thrombi resolve after 4 weeks of anticoagulation therapy. Cardioversion-related clinical thromboembolic events have been reported in 5% to 7% of patients who did not receive anticoagulation before cardioversion (this risk appears to be much lower [<1%] for AF of less than 48-hour duration).
An alternative approach that eliminates the need for prolonged anticoagulation prior to cardioversion, particularly in low-risk patients who would benefit from earlier cardioversion, is the use of TEE-guided cardioversion. Cardioversion is performed if TEE excludes the presence of intracardiac clots. Anticoagulation after cardioversion, however, is still necessary. Recently, cardiac computed tomographic (CT) angiography has emerged as a valuable alternative imaging modality for detection of LAA thrombi. However, while different studies demonstrated a high sensitivity and accuracy, other studies could not reproduce those results and also report on different levels of inter-reader variability. Therefore, currently, TEE remains the gold standard for detection of LAA thrombi.
After cardioversion, it is recommended to continue OAC therapy for at least 4 weeks. This recommendation deals only with protection from embolic events related to the cardioversion period. Subsequently, the long-term recommendations for patients who have been cardioverted to sinus rhythm but are at high risk for thromboembolism are similar to those for patients with chronic AF, even though the patients are in sinus rhythm.
A different approach with respect to anticoagulation can be used in low-risk patients (CHA 2 DS 2 -VASc score < 2) in whom there is reasonable certainty that AF has been present for less than 48 hours. Such patients have a low risk of clinical thromboembolism (0.8% in one study) if converted early, even without surveillance TEE. The ACC/AHA guidelines do not recommend long-term anticoagulation prior to cardioversion in such patients, but they do recommend heparin use at presentation and during the pericardioversion period. The optimal therapy after cardioversion in this group is uncertain, and there is currently no clear consensus. The ESC guidelines recommend 4 weeks of OAC therapy after cardioversion, whereas the HRS guidelines consider postcardioversion OAC optional. Nonetheless, in view of the known early development of prothrombotic changes after arrhythmia onset, it seems reasonable to proceed to cardioversion as early as possible in patients without OAC.
Currently, insufficient data exist to guide decisions regarding pericardioversion anticoagulation or imaging in patients with endocardial LAAO devices (Watchman or Amulet). A recent study proposed that cardioversion may be performed without the need for OAC if good device position, lack of device-related thrombus, and adequate LAA seal are confirmed on precardioversion TEE. In that study, device-related thrombus was present in 2.7%, which prompted initiation of OAC and deferring cardioversion until complete thrombus resolution. Another observational study suggested that cardioversion after LAAO appears to be safe, both in the presence as well as in the absence of guideline recommended OAC. However, larger, randomized controlled trials are required to validate the safety of these approaches. Given the fact that inadequate LAA seal and device-related thrombus can potentially increase thromboembolic risk, confirmation of adequate device positioning and LAA closure at least once before cardioversion seems rational and recommendable. Until further evidence is available, an individualized approach favoring guideline-recommended OAC seems prudent.
Percutaneous left atrial appendage device closure
Percutaneous device closure of the LAA has emerged as an alternative therapeutic approach for stroke reduction in selected patients with nonvalvular AF ( Fig. 19.2 ). The Watchman and Amulet LAA occlusion devices have the largest body of clinical randomized and nonrandomized data that has shown the safety and efficacy as an alternative to OAC for thromboembolic prophylaxis in patients with nonvalvular AF, and both devices are approved in the United States and Europe. The LAmbre LAA occluder (Lifetech, Shenzhen, China) has been approved in China and Europe. Other device such as the Wavecrest device (Biosens Webster, Diamond Bar, CA, USA) are being developed and evaluated in clinical trials, and the data regarding the safety and efficacy of these devices currently are limited. Other investigational devices include the Sideris plug patch (bioabsorbable device with polyurethane cover [Custom Medical Devices, Bakersfield, CA, USA]), the Prolipsis plug patch (a redesigned Sideris patch second-generation device [Occlutech, Helsingborg, Sweden]), the LeFort device (umbrella-shaped nitinol device [Lepu Medical Technology, Beijing, China]), the pfm device (Christmas tree-shaped pacifier device [pfm medical AG, Cologne, Germany]), and the SeaLA Occluder (umbrella-shaped nitinol plug device [Hangzhou Valued Medtech, Hangzhou, China]).
Left atrial appendage anatomy
The LAA is the only cardiac structure in the LA derived from the primitive atrium; the main LA is formed from the outgrowth of the PVs. The LAA interior surface is formed by a smooth endocardial surface and pectinate muscles that form ridges (trabeculations) and cavities. Despite the heavily trabeculated endocardium, the LAA wall is remarkably thin (approximately 1 mm). The LAA lies anteriorly in the atrioventricular sulcus in close proximity to the left circumflex artery, the great cardiac vein, the left phrenic nerve, and the left PVs. The tip of the LAA can be in a variety of positions, lying over the pulmonary trunk and the left anterior descending coronary artery, pointing posteriorly, or directed medially toward the back of the aorta.
The anatomy of the LAA is highly variable in terms of size, shape, and number of lobes. In approximately 54% of the population, the LAA is composed of two lobes, and in one-third of the population, it is composed of three lobes, with the lobes often projecting in different planes. The shape of the LAA orifice can also vary and can be classified into five types: oval (most common, 69%); foot shaped (10%); triangular (8%); waterdrop shaped (8%); and round (6%). The LAA ostium typically lies horizontal to the left superior PV but can also be superior or inferior to it.
Most often, LAAs are classified into four morphological groups ( Fig. 19.3 ): (1) chicken wing (most common, 48%): an LAA with an obvious bend in the proximal part of the dominant lobe or folding back of the LAA anatomy on itself at some distance from the perceived LAA ostium; (2) cactus (30%): an LAA with a dominant central lobe with secondary lobes extending from the central lobe in both superior and inferior directions; (3) windsock (19%): an LAA with a single dominant lobe of sufficient length (>4 cm) without a significant bend; and (4) cauliflower (3%): a short LAA (with overall length less than the LAA ostium) without a dominant lobe that branches into several lobes. These various LAA configurations can influence device/size selection and implantation success.
The LAA has long been recognized as the site of thrombus formation in most patients with nonvalvular AF. The LAA, with its trabeculations, provides the appropriate setting during fibrillation for blood stasis and thrombus formation. LAA morphology appears to be associated with different degrees of thromboembolic risk, with chicken wing morphology exhibiting the least stroke risk (4% versus 10%–18%). In addition, an increased number of lobes is associated with a higher risk of LAA thrombus. Of note, the degree of pectinate trabeculations appears to be mild in LAAs with chicken wing morphology, moderate in cases with a cactus morphology, and extensive in LAAs with a cauliflower morphology.
The specific varying shapes of the LAA and its orifice have important implications for device closure of the appendage. All current closure devices are circular in shape, which may not always conform to the LAA ostium. Furthermore, a horn-shaped configuration of the LAA (with a wide ostium and narrow “landing zone” [i.e., the area within the LAA where the device will be positioned]) can pose higher risk of device dislodgement. In these patients, choosing a device large enough to cover the ostium and yet maintain the optimal degree of oversizing in the landing zone (i.e., the area within the LAA where the device will be positioned) to secure anchorage can be a challenge. Also, LAA configuration can impact device design selection. Amulet devices are implanted in a relatively proximal position in the LAA (as compared to the Watchman device), which can be of advantage in relatively shallow LAAs and those with complex anatomy.
Left atrial appendage imaging
Preprocedural imaging
Preprocedural imaging of the LAA is used to screen suitable candidates and to define LAA morphology and dimensions as well as exclude the presence of intracardiac clots.
TEE is the gold standard for thrombus detection within the LAA, and it is also used to assess the shape and size of the LAA ostium; the width of the landing zone; the length of the LAA; and—if possible—the number, shape, and location of LAA lobes.
Cardiac CT angiography (with delayed imaging protocols to opacify the LAA) provides superior spatial resolution for assessment of LAA configuration, which has additional advantages for procedural preplanning (e.g., selecting device type, decision on device implant position and angles) aside from sizing measurements. When cardiac CT angiography shows good contrast opacification of the LAA without thrombus, confirmation with TEE is not necessary.
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