Methods

We retrospectively analyzed the 380 consecutive patients who underwent TAVI at the Tel Aviv Sourasky Medical Center between September 2008 and April 2013. Data were collected prospectively as part of the Tel-Aviv Prospective Angiography Study, after obtaining informed consent from each patient as approved by the institutional ethics committee. Severe aortic stenosis was diagnosed by a combination of clinical, echocardiographic, and hemodynamic criteria. A dedicated “heart team,” consisting of an interventional cardiologist, a cardiac surgeon, and a senior echocardiographist, decided on patient eligibility for TAVI based on predetermined criteria. TAVI was performed as previously described mainly through a transfemoral approach (98% of patients). A single team performed all procedures. After the valve was implanted, the patients were monitored at the cardiac intensive care unit where vital signs were recorded continuously during the first 24 hours after the procedure and at least 3 times daily afterward. Continuous electrocardiographic telemetry was performed throughout the hospitalization.

The diagnosis of previous AF was documented according to patient history using a prespecified registry questionnaire, current admission, and past medical records and baseline and past electrocardiograms. Unless contraindicated, a 6-month course of dual antiplatelet therapy with aspirin and clopidogrel was initiated after TAVI, and additional treatment with anticoagulants was provided according to current guidelines. NOAF was defined as AF lasting ≥30 seconds during the actual TAVI procedure or during the subsequent 30 days. In case of NOAF occurring during hospitalization or when acknowledged during follow-up, anticoagulation was introduced according to guidelines.

Baseline data collection and follow-up were performed as previously described. Stroke during hospitalization was determined by accepted clinical criteria and validated by computerized tomography. Cerebrovascular events during follow-up were adjudicated by a senior neurologist after reviewing all the hospital reports and imaging studies.

All data are displayed as mean ± SD for continuous variables and as the number and percentage of patients in each group for categorical variables. Significance for continuous variables was determined with the Student t test after Levean’s test for homogeneity. Significance for categorical variables was determined with the chi-square and Fisher’s exact tests. Logistic regression models that were fitted for NOAF was the dependent variable and adjusted to multiple possible variables contributing to the occurrence of AF after TAVI. Cox proportional hazard ratio models for all-cause mortality were adjusted to previous AF at baseline and NOAF referenced to no occurrence of AF and to other known predictors of mortality after TAVI. All the analyses were considered significant at a 2-tailed p value <0.05. The SPSS was used to perform all statistical evaluation (SPSS, Chicago, IL).

Results

We studied 380 consecutive patients who underwent TAVI between September 2008 and April 2013, with the baseline characteristics described in Table 1 . The overall rate of previous AF was 31%. In patients with previous AF, the arrhythmia was paroxysmal in 72 patients (19%) and permanent in 46 (12%) patients. CHADS ₂ and CHA ₂ DS ₂ VASC did not differ between patients with and without previous AF.

Mean follow-up time was 528 ± 364 days. Thirty-day follow-up was available for all patients, and 1-year follow-up was available for 280 (73%) patients. During follow-up, 19 (5%) new episodes of stroke occurred, of whom 6 and 18 cases occurred within 30 days and 1 year, respectively. Overall mortality during the follow-up was 68 (20%), of those 12 and 58 patients died within 30 days and 1 year, respectively. The rate of NOAF occurring within 30 days of TAVI was 8.2% (n = 31), and 6 additional patients developed AF later on. Patients with NOAF were similar to patients without NOAF in their degree of aortic disease, their co-morbidities, and procedural features ( Table 1 ). However, patients with NOAF had slightly lower ejection fraction. In multivariate analysis ( Table 2 ), reduced EF was the single significant predictor of NOAF after TAVI (p = 0.04). Not surprisingly, patients with NOAF had longer hospital stay than patients without AF or previous AF (10.5 vs 7.5 days, respectively; p = 0.04). There was no significant difference in the cumulative stroke or mortality rates between patients with NOAF versus those without NOAF or previous AF at 30 days and at 1 year ( Figure 1 ). Notably, stroke rate in our cohort was low, with just 1 patient in each group having stroke during the first 30 days after TAVI, resulting in a rate of 3% in the NOAF group and 0.4% in patients without AF.

Cumulative rates of mortality and stroke in patients with and without new-onset AF. AF = atrial fibrillation.

Comparing with patients without AF, patients with previous AF were older, had a higher rate of previously implanted pacemakers, had worse kidney function, and a higher European System for Cardiac Operative Risk Evaluation (EUROSCORE) ( Table 1 ). There was a nonsignificant trend toward increased stroke rate at 30 days (3.4% vs 0.8%, p = 0.078) and a markedly higher stroke rate at 1 year in the previous AF group (9.6% vs 2.1%, p = 0.01; Figure 2 ). In multivariate logistic regression analysis ( Supplementary Tables 1 and 2 ) adjusted for known predictors of stroke, previous AF showed a trend toward increased risk for stroke at 30 days (odds ratio = 8.7, p = 0.058) and was a significant predictor of stroke at 1 year after the procedure (odds ratio = 5.9, p = 0.015). Mortality rates at 1 year were strikingly higher in patients with previous AF at baseline (34.9% vs 8.2%; p <0.01). Multivariate adjusted Cox proportional hazard analysis ( Table 3 and Figure 3 ) showed that previous AF (HR 2.2, 95% confidence interval 1.3 to 3.8, p = 0.003), but not NOAF (HR 1.5, 95% confidence interval 0.5 to 4.1, p = 0.390), was the most significant predictor of mortality throughout the follow-up period.

Cumulative rates of mortality and stroke in patients with and without previous AF at baseline. AF = atrial fibrillation.

Table 3

Cox proportional hazard model for mortality

Coefficients	HR	95% CI		p value
		Lower	Upper
No atrial fibrillation	Reference
Prior atrial fibrillation	2.270	1.334	3.862	0.003
New onset atrial fibrillation	1.536	0.578	4.080	0.390
Gender	0.853	0.466	1.562	0.607
Age	1.073	1.010	1.141	0.024
Body mass index	0.973	0.913	1.036	0.392
Systolic heart failure	1.187	0.607	2.320	0.617
Prior coronary bypass	1.353	0.616	2.975	0.452
Pulmonary disease	1.574	0.835	2.965	0.161
EUROSCORE	1.025	1.006	1.045	0.012
Mean aortic valve pressure gradient	0.983	0.965	1.001	0.068
Previous coronary intervention	0.535	0.309	0.926	0.025
Creatinine clearance	0.996	0.976	1.016	0.710

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