Incidence and risk factors for symptomatic heart failure after catheter ...

CLINICAL RESEARCH

Europace (2016) 18, 521–530 doi:10.1093/europace/euv215

Ablation for atrial fibrillation

Incidence and risk factors for symptomatic heart failure after catheter ablation of atrial fibrillation and atrial flutter Henry D. Huang, Jonathan W. Waks, Fernando M. Contreras-Valdes, Charles Haffajee, Alfred E. Buxton, and Mark E. Josephson* Harvard-Thorndike Electrophysiology Institute, Beth Israel Deaconess Medical Center, Harvard Medical School, 185 Pilgrim Road, Baker 4, Boston, MA 02215, USA Received 4 March 2015; accepted after revision 24 May 2015; online publish-ahead-of-print 26 August 2015

Aims

To determine the incidence and risk factors for development of symptomatic heart failure (HF) following catheter ablation for atrial fibrillation (AF) and atrial flutter. ..................................................................................................................................................................................... Methods We prospectively enrolled consecutive patients undergoing pulmonary vein isolation (PVI) or cavotricuspid isthmus and results (CTI) ablation between November 2013 and June 2014. Post-discharge symptoms were assessed via telephone follow-up and clinic visits. The primary outcome was symptomatic HF requiring treatment with new/increased diuretic dosing. Secondary outcomes were prolonged index hospitalization and readmission for HF ≤30 days. Univariate and multivariable logistic regressions were used to assess the relationship between patient/procedural characteristic and post-ablation HF. Among 111 PVI patients [median age 62.0 years; left ventricular ejection fraction (LVEF) 55%], 29 patients (26.1%) developed symptomatic HF, 6 patients (5.4%) required prolonged index hospitalization, and 8 patients (7.2%) were readmitted for HF. In univariate analyses, persistent AF [odds ratio (OR) 2.97, P ¼ 0.02], AF at start of the procedure (OR 2.99, P ¼ 0.01), additional ablation lines (OR 11.07, P , 0.0001), and final left atrial pressure (OR 1.10 per 1 mmHg increase, P ¼ 0.02) were associated with HF development. Peri-procedural diuresis, net fluid balance, and LVEF were not correlated. In multivariable analyses, only additional ablation lines (ORadj 9.17, P ¼ 0.007) were independently associated with post-ablation HF. Six patients (16.7%) developed HF after CTI ablation. ..................................................................................................................................................................................... Conclusion A 26.1% of patients undergoing PVI and 16.7% of patients undergoing CTI ablation developed symptomatic HF when prospectively and uniformly assessed. 12.6% of patients experienced prolonged index hospitalizations or readmission for management of HF within 1 week after PVI. Improved understanding of risk factors for post-ablation HF may be critical in developing strategies to address during AF ablation.

----------------------------------------------------------------------------------------------------------------------------------------------------------Keywords

Atrial fibrillation † Atrial flutter † Heart failure † Ablation † Pulmonary vein isolation † Pulmonary oedema

Introduction Atrial fibrillation (AF) and atrial flutter (AFl), the most common supraventricular arrhythmias, are associated with significant morbidity and mortality.1,2 Owing to the increasing prevalence of these arrhythmias and their associated economic costs,3,4 the most recent ACC/AHA/HRS guidelines give radiofrequency (RF) catheter ablation/pulmonary vein isolation (PVI) a class I recommendation for patients with symptomatic paroxysmal AF who have failed at least 1 antiarrhythmic drug (AAD), and a class IIa indication for patients

with medically refractory, long-standing persistent AF.5 Radiofrequency ablation is also generally considered first-line therapy for patients with AFl who desire permanent restoration of sinus rhythm. Post-cardioversion pulmonary oedema is a known acute complication of direct current cardioversion (DCCV), occurring in 3– 4% of patients despite restoration of sinus rhythm and improved haemodynamic function.6 – 8 While multiple mechanisms for postcardioversion pulmonary oedema have been proposed, 9 – 13 its actual cause remains unclear.14 Development of acute pulmonary oedema and symptomatic congestive heart failure (HF) following

* Corresponding author. Tel: +1 617 632 9209; fax: +1 617 632 7620, E-mail address: [email protected] Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2015. For permissions please email: [email protected].

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What’s new? † Post-ablation HF is a frequent complication following PVI and CTI ablation procedures with 13% of patients requiring prolongation of their initial hospital stay or readmission within 1 week for management of symptomatic HF. † Development of post-ablation HF can be easily missed as symptoms may be delayed for 1–2 days following discharge from the hospital. † Creation of additional ablation lines beyond requirement for PVI was an independent risk factor for developing postablation HF, suggesting that ablation-induced injury to the atrial myocardium may play an important role. † Peri-procedural changes in left atrial pressure, net fluid balance, and the use of diuretic agents and/or low-volume irrigated ablation catheters during ablation cases were not associated with development of post-ablation HF.

PVI for AF has beenreported,15 – 17 although only anecdotally in randomized control trials,18 and its true incidence remains unclear.19 In fact, the most recent ACC/AHA/HRS guidelines do not mention HF as an expected complication of catheter ablation for AF.5 Patients referred for catheter ablation of AF and AFl likely can have different characteristics and HF risk factors compared with patients referred for DCCV. Contrary to patients undergoing DCCV, some patients undergoing ablation present in sinus rhythm, and some electrophysiologists will routinely perform extensive atrial ablation in an effort to reduce recurrence. As a result, the incidence of post-DCCV pulmonary oedema may not apply to patients undergoing catheter ablation for AF and AFl. In this study, we examined patients with AF and AFl undergoing catheter-based RF ablation to determine the incidence of post-ablation symptomatic HF and the patient and procedural characteristics associated with its development.

Methods Patient selection We prospectively enrolled consecutive patients with AF and AFl referred to Beth Israel Deaconess Medical Center (Boston, MA, USA) for PVI or AFl ablation between November 2013 and June 2014. Patients with a history of decompensated HF within 2 years of study enrolment or evidence of significant pulmonary or systemic vascular congestion on the day of scheduled ablation were excluded.

Data collection/ascertainment of outcomes Baseline characteristics and procedural parameters at the time of ablation were obtained through review of the medical record and ablation procedure reports. Cardiac imaging and an assessment of left ventricular ejection fraction (LVEF) with cardiac magnetic resonance imaging (MRI), cardiac computed axial tomography, and/or transthoracic echocardiography were performed prior to the procedure. Atrial fibrillation was defined as paroxysmal and non-paroxysmal (i.e. persistent or long-standing persistent) based on standard definitions.20 In patients undergoing PVI, direct measurement of left atrial (LA) pressure was performed prior to ablation and at the end of the case. All PVI patients had

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Foley catheters and accurate documentation of their total/net fluid status. For patients undergoing cavotricuspid isthmus (CTI) ablation, Foley catheters were not routinely used, and thus only fluid intake was assessed. The primary outcome variable was the development of new-onset, symptomatic HF requiring either new treatment or increased dosage of diuretic therapy. Secondary outcome variables included prolongation of the index hospitalization because of new-onset symptomatic HF, or readmission for a new primary diagnosis of HF ≤30 days after ablation. Patients were screened for the presence of HF symptoms via telephone contact completed on days 3 – 7 after their procedure unless they presented to the hospital for evaluation of HF symptoms prior to this time. All patients identified as having compatible symptoms during telephone follow-up were scheduled for in-person follow-up within a few days for confirmation of symptomatic HF diagnosis via history and physical exam, and electrocardiography, blood work, and radiographic testing as appropriate. As all patients had a recent assessment of LV function, echocardiograms were not routinely performed on patients who were diagnosed with HF. During the follow-up visit, a decision was made by a second, independent clinician whether to start diuretic therapy or to continue or increase the current dose of diuretic. All diagnoses of HF were independently adjudicated by one of the investigators and a second healthcare provider directly involved in the patient’s care. While providers were blinded to each other’s assessment, consensus between both providers was required for patients to be classified as having HF for the purpose of this study. The subset of patients, who developed symptoms potentially compatible with HF but were subsequently found to have symptoms attributable to recurrent tachyarrhythmia (n ¼ 2), bradycardia or heart block (n ¼ 1), pulmonary disease exacerbation (n ¼ 1), or medication non-compliance (n ¼ 2), were not considered cases of HF.

Ablation procedures Ablations were performed by six staff electrophysiologists. All patients had at least 1 month of uninterrupted therapeutic anticoagulation or the absence of atrial thrombi confirmed by the same-day transoesophageal echocardiography. For all RF PVI procedures, general anaesthesia was administered and LA access was obtained via a double transseptal approach. Isolation of left and right pulmonary veins was performed en bloc using a circumferential approach with the use of the Carto 3 electroanatomic mapping system (Biosense Webster,Diamond Bar,CA, USA) and pre-procedure cardiac MRI or cardiac computed axial tomography. Radiofrequency ablation was performed using Thermocool (R) or Thermocool (R) SF open-irrigated ablation catheters (Biosense Webster) with standard flow rates and power output between 20 and 40 W, as appropriate. Successful PVI was confirmed by documenting both entrance and exit block in all pulmonary veins. Additional empiric ablation and targeted ablation with extra ablation lines (including roof lines, box lesion sets, mitral isthmus lines, isolation of the LA appendage, or superior vena cava), or ablation of complex fractionated atrial electrograms was not routinely performed. The decision to perform additional RF ablation was at the discretion of the operator and was influenced by patient history, type of AF (persistent vs. paroxysmal), and inducibility of AF or atrial tachycardia after successful isolation of all pulmonary veins. For all cryoballoon PVI cases, general anaesthesia was administered and LA access was obtained using a single transseptal approach. The Achieve(TM) circular mapping catheter (Medtronic, Minneapolis, MN, USA) was used for electroanatomic mapping and confirmation of electrical PVI following ablation. Ablation was performed with 3 – 4-min deliveries using the Arctic Front (R) catheter (Medtronic CryoCath). All RF and cryoballoon PVI patients were anticoagulated with intravenous heparin to maintain activated clotting time .300 s.

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Patient follow-up After ablation, patients resumed their prior medications, including diuretics already prescribed. During the index hospitalization, patients were evaluated closely for the development of pulmonary vascular congestion and/or dependent oedema by symptom assessment and serial physical examination. In the absence of procedural complications, patients were routinely discharged within 24 h. The majority of patients who underwent PVI was sent home with a trans-telephonic event monitor with automatic and patient-triggered capability to record recurrence of arrhythmia for 2 – 4 weeks. All patients were contacted via telephone by one of the investigators who performed a focused history and screened for HF symptoms (dyspnoea with exertion, orthopnoea, paroxysmal nocturnal dyspnoea, new or increased lower extremity swelling, increased abdominal girth, or weight gain) 3 – 7 days after discharge. If any symptoms were compatible with HF, other potential causes were excluded by performing a detailed history and review of rhythm strips obtained from the ambulatory event monitor. Patients with suspected HF were started on a diuretic agent or had their previous diuretic dose increased and were provided with clinic follow-up within a few days for in-person assessment/examination to confirm the diagnosis of HF and assess response to diuretic therapy. In severe cases, patients were instructed to proceed to the Emergency Department for urgent evaluation.

Statistical analyses Categorical variables, reported as a number and percentage of the total, were compared using the Pearson x 2 test or Fisher’s Exact test. Continuous variables, reported as the median and interquartile range, were compared using a two-sample Wilcoxon rank sum test. To determine the correlation between patient characteristics, procedural factors, and the development of HF after RF PVI, univariate logistic regression was performed to calculate unadjusted odds ratios (ORs). For RF PVI patients, two multivariable logistic regression models were constructed with the following variables based on P , 0.1 in univariate testing, and exclusion of variables that were multicolinear: additional ablation lines or number of ablation lines (in separate models), history of persistent AF, AF at beginning of the case, total ablation time, ending LA pressure, net fluid intake, and LVEF. P-Values , 0.05 were considered significant. All analyses were performed independently by the authors using Stata version 12.1 (Stata Corp., College Station, TX, USA). All record review and data analyses were performed under the approval of the institutional review board of Beth Israel Deaconess Medical Center.

Time to onset of HF symptoms after PVI 15 13

Frequency (n)

For AFl procedures, linear ablation in the CTI from the tricuspid annulus to inferior vena cava was performed with a non-irrigated catheter: 8 mm Navistar or Celsius (Biosense Webster), or an 8 or 10 mm Blazer (Boston Scientific, Natick, MA, USA). Successful ablation was defined as bidirectional block across the CTI ablation line. The use of peri-procedural diuretics was at the discretion of the electrophysiologist performing each case, and there was no standard protocol for diuretic administration in the peri- or post-procedural period. During PVI procedures, DCCV was performed for the purpose of restoring sinus rhythm if the patient remained in AF at the end of the case or if sinus rhythm was required for catheter stability during ablation.

10

10

5 3

3

3

4

0 1

2

Days after PVI

Figure 1 Time until patients developed symptomatic HF following their PVI procedure.

Results Primary and secondary outcomes in patients with atrial fibrillation undergoing pulmonary vein isolation A total of 126 patients underwent PVI for AF during the study period. Four patients with history of decompensated HF within 2 years and two patients with significant pulmonary or systemic vascular congestion on the day of scheduled ablation were excluded from the analyses. The final study population included 111 patients with AF who underwent RF PVI and 9 patients who underwent cryoballoon PVI. No patient was lost to follow-up. Symptomatic HF occurred in 29 RF PVI patients (26.1%), and 23 of these patients (79%) developed HF within 48 h of their procedure. Nineteen PVI patients (66%) who developed post-ablation HF did so on day 2 or later, after discharge from the hospital (Figure 1). The most commonly reported symptoms when obtaining patient histories were new dyspnoea on exertion, orthopnoea, increased weight, increased lower extremity swelling, and increased or insufficient urinary output. Six patients (5.4%) required prolonged index hospitalization, and 8 patients (7.2%) required readmission for HF management within 1 week of their procedure. There was no difference in time to initial follow-up among patients with and without HF (median 4 vs. 5 days, respectively, P ¼ 0.78). Pulmonary oedema/HF occurred in two of nine (22.2%) of cryoballoon PVI patients.

Baseline patient characteristics of patients with atrial fibrillation undergoing radiofrequency pulmonary vein isolation Baseline and procedural characteristics of patients undergoing RF PVI are shown in Table 1. Patients who developed HF after PVI were more likely to have a history of persistent AF (37.9 vs. 17.1%; P ¼ 0.021) and were slightly older (median age 66.1 vs.

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Table 1 Baseline patient and procedural characteristics for patients with AF undergoing PVI All patients (n 5 111)

No HF (n 5 82)

HF (n 5 29)

Age (years) Male

62.1 (54.3–68.0) 87 (78.4%)

60.7 (54.3– 66.3) 64 (78.1%)

66.1 (60.2–70.8) 23 (79.3%)

White, non-hispanic

P-value

............................................................................................................................................................................... Patient characteristics 0.048 0.89

100 (90.1%)

73 (89.0%)

27 (93.1%)

0.73

History of persistent AF History of prior ablation

25 (22.5%) 36 (32.4%)

14 (17.1%) 28 (34.2%)

11 (37.9%) 8 (27.6%)

0.021 0.52

History of CAD

12 (10.8%)

9 (11.0%)

3 (10.3%)

0.93

History of CHF (.2 years prior) History of hypertension

7 (6.3%) 53 (47.8%)

5 (6.1%) 36 (43.9%)

2 (6.9%) 17 (58.6%)

0.88 0.17

History of diabetes

21 (18.9%)

13 (15.9%)

8 (27.6%)

0.17

History of obstructive sleep apnoea History of hyperlipidaemia

24 (21.6%) 36 (32.4%)

18 (22.0%) 25 (30.5%)

6 (20.7%) 11 (37.9%)

0.89 0.46

LV ejection fraction (%)

55 (50– 60)

55 (50– 60)

55 (40–59)

0.26

LA diameter (cm) Time of phone contact (days)

6.1 (5.4– 6.7) 5 (4– 5)

6.1 (5.4– 6.7) 5 (4–5)

6.3 (5.4– 6.8) 4 (4– 5)

0.88 0.078

AF at start of PVI DCCV during PVI

47 (42.3%) 63 (57.3%)

29 (35.4%) 44 (54.3%)

18 (62.1%) 19 (65.5%)

0.012 0.30

Number of ablation lesions

93 (60– 133)

88 (56– 124)

Additional ablation lines Number of additional ablation lines

62 (55.9%) 1 (0– 2)

36 (43.9%) 0 (0–2)

Procedural characteristics

105 (63–160)

0.104

26 (89.7%) 2 (1– 3)

,0.0001 ,0.0001

Total ablation time (min)

68 (50– 90)

63 (47– 81)

95 (61–107)

0.0004

ThermoCool SF catheter use (vs. non-SF) Lasix administered during procedure

66 (61.1%) 26 (23.4%)

47 (58.8%) 22 (26.8%)

19 (67.9%) 4 (13.8%)

0.40 0.21

LA pressure start (mmHg)

15 (12– 18)

14 (12– 17)

17 (13–22)

0.026

LA pressure end (mmHg) Change in LA pressure (mmHg)

15 (12– 19) 0 (22 to 2)

15 (11– 18) 1 (22 to 2)

18 (15–21) 0 (22 to 2)

0.015 0.80

Fluid intake (L)

2.95 (2.20–3.80)

3.30 (2.40– 3.80)

2.90 (2.20–3.70)

0.36

Fluid net (L) Case duration (min)

2.01 (1.34–2.68) 262 (207–317)

1.83 (1.20– 2.57) 250 (195–307)

2.25 (1.80–2.80) 280 (243–369)

0.045 0.024

Heart rate pre-PVI (b.p.m.)

69 (60– 81)

68 (60– 80)

73 (61–86)

0.33

Heart rate post-PVI (b.p.m.) Pressor use during PVI

72 (64– 83) 82 (82.0%)

73 (66– 84) 62 (84.9%)

71 (63–81) 20 (74.1%)

0.49 0.21

Post-procedure SBP (mmHg)

120 (111–131)

120 (111–130)

120 (110–137)

0.76

71 (62– 77) 89 (84– 96)

71 (63– 78) 86 (84– 94)

68 (60–75) 90 (84–102)

0.18 0.15

77 (72.0%) 71 (67.0%)

54 (68.4%) 53 (68.0%)

23 (82.1%) 18 (64.3%)

0.16 0.72

Post-procedure DBP (mmHg) Lowest SBP during case (mmHg) Medications Beta-blocker use pre-PVI Beta-blocker use after PVI CCB use pre-PVI

18 (16.8%)

15 (19.0%)

3 (10.7%)

0.39

CCB use after PVI History of any AAD use

16 (15.1%) 97 (87.4%)

12 (15.4%) 71 (86.6%)

4 (14.3%) 26 (89.7%)

0.89 0.67

AAD use pre-PVI

46 (43.0%)

36 (45.6%)

10 (35.7%)

0.37

AAD use after PVI

56 (52.8%)

40 (51.3%)

16 (57.1%)

0.59

Data expressed as number (%), or median (interquartile range). LV, left ventricular; DCCV, direct current cardioversion; LA, left atrial; AF, atrial fibrillation; AAD, antiarrhythmic drug; PVI, pulmonary vein isolation; CCB, calcium channel blocker; AAD, antiarrhythmic drug; HF, heart failure.

60.7 years; P ¼ 0.048). There were no significant differences in gender, race, LA diameter, prior history of PVI, or comorbidities such as coronary artery disease, congestive HF .2 years prior to ablation, hypertension, hyperlipidaemia, diabetes, or obstructive

sleep apnoea between patients who did and did not develop postablation HF. There were no significant differences in the use of beta-blockers, calcium channel blockers, and AADs prior to or after PVI.

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When procedural characteristics were evaluated, patients, who developed HF were more likely to be in AF at the start of their ablation case (62.1 vs. 35.4%, P ¼ 0.012), have additional ablation lines performed (89.7% vs. 43.9%, P , 0.0001), have higher LA pressures at the start (median 17 vs. 14 mmHg, P ¼ 0.026) and the end of the case (median 18 vs. 15 mmHg, P ¼ 0.015), and were more net fluid positive (median 2.25 vs. 1.83 L, P ¼ 0.045). There was no difference in the use of DCCV to restore sinus rhythm during PVI, change in LA pressure during the case, or peri-procedural use of diuretics. There was no difference in pre- or post-procedural heart rate, peri-procedural requirement for pressor medications, or postprocedure blood pressure. Owing to procedural heterogeneity and small sample size, patients who underwent cryoballoon ablation were excluded from similar analyses. Of note, 13 of 29 patients who developed HF had reassessment of LV function via transthoracic echocardiogram during evaluation and treatment for HF, and there was no significant change in LV function before or after PVI (median 52 vs. 55%, respectively, P ¼ 0.075). All but one patient with HF had laboratories assessed prior to PVI and at the time of HF diagnosis, and there was no significant change in creatinine (1.0 mg/dL pre-PVI vs. 1.0 mg/dL postPVI, P ¼ 0.83), or haemoglobin (13.4 g/dL pre-PVI vs. 14.0 g/dL post-PVI, P ¼ 0.87) compared with their pre-ablation values.

Correlates of heart failure after radiofrequency pulmonary vein isolation Table 2 displays ORs calculated by univariate logistic regression for the development of HF after RF PVI. Notably, the strongest univariate risk factor for post-PVI HF was additional ablation lines [OR 11.07, 95% confidence interval (CI) (3.10–39.52), P , 0.0001]. History of persistent AF (OR 2.97, 95% CI (1.15–7.64), P ¼ 0.024) and AF at the start of PVI (OR 2.99, 95% CI (1.25 – 7.18), P ¼ 0.014) were also strongly associated with post-ablation HF. Risk of HF increased as more lines were created with an OR of 1.85 per line, 95% CI (1.32–2.60), P , 0.0001. Peri-procedural diuretic use, change in LA pressure during the case, and net fluid balance were not risk factors for post-ablation HF. In a multivariable logistic regression including AF at the start of the case, history of persistent AF, additional ablation lines, LVEF, net fluid balance, total ablation time, and LA pressure at the end of the procedure, only additional ablation lines (ORadj 9.17, 95% CI (1.85 – 45.53), P ¼ 0.007) remained independently associated with the development of HF (Table 3). Table 4 represents the same multivariable model, including the number of additional ablation lines rather than the dichotomized presence or absence of additional ablation lines. After multivariable adjustment, each additional ablation line was independently associated with post-ablation HF with an ORadj of 1.55, 95% CI (1.03– 2.31), P ¼ 0.034. All other variables included in the multivariable model were not significantly correlated with HF after multivariable adjustment.

Types of additional ablation lines Figure 2 demonstrates the frequency of additional ablation lines performed in addition to isolation of the pulmonary veins. Roof lines (n ¼ 25), CTI lines (n ¼ 22), and lateral mitral isthmus lines (n ¼ 17)

were the most common additional ablation lines created. Ablation in the coronary sinus, LA septum, and LA appendage were infrequently performed.

Primary and secondary outcomes and risk factors for post-ablation heart failure in patients with atrial flutter Thirty-six patients with AFl underwent ablation and symptomatic HF developed in six patients (17%). Four patients (11.1%) had prolongation of their initial hospitalization (n ¼ 2) or readmission for HF management within 1 week of ablation (n ¼ 2). Three of six patients with HF (50%) developed symptoms on day 2 after ablation. Baseline and procedural characteristics for patients undergoing catheter ablation of AFl are shown in Table 5. Patients who developed post-ablation HF were more likely to be in AFl at the start of the case (83.3 vs. 30.0%, P ¼ 0.024) and diabetic (66.7 vs. 20.0%, P ¼ 0.039). Other characteristics were similar between groups. Owing to the small number of patients that developed HF, further analysis was not performed.

Discussion Incidence of post-ablation heart failure In this prospective, single-centre study of consecutive patients referred for catheter ablation of AF and AFl, we demonstrate that 26% of patients with AF undergoing RF PVI and 17% of patients with AFl undergoing CTI ablation developed new, symptomatic HF after their procedure, and approximately half of these patients required either prolongation of their index hospitalization or readmission for HF within 1 week of their procedure. While the majority declared symptoms within 48 h, 66% of the PVI patients who developed symptomatic HF did so after 24 h, after they were already discharged from the hospital. Our results suggest that post-ablation HF has been significantly underappreciated, and although it has been recognized as a hazard of catheter ablation in small studies,15 – 18 current guidelines,5,21 which describe an average complication rate of only 3.9 – 4.5% for PVI, do not list HF as a common adverse event. Additionally, in a multi-national survey examining different practice patterns for AF catheter ablation, HF was not mentioned as a self-reported procedural complication.19 Given that an estimated 50 000 AF procedures are performed per year in the USA alone22 and that the mean cost for hospitalized management of HF is $23 000 (which often is not reimbursable given readmission soon after ablation),23 the scope and implications of post-ablation HF are significant. A lack of physician awareness likely plays a role in the underdiagnosis of post-ablation HF as early follow-up with a focused history for signs and symptoms of HF, as performed in this study, is not standard practice.19 Our findings suggest that shorter intervals of follow-up, even by telephone, aids in early identification and intervention of patients with symptomatic HF. It is possible and likely that with early systematic follow-up and outpatient intervention, some potential readmissions for HF were prevented. In the overall study population, we found that the median time to develop HF symptoms was  1 – 2 days after ablation. This time course suggests that symptoms are secondary to a gradual

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Table 2 Univariate risk factors for post-PVI heart failure Unadjusted OR (95% CI)

P-value

............................................................................................................................................................................... Patient characteristics Age (year) per 1 year increase Male

1.03 (0.98–1.08) 1.08 (0.38–3.05)

0.20 0.89

White, non-hispanic

1.66 (0.34–8.20)

0.53

History of persistent AF Prior ablation

2.97 (1.15–7.64) 0.73 (0.29–1.87)

0.024 0.52

History of CAD

0.94 (0.24–3.72)

0.93

History of CHF (.2 years prior) History of hypertension

1.14 (0.21–6.23) 1.81 (0.77–4.27)

0.88 0.18

History of diabetes

2.02 (0.74–5.53)

0.17

History of hyperlipidaemia History of obstructive sleep apnoea

1.39 (0.57–3.38) 0.93 (0.33–2.62)

0.46 0.89

LV ejection fraction (%) per 10% increase LA diameter (cm) per 1 cm increase Procedure characteristics

0.67 (0.44–1.03)

0.067

1.12 (0.71–1.76)

0.64

AF at start of PVI

2.99 (1.25–7.18)

0.014

DCCV during PVI Number of ablation lesions per 10 lesion increase

1.60 (0.66–3.86) 1.10 (1.00–1.20)

0.30 0.049

Additional ablation lines Number of additional ablation lines (per line) Total ablation time (min) per 10 min increase

11.07 (3.10–39.52)

,0.0001

1.85 (1.32–2.60) 1.39 (1.15–1.68)

,0.0001 0.001

ThermoCool SF catheter use (vs. non-SF)

1.48 (0.60–3.68)

0.40

Lasix administered during procedure LA diameter (cm) per 1 cm increase

0.44 (0.14–1.40) 1.08 (0.68–1.72)

0.16 0.74

LA pressure start (mmHg) per 1 mmHg increase

1.10 (1.02–1.18)

0.018

LA pressure end (mmHg) per 1 mmHg increase Change in LA pressure (mmHg) per 1 mmHg increase

1.10 (1.02–1.19) 1.01 (0.90–1.12)

0.019 0.91

Fluid intake (L) per 0.1 L increase

1.02 (0.98–1.05)

0.38

Fluid net (L) per 0.1 L increase Case duration (min) per 10 min increase

1.03 (0.99–1.08) 1.05 (1.00–1.10)

0.092 0.046

Heart rate pre-PVI per 10 b.p.m. increase

1.15 (0.90–1.45)

0.26

Heart rate post-PVI per 10 b.p.m. increase Post-procedure SBP (mmHg) per 5 mmHg increase

0.90 (0.63–1.29) 1.05 (0.90–1.21)

0.57 0.54

Post-procedure DBP (mmHg) per 5 mmHg increase Pressor requirement during PVI Medications

0.86 (0.69–1.09)

0.21

0.51 (0.17–1.48)

0.22

Beta-blocker use pre-PVI

2.13 (0.73–6.25)

0.17

Beta-blocker use after PVI CCB use pre-PVI

0.85 (0.34–2.10) 0.51 (0.14–1.92)

0.72 0.32

CCB use after PVI

0.92 (0.27–3.12)

0.89

History of any AAD use AAD use pre-PVI

1.34 (0.35–5.20) 0.66 (0.27–1.62)

0.67 0.37

AAD use after PVI

1.27 (0.53–3.02)

0.59

LV, left ventricular; DCCV, direct current cardioversion; LA, left atrial; AF, atrial fibrillation; AAD, antiarrhythmic drug; PVI, pulmonary vein isolation; CCB, calcium channel blocker; AAD, antiarrhythmic drug.

increase in circulating volume rather than acute, peri-procedural volume overload or pulmonary oedema.24,25 This finding is clinically important as most AF and AFl ablations are elective procedures, and the majority of patients are discharged prior to the onset of when HF symptoms would be expected. Additionally, the diagnosis of

post-discharge HF may be missed, especially when patients have normal LV systolic function and no history of symptomatic HF, because patients may confuse HF symptoms with the normal course of recovery or assume they are due to recurrent arrhythmia or another non-cardiac cause.

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Table 3 Multivariable logistic regression model of risk factors for post-PVI heart failure using dichotomized presence or absence of additional ablation lines Patient/procedure characteristics

Unadjusted OR (95% CI)

Unadjusted P-value

Adjusted OR (95% CI)

Adjusted P-value

1.10 (0.62–1.94) 1.80 (0.52–6.31)

0.74 0.36

............................................................................................................................................................................... LV ejection fraction (%) per 10% increase History of persistent AF AF at start of PVI Additional ablation lines Total ablation time per 10 min increase

0.67 (0.44– 1.03) 2.97 (1.15– 7.64)

0.067 0.024

2.99 (1.25– 7.18)

0.014

1.92 (0.59–6.22)

0.28

11.07 (3.10– 39.52) 1.39 (1.15– 1.68)

,0.0001 0.001

9.17 (1.85–45.53) 1.19 (0.94–1.50)

0.007 0.16

LA pressure at end of case (mmHg)

1.10 (1.02– 1.19)

0.019

1.01 (0.91–1.13)

0.82

Fluid net per 0.1 L increase

1.03 (0.99– 1.08)

0.092

1.03 (0.97–1.09)

0.41

Table 4 Multivariable logistic regression model of risk factors for post-PVI heart failure per additional ablation line created Patient/procedure characteristics

Unadjusted OR (95% CI)

Unadjusted P-value

Adjusted OR (95% CI)

Adjusted P-value

............................................................................................................................................................................... LV ejection fraction (%) per 10% increase

0.67 (0.44–1.03)

0.067

1.05 (0.61–1.83)

0.86

History of persistent AF

2.97 (1.15–7.64)

0.024

1.73 (0.50–6.05)

0.39

AF at start of PVI Additional ablation lines (per line increase)

2.99 (1.25–7.18) 1.85 (1.32–2.60)

0.014 ,0.0001

1.53 (0.49–4.84) 1.55 (1.03–2.31)

0.47 0.034

Total ablation time per 10 min increase

1.39 (1.15–1.68)

0.001

1.21 (0.97–1.53)

0.096

LA pressure at end of case (mmHg) Fluid net per 0.1 L increase

1.10 (1.02–1.19) 1.03 (0.99–1.08)

0.019 0.092

1.03 (0.93–1.14) 1.02 (0.97–1.08)

0.56 0.50

LV, left ventricular; LA, left atrial; AF, atrial fibrillation; PVI, pulmonary vein isolation.

Risk factors and potential mechanisms for post-pulmonary vein isolation heart failure We found that patients who developed HF after PVI were more likely to have history of persistent AF, AF at the beginning of their case, higher LA pressure, and more extensive LA ablation with additional ablation lines, although after multivariable adjustment only additional ablation lines beyond isolation of the pulmonary veins were an independent risk factor for development of HF. Neither the total number of RF lesions performed nor cumulative RF ablation time was independently correlated with HF. Although patients with persistent AF may have relatively more atriopathy at baseline and are more likely to have additional ablation performed as part of their PVI procedure, our findings suggest that extensive LA ablation rather than long-standing AF was the primary driver of post-ablation HF. These findings also suggest that the location of ablation may play an important role in development of post-ablation HF. The strong correlation between post-PVI HF and ablation lines beyond standard isolation of the pulmonary veins suggests that ablation-related damage to the LA itself might be of critical importance. This is supported by previous studies which have demonstrated that PVI can reduce LA systolic function,26 and that LA contractility and compliance are chronically impaired after extensive ablation for persistent AF, with the degree of LA dysfunction independently correlated with the extent of post-ablation LA scar detected by MRI.27

Notably, LVEF was not a risk factor for the development of postPVI HF. Although it is acknowledged that most patients with AF have some degree of diastolic dysfunction,28,29 the majority of patients who developed HF after ablation had normal LVEF and did not have a prior history of symptomatic HF. No significant difference in the peri-procedural use of intravenous diuretics was observed between those with and without post-ablation HF. While it is possible that diuretic dosing was insufficient in patients who developed symptomatic HF, neither net fluid balance, change in LA pressure during the case, nor ablation catheter choice (Thermocool vs. Thermocool SF) was associated with the development of post-PVI HF. It thus seems likely that the development of HF after RF catheter ablation for AF is related to factors beyond peri-procedural fluid management and elevated cardiac filling pressures. This is supported by data showing that 3 – 4% of patients undergoing DCCV develop post-cardioversion pulmonary oedema despite minimal intravenous fluid administration. Furthermore, despite considerably shorter procedure time and less procedural fluid administration, patients undergoing CTI ablation and cryoballoon PVI remained at risk for developing post-ablation HF (17 and 22% of patients, respectively). For patients with AF, elevated baseline LA pressure may not necessarily be a reflection of volume status but rather the degree of LA remodelling.30 In a study of 42 patients who underwent LA ablation, LA pressure did not change significantly for those whom furosemide was administered peri-procedurally and the correlation between LA

528

H.D. Huang et al.

Type of ablation lines performed in addition to PVI 25

25

22 20 17 #

15

15

15

10 7

7

7

5

3

3

3

0 f

TI

oo

LA

us m

C

R

al itr

lM

a er

t La

h st

I

LA

er

st Po

r

us m

io

al itr

h st

I

C

O

C SV

lM

a

pt

E FA

A

rR

e th

I

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at

l so

LA

n

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la Ab

A

LA

C

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Figure 2 Type and frequency of additional ablation lines used beyond that which was required for successful PVI. RA, right atrium; LA, left atrium; LAA, left atrial appendage; CS, coronary sinus; CFAE, complex fractionated atrial electrograms; CTI, cavotricuspid isthmus.

Table 5 Baseline patient and procedural characteristics for patients with AFl undergoing CTI AFl ablation All patients (n 5 36)

No HF (n 5 30)

HF (n 5 6)

P-value

66.0 (57.2–71.7) 29 (80.6%)

63.5 (57.0– 69.7) 25 (83.3%)

73.0 (62.5–82.7) 4 (66.7%)

0.23 0.57

............................................................................................................................................................................... Patient characteristics Age (years) Male White, non-hispanic

31 (86.1%)

26 (86.7%)

5 (83.3%)

1.0

9 (25.0%) 5 (13.9%)

6 (20.0%) 3 (10.0%)

3 (50.0%) 2 (33.3%)

0.15 0.19

Hypertension

21 (58.3%)

17 (56.7%)

4 (66.7%)

1.0

Diabetes Hyperlipidaemia

10 (27.8%) 16 (44.4%)

6 (20.0%) 13 (43.3%)

4 (66.7%) 3 (50.0%)

0.039 1.0 1.0

CAD History of CHF (.2 years prior to ablation)

Obstructive sleep apnoea LV ejection fraction (%) LA diameter (cm)

7 (19.4%)

6 (20.0%)

1 (16.7%)

55 (50–55) 6.1 (4.5–6.3)

55 (50– 59) 6.3 (4.4– 6.3)

43 (25– 55) 5.9 (4.5– 6.3)

0.071 0.81

14 (38.9%) 1 (2.8%)

9 (30.0%) 0 (0.0%)

5 (83.3%) 1 (16.7%)

0.024 0.17

5 (4–6)

4 (3– 4)

0.14

Procedure characteristics In AFl at start of case Lasix administered during procedure Time to phone follow-up (days)

5 (4– 6)

Data expressed as number (%), or median (interquartile range). LV, left ventricular; LA, left atrial; AFl, atrial flutter; CAD, coronary artery disease; CHF, congestive heart failure.

pressure and fluid balance was weak.31 Thus, measured LA pressure may be a poor predictor for identifying those who may require or respond to diuretic administration during PVI. In a 1000 patient study, Gibson et al. 32 showed that after extensive LA ablation 2% of patients developed ‘stiff atrial syndrome’ with severe atrial diastolic dysfunction manifesting as pulmonary hypertension,

pulmonary vascular congestion, and recurrent symptomatic HF, and existing atrial scar before the procedure was a risk factor for developing this syndrome. The natriuretic peptides atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) may also play a role in the development of post-ablation HF. Several studies have shown that ANP

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Incidence and risk factors for post-ablation heart failure

and BNP levels both decrease immediately following successful DCCV from AF to sinus rhythm,33,34 with a gradual increase in ANP levels up to 5 days after DCCV.35 Similarly in patients with persistent AF undergoing catheter ablation, Sacher et al. 36 demonstrated that there was a large decrease in ANP and BNP levels immediately following restoration of sinus rhythm. Over the next 3 days after ablation, ANP and BNP levels steadily increased and patient body weight decreased, although ANP and BNP did not return to pre-ablation levels. Conversely, Seiler et al. 31 showed that BNP levels increased from baseline in cases of LA ablation that began and ended in sinus rhythm. Thus, opposing changes in natriuretic peptide levels following ablation may be related to the correlation between starting rhythm and development of HF observed in this study. It is possible that patients who develop post-ablation HF may have a combination of delayed restoration of atrial mechanical function and an inadequate rise in ANP or BNP levels which normally occurs as a natriuretic response to HF.

initial hospital stay or readmission within 1 week for management of symptomatic HF after ablation. Development of post-ablation HF can be easily missed as symptoms may be delayed for 1 – 2 days following discharge from the hospital, but a combination of early follow-up and timely initiation of diuresis can potentially identify many of these patients and may prevent readmissions for HF. Creation of additional ablation lines beyond that required for PVI was an independent risk factor for development of post-ablation HF, suggesting that the extent of ablation-induced injury to the atrial myocardium may play an important role. Peri-procedural diuresis, change in LA pressure during the procedure, peri-procedural net fluid balance, and the use of low-volume irrigated ablation catheters were not risk independent factors for development of symptomatic HF. Future studies examining the mechanisms of and risk factors associated with post-ablation HF are needed to help elucidate improved strategies for preventing and managing post-ablation HF. Conflict of interest: none declared.

Limitations This study was performed at a single academic medical centre, and its results may therefore not be generalizable to other patient populations. Although the study prospectively examined consecutive patients undergoing ablation for AF and AFl, the study is limited by its observational nature and moderate-sized dataset. It is possible that some factors which lost significance in the multivariable model might have been shown to have a mild, independent correlation with post-PVI HF if more patients had been studied. However, even if this is possible, we can definitively conclude that additional ablation lines were by far the strongest correlate for post-PVI HF. Additionally, all ablation lines are not the same (there are variations in location, length, etc.), but we were not powered to assess the relative correlation of specific types/locations of additional ablation lines on the development of post-ablation HF. We are unable to state with certainty that ambulatory diuresis of patients who developed symptomatic HF led to prevention of some hospital readmissions, although this does seem plausible and is worthy of future study. Because this study only evaluated patients in the immediate post-procedure period, we are also unable to comment on the relationship between patient/procedure characteristics and the development of late-onset HF. This study was also not designed to examine mechanistic influences of associated HF risk factors. We are unable to comment on potential damage to the coronary arteries during ablation or plasma protein levels and if these factors might contribute to post-ablation HF in certain patients. Changes in right atrial pressure, diastolic function before and after ablation, and BNP levels were also not routinely measured, and we are unable to comment on their potential utility in terms of predicting, diagnosing, or explaining the mechanism behind postablation HF. Finally, this study was not powered to detect if there were correlations between specific types of additional ablation lines and post-ablation HF.

Conclusions This prospective, single-centre study reveals that post-ablation HF is a frequent complication of catheter ablation for atrial arrhythmias. For patients undergoing RF PVI, 13% require prolongation of their

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EP CASE EXPRESS

doi:10.1093/europace/euw058

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A pacemaker lead implantation: what if we go through the stent strut cell? Leila Riahi*, Edward E. E. Gabeler, Raluca Prisecaru, and Bruno Schwagten ZNA Middelheim, Antwerp, Belgium

* Corresponding author. E-mail address: [email protected]

We present a case report of a 78-year-old male patient, with a left arteriovenous haemodialysis fistula and left subclavian vein thrombosis treated with 2 Cordis SMART stents. Stents were implanted 2 years ago in the left subclavian vein and left innominate vein for symptomatic central vein occlusion. Doublechamber pace maker implantation was scheduled for a sick sinus syndrome on the contralateral side to avoid endangering flow in the left-sided arteriovenous fistula. After a right subclavian vein puncture, an angiogram was made revealing a long stent extending from the left subclavian vein into the superior caval vein (SVC). When advancing the classical guide wire, direct access to the SVC appeared to be impossible. However, contrast seemed to run off to the right atrium through the stent strut cells. Using a & Terumo hydrophilic 0.03-inch guide wire we managed to cross the stent reaching the right atrium and ventricle. A pre-shaped introducer sheath was advanced over the wire dilating the stent strut cell. Successively, the ventricular lead was inserted through the sheath, and implanted in the right ventricular apex. The same manoeuver was performed through a separate stent strut cell to implant the right atrial lead (Figure). The full-length version of this report can be viewed at: http://www.escardio.org/Guidelines-&-Education/E-learning/Clinical-cases/ Electrophysiology/EP-Case-Reports. Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2016. For permissions please email: [email protected].