Atrial fibrillation in cancer patients who develop stroke.

BACKGROUND: Acute ischemic stroke (Stroke) and transient ischemic attacks (TIA) are known complications in cancer patients and those with atrial fibrillation (AF). The role AF plays in Stroke/TIA in the setting of cancer is unclear. The purpose of this study was to assess the relationship between AF and Stroke/TIA in cancer patients. METHODS: We conducted a case-control study comparing all patients who developed Stroke/TIA from 2014 to 2019 following a cancer diagnosis at King Hussein Cancer Center (KHCC), matched to Stroke/TIA-free controls based on age, gender, and cancer site. RESULTS: Two hundred seventy-two patients were included (136 per group). The mean age was 63.95 ± 13.06 and 57% were females. The Stroke/TIA group had more AF at the time of event (14% vs. 4%, OR: 4.25, 95%-CI: 1.39 - 17.36) and had a larger proportion of death on study conclusion (OR: 9.4, 95%-CI: 3.74 - 23.64). On conditional logistic regression, patients in the Stroke/TIA group had higher odds of: AF (OR: 7.93, 95%-CI: 1.6 - 39.18), ischemic stroke before cancer diagnosis (OR: 9.18, 95%-CI: 2.66 - 31.74), being on active cancer treatment (OR: 3.11, 95%-CI: 1.46 - 6.62), dyslipidemia (OR: 3.78, 95%-CI: 1.32 - 10.82), and renal disease (OR: 4.25, 95%-CI: 1.55 - 11.63). On another conditional logistic regression model built to assess the role of the CHA2DS2-VASc score, a score of >=2 in males and >=3 in females significantly increased the risk of developing Stroke/TIA in cancer patients (OR: 2.45, 95%-CI: 1.08 - 5.58). CONCLUSION: AF, previous ischemic stroke, active cancer treatment, dyslipidemia, and renal disease are independent risk factors for Stroke/TIA and a higher CHA2DS2-VASc score significantly increases the risk in cancer patients regardless of AF.

Comparative safety of periablation anticoagulation strategies for atrial fibrillation: data from a large multicenter study.

BACKGROUND: There are a variety of periprocedural anticoagulation strategies for atrial fibrillation (AF) ablation, including the use of dabigatran. It is unclear which strategy is superior. OBJECTIVE: To compare the safety and efficacy of anticoagulation with uninterrupted warfarin, dabigatran, and warfarin with heparin bridging in patients undergoing ablation of AF at four experienced centers. METHODS AND RESULTS: In this retrospective analysis, 882 patients (mean age: 61 ± 11 years) underwent ablation of AF using uninterrupted warfarin (n = 276), dabigatran (n = 374), or warfarin with heparin bridging (n = 232) for periprocedural anticoagulation. The rate of total complications was 23/276 (8.3%) in the uninterrupted warfarin group, 30/374 (8.0%) in the dabigatran group, and 29/232 (12.5%) in the bridged group (P = 0.15). Major complications were more frequent in the uninterrupted warfarin group 12/276 (4.3%) compared with 3/374 (0.8%) in dabigatran and 6/232 (2.6%) in the bridged group (P = 0.01). The most common major complication was the need for transfusion or occurrence of major bleeding. Minor complications did not differ among the three groups. On multivariate analysis, female gender (odds ratio [OR] 1.93, confidence interval [CI] 1.16-3.19, P = 0.011), bridging heparin (OR 2.13, CI 1.100-3.941, P = 0.016), use of triple antithrombotic therapy (OR 1.77, CI 1.05-2.98, P = 0.033), and prior myocardial infarction (OR 2.40, CI 1.01-5.67, P = 0.046) independently predicted total complications. CONCLUSIONS: When comparing the use of uninterrupted warfarin, dabigatran, and warfarin with heparin bridging in patients undergoing catheter ablation of AF, dabigatran was not associated with increased risk, major complications were more common in the uninterrupted warfarin group, and after adjustment, warfarin with bridging increased total complications.

QTc compared to JTc for monitoring drug-induced repolarization changes in the setting of ventricular pacing.

BACKGROUND: QT prolongation is a risk factor for proarrhythmia when beginning antiarrhythmic drug therapy (AAD). However, there are no data regarding monitoring repolarization changes during a ventricular paced (VP) rhythm. OBJECTIVE: The purpose of this study was to compare serial changes in corrected QT and JT intervals, during native conduction (NC) and VP rhythms when initiating Class III AADs. METHODS: Twenty-two patients (73% men; mean age 65 ± 11 years) with an implantable device and with <10% VP were monitored during AAD initiation (16 sotalol, 6 dofetilide). QTc and JTc were measured from ECGs obtained during NC and VP at baseline (pre-AAD) and then after each AAD dose. RESULTS: During AAD loading, mean QTc increased significantly during NC (431 ± 28 ms to 463 ± 33 ms, P = .002) but not with VP (520 ± 48 ms to 538 ± 45 ms, P = .07). Mean percent increase in peak QTc during NC was significantly greater than during VP (12% vs 7%, P = .003). In contrast, peak JTc during AAD loading was not significantly different between NC and VP (P = .67). CONCLUSION: When initiating AAD, the change in QTc during VP does not correlate with the change in QTc during NC; thus, the VP QTc is inadequate for monitoring repolarization changes. However, VP JTc correlates well with JTc during NC. When initiating Class III AADs in patients with VP rhythms, the JTc, and not the QTc, interval is the useful marker for assessing repolarization.

Impact of international normalized ratio and activated clotting time on unfractionated heparin dosing during ablation of atrial fibrillation.

BACKGROUND: For ablation of atrial fibrillation, it is unclear how baseline international normalized ratio (INR) affects the dosing of unfractionated heparin (UFH). METHODS AND RESULTS: A retrospective review of 170 consecutive patients undergoing atrial fibrillation ablation with baseline activated clotting time (ACT) and INR values was performed. Patients were grouped according to INR <2.0 (G<2; n=129) and INR ≥2.0 (G≥2; n=41). Clinical variables, UFH doses, and ACT values were recorded. An equation was derived to calculate the first bolus of UFH required to achieve an ACT ≥300 seconds, and this was subsequently assessed in 168 patients. For the initial 170 patients, the baseline INR (2.47±0.31 versus 1.53±0.31) and ACT (185±26 versus 153±30 seconds) were significantly greater in G≥2 (P<0.001). The amount of UFH to achieve the first ACT ≥300 seconds was significantly higher for G<2 versus G≥2 (9701±2390 versus 8268±2366 U; P=0.0001). Baseline INR, ACT, and weight were predictors of the UFH dosage to achieve an ACT ≥300 seconds. An equation derived to achieve an ACT ≥300 seconds after a single bolus of UFH met this end point in 160 of 168 patients (95%). CONCLUSIONS: Baseline INR and ACT, in addition to weight, are the only predictors of UFH dosage needed to achieve an ACT ≥300 seconds. A derived equation predicted the UFH dosage to achieve an ACT ≥300 seconds.