Citations

AbstractIntroductionReticulated platelet (RP) content is increased in nonvalvular atrial fibrillation (NVAF). The purpose of this study was to determine if platelet content, morphology, and RP proportion are modulated by platelet genes.Methods and resultsExpression of six platelet‐predominate genes impacting platelet formation and release, platelet count, and RP content was assessed in NVAF patients before and 3–4 months after pulmonary veins isolation (PVI) and compared to normal sinus rhythm (NSR) controls. RNA from isolated platelets was reverse‐transcribed assayed against selected genes utilizing real‐time qPCR, and expressed as mean cycle threshold (ΔCt) using beta‐2‐microglobulin as endogenous control. RP content was assessed by flow cytometry. A fourfold lower expression of CFL1 gene coding for nonmuscle cofilin (7.8 ± 0.9 vs. 5.7 ± 1.6, P < 0.001) and twofold lower expression of four other genes were associated with similar platelet counts but fourfold higher (28.7+7.0 vs. 6.7+5.4, P < 0.001) RP content (%) in 97 NVAF cases compared to 51 NSR controls. Three to 4 months after PVI, RP decreased by 28%, while CFL1 gene expression increased over twofold but TUBA4A gene expression decreased almost twofold; NFE2 and MYL6 gene expression remained unchanged.ConclusionsNVAF is associated with notable downregulation of genes directing platelet production and size but increased RP content. PVI impacts the expression of many of these genes, implying a direct relationship between atrial fibrillation and platelet biogenesis.

Background: Use of magnetic resonance imaging (MRI) brain is restricted in patients with cardiovascular implantable electronic devices (CIEDs). We proposed to determine whether mortality difference exists for patients with non–MRI-conditional CIEDs undergoing brain MRI compared with controls. Methods and Results: Retrospective analysis of prospectively collected data was performed to compare all-cause mortality in patients with CIEDs undergoing brain MRI (CIED-MRI) with 3 control groups matched for age, sex, imaging year, and type of CIED: (1) no CIED, brain MRI (no–CIED-MRI); (2) CIED, brain computerized tomography (CT) scan (CIED-CT); and (3) no CIED, brain CT (no–CIED-CT). The primary outcome was a significant difference ( P <0.05) between estimated mortality rates. Secondary outcomes were changes in device function before and after brain MRI. The estimated all-cause mortality at 5 years for the CIED-MRI group [mean age (±SD), 68.2 years (15.3 years); 61.2% men] was not significantly different from patients who underwent CT with or without a device (CIED-CT group: hazard ratio, 0.814; 95% confidence interval, 0.593–1.117; P =0.2; no–CIED-CT group: hazard ratio, 1.149; 95% confidence interval, 0.818–1.613; P =0.4). There was a significant increase in mortality between CIED-MRI and no–CIED-MRI groups (hazard ratio, 1.463; 95% confidence interval, 1.019–2.099; P =0.04). Conclusions: Brain MRI in patients with CIEDs does not carry an increased mortality risk compared with brain CT and can be performed with adherence to appropriate procedural protocols.

AbstractBackgroundTransthoracic impedance measurements (TIM) is primarily used for minute ventilation rate adaptive sensors in pacemakers. With elevated impedance, the TIM electrical signal itself is oversensed, causing device malfunction.ObjectiveWe report an increased incidence of TIM oversensing.MethodRetrospective chart review. We review existing records of 18 patients who have demonstrated device malfunction with TIM oversensing.ResultsWe have found a 1.8% incidence of TIM‐related oversensing in our patient population of 959 patients with contemporary Boston Scientific (Marlborough, MA, USA) pacemakers and cardiac resynchronization therapy pacemakers. One patient experienced a syncopal episode.ConclusionOversensing with pacing inhibition is apparent with the potential of adverse effects to patients.

Background: Although the hallmark of long-QT syndrome (LQTS) is abnormal cardiac repolarization, there are varying degrees of phenotypic expression and arrhythmic risk. Our aim was to evaluate the performance of a morphological T-wave analysis program in defining breakthrough LQTS arrhythmic risk beyond the QTc value. Methods and Results: We analyzed 407 genetically confirmed patients with LQT1 (n=246; 43% men) and LQT2 (n=161; 41% men) over the mean follow-up period of 6.4±3.9 years. ECG analysis was conducted using a novel, proprietary T-wave analysis program. Time to a LQTS-associated cardiac event was analyzed using Cox proportional hazards regression methods. Twenty-three patients experienced ≥1 defined breakthrough cardiac arrhythmic events with 5- and 10-year event rates of 4% and 7%. Two independent predictors of future LQTS-associated cardiac events from the surface ECG were identified: left slope of T wave in lead V6 (hazard ratio=0.40 [0.24–0.69]; P <0.001) and T-wave center of gravity x axis (last 25% of wave) in lead I (hazard ratio=1.90 [1.21–2.99]; P =0.005), C statistic of 0.77 (0.65–0.89). When added to the QTc (C statistic 0.68 for QTc alone), discrimination improved to 0.78. Genotype analysis showed weaker association between these T-wave variables and LQT1-triggered events while these features were stronger in patients with LQT2 and significantly outperformed the QTc (C statistic, 0.82 [0.71–0.93]). Conclusion: Detailed morphological analysis of the T wave provides novel insights into risk of breakthrough arrhythmic events in LQTS, particularly LQT2. This observation has the potential to guide clinical decision making and further refine risk stratification.

Background: Recognition of rates and causes of hard, patient-centered outcomes of death and cerebrovascular events (CVEs) after heart rhythm disorder management (HRDM) procedures is an essential step for the development of quality improvement programs in electrophysiology laboratories. Our primary aim was to assess and characterize death and CVEs (stroke or transient ischemic attack) after HRDM procedures over a 17-year period. Methods: We performed a retrospective cohort study of all patients undergoing HRDM procedures between January 2000 and November 2016 at the Mayo Clinic. Patients from all 3 tertiary academic centers (Rochester, Phoenix, and Jacksonville) were included in the study. All in-hospital deaths and CVEs after HRDM procedures were identified and were further characterized as directly or indirectly related to the HRDM procedure. Subgroup analysis of death and CVE rates was performed for ablation, device implantation, electrophysiology study, lead extraction, and defibrillation threshold testing procedures. Results: A total of 48 913 patients (age, 65.7±6.6 years; 64% male) who underwent a total of 62 065 HRDM procedures were included in the study. The overall mortality and CVE rates in the cohort were 0.36% (95% confidence interval [CI], 0.31–0.42) and 0.12% (95% CI, 0.09–0.16), respectively. Patients undergoing lead extraction had the highest overall mortality rate at 1.9% (95% CI, 1.34–2.61) and CVE rate at 0.62% (95% CI, 0.32–1.07). Among patients undergoing HRDM procedures, 48% of deaths directly related to the HDRM procedure were among patients undergoing device implantation procedures. Overall, cardiac tamponade was the most frequent direct cause of death (40%), and infection was the most common indirect cause of death (29%). The overall 30-day mortality rate was 0.76%, with the highest being in lead extraction procedures (3.08%), followed by device implantation procedures (0.94%). Conclusions: Half of the deaths directly related to an HRDM procedure were among the patients undergoing device implantation procedures, with cardiac tamponade being the most common cause of death. This highlights the importance of the development of protocols for the quick identification and management of cardiac tamponade even in procedures typically believed to be lower risk such as device implantation.

AbstractAimsvon Willebrand factor (VWF) is an independent risk factor for adverse events in patients with non‐valvular atrial fibrillation (NVAF). However, it is unclear if VWF level remains elevated and predictive of stroke during entire course of NVAF.Methods and ResultsIn order to determine if VWF is a time‐dependent blood variable, VWF antigen measured by latex immunoassay in 425 NVAF patients and 100 controls with normal sinus rhythm (NSR) was analyzed according to NVAF duration (<1 month: n = 76, 1‐12 months: n = 98, and >12 months: n = 251). The mean VWF antigen level in NVAF patients with <1‐month duration (167 ± 59%) was not different compared to those with 1‐12 months (157 ± 50%, P = .24) and >12 months duration (156 ± 54%, P = .11) but higher compared to NSR controls (143 ± 48%, P = .003). Higher VWF level correlated with higher CHADS2 scores and with progressing intensity of blood stasis in the left atrium and thrombus formation in all three time periods of atrial fibrillation duration. Patients not treated with warfarin had VWF 30% higher in the first month compared to following months.Conclusionsvon Willebrand Factor is steadily elevated throughout the course of dysrhythmia in NVAF patients treated with warfarin and in those with higher intensity of left atrium blood stasis.