Circulation. Arrhythmia and electrophysiology最新文献

Background: Accurate delineation of scar patterns is valuable for guiding catheter ablation of ventricular tachycardia. We hypothesized that scar and its pattern of distribution can be determined from intracardiac electrograms using computational signal processing and that further improvements in classification can be achieved with a convolutional neural network.

Methods: A total of 5 sheep underwent anteroseptal infarction (plus 1 healthy control) with electroanatomic mapping (129±12 days post-infarct). A whole-heart histological model of the postinfarction scar was created and coregistered to ventricular electrograms. Electrograms were matched to scar pattern categories; no scar, at least endocardial scar: at least intramural scar (intramural scar sparing the endocardium), or epicardial-only scar (epicardial scar sparing the endocardium/intramural space). A suite of signal-processing features was extracted from bipolar electrograms. Furthermore, bipolar and unipolar electrograms were used to train a time series convolutional neural network (InceptionTime).

Results: A total of 11 551 electrograms were matched to 451 biopsies. Bipolar and unipolar voltage alone were poor classifiers of scar patterns. For each of the scar labels, 20 bipolar electrogram features (predominantly within the frequency domain) yielded an area under the curve of 0.815, 0.810, 0.704, and 0.681 to predict no scar, at least endocardial scar, at least intramural scar, and epicardial-only scar, respectively. Substantial improvement was achieved with a convolutional neural network trained on unipolar electrograms: areas under the curve and accuracy (averaged across wavefronts) were 0.977 and 0.929 for no scar, 0.970 and 0.919 for at least endocardial scar, 0.909 and 0.959 for at least intramural scar and 0.926 and 0.958 for epicardial-only scar.

Conclusions: Convolutional neural network-derived analysis of unipolar electrogram data has excellent predictive value for determination of scar patterns. Computational analyses of electrogram data beyond voltage and other time-domain features are necessary to improve the identification of arrhythmogenic sites in the ventricle.

Background: Wrist-worn wearables can detect irregular heart rhythms using photoplethysmography, but ECGs are required to confirm atrial fibrillation (AF). We sought to determine the frequency of a recurrent irregular heart rhythm detection (IHRD; ≥30 minutes of an irregular rhythm), estimate the potential diagnostic yield of different electrocardiographic monitoring strategies for confirming AF, and identify predictors of recurrent IHRDs.

Methods: The Fitbit Heart Study enrolled wrist-worn photoplethysmography device users without diagnosed AF. Of 455 699 participants, 1057 who wore and returned a 1-week ECG patch monitor after receiving an IHRD were analyzed. Baseline clinical data, device-derived metrics, IHRDs during follow-up, and electrocardiographic patch data were used for analysis.

Results: A total of 570 (53.9%) participants were aged 40 to 64 years, 422 (39.9%) were aged ≥65 years, and 510 (48.2%) were women. Median follow-up after ECG patch initiation was 80 days (interquartile range, 45-122 days). The frequency of another IHRD was 57.2% (95% CI, 53.1%-60.9%) at 3 months. After an initial IHRD, the estimated diagnostic yield for AF with a 10-second ECG was 7.6% (95% CI, 6.2%-9.0%), twice-daily 30-second ECGs over 1 week 19.0% (95% CI, 16.7%-21.2%), 24-hour monitor 17.4% (95% CI, 15.5%-19.3%), 1-week monitor 32.2% (95% CI, 29.4%-35.0%), 2-week monitor 46.8% (95% CI, 42.7%-50.8%), and 4-week monitor 60.8% (95% CI, 56.5%-65.1%). The risk of a recurrent IHRD was greater with older age (P<0.001), male sex (P=0.001), vascular disease (P=0.03), longer initial runs of consecutive IHRDs at detection (P=0.02), and less nightly sleep (P=0.03).

Conclusions: Irregular heart rhythms are common after initial detection using a wrist-worn wearable device. Longer electrocardiographic monitoring periods increase the likelihood of confirming AF.

Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT04380415.

Background: Differences in cardiac sarcoidosis between racial groups remain understudied. Therefore, this study aims to explore race differences in patients with cardiac sarcoidosis.

Methods: We analyzed data from the Cardiac Sarcoidosis Consortium, an international registry including over 25 centers. The primary clinical outcome was a composite end point of all-cause mortality, left ventricular assist device implantation, heart transplantation, or implantable cardioverter defibrillator therapy.

Results: A total of 619 patients were included in the study (362 White, 193 Black, and 64 other races). Black patients were diagnosed with cardiac sarcoidosis at a younger age (50.5±11.8 versus 53.7±10.5 years old; P=0.010) compared with White patients. Left ventricular ejection fraction was significantly lower in Black patients (44.6±15.4 versus 48.3±14.0; P=0.008). In addition, extracardiac involvement in the lungs (80.3% versus 72.7%; P=0.046), skin (22.8% versus 12.4%; p=0.002), and eyes (13.5% versus 5.5%; P=0.001) was more prevalent in Black patients. Patients had significantly higher rates of hypertension (69.9% versus 50.6%; P<0.001), diabetes (37.8% versus 21.0%; P<0.001), smoking (40.9% versus 26.8%; P<0.001), chronic obstructive pulmonary disease or emphysema (15.5% versus 4.1%; P<0.001), and chronic kidney disease (25.9% versus 12.4%; P<0.001). The treatment patterns including glucocorticoid (71% versus 74.3%; P=0.4), glucocorticoid-sparing (53.4% versus 59.9%; P=0.14), and implantable cardioverter defibrillator or cardiac resynchronization implantation (75.6% versus 73.8%; P=0.63), were similar. No significant differences were found in the primary outcome (29.5% in Black versus 28.5% in White; P=0.79). Subgroup analysis of the primary outcome also revealed no significant differences in both the left ventricular ejection fraction >35% group (24.1% in Black versus 25.9% in White; P=0.72) and the left ventricular ejection fraction ≤35% group (51% versus 42.5%; P=0.35).

Conclusions: Black patients with cardiac sarcoidosis exhibited significantly higher rates of lung, skin, and eye involvement and comorbidities, but had similar cardiac clinical outcomes and all-cause mortality compared with White patients. Nonetheless, ascertainment bias cannot be excluded.

Background: Ventricular arrhythmias (VAs) are a major concern in athletes. We sought to determine the prognostic role of noninvasive and invasive assessments in athletes with complex VAs.

Methods: One-hundred-ninety athletes (82% men; 28 [19-43] years; 148 [78%] competitive athletes) with frequent or exercise-induced premature ventricular complexes or nonsustained ventricular tachycardia were included in a multicenter cohort study and categorized based on VA ECG morphology into common (n=99) and uncommon (n=91) VA groups. Each athlete underwent a comprehensive diagnostic workup, including cardiac magnetic resonance in 94% (n=178) and electrophysiology study/electroanatomical mapping in 87% (n=166). The primary end point was the occurrence of sudden death or sustained VAs during long-term follow-up.

Results: Athletes with uncommon VA morphology had higher rates of abnormal findings at multimodality assessment and more final diagnoses of structural heart disease. Over a median follow-up of 6.2 (4.3-8.1) years, 7 (4%) athletes experienced a primary outcome event, including 1 sudden death. Interestingly, no events occurred in athletes with common morphology VAs. In univariable Cox models, factors associated with the primary end point included uncommon VA morphology (P=0.003), lack of VA suppression (P=0.049), and nonsustained ventricular tachycardia/ventricular tachycardia induction (P=0.010) during stress testing, late gadolinium enhancement (P=0.045), electroanatomical scar regions (P=0.022), and sustained VA inducibility by electrophysiology study (P<0.001). Incorporating findings of invasive tests improved prediction of primary outcome events over clinical/noninvasive findings in isolation (log-likelihood ratio for nested models, P=0.004). A survival tree model based on VA morphology, late gadolinium enhancement, VA response to exercise testing, and electroanatomical mapping allowed risk stratification, identifying subgroups of athletes without primary outcome events during follow-up. Among 148 competitive athletes, 101 (68%) regained eligibility after 3 months of detraining, but only 42 (28%) continued long-term.

Conclusions: A comprehensive diagnostic assessment integrating ECG, stress testing, and imaging findings, along with the selective use of invasive electrophysiology assessments, may help refine the prognostic evaluation of athletes with complex VAs.

Background: We have previously reported a novel clinical risk score (risk prediction score for shockable sudden cardiac arrest [VFRisk]) for the prediction of shockable sudden cardiac arrest, discovered and validated in 2 US west coast communities. We hypothesized that VFRisk predicts sudden cardiac death (SCD) risk in the geographically distinct FHS (Framingham Heart Study).

Methods: We performed a nested case-referents study in the FHS to test VFRisk. Cases were participants who experienced SCD among the original and offspring FHS cohorts. Referents were randomly selected from FHS participants frequency-matched (ratio of 1:3) to cases on age, sex, cohort, and exam. VFRisk was the sum of 12 risk factors, each multiplied by its respective points.

Results: Among 312 cases and 935 referents, mean ages were 69.5 and 69.7 years with 70.8% men in both groups. SCD cases had significantly higher prevalence of diabetes, heart failure, stroke, atrial fibrillation, and myocardial infarction compared with the referents group. The VFRisk score was validated with good discrimination (C-statistic, 0.71 [95% CI, 0.66-0.77]) for SCD. Cases had higher VFRisk scores than referents (3.8±2.8 versus 1.8±1.7; P<0.001). A 1-unit increase in VFRisk score was associated with a 48% increase in odds of SCD (odds ratio, 1.48 [95% CI, 1.34-1.64]). The highest VFRisk quartile had 7.8-fold higher odds of SCD than the lowest quartile.

Conclusions: The VFRisk score successfully predicted SCD in the FHS. The differences in discrimination between the 2 studies could partially be explained by the inability to distinguish shockable versus nonshockable events in the FHS.

Background: Sinoatrial node (SAN) dysfunction is commonly associated with atrial dysrhythmia (tachy-brady syndrome) and is a particularly important feature of inherited atrial cardiomyopathies leading to artificial pacemaker implantation. Essential MYL4 (myosin light chain-4) is an atrial-selective protein that associates with the myosin light chain and participates importantly in cardiacmuscle contraction. MYL4 gene variants encoding dysfunctional versions of MYL4 cause familial atrial cardiomyopathy with a high incidence of early SAN dysfunction (SND) and pacemaker requirement. In this study, we used a rat line, genetically modified to express an E11K gene mutation responsible for familial atrial cardiomyopathy, to address the mechanisms underlying SND.

Methods: Cardiac structure and function were assessed by echocardiography and in vivo telemetry recording. SAN function was studied in vivo with intracardiac electrophysiology and ex vivo with optical mapping. Mechanisms underlying SND were interrogated in vitro with the use of voltage and current clamp with tight-seal patch-clamp and Ca²⁺ imaging of isolated SAN cardiomyocytes. Gene expression was assessed by quantitative polymerase chain reaction, and fibrosis was determined with Masson's trichrome stain.

Results: Mutant Myl4-p.E11K^+/+ rats exhibited worse SAN function compared with wild-type controls. In vivo, SND was demonstrated by ≈63% increase in sinus node recovery time compared with wild type. In vitro, SAN conduction velocity was reduced by ≈ 50% for Myl4-p.E11K^+/+ compared with wild type. Isolated SAN cells showed ≈50% reduction in funny current and L-type Ca²⁺-current densities. Dysregulation of Ca²⁺ homeostasis was observed in Myl4-p.E11K^+/+, with ≈30% slower time to peak and Ca²⁺ decay. Masson's trichrome staining showed ≈45% increase in SAN region collagen deposition in Myl4-p.E11K^+/+.

Conclusions: Myl4-p.E11K^+/+ mutation causes progressive SND with aging, as a result of extensive abnormalities in the underlying determinants of SAN function, including ion-channel properties, Ca²⁺-homeostasis, and SAN structure. These observations provide new insights into the mechanisms of SAN abnormality in atrial cardiomyopathy.