The Year in Cardiovascularmedicine 2020: Arrhythmias

Harry J.G.M. Crijns; Frits Prinzen; Pier D. Lambiase; Prashanthan Sanders; Josep Brugada

Disclosures

Eur Heart J. 2021;42(5):499-507. 

In This Article

Inherited Cardiac Conditions, Risk Assessment, Implantable Defibrillators, and Sudden Death

A novel approach to the diagnosis of Brugada syndrome (BrS) described the utilization of autoantibody screening for α-cardiac actin, α-skeletal actin, keratin, and connexin-43. In total, 18/18 BrS subjects demonstrated this autoantibody profile vs. 0/8 normal controls and 0/20 cardiomyopathy cases, which included arrhythmogenic right ventricular cardiomyopathy (ARVC), hypertrophic cardiomyopathy (HCM), and dilated cardiomyopathy (DCM) patients.[50] In a subgroup of BrS patients, each of these proteins and the sodium channel protein type 5 alpha subunit (NaV1.5) aggregated in the sarcoplasm of myocardial cells. The mechanism as to why antibodies to these proteins identified BrS cases is unclear but could relate to sarcolemmal membrane damage either due to a myocarditic process in the disease course or abnormal cell adhesion resulting in an immune response. The novelty of this study is the utilisation of a serological test to identify BrS subjects, which can be challenging given the transient nature of the electrocardiogram (ECG) pattern. This paper is complemented by a study investigating polygenic risk (PRS) of ECG markers to predict a positive ajmaline response.[51] PRS for BrS, baseline QRS duration, presence of Type II or III BrS ECG at baseline and family history of BrS were independently associated with the occurrence of a Type I BrS ECG, with good predictive accuracy (optimism-corrected C-statistic 0.74). This provides the first data to enable the combination of genetic and clinical screening to predict ajmaline responses and has implications for risk stratification.

A combined clinical and electrophysiological mapping study showed that SCN5A mutation carriers exhibit more pronounced epicardial electrical abnormalities and a more aggressive clinical presentation than non-carriers.[52]

Recent data support the use of drug therapy to manage patients with catecholaminergic polymorphic VT (CPVT). In a provocative paper by Van der Werf et al.,[53] no survival benefit from ICDs was shown in young CPVT patients surviving cardiac arrest. There are a number of caveats to this study, but the main learning point was that such patients can be treated without an ICD.

PRAETORIAN compared transvenous and subcutaneous ICDs in 849 patients >18 years with a class I or Iia indication for ICD therapy for primary or secondary prevention, followed for 49.1 months.[54] S-ICD demonstrated non-inferiority of the composite primary endpoint of device-related complications and inappropriate shocks. This provides the first multicentre trial evidence that the S-ICD is as effective and safe as transvenous ICD in preventing SCD for patients not requiring brady-pacing, anti-tachycardia VT pacing, or CRT, but challenges remain including longevity of leads and ICD, and inappropriate shocks. Concerning the latter, the UNTOUCHED study of primary prevention ICD therapy supports the PRAETORIAN data by showing an inappropriate shock-free rate of 95.9%, suggesting that the new SMART PASS filter technology and appropriate high rate S-ICD programming may minimize inappropriate shocks in S-ICD recipients.[55]

Two primary prevention ICD registries applying propensity scoring showed beneficial effects but differed concerning efficacy of ICD in women and elderly.[56,57]

To predict sudden arrhythmic death (SAD) in coronary artery disease, the PRE-DETERMINE investigators integrated an ECG risk score with conventional cardiovascular parameters. A high-risk ECG score incorporating contiguous Q waves, LV hypertrophy, QRS duration, and JTc prolongation was more strongly associated with SAD than non-SAD (adjusted hazard ratios 2.87 vs. 1.38) and the proportion of deaths due to SAD was greater in the high vs. low risk groups (24.9% vs. 16.5%).[58] The addition of ECG markers to a clinical risk factor model including LVEF improved discrimination and reclassification, including correct reclassification of 28% of patients in the validation cohort. The strength of this approach is the utilization of simple bedside biomarkers to determine management, but it needs clinical validation in a randomized trial.

To conclude, The Year in Cardiovascular Medicine 2020—Arrhythmias shows significant progress in the field, much of it incremental, some of it attention gathering, and some of it clearly needing further work.

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