Transcatheter aortic valve replacement (TAVR) is a less invasive treatment option for patients that are deemed too high a risk for surgical aortic valve replacement (SAVR). The aim of this review is to evaluate the frailty tools currently being used in patients referred for TAVR. Using a literature search involving database search engines from CINAHL, PubMed, SAGE publications and European Society of Cardiology conducted from 2010 to the present, a critical evaluation of studies dealing with frailty assessment in patients referred for TAVR/SAVR is discussed. Eight studies met the criteria using frailty assessment in TAVR/SAVR patients. In all reviewed studies the impact of frailty on clinical outcome has been proved. Different instruments for measurements of frailty were used that have not been robustly evaluated. Frailty was defined differently and results may not be comparable. All reviewed studies used different cutoffs and scales and some a composite scoring system, although validity was limited. For frailty assessment implementation of validated standardized test protocols based on well-established assessment tools, covering all domains of frailty among TAVR centers is crucial for patient selection. Secondly, validated cutoffs and scoring systems are essential.

Sudden cardiac death (SCD), most often induced by ventricular arrhythmias, is one of the main reasons for cardiovascular-related mortality. While coronary artery disease remains the leading cause of SCD, other pathologies like cardiomyopathies and, especially in the younger population, genetic disorders, are linked to arrhythmia-related mortality. Despite many efforts to enhance the efficiency of risk-stratification strategies, effective tools for risk assessment are still missing. Biomarkers have a major impact on clinical practice in various cardiac pathologies. While classic biomarkers like brain natriuretic peptide (BNP) and troponins are integrated into daily clinical practice, inflammatory biomarkers may also be helpful for risk assessment. Indeed, several trials investigated their application for the prediction of arrhythmic events indicating promising results. Furthermore, in recent years, active research efforts have brought forward an increasingly large number of “novel and alternative” candidate markers of various pathophysiological origins. Investigations of these promising biological compounds have revealed encouraging results when evaluating the prediction of arrhythmic events. To elucidate this issue, we review current literature dealing with this topic. We highlight the potential of “classic” but also “novel” biomarkers as promising tools for arrhythmia prediction, which in the future might be integrated into clinical practice.

Interleukin (IL)-16, a polypeptide cytokine, plays a crucial role in the inflammatory process, acting as a chemoattractant for peripheral immune cells and has been linked to various inflammatory diseases. However, its role in patients with acute myocardial infarction (AMI) is unclear. We retrospectively analyzed serum levels of IL-16 in blood of patients with (STEMI, n = 45) and without ST-segment elevation myocardial infarction (NSTEMI, n = 42) compared with controls with excluded coronary artery disease (n = 55). Furthermore, correlation analysis with inflammatory cells, C-reactive protein (CRP) levels, dendritic cell precursors (DCPs), and other clinical and biochemical markers was performed. Compared with controls, patients with STEMI and NSTEMI evidenced higher levels of IL-16 in pg/mL (STEMI: 759.38 ± 471.54, NSTEMI: 677.77 ± 438.8, control: 500.45 ± 432.21; P = .002). IL-16 correlated with CRP (r = 0.26, P = .001), leucocytes (r = 0.38, P < .001), NT-proBNP (r = 0.20, P = .02) and hsTnT (r = 0.25, P = .004). Circulating myeloid DCPs, plasmacytoid DCPs, and total DCPs showed a significant inverse correlation to IL-16 levels (r = −0.21, P = .01; r = −0.23, P = .005; r = −0.26, P = .002, respectively). Interleukin-16 might play an important role in the inflammatory process of patients suffering from AMI and correlates with inflammatory cell activation and clinical and biochemical markers. The cytokine IL-16 might upregulate the proinflammatory response and recruitment of inflammatory cells into infarcted myocardium.

The length of the CTI as measured with help of a three-dimensional mapping system may reflect only a weak indicator for the complexity of flutter ablation procedures. The thickness of musculature and specific anatomy of the CTI seem to be the main challenges in performing a linear ablation to achieve bidirectional block.