AF is common in patients with HCM who need a CRM device. More than 50% of these patients develop de novo AF that was predominantly subclinical in our cohort.

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Background Hypertrophic cardiomyopathy (HCM) is characterized by asymmetric left ventricular hypertrophy (LVH). However, clinical signs can be subtle and differentiation from other causes of LVH is challenging. Hypothesis As diastolic dysfunction (DD) is an early sign in HCM, we aimed to find regional changes in relaxation pattern for differentiation from other entities of LVH. Methods In 148 patients (81 HCM, 55 arterial hypertension (AHT), 12 Fabry disease) and 63 healthy controls, relaxation patterns were assessed using regional tissue Doppler imaging. In 42 HCM patients, myocardial mass and fibrosis were quantified by cardiac magnetic resonance imaging and correlated with relaxation parameters. Results In HCM the septal to lateral isovolumic relaxation time (s/l IVRT) ratio was higher (1.5 ± 0.4) compared with AHT (1.1 ± 0.2), Fabry disease (1.0 ± 0.1), and controls (1.1 ± 0.2; P < 0.001), showing 77% sensitivity and 79% specificity to discriminate HCM‐related LVH from other entities. The s/l IVRT ratio was independent of global DD in HCM (HCM with DD: 1.5 ± 0.5, n = 52; HCM without DD: 1.5 ± 0.3, n = 29) and remained significantly different from other entities in a subgroup of HCM patients with maximum wall thickness < 20 mm (s/l ratio: 1.5 ± 0.5, n = 28). Regional IVRT did not correlate with the corresponding segmental myocardial mass or amount of fibrosis in cardiac magnetic resonance imaging. Conclusions HCM patients show a prolonged septal IVRT irrespective of the extent of LVH and even before developing global DD. The s/l IVRT ratio is significantly higher in HCM compared with AHT or Fabry disease, thus establishing segmental IVRT analysis as a potential parameter for differential diagnosis in LVH.

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Polyunsaturated fatty acids such as arachidonic acid (AA) demonstrate inhibitory modulation of Kv4 potassium channels. Molecular docking approaches using a new Kv4.2 homology model predicted a membraneembedded binding pocket for AA comprised of the S4-S5 linker on one subunit and several nearby hydrophobic residues within the internal side of S5 and S6 from an adjacent subunit. We tested the hypothesis that modulatory effects of AA on Kv4.2/KChIP channels require access to this site.