Risk for atrial fibrillation in patients with hypertrophic cardiomyopathy: Association with insulin resistance

SummaryBackgroundWe undertook a cross-sectional study to test the hypothesis that patients with hypertrophic cardiomyopathy (HCM) who have impaired left ventricular (LV) diastolic function are insulin resistant. We also evaluated the relation between the development of atrial fibrillation (AF) and insulin resistance (IR) in patients with HCM.Methods and resultsEighty-eight patients with HCM (71 men, 17 women) were enrolled in the study. IR was estimated using the homeostasis model assessment (HOMA) index. Echocardiographically determined left atrial (LA) dimension was measured as a marker of LA size. The ratio of trasmitral early LV filling velocity to early diastolic mitral annulus velocity (E/e′) was also measured as a marker of LV diastolic function. Twenty-seven patients (31%) had IR. Multivariate logistic regression analyses showed that independent determinants of AF were increased LA size [odds ratio (OR) 3.5, 95% confidence interval (CI) 1.2–9.8] and impaired LV diastolic function [OR 4.6, 95% CI 1.6–12.8]. The strongest determinant of LA size was the HOMA index (p=0.0005). Similarly, the HOMA index (p=0.0019) was an independent determinant of LV diastolic function.ConclusionIR is highly prevalent among non-diabetic patients with HCM. A possible mechanism by which IR affects the development of AF is mediated through its association with increased LA size or impaired LV diastolic function. IR may be an important underlying mechanism for the genesis of AF in HCM

Direct measurement of radial strain in the inner-half layer of the left ventricular wall in hypertensive patients

SummaryBackgroundTwo-dimensional speckle tracking echocardiography (2D-STE) is a novel technology that directly measures regional left ventricular (LV) wall contraction. This study aimed to directly measure inner-layer thickening (radial strain) of the LV using 2D-STE, and to examine the relationship between radial strain and the degree of hypertrophy.MethodsThe study enrolled 63 untreated hypertensive patients with normal geometry (N group, n=32) or concentric hypertrophy (CH group, n=31), classified according to LV mass index (LVMI) and relative wall thickness (RWT). Thirty normotensive subjects (C group, n=30) served as controls. Radial strain (ɛ) in the inner half (ɛi) and all layers of the LV wall (ɛa) were calculated from the LV short-axis view by 2D-STE.ResultsLV ejection fraction did not differ significantly among the groups. However, ɛi and ɛa were significantly lower in the CH group compared with the C and N groups (p<0.01). A ratio of ɛi to ɛa was significantly lower in the CH group compared with the C and N groups (p<0.01). A multivariate regression model that included midwall fractional shortening, E/e′, LVMI, RWT, and LV ejection fraction showed that LVMI (p=0.002) and RWT (p=0.014) were independent predictors (R2=0.59) of ɛi.ConclusionRadial strain in the inner half layer of the LV wall decreases in parallel with the degrees of LV concentricity and hypertrophy in hypertensive patients. Radial strain in the inner half layer may identify subtle systolic dysfunction even in hypertensive patients with preserved LV chamber function

Identifying the true origin of sustained monomorphic ventricular tachycardia associated with dilated-phase hypertrophic cardiomyopathy: A case of successful catheter ablation

AbstractThis case report describes sustained monomorphic ventricular tachycardia (VT) caused by a large epicardial scar, related to dilated-phase hypertrophic cardiomyopathy mimicking VT originating from the apical septum. VT resolved with epicardial catheter ablation. The exit of the VT circuit suggested that a 12-lead electrocardiogram can be remote with respect to the critical isthmus in this case. In patients with structural heart disease, it is difficult to identify the VT reentrant circuit by surface electrocardiography, which shows only the exit site. VT originating in the epicardium should be considered, even if the suspected origin is another ventricular site

In Vivo Confocal Microscopic Observations of Vortex Keratopathy in Patients with Amiodarone-Induced Keratopathy and Fabry Disease

Purpose. To compare the morphology of two types of vortex keratopathy: amiodarone-induced keratopathy and the Fabry disease-associated keratopathy. Patients and Methods. Eight patients who were receiving oral amiodarone therapy and 3 patients with Fabry disease, a mother and her 2 daughters, were examined by slit-lamp biomicroscopy and in vivo confocal microscopy (IVCM) regularly. Results. Amiodarone-induced keratopathy developed in 7 of the 8 patients, and it was detected as early as 7 days by IVCM and 14 days by slit-lamp biomicroscopy. The in vivo confocal microscopic images showed a clustering of corneal epithelial cells with a highly reflective cytoplasm in both types of keratopathy. In the amiodarone-induced keratopathy, the highly reflective epithelial cells were first found at the center of the cornea and then spread to the periphery with increasing time on amiodarone. In Fabry disease, the highly reflective epithelial cells were consistently observed extending from the limbus to the central cornea. Conclusion. These findings suggest that the corneal epithelial cells most likely endocytose amiodarone from the tear film in the amiodarone-induced keratopathy. In Fabry disease, globotriaosylceramide deposits are taken up by the lysosomes of the limbal epithelial stem cells, and they differentiate and migrate to the center of the cornea to form the whorl pattern