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PubMed2006

Decrease in the heart rate complexity prior to the onset of atrial fibrillation.

AIMS: To assess heart rate complexity changes prior to the onset of atrial fibrillation (AF) using sample entropy. It has been proposed that the autonomic nervous system might have a role in the initiation of AF. METHODS AND RESULTS: The study included 25 patients with lone AF. Each record set contained two 30 min records from 25 subjects. Each patient had 30 min records containing the ECG immediately preceding an episode of AF (pre-AF) and 30 min of ECG during a period distant from any episode of AF (AFd). Sample entropy was used for complexity analysis. The sample entropy of R-R intervals was significantly reduced in the pre-AF period compared with the AFd period (0.45+/-0.25 vs. 0.78+/-0.46, P=0.003). The pre-AF periods were divided into three successive 10 min segments. There was a significant decreasing trend in entropy towards the onset of AF with linear mixed models (P=0.002). CONCLUSIONS: The heart rate complexity is reduced with a significant decreasing trend as assessed by R-R interval entropy prior to the onset of AF. There is a need for well-defined studies with larger patient groups in order to assess the entropy changes further and to look for possible changes, which might predict impending AF episodes.

Atrial Fibrillation↗

PubMed2005

Transgenic rabbit model for human troponin I-based hypertrophic cardiomyopathy.

BACKGROUND: Transgenic and gene-targeted models have focused on the mouse. Fundamental differences between the mouse and human exist in Ca2+ handling during contraction/relaxation and in alterations in Ca2+ flux during heart failure, with the rabbit more accurately reflecting the human system. METHODS AND RESULTS: Cardiac troponin I (cTnI) mutations can cause familial hypertrophic cardiomyopathy. An inhibitory domain mutation, arginine146-->glycine (cTnI(146Gly)), was modeled with the use of transgenic expression in the rabbit ventricle. cTnI(146Gly) levels >40% of total cTnI were perinatally lethal, whereas replacement levels of 15% to 25% were well tolerated. cTnI(146Gly) expression led to a leftward shift in the force-pCa2+ curves with cardiomyocyte disarray, fibrosis, and altered connexin43 organization. In isolated cTnI(146Gly) myocytes, twitch relaxation amplitudes were smaller than in normal cells, but [Ca]i transients and sarcoplasmic reticulum Ca2+ load were not different. Detrended fluctuation analysis of the QT(max) intervals was used to evaluate the cardiac repolarization phase and showed a significantly higher scaling exponent in the transgenic animals. CONCLUSIONS: Expression of modest amounts of cTnI(146Gly) led to subtle defects without severely affecting cardiac function. Aberrant connexin organization, subtle morphological deficits, and an altered fractal pattern of the repolarization phase of transgenic rabbits, in the absence of entropy or other ECG abnormalities, may indicate an early developing pathology before the onset of more obvious repolarization abnormalities or major alterations in cardiac mechanics.

Animals↗