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Biomedical subjects

Volkan Tuzcu

Publications and source records attributed to Volkan Tuzcu.

7 recordsLinked to original sources
PubMed2006

Diagnosis of tachycardia mechanism with cryomapping in a toddler with complex congenital heart disease.

A 2.5-year-old patient with complex congenital heart disease involving dextrocardia, atrioventricular and ventriculoarterial discordance, pulmonary stenosis, ventricular septal defect (VSD), atrial septal defect (ASD), and paroxysmal supraventricular tachycardia (SVT) underwent electrophysiological study. The tachycardia mechanism was diagnosed with cryomapping. The ability of cryomapping to have transient and reversible effect on the tissue, unlike radiofrequency (RF) ablation, helped in the establishment of diagnosis in this toddler with typical atrioventricular nodal reentrant tachycardia. Cryomapping can be an additional safe diagnostic utility in young patients with complex congenital heart disease.

Catheter Ablation↗
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↗
PubMed2003

Effect of diurnal variability of heart rate on development of arrhythmia in patients with chronic obstructive pulmonary disease.

We examined the possible effect of diurnal variability of heart rate on the development of arrhythmias in patients with chronic obstructive pulmonary disease (COPD). Forty-one COPD patients (M/F: 39/2, mean age: 59+/-8.5 years) and 32 (M/F: 27/5, mean age: 57+/-11 years) healthy controls were included. Twenty-four hour ECG recordings were analyzed for atrial fibrillation (AF) or ventricular premature beats (VPB), and circadian changes in heart rate variability (HRV) were assessed by dividing the 24-h period into day-time (08:00-24:00 h) and night-time (24:00-08:00 h) periods. Night-time total (TP), low frequency (LF) and high frequency (HF) powers were similarly lower from day-time parameters in AF(-) COPD patients (HF 3.91+/-1 vs. 4.43+/-1.04 ms(2), P=0.001) and controls (HF 3.95+/-0.72 vs. 4.82+/-0.66 ms(2), P<0.001). The LF/HF ratios were also significantly reduced in the same patient groups (AF(-) COPD 1.35+/-0.21 vs. 1.27+/-0.19, P=0.04, controls 1.43+/-0.14 vs. 1.24+/-0.09, P<0.001). Night-time TP and LF were increased, HF unchanged and LF/HF significantly increased (1.11+/-0.25 vs. 1.19+/-0.27, P<0.05) in AF(+) COPD patients. Frequency of VPB was correlated with corrected QT dispersion (QTc(d)) (r=0.52, P=0.001) and the day-time/night-time HF ratio (r=0.43, P=0.02). Patients with QTc(d)>or=60 ms did not have the expected increase in night-time HF and had a statistically insignificant increase in LF/HF ratio. In COPD patients with QTc(d)<60 ms, circadian changes in HRV parameters were parallel with the controls. We concluded that COPD patients with arrhythmia had circadian HRV disturbances such as unchanged night-time parasympathetic tone and disturbed sympatho-vagal balance in favor of the sympathetic system all day long, which may explain the increased frequency of arrhythmia.

Aged↗