Biomedical subjects

Shahriar Iravanian

Publications and source records attributed to Shahriar Iravanian.

4 recordsLinked to original sources

PubMed2006

A possible mechanism of halocarbon-induced cardiac sensitization arrhythmias.

Cardiac sensitization is the term used for malignant ventricular arrhythmias associated with exposure to inhaled halocarbons in the presence of catecholamines. We investigated the electrophysiological changes associated with cardiomyocyte exposure to epinephrine and a halocarbon known to be associated with cardiac sensitization (halon 1301, CF3Br). Cardiomyocytes (CMs) were isolated from neonatal rats and grown on multielectrode arrays (MEAs). Upon exposure to epinephrine, the CM inter-spike interval (ISI) was decreased 14% at 10 microg/L (P<0.05) and 27% at 100 microg/L (P<0.05) as compared to baseline. Halon alone (50 mg/L) mildly prolonged the field potential (FP) duration (7%). CMs exposed to combinations of epinephrine (100 microg/L) and halon (50 mg/L) for 15 min showed a blunted increase in the ISI (35+/-12%) and a 38% decrease in conduction velocity (P<0.05) when compared to epinephrine alone. There was no change in field potential properties, but dephosphorylated connexin 43 (Cx43) was increased 60+/-16% with the combination as compared to epinephrine alone (P<0.05). Treatment with okadaic acid, a phosphatase inhibitor, prevented the Cx43 dephosphorylation and the reduction in conduction velocity upon exposure to halon and epinephrine. Moreover, the electrophysiological changes induced by epinephrine and halon were indistinguishable from those seen with the gap junction inhibitor heptanol. In conclusion, the combination of a halocarbon and epinephrine results in a unique electrophysiological signature including slow conduction that may explain, in part, the basis for cardiac sensitization. The slowing of conduction is most likely related to changes in the phosphorylation state of Cx43.

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PubMed2003

Functional reentry in cultured monolayers of neonatal rat cardiac cells.

Previous studies of reentrant arrhythmias in the heart have been performed in computer models and tissue experiments. We hypothesized that confluent monolayers of cardiac cells can provide a simple, controlled, and reproducible experimental model of reentry. Neonatal rat ventricular cells were cultured on 22-mm-diameter coverslips and stained with the voltage-sensitive dye RH-237. Recordings of transmembrane potentials were obtained from 61 sites with the use of a contact fluorescence imaging system. An electrical field stimulus, followed by a point stimulus, induced 39 episodes of sustained reentry and 21 episodes of nonsustained reentry. Sustained reentry consisted of single-loop (n = 18 monolayers) or figure-of-eight (n = 4) patterns. The cycle length, action potential duration at 80% repolarization, and conduction velocity were (in means +/- SE) 358 +/- 33 ms, 118 +/- 12 ms, and 12.9 +/- 1.0 cm/s for single loop and 311 +/- 78 ms, 137 +/- 18 ms, and 7.8 +/- 1.3 cm/s for figure-of-eight, respectively. Electrical termination by 6- to 13-V/cm field pulses or 15- to 20-V point stimuli was successful in 60% of the attempts. In summary, highly stable reentry can be induced, sustained for extensive periods of time, and electrically terminated in monolayers of cultured neonatal rat cardiac myocytes.

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PubMed2002

A novel algorithm for cardiac biosignal filtering based on filtered residue method.

In this paper, a new algorithm is presented for the filtering (de-noising) of cardiac bioelectrical signals. The primary target of this algorithm is the class of cardiac action potentials recorded using voltage-sensitive dyes, although the method is also applied to electrocardiographic signals. High periodicity is one of the main features of cardiac biosignals. The proposed algorithm exploits this feature in filtering signals with a minimum amount of distortion. The basic idea is to use signal averaging in time to find the stationary portion of the signal. The residue is found by subtracting the signal average from the corresponding points of the input. After passing through a low-pass filter, the filtered residue (FR) is added back to the signal average to reconstruct the output. The practical implementation of the filter residue algorithm is discussed. Stretching and shrinking operations are the basis for the conversion of quasi-periodic signals into periodic signals, which can then be subjected to the FR algorithm. Various examples are presented, and error estimation is performed to guide the selection of optimal parameters for the algorithm. The ability of the algorithm to reconstruct the variation among beats is demonstrated, and its limitations are discussed.

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PubMedDate not supplied

Role of electrophysiologic studies, signal-averaged electrocardiography, heart rate variability, T-wave alternans, and loop recorders for risk stratification of ventricular arrhythmias.

Ventricular tachycardia and fibrillation are major causes of morbidity and mortality after myocardial infarction. Frequently, sudden cardiac death is the first manifestation of such malignant rhythms. Optimal risk stratification strategies in this population are of utmost importance. In this review the authors discuss the background and clinical use of invasive tests, such as electrophysiologic study and implantable loop recorders, and noninvasive tests, such as signal-averaged electrocardiography, heart rate variability, and T-wave alternans. The utility, indications, and limitations of each test in clinical practice are discussed, especially for the purpose of postmyocardial infarction risk stratification in the elderly population.

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