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Am J Physiol Heart Circ Physiol (November 18, 2004). doi:10.1152/ajpheart.00584.2004
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Submitted on June 14, 2004
Accepted on November 16, 2004

Normal Distribution of Ventricular Pressure-Volume Area (PVA) of Arrhythmic Beats under Atrial Fibrillation in Canine Heart

Satoshi Mohri1*, Juichiro Shimizu1, Gentaro Iribe1, Haruo Ito1, Terumasa Morita2, Hiroki Yamaguchi2, Shunji Sano3, Fumihiko Kajiya1, and Hiroyuki Suga4

1 Department of Cardiovascular Physiology, Okayama University Graduate School of Medicine and Dentistry, Okayama, Okayama, Japan
2 Department of Cardiovascular Physiology, Okayama University Graduate School of Medicine and Dentistry, Okayama, Okayama, Japan; Department of Cardiovascular Surgery, Okayama University Graduate School of Medicine and Dentistry, Okayama, Okayama, Japan
3 Department of Cardiovascular Surgery, Okayama University Graduate School of Medicine and Dentistry, Okayama, Okayama, Japan
4 National Cardiovascular Center Research Institute, Suita, Osaka, Japan

* To whom correspondence should be addressed. E-mail: smohri{at}md.okayama-u.ac.jp.

We previously found the frequency distribution of the left ventricular (LV) effective afterload elastance (Ea) of arrhythmic beats to be non-normal or non-Gaussian in contrast to the normal distribution of the LV end-systolic elastance (Emax) in canine in situ LVs during electrically induced atrial fibrillation (AF). These two mechanical variables determine the total mechanical energy (PVA: systolic pressure-volume area) generated by LV contraction once the LV end-diastolic volume (EDV) is given on a per beat basis. Both PVA and Emax are the two key determinants of the LV O2 consumption per beat. In the present study, we analyzed the frequency distribution of PVA during AF by its {chi}2, significance level, skewness, and kurtosis, and compared them with those of other major cardiodynamic variables including Ea and Emax. We assumed the volume intercept (Vo) of the end-systolic pressure-volume relation needed for Emax determination to be stable during arrhythmia. We found that PVA distributed much more normally than Ea and slightly more so than Emax during AF. We compared the {chi}2, significance level, skewness, and kurtosis of all the complex terms of the PVA formula. We found that the complexity of the PVA formula attenuated the effect of the considerably non-normal distribution of Ea on the distribution of PVA along the central limit theorem. We conclude that mean ± SD of PVA can reliably characterize the distribution of PVA of arrhythmic beats during atrial fibrillation at least in canine hearts.







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