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ABSTRACT: We analyzed the frequency distribution of the left ventricular (LV) mechanical efficiency of individual arrhythmic beats during electrically induced atrial fibrillation (AF) in normal canine hearts. This efficiency is the fraction of the external mechanical work (EW) in the total mechanical energy measured by the systolic pressurevolume area (PVA). The mean, median, and mode of this efficiency (EW/PVA) were as high as 78%, 80%, and 81%, respectively, on average in six hearts. These high efficiencies were comparable to that of the regular beats in these hearts. The frequency distribution of the EW/PVA during AF tended to skew to the higher side in all the hearts. Since the EW/PVA is directly related to both the ventriculoarterial (or afterload) coupling ratio (E(a)/E(max); E(a) = effective arterial elastance, E(max) = endsystolic ventricular elastance) and the ejection fraction on a perbeat basis, we also analyzed their frequency distributions. We found them to skew enough to account for the rightward skewed frequency distribution of the EW/PVA during AF with the unexpectedly high mean EW/PVA. These results indicate that the LV arrhythmia during AF per se does not directly suppress the mean level of LV mechanical efficiency in normal canine hearts. The Journal of Physiological Sciences 09/2006; 56(4):26974. · 1.25 Impact Factor

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ABSTRACT: We have reported that the contractility index (E(max)) and the total mechanical energy (PVA) of arrhythmic beats of the left ventricle (LV) distribute normally in canine hearts under electrically induced atrial fibrillation (AF). Here, E(max) is the ventricular elastance as the slope of the endsystolic (ES) pressurevolume (PV) relation (ESPVR), and PVA is the systolic PV area as the sum of the external mechanical work within the PV loop and the elastic potential energy under the ESPVR. To obtain E(max) and PVA, we had to assume the systolic unstressed volume (V(o)) as the Vaxis intercept of the ESPVR to be constant despite the varying E(max), since there was no method to obtain V(o) directly in each arrhythmic beat. However, we know that in regular stable beats V(o) decreases by approximately 7 ml/100 g LV with approximately 100 times the increases in E(max) from ~0.2 mmHg/(ml/100 g LV) of almost arresting weak beats to approximately 20 mmHg/(ml/100 g LV) of strong beats with a highly enhanced contractility. In the present study, we investigated whether E(max) and PVA under AF could still distribute normally, despite such E(max)dependent V(o) changes. The present analyses showed that the E(max) changes were only approximately 3 times at most from the weakest to the strongest arrhythmic beat under AF. These changes were not large enough to affect V(o) enough to distort the frequency distributions of E(max) and PVA from normality. We conclude that one could practically ignore the slight E(max) and PVA changes with the Emaxdependent V(o) changes under AF. The Japanese Journal of Physiology 11/2005; 55(5):25564. · 1.04 Impact Factor

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ABSTRACT: We previously found the frequency distribution of the left ventricular (LV) effective afterload elastance (E(a)) of arrhythmic beats to be nonnormal or nonGaussian in contrast to the normal distribution of the LV endsystolic elastance (E(max)) in canine in situ LVs during electrically induced atrial fibrillation (AF). These two mechanical variables determine the total mechanical energy [systolic pressurevolume area (PVA)] generated by LV contraction when the LV enddiastolic volume is given on a perbeat basis. PVA and E(max) are the two key determinants of the LV O(2) 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 E(a) and E(max). We assumed the volume intercept (V(0)) of the endsystolic pressurevolume relation needed for E(max) determination to be stable during arrhythmia. We found that PVA distributed much more normally than E(a) and slightly more so than E(max) 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 nonnormal distribution of E(a) 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 AF, at least in canine hearts. AJP Heart and Circulatory Physiology 05/2005; 288(4):H17406. · 4.01 Impact Factor

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ABSTRACT: Left ventricular (LV) O2 consumption (V(O2)) per minute is measurable for both regular and arrhythmic beats. LV V(O2) per beat can then be obtained as V(O2) per minute minute divided by heart rate per minute minute for regular beats, but not for arrhythmic beats. We have established that V(O2) of a regular stable beat is predictable by V(O2) = a PVA + b E(max) + c, where PVA is the systolic pressurevolume area as a measure of the total mechanical energy of an individual contraction and E(max) is the endsystolic maximum elastance as an index of ventricular contractility of the contraction. Furthermore, a is the O2 cost of PVA, b is the O2 cost of E(max), and c is the basal metabolic V(O2) per beat. We considered it theoretically reasonable to expect that the same formula could also predict LV V(O2) of individual arrhythmic beats from their respective PVA and E(max) with the same a, b, and c. We therefore applied this formula to the PVA  Emax data of individual arrhythmic beats under electrically induced atrial fibrillation (AF) in six canine in situ hearts. We found that the predicted V(O2) of individual arrhythmic beats highly correlated linearly with either their V(O2) (r = 0.96 +/ 0.01) or E(max) (0.97 +/ 0.03) while both also highly correlated linearly with each other (0.88 +/ 0.04). This suggests that the above formula may be used to predict LV Vo2 of absolute arrhythmic beats from their Emax and PVA under AF. The Japanese Journal of Physiology 05/2005; 55(2):13542. · 1.04 Impact Factor

Journal of Cardiac Failure 09/1999; 5(3):8080. · 3.07 Impact Factor

Journal of Cardiac Failure 09/1998; 4(3):106106. · 3.07 Impact Factor

Journal of Cardiac Failure 09/1998; 4(3):105105. · 3.07 Impact Factor

Journal of Cardiac Failure 09/1998; 4(3):106106. · 3.07 Impact Factor