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    • br Methods br Discussion This study demonstrated

    2019-05-16


    Methods
    Discussion This study demonstrated that upgrading to CRT from RVAP improved cardiac performance and myocardial perfusion at pacing sites by SPECT. RVAP has been reported to alter left ventricular electrical and mechanical activation in a manner that is similar to the complete left bundle branch block pattern [2]. In a study utilizing SPECT, RVAP was associated with a high incidence of perfusion defects in the absence of coronary artery disease [6]. To add to the knowledge of the relationship between RVAP and coronary blood flow, Skalidis et al. reported that a significant reduction of flow velocity was observed in the epicardial coronary artery at pacing sites [2]. Furthermore, an experimental study in a canine model by Carew et al. demonstrated that the difference between the perfusion pressure in the artery and the intramyocardial pressure determined the fractional systolic and diastolic flow in the myocardial wall [7]. Another canine study by Ono et al. revealed that the diastolic–intramyocardial pressure in the septum increased significantly after induction of RVAP [8]. In general, the flow in the epicardial coronary artery shows a phasic pattern, and a large amount of flow occurs in the diastolic period. Transmural potassium channel of the intramyocardial vessels during systole and the release of the compression force during diastole cause this pattern [9]. These studies suggested that the increased septal intramyocardial pressure during the diastolic phase of the RVAP, when originally intended to decrease the intramyocardial pressure in normal electrical and mechanical sequence, led to coronary vessel resistance, thereby resulting in the reduced coronary blood flow and myocardial perfusion in the pacing sites. Although it is unclear why the septal intramyocardial pressure increases during the diastolic period while on RVAP, considering that RVAP causes an increase in QRS duration similar to a left bundle branch block pattern, this observation may be due to electrical and mechanical changes induced by RVAP. It is generally understood that RVAP induces early contraction of regions that are close to the pacing site, which stretch the remote regions that are not yet activated. This stretching further delays the shortening of these late-activating regions and increases their force of local contraction, by virtue of the Frank–Starling mechanism. Consequently, the late-activating regions impose loading on the earlier activated pacing territories, a phenomenon known as “systolic paradoxical stretch”. This non-physiological force that occurs in the diastolic period may cause increases in intramyocardial pressure that lead to reduction of the blood perfusion in the pacing site (Fig. 4). In this study, all cases of QRS duration shortened significantly, and the standard deviation of the time from the onset of QRS to end-systole in the 17 LV segments that indicate LV dyssynchrony tended to improve; furthermore, the cardiac perfusion increased at the inferoseptal region and decreased at the contrary free wall region, after upgrading to CRT. Particularly, the cardiac perfusion of segment 9 in SPECT located at the pacing lead increased in all cases. These results indicated that CRT could mechanically and electrically correct the dyssynchrony associated with RVAP, resulting in reduction in intramyocardial pressure and an increase in cardiac blood perfusion in the pacing sites. In short, CRT could restore the cardiac perfusion that was unbalanced by RVAP. An experimental MRI study in dogs showed that systolic fiber strain and external work were almost 0 at the pacing site, and more than twice that in the right atrial pacing in the contrary remote regions [10]. With echocardiography, LV wall systolic thickening at the pacing lesion is not obvious [11]. Furthermore, another study demonstrated that blood flow varied in parallel with regional function during ventricular pacing [12]. Taking these findings into consideration, RVAP would reduce the cardiac blood flow in pacing sites by increasing the intramyocardial pressure, which would impair cardiac function, this would result in increased left ventricular pressure and increased intramyocardial pressure by stretching the cardiac muscle, thereby establishing a “vicious cycle”. The current study, while including mild heart failure patients compared with the guidelines for CRT implantation, demonstrated that CRT could remodel the left ventricle with RVAP. This procedure will result in the redistribution of cardiac blood perfusion to the LV.