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Background: Preexcitation syndrome is characterized by a dominant delta wave on the baseline electrocardiogram (ECG), resulting from the change in QRS initial vector by the accessory pathway (AP). This study is to explore the effect of ventricular preexcitation on the QRS initial, maximal and terminal vector in an experimental rabbit with preexcitation syndrome induced by programmed electrical stimulation., Methods: Rabbits (n = 10) were randomized for the experimental model of ventricular preexcitation. Sensing and stimulating electrode catheters were placed in the high right atrium and along epicardial surface of atrioventricular groove of the left ventricular anterior wall, respectively. Programmed premature stimulation S 2 was synchronized with P wave and utilized to stimulate the ventricle. The ECG recorded the electrical activity of the heart. As compared with the QRS complex during sinus rhythm, paced QRS was assessed regarding the initial, maximal and terminal vector. PS 2 interval and PR interval were also measured and analyzed., Results: Preexcitation was successfully simulated by ventricular pacing in the rabbits, including (1) Complete preexcitation: PS 2 interval was less than PR interval; the difference was more than or equal to 47.00 ± 7.53 ms. (2) Incomplete preexcitation: PS 2 interval was less than PR interval; the difference was less than 47.00 ± 7.53 ms. (3) Incomplete latent preexcitation: PS 2 interval was more than or equal to PR interval; the difference was less than or equal to 13.00 ± 3.50 ms. (4) Complete latent preexcitation: PS 2 interval was more than or equal to PR interval; the difference was more than 13.00 ± 3.50 ms., Conclusions: The difference in the relative conduction velocity of the atrioventricular node versus the AP pathways determines the degree of preexcitation and different manifestation on ECG. The QRS terminal vector also reflects the ventricle preexcitation, indicating a valuable sign for the diagnosis of atypical or latent preexcitation.

This study is to investigate the effects of slow breathing on heart rate variability (HRV) and arterial baroreflex sensitivity in essential hypertension.We studied 60 patients with essential hypertension and 60 healthy controls. All subjects underwent controlled breathing at 8 and 16 breaths per minute. Electrocardiogram, respiratory, and blood pressure signals were recorded simultaneously. We studied effects of slow breathing on heart rate, blood pressure and respiratory peak, high-frequency (HF) power, low-frequency (LF) power, and LF/HF ratio of HRV with traditional and corrected spectral analysis. Besides, we tested whether slow breathing was capable of modifying baroreflex sensitivity in hypertensive subjects.Slow breathing, compared with 16 breaths per minute, decreased the heart rate and blood pressure (all P < .05), and shifted respiratory peak toward left (P < .05). Compared to 16 breaths/minute, traditional spectral analysis showed increased LF power and LF/HF ratio, decreased HF power of HRV at 8 breaths per minute (P < .05). As breathing rate decreased, corrected spectral analysis showed increased HF power, decreased LF power, LF/HF ratio of HRV (P < .05). Compared to controls, resting baroreflex sensitivity decreased in hypertensive subjects. Slow breathing increased baroreflex sensitivity in hypertensive subjects (from 59.48 ± 6.39 to 78.93 ± 5.04 ms/mm Hg, P < .05) and controls (from 88.49 ± 6.01 to 112.91 ± 7.29 ms/mm Hg, P < .05).Slow breathing can increase HF power and decrease LF power and LF/HF ratio in essential hypertension. Besides, slow breathing increased baroreflex sensitivity in hypertensive subjects. These demonstrate slow breathing is indeed capable of shifting sympatho-vagal balance toward vagal activities and increasing baroreflex sensitivity, suggesting a safe, therapeutic approach for essential hypertension.