Yano K, Hano O, Hirata T, Matsumoto Y, Hirata M, Mitsuoka T
Third Department of Internal Medicine, Nagasaki University School of Medicine, Japan.
Cardiovasc Res. 1992 Oct;26(10):988-93. doi: 10.1093/cvr/26.10.988.
The aim was to examine the effect of an increase in left ventricular systolic pressure (LVSP) on ventricular arrhythmogenicity in old canine myocardial infarction.
Fourteen mongrel dogs of either sex weighing 11 to 15 kg were used. Studies were performed 28 d after creation of myocardial infarction by ligation of the anterior descending coronary artery. Electrical induction of ventricular arrhythmia and determinations of effective refractory period (ERP) and local intraventricular conduction delay (LIVCD) were performed using the extrastimulus technique with a cycle length of 300 ms in the normal and infarcted zones of the left ventricle. Heterogeneity of ERP (delta ERP) was determined as a difference between the longest and shortest ERP values in each site. LVSP was raised by constriction of the ascending aorta in a stepwise fashion (control, level A, level B).
Incidence of electrically induced ventricular arrhythmia was increased from 28.6% at control level of LVSP [130.7(SEM 7.3) mm Hg] to 42.9% at level A [190.9(6.0) mm Hg] and to 64.3% (p < 0.05) at level B [243.3(4.0) mm Hg]. delta ERP and LIVCD were greater in the infarct zone than in the normal zone at each level of LVSP (p < 0.001). delta ERP in the infarct zone increased from 18.9(4.3) ms at control level of LVSP to 20.7(6.8) ms at level A, and to 27.1(8.1) ms at level B (p < 0.001). LIVCD in the infarct zone also increased from 22.9(6.2) ms at control level of LVSP to 26.8(4.9) ms at level A (p < 0.001), and to 36.1(6.0) ms at level B (p < 0.001). delta ERP and LIVCD in the normal zone were only slightly raised by increasing the LVSP. delta ERP and LIVCD in the infarct zone were closely correlated with incidence of electrically induced ventricular arrhythmia.
Increasing the LVSP enhances ventricular arrhythmogenicity and pre-existing electrophysiologic abnormalities of the heart in the presence of old myocardial infarction. Thus a rise in LVSP from any cause in the old myocardial infarction can be a trigger of life threatening ventricular arrhythmias.
本研究旨在探讨左心室收缩压(LVSP)升高对老年犬心肌梗死心室致心律失常性的影响。
选用14只体重11至15 kg的杂种犬,雌雄不限。在冠状动脉前降支结扎造成心肌梗死后28天进行实验。采用额外刺激技术,在左心室正常区和梗死区以300 ms的周期长度进行心室心律失常的电诱发,并测定有效不应期(ERP)和局部室内传导延迟(LIVCD)。ERP的异质性(delta ERP)定义为每个部位最长和最短ERP值之间的差值。通过逐步收缩升主动脉来升高LVSP(对照组、A水平、B水平)。
电诱发心室心律失常的发生率从LVSP对照组水平[130.7(标准误7.3)mmHg]时的28.6%增加到A水平[190.9(6.0)mmHg]时的42.9%,再到B水平[243.3(4.0)mmHg]时的64.3%(p<0.05)。在每个LVSP水平下,梗死区的delta ERP和LIVCD均大于正常区(p<0.001)。梗死区的delta ERP从LVSP对照组水平时的18.9(4.3)ms增加到A水平时的20.7(6.8)ms,再到B水平时的27.1(8.1)ms(p<0.001)。梗死区的LIVCD也从LVSP对照组水平时的22.9(6.2)ms增加到A水平时的26.8(4.9)ms(p<0.001),再到B水平时的36.1(6.0)ms(p<0.001)。正常区的delta ERP和LIVCD仅因LVSP升高而略有升高。梗死区的delta ERP和LIVCD与电诱发心室心律失常的发生率密切相关。
在存在陈旧性心肌梗死的情况下,升高LVSP会增强心室致心律失常性以及心脏原有的电生理异常。因此,在陈旧性心肌梗死中,任何原因导致的LVSP升高都可能成为危及生命的心室心律失常的触发因素。