Bacharova Ljuba, Plandorova Jana, Klimas Jan, Krenek Peter, Kyselovic Jan
International Laser Center, Bratislava, Slovak Republic.
J Electrocardiol. 2008 Nov-Dec;41(6):730-4. doi: 10.1016/j.jelectrocard.2008.01.013. Epub 2008 Mar 20.
On the basis of our previous results of animal and human studies, we assume that the discrepancies between increased left ventricular mass (LVM) and electrocardiographic (ECG) findings not exceeding the upper normal limits in left ventricular hypertrophy (LVH) are conditioned by the electrical remodeling of hypertrophied myocardium. We assumed that these discrepancies observed in the early stage of LVH in spontaneously hypertensive rats (SHR) are associated with a decreased expression of connexin 43.
Standard 12-lead ECG was recorded in 20-week-old male SHR and age-matched and sex-matched normotensive Wistar rats (Institute of Experimental Pharmacology SAV, Dobra Voda, Slovakia). The approximated maximum QRS spatial vector magnitude (QRSmax) was calculated from leads V(2), aVF, and V(5). Left ventricular mass was weighed, and the specific potential (SP) of myocardium was calculated as the QRSmax-to-LVM ratio. Left ventricular protein levels of connexin 43 were analyzed with sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blotting.
The LVM values were significantly higher in SHR than in normotensive controls (0.96 +/- 0.03 g and 0.680 +/- 0.07 g, respectively; P < .001). The QRSmax values in SHR did not follow the increase either in systolic blood pressure or in LVM. The SP values in SHR were significantly lower than those in control rats (0.92 +/- 0.11 mV/g and 1.358 +/- 0.06 mV/g, respectively; P < .01). A 37% decrease in connexin 43 level was observed in SHR.
The QRS voltage did not follow the increase in the LVM in 20-week-old SHR, and the values of connexin 43 were lower in SHR than in normotensive controls. We believe that the discrepant findings between ECG voltage and LVM can be caused by the electrical remodeling in the early stages of LVH.
基于我们之前动物和人体研究的结果，我们推测在左心室肥厚（LVH）中左心室质量（LVM）增加与未超过正常上限的心电图（ECG）表现之间的差异是由肥厚心肌的电重构所致。我们假定在自发性高血压大鼠（SHR）LVH早期观察到的这些差异与连接蛋白43表达降低有关。
对20周龄雄性SHR以及年龄和性别匹配的正常血压Wistar大鼠（斯洛伐克多布拉沃达实验药理学研究所）记录标准12导联心电图。从V(2)、aVF和V(5)导联计算近似最大QRS空间向量幅度（QRSmax）。称量左心室质量，并计算心肌的比电位（SP），即QRSmax与LVM的比值。采用十二烷基硫酸钠-聚丙烯酰胺凝胶电泳和蛋白质印迹法分析左心室连接蛋白43的蛋白水平。
SHR的LVM值显著高于正常血压对照组（分别为0.96±0.03 g和0.680±0.07 g；P<.001）。SHR的QRSmax值并未随收缩压或LVM的增加而升高。SHR的SP值显著低于对照大鼠（分别为0.92±0.11 mV/g和1.358±0.06 mV/g；P<.01）。观察到SHR中连接蛋白43水平降低了37%。
20周龄SHR的QRS电压未随LVM的增加而升高，且SHR中连接蛋白43的值低于正常血压对照组。我们认为，ECG电压与LVM之间的差异可能是由LVH早期的电重构引起的。
