WALL STRESS-INDUCED ARRHYTHMIA IS ENHANCED BY LOW POTASSIUM AND EARLYLEFT-VENTRICULAR HYPERTROPHY IN THE WORKING RAT-HEART

Objective: The aim was to investigate the effect of lowering external potassium on the sensitivity of the normal and hypertrophied rat heart to arrhythmias induced by increases in ventricular wall stress. Metho ds: The isolated working heart model was used to compare hypertrophied hearts from the spontaneously hypertensive rat (SHR) with hearts from normotensive control rats (NCR) from the Wistar and Wistar-Kyoto stra ins. Young animals [131.5(SEM 0.64) days] were used to ensure uncompli cated left ventricular hypertrophy. Arrhythmias were induced by 20 s i ncreases in ventricular wall stress. The ECG was recorded and the al-r hythmic response of each heart was compared during perfusion with Tyro de solutions containing [K] 6, 4.8, 3.6, and 2.4 mM. Results: Hypertro phied SHR hearts showed a significantly greater arrhythmic response th an control hearts at all levels of afterload increase when perfused wi th [K] 3.6 and 2.4 mM (t test P < 0.05 and P < 0.01). Both the number and complexity of arrhythmias were increased in the SHR hearts; ventri cular tachycardia occurred in 10/12 compared with 4/12 control hearts whereas ventricular fibrillation occurred in 5/12 hearts but in none o f the control hearts. Conclusions: At higher levels of [K] the sensiti vity of SHR hearts and normal hearts to wall stress induced arrhythmia s is similar. However, as [K] is lowered to 3.6 mM or below, hypertrop hied hearts show a greatly enhanced response to increases in ventricul ar wall stress They develop a larger number of ventricular ectopics an d more complex ventricular arrhythmias when compared to normal hearts. This may be of relevance to arrhythmic sudden death in hypertensive p atients in whom left ventricular hypertrophy, potassium depletion, and blood pressure lability is common. Excessive fluctuations in systolic pressure and therefore ventricular wall stress could provide a powerf ul arrhythmic stimulus in hypertensive patients with left ventricular hypertrophy, even before ischaemia, cardiac failure, or extensive extr acellular fibrosis have developed.