Wall stress induced arrhythmia is enhanced by low potassium and early left 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.


METHODS
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 strains. Young animals [131.5(SEM 0.64) days] were used to ensure uncomplicated left ventricular hypertrophy. Arrhythmias were induced by 20 s increases in ventricular wall stress. The ECG was recorded and the arrhythmic response of each heart was compared during perfusion with Tyrode solutions containing [K] 6, 4.8, 3.6, and 2.4 mM.


RESULTS
Hypertrophied SHR hearts showed a significantly greater arrhythmic response than control hearts at all levels of afterload increase when perfused with [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; ventricular tachycardia occurred in 10/12 compared with 4/12 control hearts whereas ventricular fibrillation occurred in 5/12 hearts but in none of the control hearts.


CONCLUSIONS
At higher levels of [K] the sensitivity of SHR and normal hearts to wall stress induced arrhythmias is similar. However, as [K] is lowered to 3.6 mM or below, hypertrophied hearts show a greatly enhanced response to increases in ventricular wall stress. They develop a larger number of ventricular ectopics and more complex ventricular arrhythmias when compared to normal hearts. This may be of relevance to arrhythmic sudden death in hypertensive patients 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 powerful arrhythmic stimulus in hypertensive patients with left ventricular hypertrophy, even before ischaemia, cardiac failure, or extensive extracellular fibrosis have developed.
Evans
S J
SJ
School of Medical Sciences, University of Bristol, University Walk, United Kingdom.
Levi
A J
AJ
Jones
J V
JV
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D004562:Electrocardiography; D006973:Hypertension / Q000378:metabolism / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D010477:Perfusion; D011188:Potassium / Q000378:metabolism*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D017180:Tachycardia, Ventricular / Q000378:metabolism / Q000503:physiopathology; D014693:Ventricular Fibrillation / Q000378:metabolism / Q000503:physiopathology; D017725:Ventricular Pressure / Q000502:physiology*
D011188:Potassium