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To investigate the interrelationship between arrhythmias provoked by acute pressure changes, and the presence of left ventricular hypertrophy and electrolyte imbalances.An isolated working rat heart model was used in a prospective comparison of the effects of acute pressure changes in hypertensive and normotensive hearts during perfusion with perfusate containing differing electrolyte compositions.An experimental laboratory study.Forty-four rat hearts (20 hypertensive, 24 normotensive).Hearts were subjected to sudden pressure changes of varying sizes during perfusion with two different electrolyte solutions and the arrhythmias provoked were recorded.The size of the pressure change necessary to provoke arrhythmias, and the amount and severity of arrhythmias provoked by equivalent-sized pressure changes.During perfusion with normal electrolyte concentrations, no hypertrophied hearts developed arrhythmia compared with more than half of the normal hearts during equivalent-sized pressure changes, and a much larger pressure increase was necessary to produce any arrhythmia in the hypertrophied hearts. During perfusion with cation-depleted perfusate, arrhythmias significantly increased in both groups of hearts, but the pattern was reversed; more than half of the hypertrophied hearts compared with none of the normal hearts developed ventricular tachycardia during equivalent-sized pressure increases, whilst the minimum pressure change necessary to provoke arrhythmia became significantly smaller in the hypertrophied hearts compared with, he normal hearts.Left ventricular hypertrophy plays a paradoxical role in the development of arrhythmias in this model. It appears to protect the heart from developing arrhythmias in response to sudden pressure changes when electrolyte concentrations are normal. However, it also seems to lead to a marked increase in the sensitivity of the myocardium to pressure changes during perfusion with low levels of potassium and magnesium. Under these conditions, potentially fatal arrhythmias can be readily provoked by relatively small pressure changes. These results may be of importance for the management of hypertension and may provide insight into some of the mechanisms underlying sudden death in hypertension. The findings may also be of relevance to other cardiac diseases associated with ventricular hypertrophy or abnormal wall stress.