The effect of potassium ion depletion on postinfarction canine cardiac arrhythmias.
The effect of potassium ion (K+) depletion on postmyocardial infarction ventricular arrhythmias was investigated in 32 dogs: 12 control animals, 10 animals that ate a diet extremely low in K+ for 15 days, and 10 others that, in addition to dietary K+ deprivation, received 50 mg of hydrochlorothiazide four times. The experimental myocardial infarction was created by proximal left anterior descending coronary artery ligation. In a subgroup of 24 animals selected for relatively uniform size of myocardial infarction (14% to 22% of left ventricular mass), eight animals with mean cumulative K+ balance of -4.01 +/- 2.19 meq/kg developed spontaneous ventricular fibrillation within 4 to 17 min of coronary ligation, whereas 16 animals with a mean cumulative K+ balance of -0.11 +/- 1.82 meq/kg didn't. By univariate analysis cumulative K+ deficit (p = .001) and plasma K+ concentration (p = .039) correlated significantly with spontaneous ventricular fibrillation. Multivariate analysis of the entire population of 32 animals identified cumulative K+ deficit and size of myocardial infarction as the only independent predictors of ventricular fibrillation. Cumulative K+ deficit was also an independent predictor of ventricular fibrillation induced by programmed cardiac stimulation in the conscious state 1 day after myocardial infarction.
D000818:Animals; D004285:Dogs; D004594:Electrophysiology; D005260:Female; D006852:Hydrochlorothiazide / Q000008:administration & dosage; D007473:Ion Channels / Q000378:metabolism; D009203:Myocardial Infarction / Q000150:complications*; D011188:Potassium / Q000378:metabolism / Q000502:physiology*; D011191:Potassium Deficiency / Q000150:complications*; D013223:Statistics as Topic; D014693:Ventricular Fibrillation / Q000209:etiology*
D007473:Ion Channels; D006852:Hydrochlorothiazide; D011188:Potassium