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Ventricular ectopic activity with diuretic therapy
O B Holland1, L Kuhnert, J Pollard
1Department of Internal Medicine, University of Texas Medical Branch, Galveston 77550.
Insights
Diuretic-induced hypokalemia can increase ventricular ectopic activity (VEA) in hypertensive patients. Restoring potassium levels with amiloride or potassium chloride reduced VEA, suggesting electrolyte changes cause arrhythmias.
Area of Science:
- Cardiology
- Pharmacology
- Nephrology
Background:
- Diuretic-induced hypokalemia's arrhythmogenic potential in hypertension is debated.
- Previous studies show conflicting results regarding electrolyte imbalances and cardiac arrhythmias.
Purpose of the Study:
- To investigate the arrhythmogenic effects of hydrochlorothiazide (HCTZ)-induced hypokalemia.
- To evaluate the impact of potassium repletion on ventricular ectopic activity (VEA) in hypertensive patients.
Main Methods:
- Thirty-two hypertensive patients were divided into two groups: HCTZ alone (Group 1) or HCTZ with amiloride (Group 2).
- Group 1 patients experiencing increased VEA were treated with amiloride or potassium chloride.
- Ambulatory ECG monitoring and exercise testing were used to assess cardiac rhythm.
Main Results:
- One patient in Group 1 died suddenly, with autopsy suggesting an arrhythmic cause.
- Six patients in Group 1 showed reduced VEA after potassium repletion.
- Group 2 patients, who maintained normal potassium levels, did not exhibit significant VEA increases.
Conclusions:
- Diuretic therapy, specifically HCTZ, can induce VEA primarily through induced electrolyte changes, particularly hypokalemia.
- Maintaining normal plasma potassium levels during diuretic therapy may prevent increased ventricular ectopic activity.
- Potassium repletion effectively reduces VEA in patients experiencing diuretic-induced hypokalemia.
Abstract:
The arrhythmogenic potential of diuretic-induced hypokalemia in patients with uncomplicated hypertension has been controversial. Thirty-two hypertensive patients with previous diuretic-induced hypokalemia, normal 24-hour ambulatory ECG monitoring, and normal exercise testing were treated with 100 mg hydrochlorothiazide (HCTZ) daily (Group 1) to induce hypokalemia or with a combination of HCTZ with amiloride (Group 2) to attempt to maintain plasma potassium levels in the normal range during diuretic therapy. Those Group 1 patients (Group 1A) with increased ventricular ectopic activity (VEA) during HCTZ therapy were subsequently potassium-repleted with amiloride and with supplemental potassium chloride to evaluate the effect of these treatments on VEA. One Group 1 patient died suddenly after 12 days of HCTZ therapy. Autopsy findings suggested an arrhythmic death. Six Group 1 patients who had increased VEA with HCTZ treatment had reductions in VEA with amiloride or supplemental potassium chloride. Group 2 patients did not have a significant increase in VEA. Thus, diuretic therapy appears to cause VEA primarily by electrolyte changes that are induced.