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The relationship of electrocardiographic left ventricular hypertrophy to decreased serum potassium
Peter M Okin1, Sverre E Kjeldsen, Lars H Lindholm
1Division of Cardiology, Weill Cornell Medical College, 525 East 68th Street, New York, NY 10065, USA. pokin@med.cornell.edu
Insights
Low serum potassium (K) is linked to more severe electrocardiographic left ventricular hypertrophy (LVH). This association persists even during antihypertensive treatment, indicating a significant relationship between low K and cardiac changes.
Area of Science:
- Cardiology
- Nephrology
- Clinical Research
Background:
- Low serum potassium (K) is linked to hypertension, cardiac, and renal dysfunction.
- The association between low serum K and electrocardiographic left ventricular hypertrophy (LVH) is not well understood.
Purpose of the Study:
- To investigate the relationship between low serum K and the presence/severity of Cornell product LVH.
- To assess if this association persists during antihypertensive therapy.
Main Methods:
- Examined Cornell product LVH in 8586 patients based on baseline serum K levels (lowest quartile: ≤ 3.90 mEq/l).
- Patients received losartan- or atenolol-based treatment with hydrochlorothiazide (HCTZ) as needed.
- Analyzed LVH in relation to serum K, adjusting for multiple clinical and demographic factors.
Main Results:
- Low baseline serum K was significantly associated with higher mean baseline Cornell product LVH and increased risk of LVH.
- In-treatment low serum K was linked to higher mean Cornell product LVH and increased risk of LVH at years 1-4, even after adjustments.
Conclusions:
- Low serum potassium is independently associated with increased likelihood and severity of Cornell product LVH.
- This association is evident during antihypertensive treatment, highlighting K's role in cardiac remodeling.
Background:
Low serum potassium (K) is associated with increased blood pressure, impaired cardiac function and renal dysfunction. Although lower serum K is associated with cardiac hypertrophy in animal models, the relationship of low serum K to the presence and severity of electrocardiographic left ventricular hypertrophy (LVH) is unclear.
Methods:
Baseline and yearly Cornell product LVH levels were examined in relation to low serum K (serum K ≤ 3.90 mEq/l, the lowest quartile of baseline K levels) in 8586 patients with baseline K levels. Patients were randomized to losartan-vs atenolol-based treatment and additional hydrochlorothiazide (HCTZ) therapy as needed.
Results:
After adjusting for age, sex, race, prior antihypertensive treatment, losartan vs atenolol therapy, HCTZ use, baseline diastolic and systolic pressure, body mass index, serum creatinine and urine albumin/creatinine ratio, baseline serum K ≤ 3.90 was associated with significantly higher mean baseline Cornell product LVH (2898 vs 2801 mm•ms, p = 0.001) and a 24% higher risk of Cornell product LVH > 2440 mm•ms at baseline (OR 1.24, 95% CI 1.11-1.38, p < 0.001). After also adjusting for baseline Cornell product and changes in diastolic and systolic pressure between baseline and each year of measurement, in-treatment serum K ≤ 3.90 determined yearly was associated with significantly higher mean Cornell product LVH at years 1-3 and with statistically significant 16-32% increased risks of LVH by Cornell product at years 1-4.
Conclusions:
A low serum K is independently associated with a greater likelihood and severity of Cornell product LVH during antihypertensive therapy.
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