| Popis: |
Objective Identify blood pressure (BP) response to spironolactone in patients with apparent therapy-resistant hypertension (aTRH) using electronic medical records (EMRs) in order to estimate response in a real-world clinical setting.Design Developed an algorithm to determine BP and electrolyte response to spironolactone for use in a retrospective cohort study.Setting An academic medical centre in Nashville, Tennessee.Population Patients with aTRH prescribed spironolactone.Main outcome measures Baseline BP and BP response, determined as the change in mean systolic BP (SBP) and diastolic BP (DBP) following spironolactone initiation. Additional response measures were serum sodium, potassium and creatinine, estimated glomerular filtration rate, haemoglobin A1c (HbA1c), glucose, high-density lipoprotein, low-density lipoprotein and triglycerides. Demographic characteristics included race, age, gender, body mass index (BMI), diabetes mellitus, chronic kidney disease stage 3, ischaemic heart disease and smoking.Results The mean decreases in SBP and DBP were 8.1 and 3.4 mm Hg, consistent with clinical trial data. Using a mean decrease in SBP of 5 mm Hg or in DBP of 2 mm Hg to define ‘responders’, 30.3% of patients did not respond. In univariable analyses, responders had higher BMI, baseline SBP, DBP, sodium and HbA1c, and lower creatinine. In multivariable analysis, responders were older and had significantly higher BMI and baseline SBP and DBP, and lower potassium. Increases in potassium and creatinine following spironolactone were larger in responders. When BP was evaluated as a continuous variable, decreases in SBP and DBP correlated with baseline BP, decrease in sodium and increases in potassium and creatinine following spironolactone. The decrease in SBP was associated with decreasing glucose in European Americans.Conclusions We developed an algorithm to assess BP response to a commonly prescribed medication for aTRH using EMRs. Electrolyte changes associated with the BP response to spironolactone are consistent with its mechanism of action of blocking the mineralocorticoid receptor and decreasing epithelial sodium channel activity. |
