Clinical Briefs By Louis Kuritzky, MD
Clinical Briefs
By Louis Kuritzky, MD, Clinical Assistant Professor, University of Florida, Gainesville. Dr. Kuritzky is an advisor for Endo, Kowa, Pricara, and Takeda.
When One Antihypertensive Med is Not Enough: Which Combination?
Source: Kato J, et al. J Am Soc Hypertens 2012;6:393-398.
The ALLHAT trial is the largest hypertension clinical trial ever done, originally enrolling more than 42,000 individuals. That trial concluded that a thiazide diuretic (chlorthalidone) was at least as good as — and in some situations superior to — a calcium channel blocker ([CCB] amlodipine) or an angiotensin converting enzyme inhibitor ([ACE] lisinopril), and that an alpha blocker (doxazosin) was inferior to any of the three others.
But ALLHAT also demonstrated that only about 25% of hypertensives are able to maintain control on one medication. So, when one antihypertensive med is not enough, which combination should we choose?
The ACCOMPLISH trial was the first to address this question on a large-scale basis (n = 11,506) by directly comparing ACE/CCB (benazepril/amlodipine) with ACE/diuretic (benazepril/hydrochlorothiazide). In this trial, outcomes were superior for ACE/CCB.
Not everyone can tolerate an ACE, most commonly due to cough. Kato et al performed a clinical trial to compare in 58 hypertensive elderly patients (mean age, 72 years) the efficacy of an angiotensin receptor blocker (ARB)/CCB (mostly olmesartan/amlodipine) with ARB/diuretic (mostly olmesartan/indapamide).
At the conclusion of the trial, the ARB/CCB combination provided superior blood pressure reduction to ARB/diuretic. The diuretic used in ALLHAT was chlorthalidone, which is definitely more potent than hydrochlorothiazide; whether substitution of chlorthalidone for indapamide in this trial might have tipped the scales in another direction remains unknown.
Early Identification of COPD Exacerbations
Source: Yanez AM, et al. Chest 2012; 142:1524-1529.
Acute exacerbations of chronic obstructive pulmonary disease (AE-COPD) are consequential: 10% of patients admitted to the hospital die, 25% of those admitted to the ICU die, and the mortality rate in the year following an AE-COPD hospitalization for those who are discharged home is as high as 43%. Even after successful recovery from an AE-COPD, decrements in pulmonary function from pre-event status are noted that are not regained. Early identification of AE-COPD, with an intent-to-treat with minimum delay, might possibly alter the ominous natural history of AE-COPD.
Historically, it has been shown that the increasing dyspnea characteristic of AE-COPD typically begins about 5 days before patients seek consultation from their clinician. For asthma, wider swings in variation between morning and evening peak flow rate herald an acute deterioration, even before patients are overtly symptomatic. In a similar vein of thought, the authors postulated that changes in respiratory rate would signal an impending AE-COPD.
Oxygen-dependent COPD patients (n = 89) were asked to monitor respiratory rate daily for 3 months. Monitoring of daily respiratory rate (DRR) was performed automatically by installing a monitoring device to the patients’ oxygen delivery systems. Although respiratory rate was monitored at three different times each day, only the mean DRR rate was used for evaluation.
During 3 months of follow-up, 30 of the 89 patients required hospitalization for AE-COPD. Baseline average DRR for the group as a whole was 16 breaths/minute; among the subgroup ultimately admitted for AE-COPD, baseline DRR was 15.2. In the 5 days prior to an AE-COPD admission, their DRR increased to 19.1, but no meaningful change in DRR was seen in patients not requiring hospital admission. DRR may provide a new window into early identification of AE-COPD.
Vitamin D for Osteoarthritis: NOT
Source: McAlindon T, et al. JAMA 2013; 309:155-162.
For a burgeoning population of baby-boomers who wish to continue being physically active despite advanced years, tools to provide symptomatic relief from osteoarthritis (OA) are valuable (e.g., topical and systemic NSAIDs, opioids, physical therapy), but disease-modification is really the “holy grail.” At the current time, we do not possess any disease-modifying pharmacotherapy for OA.
Since vitamin D (VID) is an important player in bone health, might it influence symptoms or disease progression of OA? McAlindon et al performed a 2-year randomized, placebo-controlled trial of VID in subjects with symptomatic OA of the knee. VID dose was titrated from 2000 IU/d up to as much as 8000 IU/d, depending on attainment of a goal plasma VID level between 36-100 ng/mL. In this population of mostly Caucasian adults (mean age, 62 years) living in the Boston area, it is perhaps not surprising that baseline levels of VID averaged 22 ng/mL.
At the end of the trial, no effect (positive or negative) was seen from supplementation with VID on either OA symptoms or evidence of disease progression as measured by degree of cartilage loss.
When One Antihypertensive Med is Not Enough: Which Combination?; Early Identification of COPD Exacerbations; Vitamin D for Osteoarthritis: NOTSubscribe Now for Access
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