Clinical Briefs
By Louis Kuritzky, MD, Clinical Assistant Professor, University of Florida, Gainesville
Dr. Kuritzky is an advisor for Endo, Kowa, Pricara, and Takeda.
Refining the Relationship Between Thyroid Hormones and Left Ventricular Mass
Source: Iida M, et al. Thyroid hormone within the normal range is associated with left ventricular mass in patients with hypertension. J Am Soc Hypertens 2012;6:261-269.
ANIMAL STUDIES HAVE SHOWN THAT THYroid hormones (T3 and T4) induce hypertrophy of cardiac myocytes through stimulation of both structural and regulatory myocyte genes, which can be prevented by ACE inhibitors or beta-blockers. Such observations have led to the question of whether there might be a relationship between cardiac mass and thyroid hormones, even within the range currently defined as normal.
Hypothyroidism and hyperthyroidism are each considered a potential secondary cause of hypertension: the former through endothelial dysfunction that leads to vasoconstrictor hyperresponsiveness and subsequent increased peripheral resistance, and the latter through increased sympathetic tone. Iida et al investigated hypertensive subjects (n = 293) who had no known thyroid disease and whose thyroid function tests (T3, T4, and TSH) were within normal limits.
Among these euthyroid hypertensive study subjects, multiple linear regression found a positive relationship between T3 and T4 and ventricular mass (the higher the thyroid hormones, the greater the ventricular mass), and an inverse relationship between TSH and ventricular mass. When compared with normotensive controls, no such relationship could be identified. This would lead to consideration that in persons with hypertension, higher levels of thyroid hormone — even within the normal range — may be related to the development of left ventricular hypertrophy.
The ORIGIN Trial: Basal Insulin vs Standard Care for Early Type 2 Diabetes
Source: The ORIGIN Trial Investigators. Basal insulin and cardiovascular and other outcomes in dysglycemia. N Engl J Med 2012;367:319-328.
TYPE 2 DIABETES REFLECTS INSULIN INsufficiency. Early in the disease process, plasma insulin levels may actually be higher than normal, but insufficient to maintain euglycemia. By the time of formal diagnosis, approximately half of beta cell mass has been lost, and as the disease progresses, insulin levels continue to fall.
The Outcome Reduction with an Initial Glargine Intervention (ORIGIN) trial randomized subjects with prediabetes or early diabetes (n = 12,537) to insulin glargine (GLAR) or standard treatment (STND) for 6.2 years (mean). The objective of the trial was to determine whether early institution of basal insulin, as compared to STND, improves cardiovascular outcomes. Standard treatment was simply treatment of diabetes as per the treating clinician’s choice; by the end of the trial, only 11% of the STND group was receiving insulin. Eighty percent of the GLAR group was on insulin at the end of the trial.
There was no difference in cardiovascular outcomes between the two treatment groups. One notable difference between treatments was the likelihood of progression from prediabetes to diabetes. The GLAR group was 28% less likely to progress than the STND group; however, there was also more hypoglycemia and weight gain in the GLAR group.
Increased incidence of cancer — a concern generated by earlier insulin trial data — was not seen in this large trial, and hence should be very reassuring.
Bronchodilators in COPD and Arrhythmias
Source: Wilchesky M, et al. Bronchodilator use and the risk of arrhythmia in COPD: Part 1: Saskatchewan Cohort Study. Chest 2012;142:298-304.
FOR CHRONIC OBSTRUCTIVE PULMONARY disease (COPD), except for the provision of oxygen in late-stage disease, no pharmacologic intervention has been confirmed to save lives. Nonetheless, since bronchodilators improve symptoms, quality of life, and exercise capacity, and reduce acute exacerbations of COPD, they play an important role in routine care. Concerns about the potential capacity for arrhythmogenicity of bronchodilators has arisen from clinical COPD trials such as the Lung Health Study (n = 5887), in which short-acting ipratropium bromide was associated with a three-fold greater incidence of arrhythmia than comparator groups. Other smaller trials have not confirmed these findings, hence clarification is needed.
Wilchesky et al analyzed data from the province of Saskatchewan, Canada, to identify COPD subjects (n = 6018) and compare the incidence of arrhythmia in new users of ipratropium, beta-agonists (short- and long-acting), and methyhlxanthines to non-users.
Short-acting anticholinergics were associated with a 2.4 relative risk of arrhythmia, and long-acting beta-agonists with a 4.5 relative risk. No statistically significant increased risk was seen with short-acting beta-agonists or methylxanthines. Despite these concerns, the authors remind us that the absolute risk increase was very small, and “in most cases would be outweighed by the therapeutic benefit accrued through symptomatic relief and consequent improvements to quality of life.”
Clinical Briefs: Refining the Relationship Between Thyroid Hormones and Left Ventricular Mass; The ORIGIN Trial: Basal Insulin vs Standard Care for Early Type 2 Diabetes; Bronchodilators in COPD and ArrhythmiasYou have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
- Award-winning Medical Content
- Latest Advances & Development in Medicine
- Unbiased Content