Author + information
- Marijana Tadic, MD, PhD∗ ( and )
- Cesare Cuspidi, MD
- ↵∗University Clinical Hospital Center “Dr. Dragisa Misovic–Dedinje”, School of Medicine, University of Belgrade, Heroja Milana Tepica 1, 11000 Belgrade, Serbia
We have read with great interest the recently published article by Jensen et al. (1) about the 2-dimensional mechanics in a large cohort of patients with type 1 diabetes mellitus (T1DM). The investigators reported significant difference in left ventricular (LV) global longitudinal strain (GLS) between the control subjects and the T1DM subjects with albuminuria, whereas the diabetic patients and those with normoalbuminuria have similar GLS as the healthy control subjects do, even though these patients have had T1DM without tight glycemic control (glycosylated hemoglobin >8%) for more than 2 decades.
We would like to discuss several important points of this investigation. The absolute value of GLS in the control group is somewhat lower than expected for the healthy mid-age population. Interestingly, diastolic blood pressure and LV mass index are higher in the control group than in the T1DM patients, especially than in the T1DM subjects with normoalbuminuria, probably due to medical therapy.
The other important issue is the lack of association between the usage of various medications and LV mechanical remodeling in T1DM. The investigators found that the treatment of statins, beta-blockers, calcium-channel blockers, angiotensin-converting enzymes, and angiotensin II inhibitors or diuretics is not associated with any improvement of GLS in the diabetic population. The data on this topic are scarce and inconsistent, and this kind of investigation with a large population of uncomplicated diabetic patients has been waiting for a long time. The previous investigations showed that all these drugs improve LV structure (reducing LV mass) and systolic and diastolic function. Is it possible that they are completely ineffective for improvement of LV longitudinal function?
Previously it was shown that statins improve LV longitudinal function and that was evaluated using different imaging techniques than speckle tracking (2). Mizuguchi et al. (3) reported that telmisartan significantly improved GLS in hypertensive patients, but only after 12 months. This finding raises the question about the duration of therapy in the present study, which was not been presented. Perhaps longer duration of therapy would change the results. Furthermore, Motoki et al. (4) recently showed that calcium-channel blockers also have favorable influence on GLS, even after only 3 months of therapy. Beta-1 blockade, induced by bisoprolol, results in the reduction of GLS (5). However, the percentage of the T1DM patients who used beta-blockers in the present study is not high enough to change the final result, especially in the subjects with normoalbuminuria.
Jensen et al. (1) showed that the usage of any of the medications was not independently associated with GLS. However, the present multivariate model consists of some variables that interact (systolic and diastolic blood pressure, body mass index and LV mass index). It would be helpful to perform a multivariate analysis considering the influence of the variables from model 3 on LV mass index and E/e′ in order to evaluate the effect of different medications on LV structure and diastolic function in this population.
The Thousand & 1 Study raises many questions that need to be resolved and confirmed, but it certainly represents a solid ground for further investigations.
Please note: The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- American College of Cardiology Foundation