Author + information
- Michael Salerno, MD, PhD∗ (, )
- Sujith Kuruvilla, MD and
- Christopher M. Kramer, MD
- ↵∗University of Virginia Health System, Department of Medicine, Cardiovascular Division, 1215 Lee Street, Box 800158, Charlottesville, Virginia 22908
We thank Drs. Tadic and Cuspidi for their interest in our study (1) evaluating the relationship between myocardial fibrosis and mechanics in hypertensive heart disease. We agree with the writers that multiple factors could affect myocardial fibrosis and extracellular volume (ECV), which require further study in a larger cohort of patients. We did not specifically exclude patients with diabetes, obesity, or metabolic syndrome from the study. There were 4 subjects with diabetes in the hypertension (HTN) non–left ventricular hypertrophy (LVH) group and 6 in the HTN LVH group. There was no significant difference in ECV between patients with diabetes and those without diabetes in our study. Glucose and lipid data were not available. With regard to obesity, there was no difference in body mass index between the groups, and there was no significant correlation between body mass index and either ECV or native T1. Thus, within the context of our study, these factors do not explain the differences in ECV and native T1 observed between the groups.
To avoid confounding conditions that could contribute to myocardial fibrosis, we excluded subjects with left ventricular (LV) ejection fraction <45%. In our study, there was no difference in LV ejection fraction among the 3 groups (63.2 ± 5.1%, 65.8 ± 8.5%, and 64.5 ± 7.4%) and no correlation between LV ejection fraction and ECV or native T1.
Regarding systolic blood pressure (SBP), concentricity (as defined by the ratio of LV mass to end-diastolic volume), and left ventricular mass index (LVMI), we chose to focus on LVMI given that LVH reflects the cumulative effect of high blood pressure on ventricular remodeling, rather than a single–time point assessment of blood pressure. From the clinical data, it is difficult to ascertain important factors, such as the duration of HTN, adequacy of blood pressure control, and the specific duration of therapy with each antihypertensive medication, whereas LV mass could be directly measured from the cardiac magnetic resonance data. This being said, as expected, there were significant correlations of SBP with ECV and native T1 (R = 0.29 and R = 0.36, respectively) and between concentricity and ECV and native T1 (R = 0.34 and R = 0.34, respectively). However, the correlations between LVMI and SBP and LVMI and concentricity were significantly higher (R = 0.69 and R = 0.74, respectively), reflecting the high degree of colinearity among LV mass, SBP, and concentricity.
Finally, it is known that renin-angiotensin-aldosterone system inhibition reduces LVH in research studies, presumably by an effect on both blood pressure and myocardial fibrosis. In our study, 51% of the HTN non-LVH patients and 85% of the HTN LVH patients were on blood pressure regimens that included either angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. There was no difference in ECV or native T1 between patients with or without renin-angiotensin-aldosterone inhibition. Again, multiple factors including variations in the antihypertensive regimens, duration of therapy, and adequacy of blood pressure control confound this assessment.
We believe that further study of myocardial fibrosis and mechanical function in patients with hypertensive heart disease is warranted and could have important implications for predicting risk in this patient population and for developing novel antifibrotic therapies for LVH and heart failure with preserved ejection fraction.
Please note: Drs. Salerno and Kramer have received research support from Siemens Healthcare. Dr. Kuruvilla has reported that he has no relationships relevant to the contents of this paper to disclose.
- American College of Cardiology Foundation