Author + information
- Jonathan C.L. Rodrigues, BSc(Hons), MBChB(Hons)∗ (, )
- Amardeep Ghosh Dastidar, MBBS,
- Julian F.R. Paton, BSc(Hons), PhD and
- David H. MacIver, MBBS, MD
- ↵∗University Hospitals Bristol National Health Service Foundation Trust, Cardiac Magnetic Resonance Department, National Institute for Health Research Bristol Cardiovascular Biomedical Research Unit, Upper Maudlin Street, Bristol BS2 8HW, United Kingdom
We read with interest the work by de Marvao et al. (1). We congratulate the investigators on the novel insights into ventricular remodeling from their extensive 3-dimensional computational analysis of 1,258 cardiac magnetic resonance studies. However, we would like to raise several points for discussion.
The investigators excluded subjects with self-reported cardiovascular disease. Subclinical hypertrophic cardiomyopathy (HCM) and genetic predilection to HCM, although likely to be rare, warrant consideration especially because hypertensive subjects with asymmetric thickening have higher incidence of HCM (2). A normal resting electrocardiograph and family history would have been additive in excluding incidental HCM. There is no mention of tissue characterization with late myocardial gadolinium enhancement, which can be a useful discriminator of causes of left ventricular (LV) hypertrophy. This is particularly important because the finding of regional myocardial function being diminished in regions that exhibit the greatest hypertrophy conflicts with previous work by Puntmann et al. (3), which demonstrated increased deformation in regions of increased wall stress in hypertensive heart disease and the opposite in HCM.
Baseline exercise activity level is another important variable to consider. Asymmetric LV thickening (segmental thickness ≥13 mm and >1.5-fold the opposing wall) has been described in 2.2% of healthy, young adult army recruits by cardiac magnetic resonance, rising to 10% following a period of physical training (4).
In addition, the study demonstrates a relationship between systolic blood pressure (BP) and cardiac remodeling. de Marvao et al. (1) suggest that rising BP might have a much earlier impact on cardiac structure than previously recognized, implying the former drives the latter while acknowledging this cannot be proven in their cross-sectional observational study design. However, there is another theoretical explanation that warrants consideration. The underlying driver for the hypertensive state may actually also be exerting a direct influence on the myocardium. Elevated sympathetic nerve activity is recognized as a potential etiology in some hypertensive subjects and can be measured by muscle sympathetic nerve activity level. Seravalle et al. (5) recently investigated muscle sympathetic nerve activity in optimal, normal, and high-normal BP subjects. They found that muscle sympathetic nerve activity was significantly higher in subjects with high-normal BP than in those with normal and optimal BP. This neurogenic alteration may be implicated in the progression to established hypertension. In parallel, it could also drive asymmetric LV changes owing to the denser sympathetic innervation of the interventricular septum relative to the lateral wall.
The relationship between BP and cardiac remodeling is likely to be complex. Time spent at a certain elevated blood pressure, rather than just the absolute systolic BP level, as well as nocturnal dipper and nondipper status, are also likely to be important factors. Differences in these variables, not investigated in the current study, may help explain why de Marvao et al. (1) were only able to demonstrate weak correlation between systolic BP and LV mass in pre-hypertension subjects and actually no significant correlation in subjects with hypertension.
Finally, we agree that we still have much to learn about hypertensive heart disease, but the advanced cardiac magnetic resonance post-processing techniques described by de Marvao et al. (1) have the potential to contribute greatly to our understanding of hypertensive heart disease and beyond.
Please note: The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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