Is inappropriate left ventricular mass related to neurohormonal factors and/or arterial changes in hypertension? a LIFE substudy

Abstract

We investigated whether inappropriately high left ventricular (LV) mass, defined as observed LV mass exceeding the level of individual LV mass predicted from gender, height, and stroke work, may be associated with an imbalance between growth-promoting and growth-inhibitory factors and/or structural vascular changes. In 53 patients with hypertension and electrocardiographic LV hypertrophy, 24-h ambulatory blood pressure (BP); echocardiographic LV mass, stroke volume and stroke work; minimal forearm vascular resistance (MFVR); and intima-media cross-sectional area in common carotid arteries (IMA) were evaluated after 2 weeks of placebo treatment. Serum insulin, plasma epinephrine, norepinephrine, endothelin, angiotensin II, aldosterone, and brain natriuretic peptide (BNP) were also measured. High observed LV mass was related to high IMA (r ¼ 0.46, Po0.001), MFVR (in men: r ¼ 0.36, Po0.05), 24-h ambulatory systolic BP (r ¼ 0.30, P ¼ 0.06), and lower plasma angiotensin II (r ¼ À0.33, Po0.05), but not to other circulating growth factors. Stroke work was similarly related to IMA (r ¼ 0.42, Po0.01), MFVR (in men: r ¼ 0.41, Po0.05), and plasma angiotensin II (r ¼ À0.32, Po0.05). Inappropriate LV mass, identified by the ratio between observed LV mass and the value predicted for gender, height, and stroke work, was not significantly related to any of the arterial or neurohormonal variables. In this small series of older hypertensive patients, inappropriate LV mass was not significantly related to arterial changes or to measured circulating growth factors, although weak relations cannot be excluded. Alternatively, inappropriately high LV mass might be related to unmeasured factors such as local myocardial alterations in growth factors and/or genetic predisposition to develop excessive LV hypertrophy.

Plasma C-terminal pro-endothelin-1 is associated with left ventricular mass index and aortic root diameter in African-American adults with hypertension

“…The results of studies that evaluated the associations of ET-1 with LVM i are not consistent. While a few small studies (n <60) reported a significant association of plasma CT-proET-1 with LVM i ,24,25,27 other studies (n =50-120) found no significant association 28-30. In our study, plasma CT-proET-1 was associated with LVM i after adjustment for adjustment for conventional cardiovascular risk factors and medication use ( P =0.002).…”

Prevalence and factors related to inappropriately high left ventricular mass in patients with rheumatoid arthritis without overt cardiac disease

“…Notably, the prevalence of iLVM we found in our RA patients was more than two-fold higher than that detected in the settings of patients mentioned above, suggesting RA disease a specific condition by which LVM is inappropriately produced together with myocardial fibrosis. The biochemical processes leading to iLVM are not known: iLVM was not significantly related to arterial changes or to any circulating growth factor traditionally measured in patients with arterial hypertension [35]. However, what we can gather from our finding is that a worrisome condition named iLVM can be easily detected by standard echocardiography at an early stage of RA disease, when the changes in cardiovascular geometry and systolic function are already evident [36][37][38][39].…”

Compensatory or inappropriate left ventricular mass in different models of left ventricular pressure overload: comparison between patients with aortic stenosis and arterial hypertension

“…Conversely, the prevalence of inappropriate LV mass was particularly high in the subgroups of patients with LV hypertrophy, and this behaviour was detected more frequently in patients with AH than aortic stenosis. It is possible that the role of nonhaemodynamic factors as determinants of LV mass inappropriateness such as proto-oncogenes and other growth factors, cytokines, plasma noradrenaline and other neurohormones has more influence in AH than aortic stenosis patients [33][34][35]. Recent studies documented a significant increase in a member of the interleukin-6 superfamily, 'cardiotrophin-1', in patients with inappropriate LV mass.…”