Insulin resistance and vascular remodelling, in relation to left ventricular mass, geometry and function: an answer to LIFE?

Abstract

Many pathophysiological processes have been intimately linked to hypertension and its complications, including insulin resistance, left ventricular mass (LVM) and geometry, central vascular hypertrophy and peripheral vascular remodelling, LV systolic and diastolic function, etc. What appears to be much less certain are the (complex) interrelations between all these diverse processes.In elderly patients with essential hypertension and LV hypertrophy (LVH), Olsen et al 1 recently reported that peripheral vascular remodelling (assessed as minimal forearm vascular resistance, MFVR), hypertrophy and low distensibility of the common carotid arteries are associated with increased systolic blood pressure (BP) but not with insulin resistance (as assessed by euglycaemic hyperinsulinaemic clamp) or hyperinsulinaemia. Their findings suggest that long-standing systolic BP load may be a far more important determinant of structural vascular changes than insulin resistance in hypertension. However, in never-treated hypertensives, insulin resistance and hyperinsulinaemia were associated with low distensibility of the common carotid arteries, independent of BP and lumen diameter; perhaps because of a direct effect of insulin on the carotid arteries, resulting in changes in collagen metabolism. 1 Indeed, the subsequent publication from Olsen et al 2 suggests that insulin sensitivity was unrelated not only to parameters of peripheral vascular remodelling, but also to endothelial function or microvascular rarefaction.In this issue of the Journal of Human Hypertension, Olsen et al 3 examine the association between insulin resistance, carotid hypertrophy and peripheral vascular remodelling on the one hand and LVH, diastolic LV filling and systolic function on the other. So, what more information can the present analysis add to their previous two publications? 1,2 We shall (hopefully) delineate these in a systematic manner.LVH by echocardiography has proved to be a strong independent predictor of cardiovascular (CV) morbidity and mortality in hypertensive patients. Patients with a concentric hypertrophy geometry (increased LVM and relative wall thickness) appear to carry the highest risk, while an eccentric hypertrophy geometry (increased LVM but normal relative wall thickness) carries an intermediate risk for target organ damage. 4,5 In addition, the former is associated with especially high arterial pressure while the latter is associated with obesity and elevated volume load. On the other hand, central vascular hypertrophy, in particular carotid intimamedia thickness (IMT) is generally regarded as 'marker' of atherosclerotic burden as well as a 'predictor' of future CV events in prospective epidemiological studies. 6 Indeed, arterial remodelling, hypertrophy, and stiffness are common alterations in hypertensive patients, as well as LV diastolic dysfunction, and all have been linked to LVH. 7 However, diastolic dysfunction is also well recognised in patients with hypertension, even in the absence of LVH, but whether its assessment ...

Diabetes, gender, and left ventricular structure in African-Americans: the atherosclerosis risk in communities study

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Nonobese, insulin-deficient Ins2Akitamice develop type 2 diabetes phenotypes including insulin resistance and cardiac remodeling

“…Our findings are consistent with the cardiovascular remodeling observed in insulin-resistant diabetic subjects (20). However, most diabetic patients exhibiting cardiac remodeling are hypertensive, a common comorbidity of diabetes that may contribute to diabetic heart disease (38).…”

Impact of Adiponectin on Left Ventricular Mass Index in Non-complicated Obese Subjects

“…Consequently, an increase in LVMI and disturbance in diastolic functions may be expected [1]. However, the common belief is that the influential mechanisms are not limited to hemodynamic changes [9]. The negative relation between adiponectin and LVMI may also contribute to this mechanism.…”

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