Kidney function and risk factors for left ventricular hypertrophy in untreated uncomplicated essential hypertension.

BACKGROUND: Left ventricular (LV) hypertrophy and decreased kidney function are well-established cardiovascular risk factors in hypertensive patients. STUDY DESIGN: We investigated the relationship between creatinine level, creatinine clearance, and estimated glomerular filtration rate (eGFR) with LV mass (LVM) in a cross-sectional study. PREDICTORS: eGFR and serum creatinine level. OUTCOME: LVM index (LVMI). SETTING & PARTICIPANTS: 400 patients with untreated uncomplicated essential hypertension. MEASUREMENTS: LVMI, eGFR (Modification of Diet in Renal Disease Study equation), Framingham risk factors, and a series of specific risk factors, ie, endothelial function (acetylcholine [ACh]-stimulated forearm blood flow [FBF]), insulin sensitivity (Homeostatic Model Assessment for insulin resistance [HOMA-R] index), C-reactive protein (CRP), and uric acid. RESULTS: Both eGFR and creatinine level were significantly related to LVMI (r = -0.34 and r = 0.35; P < 0.001). In a multiple regression model adjusting for Framingham risk factors, eGFR was independently associated with LVMI. However, this association, although highly significant, lost substantial strength after adjustment for such specific risk factors as HOMA-R index, ACh-stimulated FBF, CRP level, and uric acid level. eGFR interacted with insulin resistance in explaining the variability in LVMI (P = 0.007). LIMITATIONS: The cross-sectional nature of this study precludes cause-effect conclusions. CONCLUSIONS: Independently of other risk factors, decreased kidney function contributes to explain the variability in LVMI in patients with untreated uncomplicated essential hypertension. This association is attributable in part to the link between eGFR and such specific risk factors as HOMA-R index, ACh-stimulated FBF, CRP level, and uric acid level. Decreased kidney function and insulin resistance interact in explaining the variability in LVMI in these patients.

Interaction between vascular dysfunction and cardiac mass increases the risk of cardiovascular outcomes in essential hypertension.

AIMS: To investigate the additive prognostic impact of both forearm endothelial dysfunction and left ventricular mass (LVM) for future cardiovascular events. METHODS AND RESULTS: We enrolled 324 Caucasian, never treated, hypertensive outpatients. Endothelial function, by intra-arterial infusion of acetylcholine (ACh), and echocardiographic LVM were investigated. Patients were divided into tertiles on the basis of their increase in ACh-stimulated forearm blood flow (FBF) and LVM indexed by body surface area (LVMI). Cardiovascular events assessed were: fatal and non-fatal myocardial infarction, fatal and non-fatal stroke, transient cerebral ischaemic attack, unstable angina, coronary revascularization procedures, and symptomatic aorto-iliac occlusive disease. During a mean follow-up of 45.2+/-23.6 months, there were 47 new cardiovascular events (3.8 events/100 patient-years). The event rate was 6.8, 2.8, and 1.6% in the tertiles of ACh-stimulated FBF (log-rank test, P=0.0009), and 1.4, 3.4, and 6.6% in the tertiles of LVMI (log-rank test, P=0.0002), respectively. Besides, a significant interaction was documented between FBF and LVMI. In fact, the cardiovascular risk increases up to 11.4% in patients with low FBF and high LVMI. CONCLUSION: For the first time, we demonstrate that the co-existence of LVH and endothelial dysfunction in hypertensive patients increases significantly the risk of subsequent cardiovascular events.