Metabolic Syndrome and target organ damage

FREQUENTLY PRESENT IN EARLY STAGES OF HYPERTENSION

Cuspidi C, Meani S, Fusi V, et al. Metabolic syndrome and target organ damage in untreated essential hypertensives. J Hypertens 2004;22:1991-8.

Subjects with high blood pressure (BP) have a high prevalence of the associated metabolic risk factors defining the metabolic syndrome (high cholesterol, reduced high-density lipoprotein cholesterol [HDL-C], high triglycerides, insulin resistance, glucose intolerance, abdominal obesity, hyperuricaemia, and elevated fibrinogen). This study explored the relationship of the metabolic syndrome with cardiac and extra-cardiac target organ damage (TOD) as defined by the 2003 ESH/ESC guidelines in subjects with essential hypertension (HT). The study included 447 never-treated hypertensive patients attending a HT outpatient clinic for the first time. Inclusion criteria were: 1) recently diagnosed grade 1 and 2 HT (diastolic BP [DBP] 90-109 mm Hg or systolic BP [SBP] 140-179 mm Hg) confirmed during the first visit at the clinic; 2) absence of secondary HT, congestive heart failure, previous myocardial infarction, significant cardiac valve disease, history of coronary bypass, diabetes mellitus (antidiabetic treatment or blood glucose >126 mg/dl or >7.0 mmol/l on 2 separate occasions), renal insufficiency (serum creatinine >133 µmol/l in men, >124 µmol/l in women).

Then, the patients underwent a series of procedures during the 4 following weeks: physical examinations, clinic BP measurement, routine examinations, 24-h urine collection for microalbuminuria, 24-h ambulatory blood pressure measurement (ABPM), echocardiography, and carotid ultrasonography. The metabolic syndrome was defined using the National Cholesterol Education Program Adult Treatment Panel (NCEP ATP) III criteria (Box).

TOD was defined as the presence of microalbuminuria and ultrasonographic evidence of cardiac and vascular alterations. Left ventricular hypertrophy (LVH) was determined by echocardiography: left ventricular mass index (LVMI) >125 g/m2 in men and >110 g/m2 in women (indexation for body surface area), or >51 g/m2.7 in men and >47 g/m2.7 in women (indexation to body height).

Overall prevalence of the metabolic syndrome was 30.2%. Low HDL-C was present in 56.2% of the patients (n=248), abdominal obesity in 26.4% (n=118), hypertriglyceridaemia in 26.0% (n=116), and high fasting blood glucose in 8.3% (n=37). The two groups with (n=135, group I) and without (n=312, group II) the metabolic syndrome did not differ for the demographic and clinical characteristics (particularly for BP values, duration of HT, or prevalence of isolated HT). Significant differences were found for blood glucose, total cholesterol, HDL-C, triglycerides, uric acid levels, serum creatinine, and body mass index (BMI).
The quite high prevalence of the metabolic syndrome observed in this study, compared with that seen in other studies in Europe or in the USA (for example the NHANES III), can be explained by the fact that the patients already had HT, which is one component of the syndrome.

The prevalence of LVH plus LV concentric remodelling was higher in group I (30%) than in group II (23%), P<0.05, using the partition value of 125/110 g/m2. When using the partition value of 51/47 g/m2.7 (which detects obesity-independent and obesity-related LVH without bias due to different individual BMIs), the trend was more significant (42% vs 31.5%, P<0.01). The statistical significance persisted after adjustment for age and ambulatory SBP. The prevalence of carotid plaques and carotid intima-media thickening was higher but not significant in patients with the metabolic syndrome. Mean urinary albumin excretion was greater in group I (17.7±35.5 mg/24 h) than in group II (11.5±26.6 mg/24 h), P<0.05. More patients had microalbuminuria in group I (10.9% vs 7.9%, P<0.05), even after adjustment for age and ambulatory SBP. These findings are consistent with those of the NHANES III, showing a strong positive association between microalbuminuria and the metabolic syndrome. These results suggest that cardiac abnormalities and microalbuminuria are more sensitive indexes of early TOD in young and middle-aged subjects with essential HT and metabolic syndrome. The excess of TOD in patients with the metabolic syndrome was independent of BP (since results were adjusted for BP and age).

In conclusion, this study show that subjects with grade 1 and grade 2 HT having the metabolic syndrome also have more frequent alterations in cardiac structure and geometry, urinary albumin excretion, and serum creatinine. This excess of TOD is independent of BP and other confounding factors, and draws attention to the early negative impact of the metabolic syndrome on TOD.