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Microalbuminuria, a powerful predictor of cardiovascular events, is thought to reflect widespread subclinical vascular abnormalities. To explore the pathogenesis of increased urinary albumin excretion in primary hypertension we evaluated systemic capillary permeability and ambulatory blood pressure (BP) measurement in two groups of matched untreated patients with (n = 11) and without (n = 29) microalbuminuria.Albuminuria was measured as the mean of albumin-to-creatinine ratio (ACR) in three nonconsecutive first morning urine samples. Systemic capillary permeability was evaluated by transcapillary escape rate of albumin (TERalb) (ie, the 1-h decline rate of intravenous (125)I-albumin). Twenty-four-hour ambulatory BP, renal hemodynamics, and hormones of the renin-angiotensin-aldosterone system (RAAS) were also assessed.Patients with microalbuminuria showed greater body mass index (BMI) (P.04), higher 24-h systolic and diastolic BP levels (P = .02), and higher capillary permeability to albumin (P.02) as compared to normoalbuminurics. Renal hemodynamics and RAAS hormones were similar in the two groups. Univariate analysis showed that urinary ACR was related to ambulatory pressure components (P.02), TERalb (r = 0.31, P.05), smoking habits (r = 0.36, P = .02), and left ventricular mass index (LVMI) (r = 0.57, P.001) among the whole study group. Logistic regression analysis showed that each 1% increment in TERalb or 10 mm Hg increase in systolic BP entailed an almost three times higher risk of having microalbuminuria.Microalbuminuria is associated with greater systemic BP load and increased vascular permeability in patients with primary hypertension.

Background Urinary albumin excretion and left ventricular mass are related to each other and to the risk of cardiovascular events in patients with primary hypertension. We aimed to identify a lower threshold for albuminuria that might improve detection of patients with left ventricular hypertrophy (LVH) and cost-effectiveness in cardiovascular risk assessment. Methods Albuminuria and left ventricular mass index were assessed in 448 untreated, nondiabetic patients with primary hypertension. The impact that lower albuminuria cut-off levels might have on detecting LVH was evaluated with regard to test cost and sensitivity. This was done by a diagnostic algorithm consisting of albuminuria evaluation followed by echocardiography in the presence of normoalbuminuria. Results The area under the ROC curve of albuminuria in predicting LVH was 0.73. Using a lower albumin to creatinine ratio threshold than what is recommended by the guidelines (ie, 11.5 mg/g), the sensitivity and specificity of albuminuria in identifying patients with LVH was 39% and 92%, respectively, which translated to positive and negative predictive values of 76% and 69%, respectively. When considering only patients without electrocardiographically detected LVH, routine screening for albuminuria, followed by echocardiography in the presence of albuminuria ≤11.5 mg/g, allowed us to decrease the number of echocardiograms by 23%. Conclusion Adopting a lower threshold to define microalbuminuria could prove to be cost-effective for assessing cardiovascular risk in hypertensive patients.

The optimal management of cardiac allograft vasculopathy (CAV) remains unknown. Percutaneous coronary intervention (PCI) has been considered palliative due to high restenosis rates, but still remains an alternative to the definitive therapy of re-transplantation. Drug eluting stents (DES) were shown

Microalbuminuria, i.e., abnormal urinary excretion of albumin, which is detectable by low cost and widely available tests, is a first-line tool for identifying hypertensive patients who are at higher cardiovascular (CV) risk. Numerous studies have provided evidence that microalbuminuria is a concomitant of cardiac and vascular damage as well as a strong, independent predictor of CV events. An important, emerging issue is that the risk for CV morbidity and mortality is linearly related to urinary albumin excretion and persists well below the currently used cutoff for defining microalbuminuria. Furthermore, late-breaking evidence suggests that a reduction of albuminuria under antihypertensive treatment is paralleled by changes in CV risk. The routine search for target organ damage by means of microalbuminuria could lead to a significant improvement in the evaluation and treatment of patients with primary hypertension.

Increased arterial stiffness and the presence of metabolic syndrome (MS) have been shown to predict cardiovascular events in patients with primary hypertension. We investigated the relationship between a recently proposed index of arterial stiffness derived from ambulatory blood pressure (BP) monitoring and MS in 156 untreated, non-diabetic patients with primary hypertension. Ambulatory arterial stiffness index (AASI) was defined as 1 minus the regression slope of diastolic over systolic BP readings obtained from 24-h recordings. A modified National Cholesterol Education Program definition for MS was used, with body mass index replacing waist circumference. The prevalence of MS was 23%. Patients with MS were more frequently male (0.0291) and had increased serum uric acid (P=0.0005), high-sensitivity C-reactive protein (P=0.0259), as well as total and low-density lipoprotein (LDL)-cholesterol (P=0.0374 and P=0.0350, respectively) as compared to those without MS. After adjusting for these confounders, the association between AASI and the presence of MS was statistically significant (P=0.0257). Moreover, the prevalence of increased AASI (upper tertile, that isor=0.550) was greater in patients with MS (P=0.0156). After adjusting for age and 24-h mean BP, the presence of MS entailed a more than twofold greater risk for increased AASI (0.0280). MS is associated with increased AASI in non-diabetic patients with primary hypertension. These data support the role of this new index of arterial stiffness as a marker of risk and help to explain the high cardiovascular morbidity and mortality that is observed in hypertensive patients with MS.

Objective Arterial stiffness is a predictor of cardiovascular mortality in the general population as well as in hypertension and end-stage renal disease. We investigated the relationship between a recently proposed ambulatory blood pressure monitoring-derived index of arterial stiffness and early signs of renal damage in patients with primary hypertension. Design and setting A total of 168 untreated patients with sustained primary hypertension were studied. Ambulatory arterial stiffness index (AASI) was calculated based on 24-h ambulatory blood pressure readings. Albuminuria was measured as the albumin to creatinine ratio. Creatinine clearance was estimated using the Cockcroft-Gault formula, and the interlobar resistive index was evaluated by renal ultrasound and Doppler examination. Results AASI was positively related to urinary albumin excretion and resistive index, and was negatively related to estimated creatinine clearance and renal volume to the resistive index ratio. Patients with AASI above the median (i.e. > 0.51) showed a higher prevalence of microalbuminuria and a mild reduction in creatinine clearance. Moreover, patients with microalbuminuria or a mild reduction in creatinine clearance had significantly higher AASI values compared with those without, and the greater the renal involvement, the greater the AASI. After adjusting for several potentially confounding variables, we found that each standard deviation increase in AASI (i.e. 0.16) entails an almost twofold greater risk of renal involvement. Conclusion Increased AASI is independently associated with early signs of renal damage in patients with sustained primary hypertension. These results strengthen the usefulness of AASI and ambulatory blood pressure monitoring in cardiovascular risk assessment.

Increased arterial stiffness has been shown to predict cardiovascular mortality in patients with primary hypertension. Asymptomatic organ damage is known to precede cardiovascular events. We investigated the relationship between a recently proposed index of stiffness derived from ambulatory blood pressure (BP) and target organ damage in 188 untreated patients with primary hypertension. Ambulatory arterial stiffness index was defined as 1 minus the regression slope of diastolic over systolic BP readings obtained from 24-hour recordings. Albuminuria was measured as the albumin:creatinine ratio, left ventricular mass index was assessed by echocardiography, and carotid abnormalities were evaluated by ultrasonography. The prevalence of microalbuminuria, left ventricular hypertrophy (LVH), and carotid abnormalities was 12%, 38%, and 19%, respectively. Ambulatory arterial stiffness index was positively related to age, triglycerides, office and 24-hour systolic BP, 24-hour pulse pressure, urinary albumin excretion, and carotid intima-media thickness. Patients with microalbuminuria, carotid abnormalities, or LVH showed higher ambulatory arterial stiffness index as compared with those without it. After adjusting for confounding factors, each SD increase in ambulatory arterial stiffness index entails an &2 times higher risk of microalbuminuria, carotid abnormalities, and LVH and doubles the risk of the occurrence of ≥1 sign of organ damage. Ambulatory arterial stiffness index is associated with organ damage in patients with primary hypertension. These data strengthen the role of this index as a marker of risk and help to explain the high cardiovascular mortality reported in patients with high ambulatory arterial stiffness index.

The metabolic syndrome can be found in approximately one third of patients who do not have diabetes but have primary hypertension. Its presence has been associated with a wide range of traditional and nontraditional cardiovascular risk factors and early signs of cardiovascular and renal damage. Moreover, it was emphasized recently that the metabolic syndrome predicts an increased probability of sustaining a cardiovascular event or dying. In the clinical setting of insulin resistance, attention should be paid to the metabolic side effects of antihypertensive drugs; therefore, preference should be given to renin-angiotensin system inhibitors and calcium channel blockers rather than to beta blockers and diuretics.

Leoncini G, Ratto E, Viazzi F, Vaccaro V,Parodi D, Parodi A, Falqui V, Tomolillo C, DeferrariG, Pontremoli R (University of Genoa, Genoa, Italy).Metabolic syndrome is associated with early signs oforgan damage in nondiabetic, hypertensive patients.J Intern Med 2005; 257: 454–460.Objectives. Hypertensive patients with metabolicsyndrome (MS) are at greater risk for cardiovasculardisease. To get a better understanding of the patho-physiology underlying this association, we evaluatedthe relationship between MS and subclinical organdamage in essential hypertensive patients.Design and setting. A total of 354 untreated,nondiabetic patients with primary hypertensionwere included in the study. A modified ATP IIIdefinition for MS was used, with body mass indexreplacing waist circumference. Albuminuria wasmeasured as albumin to creatinine ratio, leftventricular mass index (LVMI) was assessed byechocardiography and carotid abnormalities byultrasonography.Results. The prevalence of MS was 25%. Patientswith MS were more likely to be smokers (P ¼ 0.004)and had higher serum uric acid levels (P ¼ 0.004).Moreover, they showed higher urinary albuminexcretion (P ¼ 0.0004) and LVMI (P ¼ 0.0006),increased intima-media thickness (P ¼ 0.045), aswell as higher prevalence of microalbuminuria(P ¼ 0.03) and left ventricular hypertrophy (LVH;P ¼ 0.003). After adjusting for age, gender andduration of hypertension, we found that thepresence of MS entails a twofold greater risk formicroalbuminuria (P ¼ 0.04), LVH (P ¼ 0.003)and carotid abnormalities (P < 0.05). Whenpatients were stratified according to the number ofcomponents of MS, albuminuria (P ¼ 0.002) andLVMI (P ¼ 0.005) increased progressively acrosscategories.Conclusions. Metabolic syndrome is associated withsubclinical organ damage in nondiabetic, essentialhypertensive patients. These data may, in part,explain the high cardiovascular morbidity andmortality that is observed in hypertensive patientswith MS.Keywords: hypertension, left ventricular hypertrophy,metabolic syndrome, microalbuminuria.

Accurate assessment of cardiovascular risk is a key step toward optimizing the treatment of hypertensive patients. We analyzed the impact and cost-effectiveness of routine, thorough assessment of target organ damage (TOD) in evaluating risk profile in hypertension. A total of 380 never-treated patients with essential hypertension underwent routine work-up plus evaluation of albuminuria and ultrasonography of cardiac and vascular structures. The impact of these tests on risk stratification, as indicated by European Society of Hypertension-European Society of Cardiology guidelines, was assessed in light of their cost and sensitivity. The combined use of all of these tests greatly improved the detection of TOD, therefore leading to the identification of a higher percentage of patients who were at high/very high risk, as compared with those who were detected by routine clinical work-up (73% instead of 42%; P < 0.0001). Different signs of TOD only partly cluster within the same subgroup of patients; thus, all three tests should be performed to maximize the sensitivity of the evaluation process. The diagnostic algorithm yielding the lowest cost per detected case of TOD is the search for microalbuminuria, followed by echocardiography and then carotid ultrasonography. Adopting lower cut-off values to define microalbuminuria allows us to optimize further the cost-effectiveness of diagnostic algorithms. In conclusion, because of its low cost and widespread availability, measuring albuminuria is an attractive and cost-effective screening test that is especially suitable as the first step in the large-scale diagnostic work-up of hypertensive patients.

Mild renal dysfunction (MRD) is an often overlooked but relatively common condition in patients with primary hypertension (PH), and is associated with high cardiovascular morbidity and mortality. Whether MRD is also associated with abnormalities in renal vascular resistance is currently unknown.Two hundred ninety-one untreated patients with PH were studied. The MRD was defined as a creatinine clearanceor=60 mL/min but90 mL/min (Cockcroft-Gault formula) or the presence of microalbuminuria. Albuminuria was measured as the albumin-to-creatinine ratio in first morning urine samples. Renal resistive index (RI) was evaluated by ultrasound Doppler of the interlobar arteries.The prevalence of MRD in our cohort was 63%. Patients with MRD were older, had higher mean blood pressure (BP), pulse pressure, and total cholesterol, longer history of hypertension, and were more likely to be men. Renal RI was positively related to female gender, age, systolic BP, pulse pressure, total cholesterol, albuminuria, and to carotid wall thickness and cross-sectional area, whereas it was inversely related to diastolic BP and creatinine clearance. Patients with the highest renal resistance (upper quartile,or=0.63) showed a greater prevalence of renal dysfunction (P=.0005). After adjusting for age, pulse pressure, and LDL-cholesterol, we found that the risk of MRD increased twofold (P=.04) when renal RI wasor=0.63.A reduction in creatinine clearance and the presence of microalbuminuria are associated with increased renal vascular impedence, as well as with signs of extrarenal arterial stiffness.

A reduction in renal function is associated with high cardiovascular morbidity and mortality in hypertension. The aim of the present study was to investigate the relationship between creatinine clearance and subclinical organ damage in 957 never previously treated, middle-aged patients with primary hypertension. Renal function was estimated by means of the serum creatinine level using the Cockcroft-Gault formula; left ventricular hypertrophy (LVH) was determined according to electrocardiographic criteria; and retinal vascular changes were evaluated by direct ophthalmoscopy. Creatinine clearance was, on the average, 83+/-21.2 ml/min, and the prevalence of LVH and retinopathy was 13 and 49%, respectively. Creatinine clearance was inversely related to the duration of disease (r=-0.132, P

Objective To assess the impact and cost-effectiveness of microalbuminuria and cardiovascular ultrasonography in evaluating the risk profile in primary hypertension. Methods Four hundred and five untreated patients with primary hypertension underwent a routine, traditional work-up plus evaluation of albuminuria and ultrasound (US) assessment of cardiac and vascular structures. Albuminuria was measured as the albumin to creatinine ratio in three non-consecutive first-morning urine samples. Left ventricular mass index was assessed by MB-mode echocardiography and carotid intima–media thickness by high-resolution US scan. The impact of these tests on patient risk classes, as indicated by European Society of Hypertension–European Society of Cardiology (ESH–ESC) guidelines, was assessed with respect to their cost and sensitivity. Results The prevalence of microalbuminuria, left ventricular hypertrophy and carotid intima–media thickening or carotid plaque was 13, 49 and 32%, respectively. The combined use of albuminuria, cardiac and vascular ultrasonography led to the detection of a significantly higher percentage of patients at high/very high risk. The three tests differ in sensitivity (albuminuria, 20%; echocardiography, 65%; and carotid ultrasound, 41%). The signs of target organ damage (TOD) only partly cluster within the same subgroup of patients and, thus, all three tests should be performed in order to maximize the sensitivity of the evaluation process. The diagnostic algorithm yielding the lowest cost per detected case of TOD is the search for microalbuminuria followed by cardiac and carotid ultrasound assessment. Conclusions Ultrasonographic detection of TOD is a sensitive tool in the identification of high-risk patients, but should be preceded by a routine search for microalbuminuria in order to optimize the cost-effectiveness of the diagnostic work-up.

Mild renal dysfunction, defined as GFR