The degree of albuminuria is related to left ventricular hypertrophy in hypertensive diabetics and is associated with abnormal left ventricular filling: a pilot study

The association of albuminuria and left ventricular (LV) hypertrophy (LVH) in diabetics aggravates the prognosis. The authors studied the relation between LVH and the degree of albuminuria in diabetics and investigated the relationship of albuminuria to LV filling. A comparison was made between 30 hypertensive diabetics, 10 of whom had microalbuminuria (MIC) and 20 had macroalbuminuria (MAC), and 18 diabetics who were normotensive and normalbuminuric (NOR). LV mass index (LVMI) and LV ejection fraction (LVEF) were measured during echocardiography. LV filling pattern at rest and at peak standardized isometric exercise (IME) using handgrip was assessed by measuring E/A (peak velocity of the early/atrial filling waves) of the transmitral flow during Doppler and echocardiography. Each patient underwent a stress ECG test. LVMI was higher in MAC (132.3 +/- 55.4) than in MIC (115.6 +/- 32.5) or NOR (90.0 +/- 31.8) (p<0.01). There were more patients in MAC with LVH (n = 13) and abnormal filling (n = 9 at rest and 16 with IME) than in MIC (LVH = 5, abnormal filling = 1 at rest and 10 during IME) or NOR (LVH = 3, abnormal filling = 1 at rest and 9 during IME) (p < 0.02). LVMI was not related to LVEF. Although blood pressure was not different between MAC and MIC groups, it was significantly higher than in the NOR group. This study suggests that a high degree of albuminuria in hypertensive diabetics is associated with greater value for LVMI and an increased incidence of LVH independent of blood pressure level or systolic LV function. LVH is associated with abnormal LV filling. The degree of albuminuria may predict LVMI and LVH, which are associated with abnormal LV filling. This association of abnormal LV filling with albuminuria in hypertensive diabetic patients may account for their high risk of cardiovascular events.     

Inappropriate left ventricular mass is associated with microalbuminuria independently of left ventricular hypertrophy in primary hypertension

OBJECTIVE: Inappropriate left ventricular mass (LVM) and microalbuminuria predict cardiovascular events in hypertension. We attempted to evaluate the relationship between inappropriate LVM and albuminuria in hypertensive patients. PATIENTS AND METHODS: Four hundred and two nondiabetic, untreated patients with primary hypertension were studied. The appropriateness of LVM to cardiac workload was calculated by the ratio of observed LVM to the predicted value using the reference equation. Albuminuria was evaluated by the urinary albumin to creatinine ratio. RESULTS: The deviation of LVM from the predicted value was positively related to albuminuria (P < 0.0001). Multiple regression analysis showed that albuminuria (0.0182), pulse pressure (P < 0.0001) and left ventricular hypertrophy (LVH) (P < 0.0001) were the only independent predictors of observed/predicted LVM. When subjects were divided into subgroups on the basis of the presence/absence of inappropriate LVM, patients with inappropriate LVM showed higher urinary albumin excretion (P < 0.0001), regardless of potential confounding factors, including LVH (analysis of covariance, P = 0.0453), and higher prevalence of microalbuminuria (P = 0.0024) compared to those without it. Analogous results were obtained by looking at the study patients on the basis of the presence of micro- or normoalbuminuria. Indeed, patients with microalbuminuria showed higher prevalence of inappropriate LVH compared to other left ventricular geometries (appropriate LVH and absence of LVH) (P < 0.0001). After adjusting for confounders, microalbuminuria entailed a three- and five-fold greater risk of having appropriate and inappropriate LVH, respectively. CONCLUSIONS: Inappropriate LVM is associated with albuminuria in hypertension. These data strengthen the role of microalbuminuria as an indicator of high cardiovascular risk.     

Microalbuminuria and Cardiovascular Risk Assessment in Primary Hypertension: Should Threshold Levels Be Revised?

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 相似文献   

Prevalence and correlates of advanced retinopathy in a large selected hypertensive population. The Evaluation of Target Organ Damage in Hypertension (ETODH) study

OBJECTIVE: To describe the prevalence of advanced retinal microvascular lesions and their associations with cardiac and extracardiac signs of target organ damage (TOD) in a large selected hypertensive population. METHODS: A total of 2172 non-diabetic untreated and treated uncomplicated essential hypertensives consecutively attending for the first time our hospital outpatient hypertension clinic and included in the Evaluation of Target Organ Damage in Hypertension (ETODH), an observational ongoing registry of hypertension-related TOD, were considered for this analysis. Advanced hypertensive retinopathy was defined by the presence of any of the following lesions: flame-shaped haemorrhages, soft exudates or cotton wool spots and papilloedema. Left ventricular hypertrophy (LVH), carotid structural abnormalities, such as plaques and intima media (IM) thickening, and microalbuminuria were diagnosed according to the 2003 ESH/ESC guidelines criteria. RESULTS: Among the whole study population, 33 patients (1.5%) were found to have advanced hypertensive retinopathy. Patients with these retinal lesions were similar to those without for age, body mas index, known duration of hypertension, smoking habit, total serum cholesterol, fasting blood pressure and prevalence of antihypertensive treatment; whereas mean systolic and diastolic blood pressures were higher in the former group. The prevalence rates of LVH, carotid plaques, carotid IM thickening and microalbuminuria in patients with and without retinopathy were 57%, 67%, 69%, 19% and 25%, 47%, 44%, 12%, respectively. In a multivariate logistic regression analysis, advanced retinopathy was significantly associated with LVH (OR = 4.0), carotid IM thickening (OR = 2.9), carotid plaques (OR = 2.8), but not with microalbuminuria. CONCLUSIONS: Our study indicated that: (i) advanced retinopathy is a rare finding in non-diabetic hypertensive patients seen in a specialist setting; (ii) a strong relation exists between retinal microvascular lesions and cardiac and macrovascular markers of TOD.     

Prognostic significance of microalbuminuria in non-diabetic patients with acute myocardial infarction

BACKGROUND: The aim of this study was to examine whether the presence of microalbuminuria (20-200 microg/min) can predict in-hospital morbidity and mortality in non-diabetic patients with acute myocardial infarction. METHODS: Two hundred twenty-three (172 men and 51 women) non-diabetic patients with acute myocardial infarction were studied prospectively. The main outcome measures of the study were based on a comparison of in-hospital mortality and major non-fatal in-hospital events (pulmonary edema, post-infarction angina, infarct extension, mechanical complications, conduction disturbances and ventricular arrhythmias) between microalbuminuric and normoalbuminuric patients. RESULTS: A significant proportion of patients (33.6%) had microalbuminuria. Seventy-six patients (34%) developed an in-hospital event (fatal or non-fatal). Six patients (2.7%) with acute myocardial infarction died in the hospital. Patients with microalbuminuria had a higher mortality rate in comparison with normoalbuminuric patients (6.6% vs. 0.68%, p = 0.01). For non-fatal events, the incidence of pulmonary edema and ventricular arrhythmias was significantly higher in patients with microalbuminuria (14.6% vs. 3.4%, p < 0.001 and 12% vs. 3.4%, p = 0.01, respectively). The combined end-point of the total number of fatal and non-fatal events was significantly higher in patients with microalbuminuria (57.3% vs. 22.3%, p < 0.001). In multiple logistic regression analysis, microalbuminuria (p < 0.001) and ejection fraction (p = 0.01) were independently related to the occurrence of major in-hospital events. CONCLUSIONS: Microalbuminuria is a significant predictor of in-hospital morbidity and mortality in non-diabetic patients with acute myocardial infarction.     

Intraventricular septal hypertrophy in type 1 diabetic patients with microalbuminuria or early proteinuria

To investigate whether the slightly increased blood pressure that occurs in early diabetic renal disease is associated with hypertensive left ventricular hypertrophy, M-mode echocardiograms were recorded in 11 non-diabetic control subjects and four groups of Type 1 diabetic patients. These were 15 patients without microvascular complications, 10 with microalbuminuria, 12 with early persistent proteinuria, and 8 with established renal impairment. Mean blood pressure was 133/80 mmHg (uncomplicated patients), 143/85 mmHg (microalbuminuria), 147/92 mmHg (early proteinuria) and 158/85 mmHg (renal impairment). Mean intraventricular septal width in the uncomplicated diabetic patients was 9.8 (SE 1.2) mm which did not differ from non-diabetic control subjects. Mean septal width was significantly greater in the other groups (microalbuminuria, 12.7 (1.1) mm, p less than 0.02; proteinuria, 12.0 (0.7) mm, p less than 0.05; renal impairment, 15.5 (1.8) mm, p less than 0.001). Left ventricular mass increased progressively between groups and was significantly increased in those with renal impairment (140 (21) vs 103 (5) g m-2 in uncomplicated patients, p less than 0.05). Septal width in the diabetic population not receiving antihypertensives (n = 37) was significantly correlated with systolic blood pressure (r = 0.45, p less than 0.005) which was the only variable independently related to septal width and ventricular mass. It appears that the slight increase in blood pressure that occurs in microalbuminuria and early proteinuria is frequently associated with hypertensive left ventricular hypertrophy.     

Metabolic syndrome is associated with early signs of organ damage in nondiabetic, hypertensive patients

OBJECTIVES: Hypertensive patients with metabolic syndrome (MS) are at greater risk for cardiovascular disease. To get a better understanding of the pathophysiology underlying this association, we evaluated the relationship between MS and subclinical organ damage in essential hypertensive patients. DESIGN AND SETTING: A total of 354 untreated, nondiabetic patients with primary hypertension were included in the study. A modified ATP III definition for MS was used, with body mass index replacing waist circumference. Albuminuria was measured as albumin to creatinine ratio, left ventricular mass index (LVMI) was assessed by echocardiography and carotid abnormalities by ultrasonography. RESULTS: The prevalence of MS was 25%. Patients with MS were more likely to be smokers (P = 0.004) and had higher serum uric acid levels (P = 0.004). Moreover, they showed higher urinary albumin excretion (P = 0.0004) and LVMI (P = 0.0006), increased intima-media thickness (P = 0.045), as well as higher prevalence of microalbuminuria (P = 0.03) and left ventricular hypertrophy (LVH; P = 0.003). After adjusting for age, gender and duration of hypertension, we found that the presence of MS entails a twofold greater risk for microalbuminuria (P = 0.04), LVH (P = 0.003) and carotid abnormalities (P < 0.05). When patients were stratified according to the number of components of MS, albuminuria (P = 0.002) and LVMI (P = 0.005) increased progressively across categories. CONCLUSIONS: Metabolic syndrome is associated with subclinical organ damage in nondiabetic, essential hypertensive patients. These data may, in part, explain the high cardiovascular morbidity and mortality that is observed in hypertensive patients with MS.     

Relationship between hypertensive left ventricular hypertrophy and levels of endothelin and nitric oxide.

To investigate the relationship between hypertensive left ventricular hypertrophy (LVH) and levels of endothelin (ET) and nitric oxide (NO), and to provide an experimental basis for prevention and treatment of hypertensive LVH. Fifty eight hypertensive patients and 14 healthy controls were studied. All patients were examined by echocardiography. Left ventricular mass (LVM) and left ventricular mass index (LVMI) were calculated using Devereux RB formula. Hypertensive patients were divided into a LVH (+) group (n= 21) and a LVH (-) group (n=37), and the levels of endothelin and nitric oxide in the peripheral venous blood were measured. The mean ET level was significantly higher in the LVH (+) group than in LVH (-) group (p < 0.05), but the NO level was significantly lower in the LVH (+) group. The ET/NO ratio was significantly higher in the LVH (+) group than in LVH (-) group (p< 0.01). For the stepwise multiple regression analysis, the LVMI of hypertensive patients served as a dependent variable, and age, sex, BMI, MAP, ET, NO, and ET/NO served as independent variables. Only MAP, ET, and NO were found to have significant correlation to hypertensive LVH. ET had a significant positive correlation, and NO a significant negative relation to LVMI, but ET/NO showed no correlation to hypertensive LVH. ET and NO are involved in hypertensive LVH; the independent action of ET and NO in the pathogenesis of hypertensive LVH may weaken the relation between ET/NO and hypertensive LVH.     

Technetium-99m sestamibi cavity/myocardium count ratio in the detection of left ventricular hypertrophy

BACKGROUND AND HYPOTHESIS: Left ventricular hypertrophy (LVH) is an independent risk factor for cardiovascular mortality and morbidity. This study was designed to assess whether technetium-99m (99mTc) sestamibi cavity-to-myocardium count (c/m) ratio would differentiate LVH from normal geometry, and discriminate between the two patterns-concentric and eccentric--of LVH. METHODS: In all, 72 patients including 32 hypertensive patients with both normal 99mTc sestamibi single-photon emission computed tomography imaging and good-quality echocardiographic recordings were studied retrospectively. Four different patterns of left ventricular (LV) geometry were defined: normal (n = 47), concentric remodeling (n = 3), eccentric LVH (n = 13), and concentric LVH (n = 9). RESULTS: Left ventricular hypertrophy was detected in 22 of 32 hypertensive patients. The c/m ratio calculated on midventricular short-axis slices of dipyridamole-stress 99mTc sestamibi images was significantly decreased in patients with LVH compared with subjects with normal geometry (0.05 +/- 0.02 vs. 0.17 +/- 0.08, p = 0.001). A c/m ratio of <0.124 yielded a sensitivity of 86%, a specificity of 64%, and an overall diagnostic accuracy of 68% for detecting LVH. Negative correlations of c/m ratio were found to LV mass-index (r = -0.44, p = 0.004), septal width (r = -0.42, p = 0.008), posterior wall thickness (r = -0.39, p = 0.001), and relative wall thickness (r = -0.40, p = 0.001). Multiple linear regression analysis revealed that LV mass index was the single independent predictor of c/m ratio. Although both groups with concentric and eccentric LVH had a significantly lower mean c/m ratio than those with normal geometry (p = 0.01 and p = 0.01, respectively), no significant difference of c/m ratio was found between the two patterns of LVH. CONCLUSION: A new index, c/m ratio on 99mTc sestamibi images, has a potential to discriminate between LVH and normal geometry in subjects free of myocardial ischemia.     

Relation of left ventricular hypertrophy with systemic inflammation and endothelial damage in resistant hypertension

The relation between left ventricular hypertrophy (LVH) and unfavorable cardiovascular prognosis may involve systemic inflammation and endothelial dysfunction/damage. The aim of this study was to investigate in a cross-sectional design the relationships of LVH with C-reactive protein (CRP) levels (a marker of systemic low-grade inflammation) and with microalbuminuria (a marker of glomerular endothelial damage) in 705 patients with resistant hypertension. At baseline, all were submitted to a laboratory evaluation including 24-hour urinary albumin excretion, 2D echocardiogram, and 24-hour ambulatory blood pressure monitoring. A total of 463 patients also had high-sensitivity CRP levels determined. LVH was defined as an indexed left ventricular mass >110 g/m(2) in women and >125 g/m(2) in men. Microalbuminuria was evaluated in 3 categories: low normal (<15 mg/24 hours), high normal (between 15 and 29 mg/24 hours), and abnormal (between 30 and 299 mg/24 hours). CRP was dichotomized at the median value (3.7 mg/L). Associations with LVH were examined after adjustment for all of the potential confounders by multivariate logistic regression. A total of 534 patients (75.7%) had LVH. After full adjustment, both abnormal microalbuminuria (odds ratio: 1.97; 95% CI: 1.04 to 3.73) and high CRP (OR: 1.76; 95% CI: 1.06 to 2.93) were independently associated with LVH occurrence. The high-normal albuminuria was associated with a borderline significant 46% increased chance of having LVH. Furthermore, the association between high CRP and LVH was observed exclusively in the subgroup with normal albuminuria. In conclusion, both systemic inflammation and endothelial damage were associated with LVH occurrence. These relationships offer insight into the pathophysiological mechanisms linking LVH to atherosclerosis and to increased cardiovascular morbidity and mortality.     

Hypertensive smokers have a worse cardiovascular risk profile than non-smokers in spite of treatment--a national study in Sweden

Smoking is a well-established risk factor for cardiovascular disease. Studies have indicated that smoking may outweigh the benefit of blood pressure (BP) control. Our aim was to compare cardiovascular risk factors in smokers vs non-smokers from a national sample of treated hypertensives. Data were collected on smoking habits, BP control, total and low-density lipoprotein (LDL) cholesterol, diabetes, left ventricular hypertrophy (LVH), and microalbuminuria (MA), from records of 4424 consecutive patients by 189 physicians. All technical methods were local. Treated hypertensives who smoked had microalbuminuria significantly more often than non-smokers, 26.2% vs 20.5% (p<0.05), and a higher proportion of smokers were suboptimally controlled (DBP > or = 90 mmHg), 32.7% vs 25.0% (p<0.01). Smoking males had a higher prevalence of LVH (25.7% vs 20.1; p<0.05), microalbuminuria (29.7% vs 24.7%; p<0.01), and a higher proportion of subjects with uncontrolled systolic BP (> or = 140 mmHg) (72.8% vs 68.9%; p<0.01). Both DBP and total cholesterol were higher in smoking vs non-smoking females. An increased prevalence of LVH and microalbuminuria was independently associated with smoking. In summary, smokers with treated hypertension show a higher proportion of LVH (men), microalbuminuria and worse diastolic BP control than non-smokers. This may hypothetically reflect either less compliance with drug treatment in smokers or that smoking impairs the pharmacological effects of antihypertensive drugs.     

Global risk stratification in primary hypertension: the role of the kidney

OBJECTIVE: Microalbuminuria and a reduction in creatinine clearance are well known, independent predictors of unfavourable cardiovascular prognosis. Our aim was to evaluate the impact of renal damage on global risk stratification in 459 non-diabetic, untreated hypertensive patients (64% men, mean age 47.3 years). METHODS: Renal damage was defined as creatinine clearance < 60 ml/min per 1.73 m2 (Cockcroft-Gault formula) or the presence of microalbuminuria (albumin to creatinine ratio). Cardiac and vascular organ damage was assessed by ultrasound scan. We evaluated the impact of renal damage, left ventricular hypertrophy and carotid atherosclerosis on risk stratification as recommended by the 2007 European Society of Hypertension-European Society of Cardiology Guidelines. RESULTS: The prevalence of renal damage, microalbuminuria and creatinine clearance < 60 ml/min per 1.73 m2 was 24, 12 and 13%, respectively. There was no correlation between albuminuria and estimated creatinine clearance, and only 0.9% of patients showed microalbuminuria and reduced creatinine clearance simultaneously. The presence of renal damage entailed a 3.3 times higher risk of having cardiovascular abnormalities. Based on routine work-up, 58% of our study patients were classified as high-very high risk. The simultaneous evaluation of albuminuria and creatinine clearance resulted in a significant change in risk stratification, since 68% of patients were classified in the high-very high risk class. The search for left ventricular hypertrophy or carotid atherosclerosis by ultrasonography did not improve risk stratification significantly as compared to the assessment of renal damage. CONCLUSIONS: Our findings support the assessment of renal abnormalities as the first step when evaluating target organ damage for cardiovascular risk assessment in hypertensive patients.     

Albuminuria and other target organ damage in Chinese patients with hypertension and diabetes: A data analysis based on the ATTEND study

AimsThe relationship between albuminuria and left ventricular hypertrophy (LVH) was well characterized in hypertension (HTN), but not in diabetes. Moreover, most studies have described the correlation between albuminuria and cardiovascular mortality, but not cardiovascular diseases (CVD) morbidity. This study aimed to explore the relationship between albuminuria and LVH, CVD morbidity in patients with HTN, diabetes mellitus (DM) or HTN + DM.MethodsConducted a data analysis based on the demographic, medical history and laboratory data of 2504 patients from the ATTEND study, a national registry study on HTN and DM in Chinese outpatients.ResultsThe prevalence of LVH and CVD was 7.7% and 21.5% in HTN + DM, 7.6% and 17.6% in HTN, 3.9% and 5.2% in DM patients. Subjects with HTN + DM implied higher risk of LVH (P = 0.023), CVD (P = 0.001) and 10-year coronary heart disease (CHD) (P < 0.001) than those with DM only. There was no significant relationship between albuminuria and LVH or CVD.ConclusionsMore than one-fifth of HTN and/or DM patients with microalbuminuria suffered from CVD. Comorbidity of DM and HTN significantly increases cardiovascular events than DM only. No statistical association between albuminuria and LVH or CVD was found.     

Elevated plasma fibrinogen levels in patients with essential hypertension are related to vascular complications.

AIM: We investigated whether or not fibrinogen is related to the cardiovascular risk profile and complications in hypertensive subjects. METHODS: Plasma fibrinogen and laboratory tests including factor VII, homocysteine and microalbuminuria were evaluated in 127 consecutive hypertensive subjects stratified according to cardiovascular risk. Parameters were age, gender, smoking, cholesterol, diabetes, target organ damage: left ventricular hypertrophy (LVH), carotid atherosclerotic complications and retinical vessels. RESULTS: Fibrinogen levels were significantly different between patients according to risk levels (low 290+/-73, n=20, high 342+/-94 mg/dl, n=39, very high risk 350+/-72, n=29, p=0.01), hypertension grade (II-III) and organ damage. Fibrinogen was significantly higher in patients with more severe carotid atherosclerotic lesions and vascular retinal lesions (grades II-III vs 0 and I). Also in patients, matched for age and sex, without and with carotid atherosclerotic lesions, fibrinogen was significantly higher in the latter group. No significant differences were found on the basis of IVS, creatinine and microalbuminuria. In hypertensive patients, fibrinogen directly correlated with age, by multiple linear regression. In hypertensive patients with diabetes, fibrinogen was significantly higher (466+/-176 mg/dL, n=14) than in those hypertensive without diabetes (333+/-87 mg/dL, n=113, p=0.001) and in all patients there was a a significant correlation (r=0.474, p<0.001) between blood glucose and fibrinogen. CONCLUSION: Hyperfibrinogenemia is a marker of vascular damage and could be an important factor contributing to the evolution of the complications.     

伊贝沙坦对老年原发性高血压患者血压昼夜节律与左心室肥厚的影响

目的 :探讨伊贝沙坦对老年原发性高血压患者的血压昼夜节律及左心室肥厚 (LVH)的影响。　　方法 :选择 93例年龄≥ 60岁的老年原发性高血压患者 ,通过 2 4小时动态血压监测了解其血压昼夜节律变化 ,通过超声心动图观察左心室内径、室间隔和左心室后壁厚度 ,并测算左心室重量指数。选择血压昼夜节律消失的 5 4例患者随机分为伊贝沙坦治疗组 (伊贝沙坦组 ) 3 0例 ,吲达帕胺对照组 (吲达帕胺组 ) 2 4例。治疗 12周后两组患者再次接受动态血压监测和超声心动图检查 ,对比治疗前后血压昼夜节律及左心室参数的变化。　　结果 :93例老年原发性高血压患者中合并左心室肥厚者 5 3例 ,其中血压昼夜节律消失者为 42例 (79 2 % ) ;40例无LVH患者中昼夜节律消失者为 12例 (3 0 0 % ) ,合并LVH者中血压昼夜节律消失者显著多于无LVH者 (P <0 0 0 5 ) ,有极显著性差异 ;5 4例血压昼夜节律消失者治疗 12周后昼夜节律恢复者伊贝沙坦组 2 2例 (2 2 /3 0 ) ,吲达帕胺组 9例 (9/2 4) ,两组比较有极显著性差异 (P <0 0 1) ;伊贝沙坦组高血压合并LVH者治疗后室间隔、左心室后壁厚度无显著性改变 ,但左心室重量指数与治疗前及吲达帕胺组比较均有下降 (P均 <0 0 5 ) ,均有显著性差异。　　结论 :在血压昼夜节律消失的老年原发     

B-type natriuretic peptide and left ventricular hypertrophy in hypertensive patients.

AIM: To assess the accuracy of B-type natriuretic peptide (BNP) plasma levels for the diagnosis of left ventricular hypertrophy (LVH) in hypertensive patients. PARTICIPANTS AND METHODS: We studied a sample of 409 adults aged 45 years or older, recruited from residents of Porto by random digit dialing. Data were collected by clinical interview and physical examination, ECG, echocardiogram and venous blood sampling for the measurement of plasma concentrations of BNP. Hypertension (HT) was defined as blood pressure > or = 140/90 mmHg on the day of interview and/or self-reported HT if treated with any antihypertensive medication; LVH was defined as left ventricular mass index (LVMI) > or = 125 g/m2 in men and 110 g/m2 in women. The participants were further classified in four strata according to left ventricular morphology--normal, concentric remodeling, eccentric LVH or concentric LVH. RESULTS: Two hundred and thirty-two (56.7%) individuals were hypertensive, and among these 73 (31.5%) had LVH. BNP levels were significantly higher in these individuals (median [P25-P75] = 55.8 pg/ml [22.6-88.4]) than in hypertensive patients without LVH (29.9 pg/ml [10.0-62.8]), p = 0.003. BNP levels also differed significantly across strata of left ventricular geometry, the main difference depending on the presence or absence of LVH. There was a positive correlation between plasma BNP levels and LVMI (Spearman's P 0.185, p = 0.005). The area under the ROC curve--a parameter for diagnostic accuracy quantification--was 0.62 (95% confidence interval 0.54-0.70), indicating low discriminatory power between normal and abnormal LVMI. CONCLUSION: In the assessed population, BNP levels were higher in hypertensive patients with LVH than in the absence of LVH. However, BNP did not perform well in discriminating between the presence or absence of LVH.     

Left ventricular hypertrophy is associated with an attenuated endothelium-dependent vasodilation in hypertensive men

To investigate the relationship between left ventricular hypertrophy (LVH) and endothelium-dependent vasodilation (EDV), 30 untreated hypertensive patients, 18 treated hypertensives (53 +/- 7 years, all males) and 26 age-and sex-matched healthy normotensive controls, underwent evaluation of EDV and endothelium-independent vasodilation (EIDV) in the forearm, by means of local intra-arterial infusions of methacholine (MCh, evaluating EDV) and sodium nitroprusside (SNP, evaluating EIDV). Forearm blood flow was measured by venous occlusion plethysmography and LVH was measured by echocardiography. The reduction in forearm vascular resistance during MCh infusion (4 microg/min) was significantly smaller in the hypertensive patients with LVH when compared to those without LVH, both in the untreated (-61 +/- 12%, n = 19 vs -72 +/- 4%, n = 11, p < 0.01) and in the treated group (-60 +/- 15%, n = 11 vs -75 +/- 5%, n = 7, p < 0.01). Thereby, EDV was significantly impaired only in the hypertensive patients with LVH when compared to controls (-77 +/- 7% at MCh 4 microg/min, p < 0.001). EIDV was not significantly different between patients with and without LVH and controls. In conclusion, the presence of LVH was related to endothelial dysfunction, both in untreated and treated hypertensive patients, suggesting either a role for endothelial function in the development of LVH, or that a dysfunctional endothelium and LVH are coexisting markers of a more severe hypertensive disease.     

Left ventricular hypertrophy in hypertensive African blacks: echocardiographic study of 452 patients

OBJECTIVE: The aim of this study was to define in a population of hypertensive Black African, the frequency of left ventricular hypertrophy (LVH), the different kind of LVH, and the factors of LVH occurring. METHODS: Clinical and echographic (according to Penn convention) data was collected in 452 consecutive hypertensive patients (193 women and 259 men). LVH was defined as an indexed left ventricular mass (ILVM) > 134 g/m2 in man and 110 g/m2 in woman. RESULTS: The mean systolic blood pressure was 187 mmHg, and the mean diastolic, 111 mmHg. The mean ILVM was 135.25 g/m2. LVH was present in 53.3% of the patients. Concentric LVH represented 48.5%, eccentric LVH 41.1%, and asymmetric hypertrophy of the septum, 10.4%. LVH increased with patient's age (p = 0.008), hypertension severity (p = 0.0001), and the ancientness of the hypertension (p = 0.0001). CONCLUSION: LVH is frequent in hypertensive black African, and concentric LVH is the most frequent kind of LVH. Factors of LVH occurring are patient's age, severity and the ancientness of the hypertension.     

Microalbuminuria,a parameter independent of metabolic influences in hypertensive men

OBJECTIVE: To evaluate the relationship of albuminuria and microalbuminuria (overnight urine albumin > or = 15 micro g/min) with insulin resistance and related metabolic abnormalities in patients with essential hypertension. DESIGN: Cross-sectional evaluation of 271 (age range, 19-77 years) never-treated, non-diabetic, uncomplicated hypertensive men. MAIN OUTCOME MEASURES: Triplicate overnight urine albumin determination and homeostasis model assessment (HOMA) of insulin resistance as a surrogate measure of insulin sensitivity. Additional parameters were fasting and post-load circulating glucose and insulin, lipids, body mass index, blood pressure and echocardiographic left ventricular mass. RESULTS: HOMA, fasting and post-challenge glucose and insulin, percentages of glucose-intolerant patients, triglycerides and high-density lipoprotein cholesterol levels did not differ across ascending urine albumin quartiles. Body mass index, blood pressure and ventricular mass were significantly greater in the upper quartiles, and the prevalence of obesity fivefold more frequent in the top as compared with the bottom urine albumin fourth. The statistical trend was unchanged after adjustment for HOMA, while accounting for systolic blood pressure and left ventricular mass by co-variance analysis abolished it. Eighty-eight patients bearing the phenotypic traits of the metabolic syndrome and a striking degree of insulin resistance and hyperinsulinemia showed urine albumin rates and prevalence of microalbuminuria comparable with the 183 patients who were not affected by that syndrome. CONCLUSIONS: Albuminuria is independent of insulin resistance and other phenotypic components of the metabolic syndrome in never-treated, non-diabetic essential hypertensive men. Microalbuminuria is more frequent in obese hypertensives but this association is explained by higher blood pressure more than insulin resistance.     

Comparative effects of valsartan versus amlodipine on left ventricular mass and reactive oxygen species formation by monocytes in hypertensive patients with left ventricular hypertrophy

OBJECTIVES: To compare the effects of the angiotensin receptor blocker (ARB) valsartan versus the calcium channel blocker amlodipine, reactive oxygen species (ROS) formation by monocytes, C-reactive protein (CRP), and left ventricular (LV) mass were studied in 104 hypertensive patients with left ventricular hypertrophy (LVH). BACKGROUND: There is evidence that ARBs have blood pressure (BP)-independent effects on LV mass. Whether regression of LV mass by ARBs is correlated to ROS formation by monocytes and CRP is not fully understood yet. METHODS: A cross-sectional and prospective study was performed. Participants were randomly assigned to either the 80-mg valsartan (n = 52) or 5-mg amlodipine (n = 52) group and were treated for eight months. The left ventricular mass index (LVMI) was calculated from two-dimensional M-mode echocardiography. Formation of ROS by monocytes was measured by gated flow cytometry. In addition, CRP, plasma renin activity, plasma aldosterone, and traditional risk factors were assessed. RESULTS: Multiple regression analysis showed a significant correlation between LVMI and ROS formation by monocytes and between LVMI and CRP. Treatment reduced BP to a similar extent in both groups. Valsartan significantly reduced LVMI after eight months, but amlodipine had less effect (16% vs. 1.2%, n = 50, p < 0.01). Formation of ROS by monocytes was reduced to a greater extent with valsartan than with amlodipine (28% vs. 2%, n = 50, p < 0.01). Valsartan but not amlodipine reduced CRP levels. A significant correlation between changes in ROS formation by monocytes and LVMI or between CRP and LVMI was observed. CONCLUSIONS: The ARB valsartan has BP-independent effects on LVH, ROS formation by monocytes, and CRP in hypertensive patients with LVH.