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Treatment and prevention of target organ damage.

Target organ damage to the brain, heart or kidneys due to hypertension appears to differ in various ethnic groups. Prevention of such damage is by early recognition of mild hypertension and institution of treatment primarily by non-pharmacologic and if required drugs. Treatment of established damage is by both these methods. In the choice of drugs 24-hour control of blood pressure is essential as is regression of left ventricular hypertrophy. Other desirable qualities of the drugs are their anti-ischaemic and anti-atherogenic effects.

Brain Diseases↗

Enhancement of endogenous defenses against ROS by supra-nutritional level of selenium is more safe and effective than antioxidant supplementation in reducing hypertensive target organ damage.

Hypertension-induced target organ damage (TOD), is one of the leading causes of morbidity and mortality. Reactive oxygen species (ROS) play an important role in the pathogenesis and development of hypertension. It has been suggested that hypertension-induced TOD is related to the level of oxidative stress, but is in part independent of the level of blood pressure. Therefore, in addition to anti-hypertensive drug therapy, novel strategies against ROS, will provide additional benefits to patient with hypertension. Vitamin E has long been supplemented as an effective antioxidant. However, the potential hazardous effects of vitamin E supplementation as antioxidant revealed by recent studies make its clinical and routine use prudent. Therefore, novel approaches capable of enhancing endogenous system to defend against ROS are required. Here, we propose that enhancement of intrinsic defenses against ROS by supra-nutritional level of selenium is more safe and effective than antioxidant supplementation in reducing hypertensive target organ damage, owing to its role in activating and constitution of native vital proteins and/or enzymes against oxidative stress, and the fact that scarcity of selenium can not be supplemented by normal food, and potentially extra benefits by supra-normal intake.

Antioxidants↗

High prevalence of cardiac and extracardiac target organ damage in refractory hypertension.

OBJECTIVE: Target organ damage (TOD) in chronically treated hypertensives is related to effective blood pressure (BP) control. The aim of this study was to evaluate the prevalence of cardiac and extracardiac TOD in patients with refractory hypertension (RH) compared with well-controlled treated hypertensives (C). METHODS: Fifty-four consecutive patients with RH (57 +/- 10 years), selected according to WHO/ISH guidelines definition, and 51 essential hypertensives (55 +/- 10 years) with satisfactory BP control obtained by association therapy, underwent the following procedures: (1) clinic BP measurement; (2) blood sampling for routine chemistry examinations; (3) 24 h urine collection for microalbuminuria; (4) non-mydriatic retinography; (5) echocardiogram; (6) carotid ultrasonogram. In order to exclude 'office resistance' (defined as clinic BP > 140/90 mmHg and average 24 h BP </= 125/79 mmHg), all patients with RH were subjected to 24-hour ambulatory BP monitoring. RESULTS: Both groups were similar for age, gender, body surface area, smoking habit and duration of hypertension, glucose, creatinine and lipid levels. By definition, clinic BP was significantly higher in RH than C (161 +/- 19/96 +/- 9 versus 127 +/- 6/80 +/- 5 mmHg, respectively, P < 0.01). The increased prevalence of left ventricular hypertrophy (LVH) and carotid intima-media (IM) thickening (40 versus 12%, P < 0.01, according to a non-gender-specific partition value of 125 g/m2; and 36 versus 14%, P < 0.01, according to IM thickness > or =1.0 mm, respectively); a higher prevalence of carotid plaques (65 versus 32%, P < 0.05), a more advanced retinal involvement (grade II and III, 73 and 5% versus 38 and 0%, P < 0.01) and a greater albumin urinary excretion (22 +/- 32 mg/24 h versus 11 +/- 13 mg/24 h, P < 0.01) were found in RH compared to C. CONCLUSIONS: Our study suggests that RH is a clinical condition associated with a high prevalence of TOD at cardiac, macro- and microvascular level and consequently with high absolute cardiovascular risk, which needs a particularly intensive therapeutic approach aimed to normalize BP levels and to induce TOD regression.

Albuminuria↗

Left ventricular hypertrophy precedes other target-organ damage in primary aldosteronism.

To elucidate whether there is a difference in the progression of target-organ damage between primary aldosteronism and essential hypertension, we compared left ventricular hypertrophy and extracardiac target-organ damage in 23 patients with primary aldosteronism and 116 patients with essential hypertension. The severity of hypertensive retinopathy and the renal involvement in primary aldosteronism were subclinical and similar to those in essential hypertension without left ventricular hypertrophy but significantly milder than those in essential hypertension with left ventricular hypertrophy. There was a strongly significant correlation between the degree of left ventricular mass index and the severity of hypertensive retinopathy and renal involvement independent of office blood pressure in essential hypertension. In contrast, left ventricular hypertrophy markedly progressed despite the mild extracardiac target-organ damage in primary aldosteronism. Left ventricular end-diastolic dimension index in primary aldosteronism (3.16+/-0.50 cm/m2) was significantly larger than in essential hypertension without (2.87+/-0.23) and with (2.88+/-0.22) left ventricular hypertrophy. On the other hand, there was no difference in extracardiac target-organ damage between 13 primary aldosteronism patients with eccentric left ventricular hypertrophy and the 26 essential hypertensive patients with eccentric left ventricular hypertrophy. The results suggest that predominantly volume load, be it due to aldosteronism or other mechanisms, resulting in eccentric left ventricular hypertrophy is less likely to cause extracardiac target-organ damage than hemodynamic or nonhemodynamic mechanisms resulting in concentric left ventricular hypertrophy.

Adult↗

Home blood pressure telemonitoring reveals race-specific patterns of target organ damage.

BACKGROUND: Racial differences in cardiac and renal target organ damage (TOD) may persist at comparable blood pressure levels. This study compared TOD in high-risk, non-African-American Black and White patients in relation to the home blood pressure (HBP). METHODS: UPRIGHT-HTM (NCT04299529) is an ongoing international trial comparing risk stratification strategies in asymptomatic patients, aged 55-75 &#x200a;years, with &#x2265;5 risk factors. Patients engage in HBP telemonitoring (OMRON HEM 9210-T). After 34.7&#x200a;months (median), 287 Black and 154 White patients underwent echocardiography. At baseline, their chronic kidney disease (CKD) grade was assessed by cross-classification of the race-free estimated glomerular filtration rate and albuminuria (2024 KDIGO guideline). HBP was stratified by the 2024 ESC thresholds. Linear and logistic regression models, including a race-by-HBP interaction term, were applied to assess associations with the home systolic HBP. RESULTS: The number of HBP readings was 252 215. Median systolic/diastolic HBP was 127/77&#x200a;mmHg with 142 patients (32.2%) having home hypertension. Fewer Black patients received statins or combination therapy for hypertension or diabetes. Among nonhypertensive White compared to Black patients, left atrial dimensions, mitral annular s', and stroke volume had a steeper slope in relation to systolic HBP. All patients had concentric left ventricular remodeling, but only 4 Black and 13 White patients had an ejection fraction&#x200a;<&#x200a;50%. CKD grade was worse in Black than White patients without association with HBP. CONCLUSIONS: TOD primarily affects the kidney in Black and the heart in White patients. Intensifying pharmacological treatment in sub-Saharan Africa, including antihypertensives, lipid-lowering agents, antidiabetic medications, and aspirin, should create an opportunity for improved overall cardiovascular and metabolic prevention.

Aged↗

Nitric oxide synthase inhibition accelerates the pressor response to low-dose angiotensin II, exacerbates target organ damage, and induces renin escape.

Because nitric oxide may attenuate both the pressor and cytotoxic effects of angiotensin II (Ang II), we investigated whether nitric oxide synthase (NOS) inhibition might accelerate the slow pressor effect of Ang II, and augment target organ damage. Using conscious, chronically catheterized rats, we previously observed that low-dose Ang II (10 ng/kg/min) rapidly increased mean arterial pressure (MAP) by approximately 25 mm Hg. The MAP then remained at this level for 2 to 4 days, and then increased again during the next 5 days by a further 25 mm Hg to a second plateau. In the present study, 7 days of N(omega)-nitro-l-arginine methyl ester (L-NAME; 10 microg/kg/min) alone increased MAP by 16 mm Hg. When Ang II was added to L-NAME, MAP increased as much as with Ang II alone, but then continued to increase until day 4, reaching a plateau as high as that reached only on day 9 of Ang II alone. In approximately half the rats infused with L-NAME + Ang II, plasma renin escaped from Ang II-induced suppression after day 4 of Ang II, and continued to increase for the duration of the study. On the first day that Ang II was added to L-NAME, urinary protein excretion and plasma cardiac troponin T increased, indicating early target organ damage. By the end of the study, all rats treated with L-NAME + Ang II developed tubulointerstitial and glomerular injuries, fibrosis of the renal and cardiac arteries, and cardiac interstitial fibrosis. Target organ damage was greater in rats that developed renin escape than in those in which plasma renin remained suppressed, but was minimal in rats infused with Ang II or L-NAME alone. Taken together, these findings suggest that endogenous NO normally attenuates the pressor response to low-dose Ang II for several days, and protects from Ang II-induced target organ damage. Under conditions of reduced NO bioavailability, which may result from endothelial insufficiency, relatively small changes in circulating Ang II levels may damage target organs. Moreover, renal damage leading to renin escape may initiate a vicious cycle of elevated Ang II production, leading to higher blood pressure and greater target organ damage.

Angiotensin II↗

Ethnic differences in skin microvascular function and their relation to cardiac target-organ damage.

BACKGROUND: People of Black African descent have increased risks of vascular target-organ damage not explained by greater blood pressures. OBJECTIVE: To study ethnic differences in the microvasculature. DESIGN AND METHODS: Flow (flux) in microcirculatory skin vessels was assessed using laser Doppler fluximetry in 181 Afro-Caribbean and European men and women aged 40-65 years from the general population in London, UK. Flux in response to maximal heating (maximal hyperaemic response) was measured and minimum vascular resistance calculated. Peak flux and time to peak after an ischaemic stimulus were also measured. Target-organ damage was assessed using echocardiographic interventricular septal thickness (IVST). RESULTS: In men, maximum hyperaemic response was attenuated in Afro-Caribbeans [109 arbitrary units (au), 25th and 75th percentiles 101, 117] compared with Europeans [165 (155, 179) au; P = 0.008]. Minimum vascular resistance was greater in Afro-Caribbeans, significantly so in men [(1.22 (1.18, 1.28) au/mmHg compared with 0.80 (0.77, 0.83) au/mmHg; P = 0.006]. Peak ischaemic response was attenuated in Afro-Caribbean men and women compared with Europeans (35.6 au compared with 49.5 au; P < 0.001) and time to peak was prolonged (14.1 s compared with 12.5 s; P = 0.07). These ethnic differences could not be accounted for by standard cardiovascular risk factors. IVST was greater in Afro-Caribbeans than in Europeans. Minimum vascular resistance and peak response accounted for a small proportion of this ethnic difference, in addition to conventional factors. CONCLUSIONS: Afro-Caribbeans have poorer microvascular structure and function, unexplained by conventional risk factors, which may contribute to greater rates of vascular target-organ damage.

Adult↗

Fibrinogen and preclinical echocardiographic target organ damage: the strong heart study.

Relations of fibrinogen to preclinical target organ damage, such as left ventricular hypertrophy, systolic dysfunction, and increased arterial stiffness while accounting for traditional risk factors, are unknown in a population-based sample free of clinically overt coronary heart disease. Therefore, we studied clinical and echocardiographic characteristics of 2709 American Indians participating in the Strong Heart Study without symptomatic atherosclerosis. The study sample was divided into tertiles of fibrinogen (cut-points, 3.24 and 3.83 g/L). Mean age, body mass index, proportion of women, and prevalences of hypertension and diabetes increased from the first to third tertile of fibrinogen. After adjustment for covariates, systolic and pulse pressures did not significantly differ among tertiles of fibrinogen, whereas diastolic pressure was slightly lower in the third than in lower tertiles of fibrinogen. HDL cholesterol was lower and plasma creatinine and urinary albumin/creatinine ratio was higher in the third tertile of fibrinogen. Left ventricular mass index, pulse pressure/stroke index, an estimate of arterial stiffness, and cardiac index were higher and left ventricular systolic function and total peripheral resistance were lower in the third than in two lower tertiles of fibrinogen independent of major covariates. In multiple regression analyses, left ventricular mass and pulse pressure/stroke index were positively associated with, and stress-corrected midwall shortening negatively associated with fibrinogen, independent of major covariates. Participants with fibrinogen >3.83 g/L were more likely to have at least 1 preclinical cardiovascular abnormality such as left ventricular hypertrophy, elevated arterial stiffness, or systolic myocardial dysfunction independent of covariates including renal dysfunction (adjusted odds ratio, 1.38; P<0.001). Thus, in a population sample of adults without clinically overt coronary heart disease, elevated fibrinogen is an independent correlate of prognostically relevant cardiovascular target organ damage.

Arteries↗

Mechanisms of target organ damage caused by hypertension: therapeutic potential.

Hypertension is a major risk factor for cardiovascular mortality and morbidity through its effects on target organs like the brain, heart, and kidney. Structural alterations in the microcirculation form a major link between hypertension and target organ damage. In this review, we describe damages related to hypertension in these target organs and the mechanisms involved in the pathogenesis of hypertension-induced cardiovascular diseases such as dementia, cardiac ischemia and remodeling, or nephropathy. We also focus on the therapeutical potential on the basis of such mechanisms. Several antihypertensive agents like diuretics, angiotensin converting enzyme (ACE) inhibitors, angiotensin II (Ang II) receptor antagonists, beta-blockers, or calcium channel blockers (CCBs) have been shown to reduce effectively hypertension associated cardiovascular events and to improve end organ damage. More recently, aldosterone antagonism has also shown beneficial effects. Part of the favorable effects of these agents is due to blood pressure lowering as such. Other mechanisms such as oxidative stress, inflammation, or endothelial dysfunction have appeared to play a key role in the pathogenesis of target organ damage and therefore represent another important pathway for therapy. In this review, we discuss the different therapeutic approaches aiming at reducing cardiovascular events and damages induced by hypertension.

Animals↗

Influence of isolated diastolic hypertension identified by ambulatory blood pressure on target organ damage.

Clinical decisions and controlled studies in regard to hypertension have long emphasized the casual diastolic blood pressure (DBP). The influence of superimposition of high systolic blood pressure (SBP) on the target organ damage has been less studied. To assess the role of isolated diastolic hypertension without interference of superimposition of systolic hypertension, 171 subjects with normal blood pressure, isolated diastolic hypertension (SBP < 140 and DBP > or = 90 mmHg) isolated systolic hypertension (SBP > or = 140 and DBP < 90 mmHg) or combined hypertension (SBP > or = 140 and DBP > or = 90 mmHg) determined by mean 24-h ambulatory blood pressure were compared in relation to target organ damage including ECG abnormality related to hypertension, cardiac enlargement by chest X-ray, proteinuria and retinopathy. The incidence of target organ damage was lower in subjects with normal BP than in the other three groups. The incidence of target organ damage was almost significantly higher in patients with isolated systolic hypertension than in those with isolated diastolic hypertension. No significant difference in the incidence of complications existed between patients with isolated systolic and combined hypertension. These findings demonstrate that the severity of hypertensive complications is more closely related to mean ambulatory SBP than mean ambulatory DBP. The level of systolic BP is important for predicting the severity of target organ damage in patients with high diastolic BP, because there is a significant difference in the incidence of target organ damage between isolated diastolic hypertension and combined hypertension.

Arrhythmias, Cardiac↗

Evaluation of target organ damage in arterial hypertension: which role for qualitative funduscopic examination?

BACKGROUND: The objective of this study was to compare the prevalence of quantitative markers of target organ damage, such as echocardiographically documented left ventricular hypertrophy (LVH), carotid structural changes and microalbuminuria with that of retinal abnormalities detected by qualitative funduscopic examination in a large selected population of patients with essential hypertension. METHODS: Eight hundred consecutive untreated (n = 232) and treated (n = 568) hypertensive patients (386 men, 414 women, mean age 52.7 +/- 11.8 years) referred for the first time to our out-patient clinic were included in the study. In order to search for target organ damage, they were submitted to the following procedures: 1) amydriatic retinography, 2) 24-hour urine collection for microalbuminuria, 3) echocardiography, and 4) carotid ultrasonography. Retinal changes were evaluated according to the Keith, Wagener and Barker (KWB) classification by two physicians, who had no knowledge of the patients' characteristics. Microalbuminuria was defined as a urinary albumin excretion > 30 and < 300 mg/24 hours, LVH as a left ventricular mass index > or = 134 g/m2 in men and > or = 110 g/m2 in women; finally carotid plaque was defined as a focal thickening > 1.3 mm. RESULTS: Hypertensive retinopathy was the most frequent (KWB grade I 46%, II 32%, III-IV < 2%) marker of target organ damage, followed by carotid plaques (43%), LVH (22 %, eccentric LVH was the prevalent type and was 1.8 times as frequent as the concentric one) and microalbuminuria (14%). CONCLUSIONS: At variance with the markers of cardiac, macrovascular and renal damage, an extremely high prevalence of retinal abnormalities (narrowings and initial arterio-venous crossings) were found in our population. If, as suggested by the WHO/ISH guidelines, these retinal abnormalities were considered as a reliable marker of target organ damage, then almost all patients would be affected by hypertensive vascular disease. Based on this evidence it is suggested that retinal abnormalities included in funduscopic grades I and II of the KWB classification should not be considered among the criteria for the quantitative detection of target organ damage.

Adult↗

p38 mitogen-activated protein kinase inhibition ameliorates angiotensin II-induced target organ damage.

We investigated whether or not p38 mitogen-activated protein kinase inhibition ameliorates angiotensin II-induced target organ damage. We used double transgenic rats harboring both human renin and angiotensinogen genes (dTGRs). dTGR, with or without p38 inhibitor (BIRB796; 30 mg/kg per day in the diet), and nontransgenic Sprague-Dawley rats were studied in 2 protocols. In protocol 1 (week 7), systolic blood pressure of untreated dTGRs was 204+/-4 mm Hg, but partially reduced after BIRB796 treatment (166+/-7 mm Hg), whereas Sprague-Dawley rats were normotensive. The cardiac hypertrophy index was unchanged in untreated and BIRB796-treated dTGRs. The beta-myosin heavy chain expression of BIRB796-treated hearts was significantly lower in BIRB796 compared with dTGRs, indicating a delayed switch to the fetal isoform. BIRB796 treatment significantly reduced cardiac fibrosis, connective tissue growth factor, tumor necrosis factor-alpha, interleukin-6, and macrophage infiltration. Albuminuria was not reduced in BIRB796-treated dTGRs. Tubular and glomerular damage with tumor necrosis factor-alpha expression was unaltered, although serum creatinine and cystatin C were normalized. Renal macrophage infiltration, fibrosis, and vessel damage were reduced. In protocol 2 (week 8), we focused on mortality and arrhythmogenic electrical remodeling. Mortality of untreated dTGRs was 100% but was reduced to 10% in the BIRB796 group. Cardiac magnetic field mapping showed prolongation of depolarization and repolarization in untreated dTGRs compared with Sprague-Dawley rats with a partial reduction by BIRB796. Programmed electrical stimulation elicited ventricular tachycardias in 81% of untreated dTGRs but only in 48% of BIRB796-treated dTGRs. In conclusion, BIRB796 improved survival, target organ damage, and arrhythmogenic potential in angiotensin II-induced target organ damage.

Angiotensin II↗

Comparison of early target organ damage between blacks and whites with mild systemic arterial hypertension.

As greater mortality and morbidity from target organ damage in arterial hypertension have been reported for black than for white hypertensives, we examined in a matched-pair analysis whether race per se affected markers of early target organ damage at similar levels of blood pressure. After controlling for the confounding factors such as age, sex, weight, and arterial pressure that interact with hypertension-related target organ damage, no racial disparities could be detected between matched black and white hypertensive patients.

Adult↗

[Target organ damage in children with newly diagnosed and untreated essential hypertension].

UNLABELLED: Target organ damage in the course of essential hypertension (EH) may develop already in childhood. The aim of the study was to determine the prevalence of left ventricular hypertrophy (LVH) and arterial damage and its main determinants in children with newly diagnosed, untreated EH. PATIENTS (pts): 87 children (22 girls and 65 boys) with EH, age 14.4 +/- 3 (5-18) yrs. CONTROL GROUP: 104 healthy children (51 girls and 53 boys) aged 13.3 +/- 3.3 (5-20) yrs. STUDY DESIGN: cross-sectional, controlled study. METHODS: evaluation of anthropometrical data, birth weight, family history towards cardiovascular diseases, serum biochemical cardiovascular risk factors (lipids, sCRP, homocysteine, uric acid), carotid (cIMT) and superficial femoral artery intima-media thickness (fIMT). In EH children ambulatory blood pressure monitoring (ABPM), echocardiography, ophthalmoscopy, microalbuminuria were evaluated. RESULTS: EH pts were significantly higher, heavier and had greater body mass index (BMI) (p<0.05). 59% of pts were overweight compared to 19% in control group (p<0.05). Carotid (cIMT) and superficial femoral artery intima-media thickness (fIMT) was greater in children with EH (0.47 +/- 0,05 v 0.43 +/- 0.04 and 0.36 +/- 0.04 v 0.33 +/- 0.04) (p<0.05) respectively. 41% and 19% of pts had cIMT and fIMT above 2 SDS of normal values respectively. The prevalence of LVH was 45%, and in 12% of pts severe (left ventricular mass index--LVMi > 51 g/m2.7) LVH was diagnosed. Pts with LVH had higher birth weight than other pts 3525 < or = 598 v 3136 +/- 635 g (p=0.04) and LVMi correlated with higher birth weight (p=0.0001; r=0.358), 24-hour heart rate (p=0.01; r= -0.361), serum uric acid (p=0.01; r=0.286), homocysteine (p=0.01; r=0.309) and apolipoprotein B (p=0.0001; r=0.258). LVMi correlated with fIMT (p=0.02; r=0.292), but not with cIMT. cIMT correlated with 24-hour systolic blood pressure (SBP)(p=0.01; r=0.305), SBP load (p=0.01; r=0.377), puls pressure (PP) (p=0.01; r=0.292), and heart rate (HR) (p=0.01; r=-0.285). 46% of pts had primary retinopathy, and 1 boy had secondary retinopathy. All pts had normal renal function, and mean microalbuminuria was 29.3+/-11.4 mg/d. Positive family history towards EH was confirmed in 80% of pts vs 29% in controls (p<0.05). CONCLUSIONS: 1. Target organ damage is present already at the time of diagnosis in significant number of children with EH. 2. Overweight was 59% of pts and only 19% of healthy children. 3. LVMi and markers of arterial injury correlate with SBP, PP and HR, fIMT, uric acid, homocysteine, apolipoprotein B and birth weight.

Adolescent↗

Clinical evidence for an association between left ventricular geometric adaptation and extracardiac target organ damage in essential hypertension.

OBJECTIVES: To elucidate an association between left ventricular geometric adaptation to sustained hypertension and preclinical extracardiac target organ damage in essential hypertension. We also studied the clinical significance of neurohumoral factors for cardiovascular structural changes. DESIGN: One hundred and forty patients with essential hypertension were divided into four subgroups, based on left ventricular mass index and relative wall thickness. With respect to extracardiac target organ damage, we measured the funduscopic grade of retinal changes and serum creatinine levels. RESULTS: Among the hypertensive patients, only 19 (14%) had a typical concentric hypertrophy (increase in left ventricular mass index and relative wall thickness). Hypertensive patients with concentric hypertrophy had the most advanced funduscopic abnormalities and the greatest renal involvement, and hypertensive patients without left ventricular hypertrophy had the least extracardiac target organ damage. Plasma renin activity and plasma aldosterone concentration were higher in hypertensive patients with than in those without concentric hypertrophy. In a multiple regression model there was a strongly significant correlation between the degree of left ventricular mass index and the severity of hypertensive retinopathy and renal involvement, independent of office blood pressure. CONCLUSIONS: These results clearly demonstrate that echocardiographically determined left ventricular mass and geometry stratify extracardiac target organ damage in patients with essential hypertension more closely than office blood pressure. The present study also suggests that, in addition to blood pressure load, the renin-angiotensin-aldosterone system appears to play an important role in myocardial hypertrophy and peripheral vascular damage in hypertension.

Aldosterone↗

Low frequency of target organ damage in Taiwanese with white coat hypertension.

BACKGROUND AND PURPOSE: The clinical importance of white coat hypertension (WCH) remains to be clarified. This study investigated the target organ damage in Taiwanese with WCH. METHODS: A total of 188 consecutive Taiwanese (88 men and 100 women), aged 26 to 75 years who had an abnormal office casual blood pressure (systolic blood pressure >/= 140 mm Hg or diastolic blood pressure >/= 90 mm Hg or both) and a normal ambulatory blood pressure (ABP) average (systolic ABP average < 140 mm Hg and diastolic ABP average < 90 mm Hg) at the outpatient clinic or from a mass survey were enrolled. Office casual blood pressure measurements were obtained by standard sphygmomanometric methods. Twenty-four-hour blood pressures were recorded by a commercial ambulatory pressure recorder (Del Mar Avionics, Model 1990 Pressurometer IV System). Hypertension-related target organ complications were assessed by electrocardiogram, chest X-ray, urinalysis and eye fundus examinations. RESULTS: Target organ damage was found in 6.4% of subjects with WCH. Roentgenographic left ventricular hypertrophy (LVH) was found in 1.1% of subjects and electrocardiographic LVH in 2.7%. Proteinuria was found in 1.6% of subjects and retinopathy in 1.1%. The frequencies of various target organ damage were not significantly associated with age, gender and the definition of normal ABP average as 135/85 mm Hg or 140/90 mm Hg. CONCLUSIONS: WCH represents a low-risk stratum for target organ damage in Taiwanese. These subjects should be identified and followed up regularly. The factors responsible for the low frequency of target organ damage in Taiwanese with WCH need further study.

Adult↗

Comparison of target organ damage in renovascular and essential hypertension.

In many reports, the prevalence of target organ damage in renovascular hypertension (RVH) appears to be higher than in essential hypertension (EH). Since in most studies the renal artery stenosis is part of a diffuse atherosclerotic disease, it is not known whether these complications are due to RVH itself or to the vascular disease. We have undertaken a case control study of 92 patients divided into two groups (46 in each), one with RVH and the other with EH and abdominal aortic aneurysm, with a comparable degree of diffuse atherosclerotic vascular disease. The vascular state of the extracranial carotid arteries and abdominal and inferior limb districts was investigated with angiography and sonography. The prevalence of left ventricular hypertrophy (LVH) and ischemic heart disease (IHD) were assessed by electrocardiography. Serum creatinine and urinary protein excretion were employed in the renal evaluation. While the analysis of the results confirmed an even diffusion of atherosclerotic vascular disease between the two groups, a significant difference was found in the prevalence of heart and renal damage. LVH was present in 32.6% of RVH patients versus 10.8% in EH (P = .02). Serum creatinine > 1.4 mg/dL was found in 50% of RVH and in 23.9% of EH, (P = .01). The prevalence of proteinuria in RVH was also higher although not reaching the statistical significance. The results suggest that, in patients with comparable degrees of atherosclerotic vascular disease, RVH is responsible for the higher prevalence of target organ damage in this condition compared to those with EH.

Aged↗

Gender-related differences in target organ damage in untreated patients with essential hypertension.

We examined the gender-related differences in target organ damage in 220 untreated patients with essential hypertension (106 men and 114 women). As the indices of target organ damage, we examined the left ventricular mass index and the intima-media thickness in the carotid and femoral arteries obtained from echocardiography. In a multiple regression model, there was a significant positive correlation between the intima-media thickness and age in both groups. In men, there was a significant positive correlation between the left ventricular mass index and age, as well as the diastolic blood pressure, and body mass index. In women, there was a significant positive correlation between the left ventricular mass index and age, as well as plasma renin activity and smoking. In conclusion, there are gender-related differences in the contributing factors, which relate to left ventricular hypertrophy in patients with essential hypertension.

Aged↗