Who contributes to the public health function?

OBJECTIVES: To describe patterns of hypertension history in patients with various types of end-stage renal disease (ESRD) and in persons with normal kidney function; and to identify risk factors for the diagnosis 'hypertensive ESRD'. DESIGN: A case-control study. SETTING: Population-based. PARTICIPANTS: Patients with ESRD due to hypertension (n = 214), diabetes (n = 239), other specified causes (n = 181), unknown causes (n = 82) and control subjects drawn from the general population (n = 361). MAIN OUTCOME MEASURES: Participants' history of hypertension. RESULTS: The prevalence of hypertension was 90% in ESRD patients and 27% in controls. Only 6% of patients with hypertensive ESRD had a history of malignant hypertension. Patients with hypertensive ESRD were more likely to have been hospitalized because of hypertension (36%) than were other ESRD patients (18%) or controls (5%). ESRD of any cause was more strongly associated with hypertension of > or = 25 years duration (odds ratio 51.0, compared with normal blood pressure) than it was with hypertension of shorter duration (15-25 years: odds ratio 31.8, 5-15 years: odds ratio 16.0, < 5 years: odds ratio 21.2). Among patients who had both hypertension and ESRD, the diagnosis of 'hypertensive ESRD' was associated independently with a long duration of hypertension, greater severity of hypertension, the absence of diabetes, black race, and limited education. CONCLUSIONS: Hypertension is common among patients with ESRD. The risk of ESRD from any cause increases progressively with the duration of hypertension, and with indicators of severe hypertension. This result supports the hypothesis that nonmalignant hypertension of long duration may cause renal insufficiency. The criteria used to diagnose hypertensive ESRD are consistent with pathophysiologic and epidemiologic evidence.     

Cardiac function and dysfunction in hypertension

BACKGROUND: Hypertension is the most common condition of increased left ventricular afterload that affects the cardiovascular system. OBJECTIVE: To review the effects of increased blood pressure on cardiac function. SUMMARY: In early or borderline hypertension, cardiac output increases but intravascular volume remains normal. In uncomplicated established hypertension, left ventricular systolic function is generally normal at rest; however, the left ventricular filling rate is reduced in approximately 30% of hypertensive patients without associated alterations in systolic function. In the presence of left ventricular hypertrophy, overall left ventricular systolic performance remains within normal limits; however, left hypertrophy in hypertension is associated with a high morbidity rate, possibly due to increased collagen concentration leading to reduced left ventricular compliance, fewer adrenergic receptors, reduced responsiveness of the adenylate cyclase system, and reduced coronary flow reserve. Acute increases in blood pressure in a hypertensive patient may worsen cardiac function, particularly in the presence of medications that interfere with the adrenergic support of the heart. New, accurate, noninvasive techniques can assess cardiac structural and functional aspects of hypertension under precise circumstances. CONCLUSIONS: Assessing both systolic and diastolic function is important in the follow-up of hypertensive patients and in the choice of therapy.     

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.     

Left ventricular geometric patterns and QT dispersion in untreated essential hypertension

The spectrum of left ventricular adaptation to hypertension, different types of hypertrophy patterns, and QT dispersion in different types of hypertrophy was investigated in 107 patients with untreated essential hypertension and 30 age- and gender-matched normal adults studied by 12-derivation electrocardiogram (ECG), two-dimensional, and M-mode echocardiography. Left ventricular mass (LVM), body mass index, total peripheral resistance (TPR), relative wall thickness (RWT), and QT dispersion were found to be statistically significantly higher in the hypertension group (P < .001 for all). Among hypertensive patients, 41.1% had both normal LVM and RWT, here called normal left ventricle in hypertension; 10.3% had concentric hypertrophy with increased LVM and RWT; 14.95% had eccentric hypertrophy with increased LVM and normal RWT; and 32.7% had concentric remodeling with normal LVM and increased RWT. Echocardiographically derived cardiac index was higher in the concentric hypertrophy and eccentric hypertrophy patterns (P = .002 and P < .0001, respectively), whereas TPR was higher in the concentric hypertrophy and concentric remodeling patterns (P = .017 and .02, respectively). QT dispersion values were found to be increased in the hypertensive group (P = .001), whereas similar values were calculated for different types of hypertrophy patterns. We conclude that the more common types of ventricular adaptation to essential hypertension are eccentric hypertrophy and concentric remodeling. Concentric hypertrophy is found to be associated with both volume and pressure overload, whereas eccentric hypertrophy is associated with volume overload only and concentric remodeling is associated with pressure overload. But different left ventricular geometric patterns seem to have similar effects on QT dispersion.     

Appearance of the interventricular septum in obstructive lesions of the left ventricular outflow tract

Measurements of the thickness of the septum were made in 26 cardiac specimens and in 13 patients. There were 10 normal specimens, five with aortic stenosis, two with asymmetric septal hypertrophy, four with hypertensive cardiovascular disease, and five with idiopathic cardiomyopathy. Patient measurements were obtained by visualizing the septum during simultaneous left and right ventriculography on angiograms obtained in the left anterior oblique projection. Four patients were normal, five had aortic stenosis, and four had a symmetric septal hypertrophy. Measurements derived from normal cardiac specimens and angiographic appearance suggested that the normal septum is a smooth-walled structure with right and left ventricular surfaces parallel, diverging only slightly at the apex of the ventricle. In aortic stenosis and idiopathic cardiomyopathy, the septum tends to be biconvex with maximal thickening in its middle third. Hypertensive cardiovascular disease produces uniform septal thickening, resembling an exaggeration of normal. However, in asymmetric septal hypertrophy no consistent patterns of hypertrophy or septal thickening are evident; bulging can be present at any point along the left ventricular surface of the septum.     

Surgical repair of fecal incontinence. Correlation of sonographic anal sphincter integrity with subjective cure

We examined the relationship between left ventricular hypertrophy (LVH) and renal and retinal damage in 174 untreated patients with essential hypertension. As an index of renal and retinal damage, we examined proteinuria and retinal vascular change. LVH was diagnosed according to left ventricular mass obtained from echocardiography. Of the hypertensive patients, 111 patients (64%) had LVH. The incidences of proteinuria and advanced retinal vascular change were higher in patients with LVH than in those without LVH. In a multiple regression model, there was a significant positive correlation between left ventricular mass and proteinuria, as well as diastolic blood pressure, sex, age and body mass index. In conclusion, proteinuria is related to elevated left ventricular mass in patients with essential hypertension.     

Exercise renography in untreated subjects with essential hypertension

Exercise induced renal dysfunction is reported to occur in treated hypertensive patients but not seen normotensive subjects. It is unclear if this phenomenon is related to the disease or to treatment. METHODS: Four normal volunteers and 15 hypertensive subjects (antihypertensive medications were discontinued for more than 4 wk) were studied with upright radionuclide renography at rest and during bicycle exercise. The amount of exercise was sufficient to increase the heart rate at least 20 bpm above the resting value. All subjects were healthy, without evidence of left ventricular hypertrophy renal disease or hypertensive retinal disease. BUN, serum creatinine concentration and urinalysis were normal in all subjects. Renograms were performed for 12-15 min after injection of either 1 mCi[123]orthoidohippurate (OIH) or 2-7 mCi 99mTc-mercaptoacetyltriglycine (MAG3). Visual analysis and mean transit time calculation were performed on the rest and exercise studies. RESULTS: Seven of 14 hypertensive subjects and none of the normal volunteers demonstrated abnormal prolongation in renal transit during exercise which was not seen on the resting renogram. Four of these seven subjects had a history of hypertension for 2 yr or less. CONCLUSION: About 50% of individuals with mild-to-moderate hypertension and normal renal function may have abnormal renal transit of renal excretion agents during exercise, although their baseline studies are normal. This finding is unassociated with therapy and appears to be related directly to the pathophysiology of essential hypertension.     

Angiotensin converting enzyme gene I/D polymorphism in essential hypertension and nephroangiosclerosis

An insertion/deletion (I/D) polymorphism of the angiotensin converting enzyme (ACE) gene significantly influences circulating ACE levels and plays a role in the development of target organ damage, that is, left ventricular hypertrophy in essential hypertension (EH), and microalbuminuria in diabetes mellitus. We have examined the role of the I/D polymorphism in essential hypertensive patients with renal involvement. The study was divided in two independent protocols. In protocol 1, we retrospectively analyzed the ACE genotypes in 37 essential hypertensive patients with a clinical and histopathological diagnosis of nephroangiosclerosis. In protocol 2, ACE genotypes as well as microalbuminuria and renal hemodynamic parameters were investigated in 75 patients with EH with normal renal function and a strong family history of hypertension. As control group, 75 healthy subjects with BP < 130/85 mm Hg and no family history of cardiovascular diseases were studied. The ACE variants were determined by PCR and the genotypes were classified as DD, DI and II. In protocol 1, patients with nephroangiosclerosis displayed a significant difference in the genotype distribution (57% DD, 27% DI, 16% II) when compared to the control population (25% DD, 64% DI, 11% II; P < 0.001). There was no significant difference in genotype distribution between hypertensive patients with normal renal function (protocol 2; 33% DD, 59% DI, 8% II) and the control group. There were no differences in age, blood pressure, microalbuminuria and duration of the disease among the three genotypes in the EH group from protocol 2. Taken together, these findings suggest that the DD genotype of ACE is associated with histopathologic-proven kidney involvement in patients with EH and that this polymorphism could be a potential genetic marker in hypertensives at risk of renal complications.     

Magnito-, electro- and echocardiography in detecting symptoms of the "hypertensive heart"

The study compared diagnostic potential of magnetocardiography (MCG), electrocardiography (ECG) and echocardiography (echo-CG) in 18 patients with arterial hypertension (AH). 32 healthy males served as control. Elements of MCG from normal subjects have been analyzed morphologically in 36 points of precordial leads. Left ventricular hypertrophy was registered at echo-CG, MCG, ECG in 11 (61%), 16 (84%) and 7 (34%) of the AH patients, respectively. Left atrial hypertrophy was discovered primarily by echo-CG and MCG. Defects in ventricular repolarization were recorded by MCg in 7 (39%) patients basing on MCG, echo-CG and rarely ECG signs of left ventricular hypertrophy. MCG is recommended as an effective tool in diagnosis of "hypertensive heart".     

Direct evidence of impaired cardiac sympathetic innervation in essential hypertensive patients with left ventricular hypertrophy

Increased sympathetic nervous activity has been proposed as one of the causes of left ventricular hypertrophy (LVH) associated with hypertension. However, the precise relationship is not fully understood. METHODS: To elucidate the relationship between myocardial sympathetic nervous activity and LVH in patients with essential hypertension EHT), we performed 123I-metaiodobenzylguanidine (MIBG) myocardial scintigraphy in 49 patients with EHT and 17 normotensive control subjects. Sympathetic innervation of the left ventricle was evaluated using SPECT, and the whole heart uptake of the tracer was quantitatively assessed as the heart-to-mediastinum uptake ratio on both the early (15-min) and delayed (5-hr) images. Myocardial washout rate (MWR) of the tracer from 15 min to 5 hr after the isotope administration was also calculated. The left ventricular mass index (LVMI) was determined echocardiographically. RESULTS: In 49 hypertensive patients, there was a negative correlation between LVMI and heart-to-mediastinum uptake ratio on both the early and delayed images (r=-0.55, p < 0.0001; r=-0.63, p < 0.0001, respectively). In addition, there was a positive correlation between the LVMI and MWR of 123I-MIBG in these hypertensive patients (r=0.59, p < 0.0001). As for the regional uptake of the tracer, there was no significant difference between control subjects and hypertensive patients without cardiac hypertrophy, but a significant decrease of the uptake in the inferior and lateral regions was observed in hypertensive patients with cardiac hypertrophy. CONCLUSION: Patients with EHT had decreased accumulation and increased MWR of 123I-MIBG in proportion to the degree of LVH. Hypertensive patients with cardiac hypertrophy had impaired sympathetic innervation in the inferior and lateral regions of the left ventricle.     

Cruciferous vegetables in relation to renal cell carcinoma

In the general population and in patients with essential hypertension the presence of left ventricular hypertrophy is a powerful predictor of cardiovascular events, independent of blood pressure and other cardiovascular risk factors. The prevalence of left ventricular hypertrophy increases with age and with the severity of renal impairment. Left ventricular hypertrophy is also a sensitive indicator of vascular structural changes in both large and small arteries. The possibility of reversing left ventricular hypertrophy therefore represents a major therapeutic goal for the treatment of hypertensive patients. Several studies examining the characteristics of left ventricular hypertrophy in the elderly, the interrelations between cardiac and vascular hypertrophy, the possibility of reversing left ventricular hypertrophy and its consequent prognostic value will be reported and commented on in the present review.     

Aging and regression of cardiac hypertrophy in the hypertensive patient

OBJECTIVE: This study was aimed at determining factors acting on the regression of left ventricular hypertrophy due to essential hypertension. METHODS: It was a non-randomized, echocardiographic study of 60 previously untreated hypertensive subjects (20 to 75 years of age). RESULTS: Following a 5-year therapy, the decrease in the left ventricular mass was 14%. Normalization of blood pressure and reversal of left ventricular hypertrophy were obtained in 50% and 58% of patients, respectively. Patients of the non-responder group (non-response being defined as a less than 10% decrease in the left ventricular mass) were older and had a longer history of high blood pressure. A positive correlation was observed between age and decrease in the left ventricular mass, the latter being less marked in older patients. Antihypertensive drugs classes had no influence on reversal of left ventricular hypertrophy. CONCLUSION: Ageing may be a factor of resistance to the decrease in left ventricular mass with therapy. These results suggest that early screening and management of hypertension are essential.     

Glucose intolerance exaggerates left ventricular hypertrophy and dysfunction in essential hypertension

The influence of glucose intolerance, the preclinical stage of diabetes mellitus, on the progression of left ventricular hypertrophy and left ventricular dysfunction in essential hypertension, was assessed with two-dimensional M-mode echocardiography in age- and sex-matched essential hypertensive patients with (n = 28) or without (n = 44) glucose intolerance, and normotensive control subjects (n = 29). Left ventricular mass index in hypertensive patients with glucose intolerance was significantly higher than that in hypertensive patients without glucose intolerance (mean +/- SD, 115.6 +/- 28.2 v 102.1 +/- 22.1 g/m2; P < .05). Left ventricular diastolic function as reflected by peak lengthening rate was reduced in glucose-intolerant hypertensive patients than in hypertensive patients without glucose intolerance (2.68 +/- 0.71 v 3.16 +/- 0.82/sec; P < .05). End-systolic wall stress/left ventricular end-systolic volume index, an index of left ventricular contractility, was reduced more in glucose-intolerant hypertensive patients than in hypertensive patients without glucose intolerance (2.75 +/- 0.55 v 3.13 +/- 0.55 10(3) dyn.m2/cm2.mL-1; P < .01). These findings suggest that glucose intolerance accelerates progression of left ventricular hypertrophy and deteriorates left ventricular diastolic function and contractility in essential hypertension.     

Changes in left ventricular structure and function in patients with white coat hypertension: cross sectional survey

OBJECTIVES: To assess the relation between white coat hypertension and alterations of left ventricular structure and function. DESIGN: Cross sectional survey. SETTING: Augsburg, Germany. SUBJECTS: 1677 subjects, aged 25 to 74 years, who participated in an echocardiographic substudy of the monitoring of trends and determinants in cardiovascular disease Augsburg study during 1994-5. OUTCOME MEASURES: Blood pressure measurements and M mode, two dimensional, and Doppler echocardiography. After at least 30 minutes' rest blood pressure was measured three times by a technician, and once by a physician after echocardiography. Subjects were classified as normotensive (technician <140/90 mm Hg, physician <160/95 mm Hg; n=849), white coat hypertensive (technician <140/90 mm Hg, physician >=160/95 mm Hg; n=160), mildly hypertensive (technician >=140/90 mm Hg, physician <160/95 mm Hg; n=129), and sustained hypertensive (taking antihypertensive drugs or blood pressure measured by a technician >=140/90 mm Hg, and physician >=160/95 mm Hg; n=538). RESULTS: White coat hypertension was more common in men than women (10.9% versus 8.2% respectively) and positively related to age and body mass index. After adjustment for these variables, white coat hypertension was associated with an increase in left ventricular mass and an increased prevalence of left ventricular hypertrophy (odds ratio 1.9, 95% confidence interval 1.2 to 3.2; P=0.009) compared with normotensive patients. The increase in left ventricular mass was secondary to significantly increased septal and posterior wall thicknesses whereas end diastolic diameters were similar in both groups with white coat hypertension or normotension. Additionally, the systolic white coat effect (difference between blood pressures recorded by a technician and physician) was associated with increased left ventricular mass and increased prevalence of left ventricular hypertrophy (P<0.05 each). Values for systolic left ventricular function (M mode fractional shortening) were above normal in subjects with white coat hypertension whereas diastolic filling and left atrial size were similar to those in normotension. CONCLUSION: About 10% of the general population show exaggerated inotropic and blood pressure responses when mildly stressed. This is associated with an increased risk of left ventricular hypertrophy.     

Parallel increase in carotid, brachial and left ventricular cross-sectional areas in arterial hypertension

Few data have been published about the relation between the vessels geometry and development of left ventricular (LV) hypertrophy in patients with arterial hypertension. The aim of this study is to describe arterial and LV geometry changes due to mild-to-moderate arterial hypertension in an untreated hypertensive population. In 95 untreated patients with mild-to-moderate hypertension and 23 age- and sex-matched healthy normotensives, we measured the end-diastolic diameter and wall thickness of the left ventricle and the internal diameter and intimal-medial thickness (IMT) of carotid and brachial arteries. From these data, the cross-sectional areas (CSAs) of arterial and myocardial walls were calculated. Hypertensive patients were further subdivided on the basis of the presence of LV hypertrophy defined according to Devereux et al as anatomical LV mass >125 g/m. In hypertensive patients with hypertrophy, carotid and brachial CSAs increased, without significant changes in thickness/diameter ratio (arterial 'enlargement'), while the left ventricle developed 'concentric' hypertrophy. Arterial and LV CSAs showed a significant direct correlation with systolic blood pressure (BP). However, when data were corrected for BP, the correlation between the increase in arterial and LV CSAs became much improved than for the raw data. In conclusion patients with untreated mild-to-moderate hypertension, both carotid and brachial arterial walls showed an enlargement that was proportional to the development of LV hypertrophy. These results suggest that the effects of arterial hypertension on carotid, brachial and LV wall geometry have a common modulation.     

Relation of endothelium, thrombogenesis, and hemorheology in systemic hypertension to ethnicity and left ventricular hypertrophy

Although the arterial tree is exposed to increased pressure in hypertensive patients, paradoxically, the complications of hypertension (heart attacks, stroke) are mainly thrombotic rather than hemorrhagic. Patients with left ventricular (LV) hypertrophy are at high risk of the complications of hypertension. We performed a cross-sectional study of 178 patients attending a hypertension clinic in a city center teaching hospital, and measured plasma levels of the soluble adhesion molecule P-selectin (associated with platelet activity/function and atherosclerosis), the von Willebrand factor (vWf; a marker of endothelial dysfunction), fibrin D-dimer (an index of thrombogenesis), plasminogen activator inhibitor (PAI, an index of fibrinolysis), lipoprotein(a) (Lp(a), associated with thrombogenesis and atherogenesis) and hemorheological indexes (fibrinogen, hematocrit, plasma viscosity, hemoglobin) in patients with essential hypertension, in whom the LV mass and LV mass index were determined using echocardiography. The 178 patients (86 men, mean age 54 +/- 15 years) were compared with 47 normotensive healthy controls (aged 56 +/- 20 years). Hypertensive patients had higher P-selectin, PAI, vWf, fibrin D-dimer, Lp(a), plasma fibrinogen, and plasma viscosity when compared with controls. Black hypertensive patients had higher Lp(a) levels and LV septal and posterior wall thickness on echocardiography, but lower plasma PAI levels. Patients with LV hypertrophy (defined as a LV mass index > 134 g/m2 in men or > 110 g/m2 in women) had higher plasma fibrinogen compared with those without LV hypertrophy. Systolic blood pressures were significantly correlated to age, plasma viscosity, plasma fibrinogen, and vWf. Diastolic blood pressures were significantly correlated with age and plasma fibrinogen. Fibrinogen levels were correlated with LV mass, LV mass index, left atrial size, plasma viscosity, and vWf. Fibrin D-dimer levels were significantly correlated with vWf and fibrinogen levels. Thus, hypertensive patients have high plasma fibrinogen levels, thrombogenesis, and impaired fibrinolysis (as indicated by high D-dimer and PAI levels, respectively), platelet activation (raised soluble P-selectin), and endothelial dysfunction (high vWF). The high plasma fibrinogen levels were related to blood pressures, LV mass index (and LV hypertrophy), and left atrial size. These abnormalities in hemorheologic factors and markers of thrombogenesis and endothelial function may act synergistically to increase the risk of thrombogenesis and atherosclerosis in hypertensive patients.     

Angiotensin receptors in cardiac and renal hypertrophy in rats

Angiotensin II mediates its effects through activation of specific angiotensin (AT) receptors which can be regulated during cardiovascular disease. This study has investigated whether an increased cardiac and renal AT receptor density is important in the development of left ventricular and renal hypertrophy in three rat models of hypertension [spontaneous hypertensive (SHR), deoxycorticosterone acetate (DOCA)-salt and 2K1C renal hypertensive rats]. Although all hypertensive rats developed left ventricular and renal hypertrophy, AT receptor density increased only in the left ventricle and kidney of SHR during the development of hypertension. Thus, cardiac and renal hypertrophy per se do not increase AT receptor density. AT receptors were increased in the liver of DOCA-salt rats, 2K1C rats and 52-week-old SHR and in adrenal glands of DOCA-salt rats and SHR. A plausible explanation for tissue-dependent AT receptor regulation involves tissue-selective control of local renin-angiotensin systems independent of circulating hormone levels, combined with disease-induced cell damage.     

Lectin histochemistry of fallopian tube epithelial cells. Relation to ovum transport and ovum pickup

BACKGROUND: This study was designed to investigate whether collagen type I degradation is altered in patients with essential hypertension and whether this alteration could be related to disturbances in the serum matrix metalloproteinase pathway of collagen degradation. A second aim of the study was to assess whether some relation exists between serum markers of collagen type I degradation and left ventricular hypertrophy in hypertensive patients. METHODS AND RESULTS: We measured serum concentrations of carboxy-terminal telopeptide of collagen type I (CITP) as a marker of extracellular collagen type I degradation, of total matrix metalloproteinase-1 (MMP-1), or collagenase, of total tissue inhibitor of metalloproteinases 1 (TIMP-1), and of MMP-1/TIMP-1 complex in 37 patients with never-treated essential hypertension and in 23 normotensive control subjects. Serum concentrations of free MMP-1 and free TIMP-1 were calculated by subtracting the values of MMP-1/TIMP-1 complex from the values of total MMP-1 and total TIMP-1, respectively. Measurements were repeated in 26 hypertensive patients after 1 year of treatment with the ACE inhibitor lisinopril. Baseline free MMP-1 was decreased (P<0.001) and baseline free TIMP-1 was increased (P<0.001) in hypertensives compared with normotensives. No significant differences were observed in the baseline values of CITP between the 2 groups of subjects. Hypertensive patients with baseline left ventricular hypertrophy exhibited lower values of free MMP-1 (P<0.01) and CITP (P<0.05) and higher (P<0.001) values of free TIMP-1 than hypertensive patients without baseline left ventricular hypertrophy. Treated patients attained an increase (P<0.001) in free MMP-1 and a decrease (P<0.05) in free TIMP-1. In addition, serum CITP was increased (P<0.05) in treated hypertensives compared with normotensive subjects. CONCLUSIONS: These findings suggest that systemic extracellular degradation of collagen type I is depressed in patients with essential hypertension and can be normalized by treatment with lisinopril. A depressed degradation of collagen type I may facilitate organ fibrosis in hypertensive patients, namely, in those with left ventricular hypertrophy.     

Continuous ambulatory measurement of blood pressure in children--personal experience

Ambulatory blood pressure monitoring (ABPM) during normal daily activities and during night, when the patient is asleep, is a new method of measuring blood pressure (BP) in children, used for better diagnosis and treatment of hypertension. Compared to casual BP measurements, it documents normal daily BP variations, BP during sleep, the influence of emotional and physical stress on BP and is a better predictor of hypertension associated with end-organ damage. However, the experience in ABPM in children is still limited. In our country ABPM has been used since recently, and first results are referred to children with end-stage renal failure. SUBJECTS AND METHODS: ABPM was performed in two groups of children: group A consisted of 61 children, aged 14.3 +/- 2.9 (mean +/- SD) yrs in whom intermittent outpatient BP measurements (for at least 3 months) suggested the diagnosis of hypertension (according to the data of Second Task Force); group B consisted of 52 patients (pts), aged 12.8 +/- 4.6 yr with renal disease. Four pts from group A (6.6%) and 20 pts from group B (38.5%) received antihypertensive therapy (captopril, nifedipine, furosemide and propranolol ). All children from group A and half of the children from group B had normal renal function. Eighteen pts from group B were on chronic haemodialysis (34.6%). Blood pressure was recorded during a 24-hour period except in haemodialyzed pts (48 h) (Table 1). Results of BP measurements are presented as the mean values of BP during a 24-hour period, during normal daily activities and during sleep. We used the age- and gender-appropriate 95th percentile from the Task Force Study as the daytime upper-limit of normal and 10% lower for the upper-limit at night. According to BP load (the percentage of BPs exceeding the upper limits of normal for age), children were assumed to have mild-to-moderate hypertension (BP load between 20% and 40%) or severe hypertension (BP load more than 40%). The success of antihypertensive therapy was evaluated after 1-3 months in 11 pts (twice in 10 pts and three times in one pt). RESULTS: In group A 39.4% of pts were normotensive and 36.1% were without antihypertensive therapy, 58.4% of normotensive and 40.5% of hypertensive pts had blunted circadian BP rhythm (nocturnal BP reduction of less than 10% of diurnal values) (Graph. 1). In group B 38.5% of pts were normotensive and 27% were without antihypertensive therapy. In the group of normotensive pts alteration of circadian BP rhythm was found in 40% of pts with normal renal function, 80% of pts with chronic renal failure and in 100% of pts with terminal renal failure, while in the hypertensive group, altered circadian BP rhythm had 68%, 100% and 92% of pts, respectively (Graph 2). Mild-to-moderate hypertension had 54% of hypertensive pts from group A and 37.5% of hypertensive pts from group B. Severe hypertension was more frequent in group B (62.5%) comparing to group A (46%). The effectiveness of antihypertensive therapy was assessed in 11 pts. In 69.2% of pts BP became normal or was significantly decreased, in 23.1% of pts BP was not changed and 7.7% of pts had higher values of BP. DISCUSSION: ABPM is very useful for diagnosing white coat hypertension. Like other authors, we have pointed out that more than one third of pts who were hypertensive according to usual BP measurements had normal 24-hour BP and we classified them as white coat hypertensives. More than a half of the pts had blunted circadian BP rhythm, and as it is not certain whether they will become hypertensive in adulthood they should be periodically controlled. There are several proofs that results of ABPM have a better correlation with hypertensive end-organ damage; therefore ABPM is used for assessing the severity of hypertension. In our former work, we showed excellent correlation of BP with left ventricular mass index in children with end-stage renal failure. (ABSTRACT TRUNCATED)     

HSP27 locus cosegregates with left ventricular mass independently of blood pressure

Left ventricular hypertrophy remains a significant clinical problem and a predictor of fatal outcome in hypertension. Blood pressure per se and environmental modifiers including stress affect cardiac mass. Heat shock proteins are involved in the stress response as well as in the regulation of cardiac growth and cytoprotection. The present study evaluates heat shock protein 27 as a locus marker or candidate gene of cardiac hypertrophy in hypertension. The spontaneously hypertensive rat allele of heat shock protein 27 was associated with about a 6% increase in relative left ventricular weight (P = .0112) in 30 recombinant inbred strains from crosses of Brown Norway and spontaneously hypertensive rats. In 336 F2 crosses of spontaneously hypertensive and Wistar-Kyoto rats, the hypertensive allele was dominant and cosegregated with a similar 6% increase in the ratio of left ventricular weight to body weight (P = .0058) in rats fed a normal salt diet, but its contribution to left ventricular weight decreased in rats kept on a high salt diet. The contribution of the heat shock protein 27 allele was independent of blood pressure. We suggest that heat shock protein 27 represents a candidate gene/locus marker of cardiac hypertrophy in hypertension.