Effect of surgical treatment on myocardial strain in patients with pheochromocytoma and paraganglioma: a mini-review and meta-analysis.

AIM: Information on systolic dysfunction, as assessed by left-ventricular (LV) mechanics, in patients with pheochromocytoma after surgical treatment is scanty. We performed a systematic meta-analysis of speckle tracking echocardiographic studies to provide an updated comprehensive information on this issue. METHODS: The PubMed, OVID-MEDLINE, and Cochrane library databases were analyzed to search for articles published from the inception up to May 31st 2021. Studies were identified using MeSH terms and crossing the following search items: "myocardial strain" "left ventricular mechanics", "speckle tracking echocardiography", "systolic dysfunction", "pheochromocytoma", and "paraganglioma". RESULTS: A total of 92 surgically treated patients with pheochromocytoma/paraganglioma were included in 3 longitudinal studies. Successful surgical treatment was associated with a decrease in relative wall thickness (SMD - 0.25 ± 0.10, CI - 0.45/- 0.05, p < 0.01) and an improvement in global longitudinal strain (SMD - 0.45 ± 0.10, CI - 0.66/- 0.24, p < 0.0001). The favorable effects of treatment on LV geometry and mechanics were not accompanied by significant changes in ejection fraction (SMD - 0.07 ± 0.10, CI - 0.27/0.12, p = 0.44). CONCLUSIONS: This meta-analysis adds a new piece of evidence, suggesting that surgical treatment of patients with pheochromocytoma impacts favorably on LV geometry and LV mechanics, and, more importantly, the assessment of LV changes in this setting can no longer rely on conventional echocardiographic parameters such as ejection fraction.

Metabolic syndrome and biventricular hypertrophy in essential hypertension.

The metabolic syndrome (MS) is associated with structural and functional alterations of the left ventricle (LV); no evidence is available on the impact of the MS on the right ventricle (RV). To assess whether MS, as defined by the ATP III report, is associated with biventricular hypertrophy, a total of 286 hypertensive subjects (mean age 58.7+/-12.2 years) attending our outpatient clinic underwent the following procedures: (1) physical examination and standard clinic blood pressure (BP) measurement; (2) routine laboratory investigations; (3) M-mode, two-dimensional and Doppler echocardiography. LV hypertrophy (LVH) was defined by LM mass index>or=51/47 g m(-2.7) in men and women, respectively. Right-sided chambers were measured in parasternal long axis at the outflow tract and subcostal view; RV hypertrophy (RVH) was defined by anterior RV wall thickness>or=6.0/5.5 mm in men and women, respectively. Filling velocities of both ventricles were assessed by pulsed Doppler echocardiography. Structural cardiac alterations were more pronounced in hypertensive men and women with MS than in their non-MS counterparts and involved both ventricles as shown by the differences in continuous variables as well as in prevalence rates of LVH (58 and 48% vs 28 and 30%, respectively, P<0.01) and RVH (48 and 54% vs 25 and 35%, respectively, P<0.01). Both LV and RV filling in MS hypertensives were more dependent on the atrial systole. Our study shows that in human hypertension, structural and functional cardiac changes induced by MS are not limited to the LV but also involve the right one.

Prevalence and correlates of multiple organ damage in referred treated hypertensives: data from the ETODH study.

This study, carried out in a large cohort of treated essential hypertensives attending an out-patient hospital hypertension clinic, extends previous observations by showing that a clustering of two or three markers of organ damage (OD) has a higher prevalence than a single organ involvement. These findings call for a systematic evaluation of cardiac and extracardiac OD in treated hypertensive patients referred to a specialist setting.

Ambulatory heart rate and target organ damage in never-treated essential hypertensives.

Limited evidence is available about the relationship between ambulatory heart rate (HR) and target organ damage (TOD) in uncomplicated hypertension. We sought to investigate the association between ambulatory HR and subclinical cardiac, vascular and renal markers of TOD in never-treated essential hypertensives. A total of 580 subjects with recently diagnosed (

Ambulatory blood pressure, target organ damage and aortic root size in never-treated essential hypertensive patients.

The relationship between ambulatory blood pressure (ABP), target organ damage (TOD) and aortic root (AR) size in human hypertension has not been fully explored to date. We investigated the relationship between ABP, different markers of TOD and AR size in never-treated essential hypertensive patients. A total of 519 grade 1 and 2 hypertensive patients (mean age 46+/-12 years) referred for the first time to our outpatient clinic underwent the following procedures: (1) routine examination, (2) 24 h urine collection for microalbuminuria (MA), (3) ambulatory blood pressure monitoring over two 24 h periods within 4 weeks, (4) echocardiography and (5) carotid ultrasonography. AR dilatation was defined by sex-specific criteria (> or =40 mm in men and > or =37 mm in women). AR diameter was increased in 3.7% of patients. Demographic variables (body mass index, age and male gender), average night-time diastolic blood pressure (BP) (but not clinic or average 48 h BP), left ventricular mass index and carotid intima-media (IM) thickness showed an independent association with AR size in both univariate and multivariate analyses. When TOD data were analysed in a categorical way, a stepwise increase in the prevalence of left ventricular hypertrophy (LVH) (I=17.5%, II=27.6%, III=35.8%) and carotid IM thickening (I=20.9%, II=28.8%, III=34.4%), but not in MA (I=6.8%, II=9.1%, III=8.7%) was found with the progression of AR size tertiles. Our results show that (1) AR enlargement in uncomplicated never-treated hypertensive patients has a markedly lower prevalence than traditional markers of cardiac and extracardiac TOD; (2) night-time BP, LVH and carotid IM thickening are independent predictors of AR dimension.

Midwall mechanics are improved after regression of hypertensive left ventricular hypertrophy and normalization of chamber geometry.

BACKGROUND: It is still unclear whether substantial regression of hypertensive left ventricular hypertrophy (LVH) and normalization of chamber geometry are associated with improved left ventricular (LV) myocardial function. METHODS AND RESULTS: Midwall mechanics were evaluated in 152 patients undergoing 1 year of effective antihypertensive treatment. Two-dimensionally directed M-mode echocardiography was performed as follows: (1) after a 4-week placebo "run-in" period, (2) after 1 year of treatment with 20 mg/d lisinopril (alone or associated with 12.5 to 25 mg/d hydrochlorothiazide), and (3) after a final 1-month placebo period to allow blood pressure (24-hour average ambulatory monitoring) to return to pretreatment levels. Treatment-induced reductions in blood pressure (from 149+/-16/95+/-11 to 131+/-12/83+/-10 mm Hg, P:<0.05) and circumferential end-systolic wall stress (from 84+/-22 to 72+/-19 g/cm(2), P:<0.05) were associated with a marked reduction in LV mass index (from 159+/-30 to 133+/-26 g/m(2), P:<0.05). LVH regression was accompanied by an increase in midwall fractional shortening (from 19.7+/-2.7% to 20.9+/-2.7%, P:<0.05) and by a decrease in relative wall thickness (from 48.2+/-7.7% to 44.1+/-6.7%, P:<0.05). The improvement in midwall function associated with afterload reduction and substantial LVH regression persisted after antihypertensive therapy withdrawal and restoration of the hypertensive state. Despite a significant increase in end-systolic wall stress, further LV chamber remodeling did not occur. The preservation of relative wall thickness was associated with a persistent improvement in midwall systolic function. CONCLUSIONS: Regression of concentric LVH is associated with an improvement of midwall systolic function, which is more dependent on the normalization of LV geometry than on the reduction in LV systolic stress.

Isolated ambulatory hypertension and changes in target organ damage in treated hypertensive patients.

Isolated ambulatory hypertension is a condition characterized by elevated ambulatory but normal clinic blood pressure (BP), and has been reported to be associated with increased cardiovascular risk in untreated subjects. However, little is known about the relationship between this condition and intermediate end points such as target organ damage (TOD) in treated hypertensives. We investigated the impact of isolated ambulatory hypertension on left ventricular hypertrophy (LVH) and microalbuminuria (MA) in a selected sample of treated nondiabetic hypertensives with effective and prolonged clinic BP control (BP<140/90 mmHg). Clinic BP measurements, routine diagnostic procedures, echocardiography and 24-h urine collection for MA, were undertaken in 80 patients (mean age 53+/-8 years) with essential hypertension attending our hospital outpatient centre at baseline and after an average follow-up of 30 months. At follow-up evaluation BP status was assessed by self-measurement of BP and ambulatory BP monitoring (ABPM). At the follow-up visit, 51 out of 80 patients (63.7%) reached a BP control according to ABP (average daytime BP<132/85 mmHg) criteria (group I) whereas the remaining 29 did not (group II); home BP was controlled (BP<135/85 mmHg) in all members of group I and in 86% of group II. In the overall study population, mean Sokolow voltage, LV mass index (LVMI) and urinary albumin excretion (UAE) decreased compared to baseline from 24.1+/-5.0 to 18.9+/-5.1 mm (P<0.05), 115.6+/-24.1 to 97.7+/-21.6 g/m(2) (P<0.01), 11.8+/-23.7 to 5.8+/-14.9 mg/24 h (P<0.05), respectively. The prevalence of ECG LVH, altered LV patterns and MA fell from 7.5 to 2.5% (P=NS), from 45 to 25 (P<0.01) and from 13.7 to 5.1% (P<0.05), respectively. However, when data were analysed separately for the two groups a significant decrease of echo LVH and MA was found only in patients with controlled ABP. LVMI and MA decreased from 117.1+/-23.1 to 95.9+/-22.1 g/m(2) (P<0.01) and 12.8+/-24.7 to 4.1+/-5.7 mg/24 h (P<0.05) in group I, and from 114.1+/-24.8 to 102.3+/-20.3 (P=NS) and 11.9+/-22.1 to 6.3+/-18.1 mg/24 h (P=NS) in group II. In conclusion, in the present study isolated ambulatory hypertension in treated patients is associated with a lack of regression in cardiac and extracardiac TOD, suggesting that a tight BP control throughout the 24 h plays a key role in lowering hypertension-induced structural and functional alterations at cardiac and renal level.

Cardiopulmonary receptor modulation of plasma renin activity in normotensive and hypertensive subjects.

Cardiopulmonary receptors modulate renin release in several animals species. However, their involvement in reflex control of this humoral substance in humans is controversial. Furthermore, no information is available on the alteration of this control in hypertension. We studied the modulation of plasma renin activity (radioimmunoassay) in 12 normotensive subjects and in 12 age-matched subjects with untreated hypertension of mild or moderate degree. Cardiopulmonary receptors were stimulated by increasing central venous pressure (right atrial catheter) and cardiac volume (echocardiographic measurement) through passive leg raising and deactivated by reducing central venous pressure and cardiac volume through lower body negative pressure. The stimuli were maintained for 20 to 30 minutes, and their degree was set to avoid changes in blood pressure (indirect or direct measurements) and heart rate, thus avoiding involvement of arterial baroreceptors. In normotensive subjects, deactivation of cardiopulmonary receptors induced a progressive rise in plasma renin activity and stimulation of cardiopulmonary receptors induced a progressive fall. The reflex gain (ratio between plasma renin activity and central venous pressure or cardiac volume changes) was similar for deactivation and stimulation. During cardiopulmonary receptor deactivation, the gain corresponded to that obtained by dividing the increase in plasma renin by the reduction in central venous pressure induced by tilting. Cardiopulmonary receptor deactivation and stimulation also induced clear-cut changes in plasma renin activity in hypertensive subjects, but the percent magnitude of the reflex plasma renin activity excursion was less than that in normotensive subjects. These observations indicate that cardiopulmonary receptors modulate plasma renin activity in humans.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiopulmonary reflex before and after regression of left ventricular hypertrophy in essential hypertension.

Studies that have examined the cardiopulmonary receptor control of circulation in hypertension have produced conflicting results. In 10 normotensive subjects and in age-matched essential hypertensive subjects without (n = 10) or with left ventricular hypertrophy (n = 12), as well as in seven subjects of the latter group restudied after 1 year of treatment that induced regression of cardiac hypertrophy, we examined the cardiopulmonary reflex by increasing central venous pressure and stimulating cardiopulmonary receptors through passive leg raising and by reducing central venous pressure and deactivating cardiopulmonary receptors through nonhypotensive lower body negative pressure. Reflex responses were measured as changes in forearm vascular resistance (mean blood pressure divided by plethysmographically measured blood flow), plasma norepinephrine concentration, and plasma renin activity. In hypertensive subjects without left ventricular hypertrophy, stimulation and deactivation of cardiopulmonary receptors caused changes in forearm vascular resistance, norepinephrine concentration, and plasma renin activity that were modestly reduced as compared with those in normotensive subjects. However, all these changes were markedly reduced in hypertensive subjects with left ventricular hypertrophy. Following regression of left ventricular hypertrophy, the changes in vascular resistance, plasma norepinephrine, and plasma renin activity induced by cardiopulmonary receptor manipulation all improved markedly. These results demonstrate that cardiopulmonary receptor regulation of peripheral vascular resistance and of neurohumoral variables is impaired in essential hypertension and that the impairment is much more pronounced when this condition is associated with cardiac structural alterations. Therapeutic regression of these alterations, however, leads to a marked improvement of this reflex, with consequent favorable effects on circulatory homeostasis.

Effects of amlodipine on sympathetic nerve traffic and baroreflex control of circulation in heart failure.

Short-acting calcium antagonists exert a sympathoexcitation that in heart failure further enhances an already elevated sympathetic activity. Whether this is also the case for long-acting formulations is not yet established, despite the prognostic importance of sympathetic activation in heart failure. It is also undetermined whether in this condition long-acting calcium antagonists favorably affect a mechanism potentially responsible for the sympathetic activation, ie, the baroreflex impairment. In 28 heart failure patients (NYHA functional class II) under conventional treatment we measured plasma norepinephrine and efferent postganglionic muscle sympathetic nerve activity (microneurography) at rest and during arterial baroreceptor stimulation and deactivation induced by stepwise intravenous infusions of phenylephrine and nitroprusside, respectively. Measurements were performed at baseline and after 8 weeks of daily oral amlodipine administration (10 mg/d, 14 patients) or before and after an 8-week period without calcium antagonist administration (14 patients). Amlodipine caused a small and insignificant blood pressure reduction. Heart rate, left ventricular ejection fraction, and plasma renin and aldosterone concentrations were not affected. This was the case also for plasma norepinephrine (from 2.43+/-0.41 to 2.50+/-0.34 nmol/L, mean+/-SEM), muscle sympathetic nerve activity (from 54.4+/-5.9 to 51.0+/-4.3 bursts/min), and arterial baroreflex responses. No change in the above-mentioned variables was seen in the control group. Thus, in mild heart failure amlodipine treatment does not adversely affect sympathetic activity and baroreflex control of the heart and sympathetic tone. This implies that in this condition long-acting calcium antagonists can be administered without untoward neurohumoral effects anytime conventional treatment needs to be complemented by drugs causing additional vasodilatation.

Reflex vasopressin and renin modulation by cardiac receptors in humans.

Animal studies have shown that vasopressin secretion is modulated by arterial baroreceptors and cardiopulmonary volume receptors. Whether this is the case also in humans is controversial, however. To determine whether vasopressin is reflexly modulated by cardiac volume receptors, we studied the effect on plasma vasopressin (venous blood, radioimmunoassay) of reducing venous return and left ventricular end-diastolic diameter (echocardiography) by producing a 20-minute lower body negative pressure in 14 healthy subjects (aged 49.3 +/- 3.8 years, mean +/- SEM). The data were compared with those of 14 age-matched heart-transplant recipients, i.e., subjects with cardiac denervation. In healthy subjects, lower body negative pressure at -15 mm Hg caused a modest reduction in left ventricular end-diastolic diameter (-5 +/- 3.4%) and no change in vasopressin, whereas lower body negative pressure at -37.5 mm Hg caused a more marked reduction in left ventricular end-diastolic diameter (-12 +/- 2.5%) and a small, variable, but overall statistically significant (p < 0.05) increase in vasopressin (+145 +/- 46%, p < 0.01). The left ventricular end-diastolic diameter changes induced by the two lower body negative pressure stimuli were similar in heart-transplant recipients, but the vasopressin increase seen with the lower body negative pressure at -37.5 mm Hg was abolished. The marked increase in plasma renin activity and forearm vascular resistance induced by lower body negative pressure in healthy subjects was also abolished or drastically attenuated in heart-transplant recipients.(ABSTRACT TRUNCATED AT 250 WORDS)

Early 24-hour blood pressure elevation in normotensive subjects with parental hypertension.

Subjects with a family history of parental hypertension are reported to have a slightly higher office blood pressure in the prehypertensive stage. Whether this reflects a hyperreactivity to blood pressure measurement or a more permanent blood pressure elevation, however, is not known. In the present study, blood pressure was measured in 15 normotensive subjects whose parents are both hypertensive (FH++), 15 normotensive subjects with one hypertensive parent (FH(+)-), and 15 normotensive subjects whose parents are not hypertensive (FH--); among the three groups, subjects were matched for age, sex, and body mass index. The measurements were made in the office during a variety of laboratory stressors and during a prolonged resting period, and for a 24-hour period (ambulatory blood pressure monitoring). Office blood pressure was higher in the FH++ group than in the FH-- group (p less than 0.05). The pressor responses to laboratory stressors were similar in the two groups, but the FH++ group had higher prolonged resting and 24-hour blood pressure than the FH-- group; the difference was always significant (p less than 0.05) for systolic blood pressure. The FH++ group also had a greater left ventricular mass index (on echocardiographic examination) than the FH-- group (p less than 0.01). The blood pressure values and echocardiographic values of the FH(+)- group tended to be between those of the other two groups. Thus, the higher blood pressure shown by individuals in the prehypertensive stage with a family history of parental hypertension does not reflect a hyperreactivity to stress but an early permanent blood pressure elevation.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiopulmonary receptor regulation of renin release.

Cardiopulmonary receptors have been shown to modulate renin release in animals. However, their involvement in reflex control of renin in humans has never been unequivocally established. This report reviews data on the effects on plasma renin activity of maneuvers (lower body negative pressure and passive leg raising) that reduce and increase central venous pressure and cardiac diameter without affecting blood pressure and heart rate, thereby deactivating and stimulating cardiopulmonary receptors with little or no involvement of the arterial baroreceptors. In normotensive subjects, reduction in central venous pressure was accompanied by an increase in plasma renin activity that was similar to the increase observed during tilt that reduced central venous pressure to a similar extent. Conversely, an increase in central venous pressure was accompanied by a reduction in plasma renin activity. The increase in plasma renin activity that followed the reduction in central venous pressure was drastically attenuated in four patients who had undergone cardiac transplantation, along with other reflex effects (changes in forearm vascular resistance and plasma norepinephrine) of cardiopulmonary receptor manipulations. There was a modest reduction in the overall reflex changes in plasma renin activity in patients with mild to moderate essential hypertension compared with normotensive subjects. However, patients with essential hypertension and cardiac hypertrophy showed marked attenuation of all reflex influences of the cardiopulmonary receptors. In five subjects, therapeutic regression of this structural alteration was associated with a clear improvement in the cardiopulmonary reflex. Thus, in humans, cardiopulmonary receptors exert an important reflex control of renin release. This control (which is due in part to receptors located in the cardiac walls) is moderately affected by a mild to moderate blood pressure elevation but is markedly impaired when the elevation produces structural alterations in the heart. Preliminary evidence, however, suggests that the cardiopulmonary reflex may be improved by a reduction in cardiac hypertrophy.

Prognostic value of 24-hour blood pressure variability.

OBJECTIVES: Evaluation of the prognostic value of 24-h blood pressure averages and 24-h blood pressure variability. DESIGN: After an initial thorough clinical and laboratory evaluation which included 24-h continuous ambulatory blood pressure monitoring, a group of hypertensive patients were re-examined after an average of 7.4 years. End-organ damage at the follow-up visit was related to different measures of blood pressure levels and variability obtained at the initial or the follow-up visit or both. METHODS: Seventy-three patients with essential hypertension of variable severity, in whom ambulatory blood pressure was monitored intra-arterially for 24 h (Oxford technique) were re-examined at a follow-up visit (including echocardiographic assessment of left ventricular mass index) 1-13 years later (mean 7.4 years). The severity of end-organ damage was quantified by a score and related to clinic blood pressure at follow-up and to (1) clinic blood pressure, (2) 24-h blood pressure mean, (3) 24-h short-term and long-term blood pressure variability, and (4) end-organ damage, all assessed at the initial visit (multiple regression analysis). RESULTS: The set of independent variables considered was significantly related to end-organ damage at follow-up (R = 0.51). The individual variables most important in determining end-organ damage at follow-up were clinic blood pressure at the follow-up visit (P < 0.01), the initial level of end-organ damage (P < 0.05) and long-term blood pressure variability (among half-hour standard deviation of 24-h mean blood pressure) at the initial evaluation (P < 0.05). The prognostic individual weight of the other haemodynamic parameters considered was less and not statistically significant. CONCLUSIONS: The results confirm that the level of blood pressure achieved by treatment and the degree of end-organ damage at the time of initial evaluation are important determinants of future end-organ damage related to hypertension. They also constitute the first longitudinal evidence that the cardiovascular complications of hypertension may depend on the degree of 24-h blood pressure variability.

Similarities and differences in structural and functional changes of left ventricle and carotid arteries in young borderline hypertensives and in athletes.

OBJECTIVE: To investigate the association between increased left ventricular mass and the intima-media thickening of carotid arteries in hypertensive patients and the simultaneous involvement of the heart and the conductance vessels by the hypertensive process. METHODS: Because no data are available concerning the ultrasonographic characteristics of large arteries in athletes with physiological increases in left ventricular mass, we measured the intima-media thickness (IMT) of the common carotid artery (CCA) in 14 normotensive subjects (group I, aged 22 +/- 4 years), in 14 borderline hypertensives (group II, aged 24 +/- 6 years) and in 14 Japanese wrestling players (group III, aged 23 +/- 4 years). The IMT of the posterior wall of the CCA was measured at 5, 10 and 20mm caudally to the bifurcation and the measurements were averaged. Left ventricular diameters and thicknesses of the interventricular septum and posterior wall were obtained from two-dimensionally guided M-mode tracings and measured according to the Penn convention. Left ventricular mass was calculated by the formula of Devereux. Left ventricular filling was measured by a pulsed Doppler technique. RESULTS: Both systolic and diastolic blood pressure values were significantly higher in group II (145 +/- 7/91 +/- 5 mmHg) than they were in group I (116 +/- 11/75 +/- 5 mmHg) and in group III (120 +/- 8/78 +/- 6 mmHg). In athletes and hypertensives both the left ventricular mass index and the IMT of the CCA were significantly greater than they were in control subjects (80 +/- 12 g/m2 and 0.45 +/- 0.05 mm in group I; 106 +/- 15 g/m2 and 0.57 +/- 0.08 mm in group II; and 122 +/- 17 g/m2 and 0.55 +/- 0.05 mm in group III). The mitral early:late peak flow velocity ratio was significantly lower in group II (1.9 +/- 0.58) than it was in the other two groups (2.3 +/- 0.66 in group I and 2.6 +/- 0.64 in group III). CONCLUSIONS: The results of our study suggest that both hypertension and physical training can induce parallel changes in cardiac and in arterial walls, and that physiological left ventricular hypertrophy in athletes is accompanied by a normal diastolic filling pattern in contrast to the pathological pattern found in hypertensives. Further investigation is required to explore possible differences in carotid structure and function between these two conditions.

Cardiac and carotid structure in patients with established hypertension and white-coat hypertension.

AIM: The introduction of ambulatory blood pressure monitoring in the clinical practice has defined a new subgroup of hypertensive patients called white-coat hypertensives. It has been reported that white-coat hypertensives have less cardiac involvement than established hypertensive patients. This study was designed to examine the extent of cardiac and vascular involvement in patients with white-coat hypertension and established hypertension. PATIENTS AND METHODS: We studied 82 patients with mild essential hypertension, never previously treated, using 24-h ambulatory blood pressure monitoring and an echocardiographic and vascular ultrasonographic study. Left ventricular dimensions and mass were obtained according to the Penn convention. The intima-media thickness of the posterior wall of both common carotid arteries was measured 5, 10 and 20 mm caudally to the flow-divider and the average value was used for analysis. RESULTS: Of the 82 patients, 31 (mean +/- SD age 35 +/- 10 years) had average 24-h systolic/diastolic blood pressure values of below 132/85 mmHg (white-coat hypertensives) and 51 (aged 42 +/- 2 years) had a consistently elevated diastolic blood pressure. Both groups had similar body surface area (1.82 +/- 0.22 versus 1.81 +/- 0.22 m2), sex distribution (20 males and 11 females versus 32 males and 19 females), duration of hypertension, metabolic parameters and smoking habit. The 24-h ambulatory blood pressure monitoring values were, by definition, significantly higher in established hypertensives than in white-coat hypertensives (142 +/- 10/94 +/- 6 versus 127 +/- 6/79 +/- 4 mmHg, P<0.001). The left ventricular mass index and intima-media thickness were significantly higher in the established hypertensives (112 +/- 17 g/m2, 0.67 +/- 0.11 mm, respectively) than in the white-coat hypertensives (98 +/- 18 g/m2, 0.58 +/- 0.09 mm; P<0.001 for both). CONCLUSIONS: The prevalence of left ventricular hypertrophy and cardiac remodeling was significantly more frequent in established hypertensives (51%) compared to white-coat hypertensives (19%). These confirm that structural changes in the left ventricle in white-coat hypertensives are more limited than in established hypertensives and show that in white-coat hypertensives there is significantly less involvement of the conductance vessels than in established hypertensives.

Left ventricular concentric remodelling and carotid structural changes in essential hypertension.

AIM: Left ventricular concentric remodelling defines a modified left ventricular geometry in the presence of a normal left ventricular mass; it is an early and frequent adaptation in arterial hypertension. The present study was designed to evaluate the extent of carotid structural changes in essential hypertensives with left ventricular remodelling. PATIENTS AND METHODS: Two groups of hypertensive patients, who had never previously received anti-hypertensive treatment, 14 with left ventricular concentric remodelling (group I, relative wall thickness 0.48 +/- 0.02) and 48 with normal left ventricular geometry (group II, relative wall thickness 0.37 +/- 0.04) underwent clinical and laboratory examination, echocardiography, carotid artery ultrasonography and 24 h ambulatory blood pressure monitoring (ABPM). The left ventricular dimensions and mass were obtained according to the Penn convention. The intima-media thickness (IMT) of the posterior wall of both common carotid arteries was measured 5, 10 and 20 mm caudally to the bulb and the average value was used for analysis. RESULTS: In both groups age (group I 44 +/- 9 years; group II 40 +/- 9 years), body surface area (group I 1.85 +/- 0.2 m2; group II 1.80 +/- 0.2 m2), duration of hypertension (group I 4.4 +/- 4; group II 3.8 +/- 3.9 years), metabolic parameters and smoking habits were similar. Both clinic and 24 h ABPM values were higher in group I (clinic 157 +/- 12/102 +/- 5; 24 h ABPM 145 +/- 10/95 +/- 7 mmHg) than they were in group II (clinic 146 +/- 11/97 +/- 5; 24 h ABPM = 134 +/- 10/87 +/- 8 mmHg, P < 0.01). The left ventricular mass index (LVMI) and IMT were found to be slightly but significantly greater in group I than they were in group II (LVMI 106 +/- 7 versus 98 +/- 12 g/m2, P < 0.05; IMT 0.68 +/- 0.13 versus 0.61 +/- 0.10 mm, P < 0.05). A significant correlation was found between LVMI and common carotid IMT in the whole group of hypertensive patients (r = 0.43, P < 0.01). CONCLUSIONS: Our results indicate that left ventricular concentric remodelling does not represent the only early cardiovascular change in arterial hypertension but rather is associated often with carotid intima-media thickening.

Reproducibility and clinical value of nocturnal hypotension: prospective evidence from the SAMPLE study. Study on Ambulatory Monitoring of Pressure and Lisinopril Evaluation.

OBJECTIVE: To assess whether modifications in the nighttime blood pressure fall caused by antihypertensive treatment predict the regression of end-organ damage of hypertension. METHODS: The analysis was performed in patients with essential hypertension and echocardiographically detected left ventricular hypertrophy involved in the SAMPLE study. For each patient, ambulatory blood pressure monitoring and echocardiographic determination of left ventricular mass index were performed at the end of a 4-week wash-out pretreatment period, after 3 and 12 months of treatment with lisinopril or with lisinopril plus hydrochlorothiazide and after a final 4-week placebo period. For each ambulatory blood pressure monitoring the 24 h average, daytime average (0600-2400 h), night-time average (2400-0600 h) and day-night difference was computed. The percentages of dipper and non-dipper patients (i.e. the patients with night blood pressure falls greater and less than 10% of the daytime average, respectively) were also computed. RESULTS: The reproducibility of the day-night difference was low, both for comparison of the pretreatment and final placebo periods (n = 170) and for comparison of the third and the 12th month of treatment (n = 180). The reproducibility of the dipper-non-dipper dichotomy was also low, 35-40% of patients becoming non-dippers if they were dippers and vice versa, both with and without treatment The changes in left ventricular mass index after 12 months of treatment were significantly (P<0.01) related to the changes in 24 h, daytime and night-time blood pressure (r always > 0.33), but this was not the case for the treatment-induced modification of the day-night difference (r= -0.03 and -0.008 for systolic and diastolic blood pressures, respectively). CONCLUSIONS: Our results show that day-night blood pressure changes and the classification of patients into dippers and non-dippers are poorly reproducible over time. It also provides the first prospective evidence that treatment-induced changes in day-night blood pressure difference are not related to treatment-induced regression of left ventricular mass index, thus having a limited clinical significance.

Prevalence of target organ damage in treated hypertensive patients: different impact of clinic and ambulatory blood pressure control.

OBJECTIVES: First, to evaluate the prevalence of left ventricular (LV) hypertrophy, LV concentric remodelling and microalbuminuria in a selected sample of treated hypertensive patients with effective and prolonged clinic blood pressure (BP) control (BP < 140/90 mmHg). Second, to compare the prevalence of these markers of organ damage in patients with and without ambulatory BP (ABP) control, defined as average daytime BP < 132/85 mmHg). DESIGN AND METHODS: Fifty-eight consecutive hypertensive patients who attended our hypertension outpatient clinic over a period of 3 months and were regularly followed up by the same medical team were included in the study. Obesity, diabetes mellitus, history or signs of cardiovascular or renal complications and major noncardiovascular diseases were the exclusion criteria from the study. Each patient underwent 24 h ABP monitoring, echocardiography and 24 h urine collection for albumin measurement. RESULTS: The prevalence of LV hypertrophy (LV mass index > 125 g/m2 in both sexes), LV concentric remodelling (relative wall thickness > 0.45) and microalbuminuria (urinary albumin excretion < 300 mg/ 24 h) in this selected group of patients (32 men, 26 women; mean age 53 +/- 9 years; mean clinic BP 122 +/- 9/ 78 +/- 6 mmHg) was markedly low (6.9, 8.6 and 5.1%, respectively). The 26 patients with effective ABP control (group I) were similar to the 32 patients without effective ABP control (group II) in age, gender, body surface area, clinic BP, smoking habit, glucose, cholesterol and creatinine plasma levels. Prevalence of LV hypertrophy, LV concentric remodelling and microalbuminuria was lower in group I than in group II (0 versus 12.9% P< 0.01, 7.7 versus 9.4% NS, 3.8 versus 6.2% NS, respectively). CONCLUSIONS: This study demonstrates that nonobese, nondiabetic hypertensive patients with an effective clinic BP control have a very low prevalence of target organ damage and that LVH is present only in individuals with insufficient ABP control.

Impact of nocturnal fall in blood pressure on early cardiovascular changes in essential hypertension.

OBJECTIVE: To evaluate in a selected population of subjects with a recent diagnosis of hypertension whether a blunted nocturnal fall in blood pressure is associated with more advanced cardiac and vascular damage. METHODS: One hundred and eleven recently diagnosed and never-treated patients with mild essential hypertension underwent 24-h ambulatory blood pressure monitoring (ABPM), echocardiography and carotid ultrasonography. RESULTS: The 78 patients with normal (> 10%) night-time fall in systolic blood pressure (SBP) and diastolic blood pressure (DBP) (dippers) were similar to the 33 patients with a small (< or = 10 %) fall (non-dippers) for age, sex, body surface area, smoking habit, clinic and 24-h blood pressure. There were no differences between dippers and non-dippers in left ventricular mass index (104 versus 105 g/m2), common carotid internal diameter (5.8 versus 5.9 mm), intima-media thickness (0.66 versus 0.64 mm) and carotid plaques prevalence (25 versus 29%). Furthermore, no differences were found in the correlation of daytime and night-time SBP and DBP with left ventricular mass and carotid wall thickness. When the 77 men and 34 women were analysed separately, similar results were obtained. CONCLUSION: These results suggest that a blunted reduction in night-time blood pressure does not play a major role in the development of cardiovascular changes during the early phase of essential hypertension.