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Only 20-30% out of the treated hypertensive patients in Europe are achieving blood pressure (BP) control. Among other recognized factors, these poor results could be attributable to the fact that for many doctors it is very difficult to detect which is the predominant hemodynamic cause of the hypertension (hypervolemia, hyperinotropy or vasoconstriction). The aim of the study was to use non-invasive thoracic electrical bioimpedance (TEB) to evaluate hemodynamic modulators and subsequent hemodynamic status in uncontrolled hypertensive patients, receiving at least two antihypertensive drugs. A number of 134 uncontrolled hypertensive patients with essential hypertension were evaluated in nine European Hypertension Excellence centers by means of TEB (the HOTMAN® System). Baseline office systolic and diastolic BP averaged 156/92 mmHg. Hemodynamic measurements show that almost all patients (98.5%) presented at least one altered hemodynamic modulator: intravascular hypervolemia (96.4%) and/or hypoinotropy (42.5%) and/or vasoconstriction (49.3%). Eleven combinations of hemodynamic modulators were present in the study population, the most common being concomitant hypervolemia, hypoinotropy and vasoconstriction in 51(38%) patients. Six different hemodynamic states (pairs of mean arterial pressure and stroke index) were found. Data suggest that there is a strong relation between hypertension and abnormal hemodynamic modulators. This method might be helpful for treatment individualization of hypertensive patients. [ABSTRACT FROM AUTHOR]

Little information is available about the burden of hypertension on echo-lab activity in current practice. The aim of the present nation-wide survey in outpatient echo-labs was to investigate the prevalence rates of (1) echo examinations performed for the evaluation of hypertensive cardiac damage; (2) reports providing quantitative data on left ventricular (LV) structure and geometry; (3) LV hypertrophy (LVH) in hypertensives referred to echo labs. The study was carried out in 14 outpatient echo-labs across Italy. Prescriptions written by general practitioners were used to identify the indications for the examinations. Estimates of LVH were derived from original echo reports or were calculated from LV primary measures, when available, with Devereux's formula in a post-analysis. Echo examination was performed in 2449 subjects (1245 men and 1204 women); hypertension was the indication for echo in 745 (30.4%) cases. In this subgroup, LV mass (LVM), LVM indexed to body surface area, LVM indexed to height2.7 and relative wall thickness ratio were reported in 58, 59, 54 and 52%, respectively. LVH was present in 53% of untreated hypertensives and, among treated patients, in 45 and 65% of those with and without blood pressure control, respectively. Our findings show that (1) hypertension accounts for approximately one-third of echo examinations performed in clinical practice; (2) a large fraction of echo reports do not provide quantitative data on LVM and LV geometry, (3) LVH is highly prevalent in hypertensives referred to echo labs for assessment of cardiac damage. [ABSTRACT FROM AUTHOR]

Macrovasculature, microvasculature and the heart determine the structure and function of the circulatory system. Due to the viscoelastic properties of large arteries, the pulsatile pressure and flow that result from intermittent ventricular ejection is smoothed out, so that microvasculature mediates the delivery of nutrients and oxygen to tissues steadily. The disruption of this function, which occurs when microvascular structure develops in response to hypertension, leads to end-organ damage. Microvascular structure is not only the site of vascular resistance, but also the origin of most of the wave reflections generating increased central systolic blood pressure (SBP) in the elderly. Nowadays many data of the literature suggest that hypertension-related damage to the micro and macrovascular system may be manageable through pharmacological agents. Among them, β-blocking agents and diuretics poorly modify microvascular structure, whereas angiotensin and calcium entry blockade has an opposite effect, thereby reducing central wave reflections and, finally, causing a selective SBP reduction.Journal of Human Hypertension (2008) 22, 590–595; doi:10.1038/jhh.2008.43; published online 29 May 2008 [ABSTRACT FROM AUTHOR]

The article presents an examination of the maternal cardiovascular function in pregnancies complicated by intrauterine growth restriction (IUGR). It aims to evaluate maternal cardiovascular function by means of both echocardiography and ambulatory blood pressure monitoring in pregnancies complicated by IUGR.

To assess the prevalence of genetic mutations in nonsyndromic pheochromocytoma/paraganglioma (PHEO/PGL) patients we have performed a systematic search for mutations in the succinate dehydrogenase (SDH) B, C, and D subunits, von Hippel–Lindau (VHL), and RET genes by direct bidirectional sequencing. Patients were selected from the medical records of hypertension centers. After exclusion of syndromic patients, 45 patients with familial (F+, n= 3) and sporadic (F−, n= 42) cases of isolated PHEO/PGL were considered. They included 35 patients with PHEO, 7 with PGL, and 3 with head/neck PGL (hnPGL). Three patients with PHEO (2F−, 1F+) presented VHL mutations (P86A, G93C, and R167W), six with PGL (4F−, 2F+) were positive for SDH or VHL mutations (SDHB R230G in two patients, SDHB S8F, R46Q, R90Q, and VHL P81L in one subject each), and one with hnPGL carried the SDHD 348–351delGACT mutation. We have also detected missense (SDHB S163P, SDHD H50R and G12S), synonymous (SDHB A6A, SDHD S68S), and intronic mutations that have been considered nonpathological polymorphic variants. No mutation was found in SDHC or RET genes. Our data indicate that germline mutations of VHL and SDH subunits are not infrequent in familial as well as in sporadic cases of nonsyndromic PHEO/PGL (overall, 12 of 45 probands, 22%). Accordingly, screening for such mutations seems to be justified. However, a more precise characterization of the functional relevance of any observed sequence variant and of other genetic and environmental determinants of neoplastic transformation is essential in order to plan appropriate protocols for family screening and follow-up. [ABSTRACT FROM AUTHOR]

Hypertension and non insulin-dependent diabetes mellitus (NIDDM) are well-known risk factors for atherosclerotic disease. Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) may exert a relevant role in the pathogenesis of atherosclerosis; their prognostic relevance has been recently demonstrated. The aim of the study was to investigate possible inter-relation between circulating adhesion molecule levels, carotid artery structure and endothelial function in 15 patients with NIDDM, as well as in 15 patients with both NIDDM and essential hypertension (NIDDM+EH) compared with 15 normal subjects (NS) and 15 euglycaemic patients with EH, matched for age, sex and body weight. All subjects were submitted to a biopsy of the gluteal subcutaneous fat. Small arteries were dissected and mounted on a micromyograph, and the media-to-lumen (M/L) ratio was then calculated. Carotid artery structure was investigated by Doppler ultrasound. Endothelial function was evaluated by investigation of the flow-mediated dilatation (FMD) of the brachial artery. ICAM-1 and VCAM-1 plasma levels were measured by ELISA. ICAM-1 and VCAM-1 plasma levels were significantly greater and FMD smaller in EH, NIDDM and NIDDM+EH than in NS, but no difference was observed among the three pathological groups. Carotid artery structural changes were more pronounced in NIDDM+EH. No significant difference was observed among NIDDM, EH and NS. The M/L ratio of subcutaneous small resistance arteries was significantly greater in NIDDM+EH than in NIDDM or EH. NS had a smaller M/L ratio than the other groups. Significant correlations were observed between ICAM-1 plasma levels and indices of carotid artery structure in diabetic patients. However, the relations were close only in NIDDM+EH. In conclusion, our data suggest that NIDDM+EH may present more pronounced vascular structural alterations than NIDDM, and that adhesion molecules plasma levels are closely inter-related with... [ABSTRACT FROM AUTHOR]

The aim was to determine, in a cross-sectional study, the relation between structural alterations in the heart and carotid arteries, and blood pressure (BP) changes from day to night time, measured by ambulatory BP (ABP). In 225 untreated subjects (107 F, 118 M, age range 48-64 years) and 59 treated subjects (24 M, 35 F, age range 50-64), living in a small town of northern Italy (Vobarno, Brescia) carotid intima media thickness as well as the occurrence of plaque, were evaluated by ultrasound. Echocardiographic left ventricular (LV) mass was measured according to the Penn Convention. BP was determined by clinic measurement and by 24-h non-invasive ABP monitoring. Subjects were divided in two groups, according to the decrease of night time systolic BP (SBP) 'dippers' (SBP decreased by at least 10% during night time) and 'non-dippers' (decrease of night time SBP <10%). The intima-media thickness in the common carotid, in the carotid bifurcation, in the internal carotid artery and average intima-media thickness were significantly greater in untreated non-dippers as compared with dipper subjects (ANOVA P < 0.05). A significantly higher prevalence of plaque was observed in untreated non-dippers as compared with dippers (P = 0.002). After adjusting for age, sex, 24-h SBP, and smoking, IMT in the carotid bifurcation and average intima-media thickness remained significantly greater in non-dipper subjects (P < 0.05 for all comparisons). No significant differences in LV mass were observed between dippers and non-dipper subjects. In conclusion, in a general population of unselected middle-aged subjects, night time BP values, among other risk factors, seem to represent an important determinant of carotid wall structure. [ABSTRACT FROM AUTHOR]

Objective: The aim of this study was to compare the efficacy and tolerability of the new angiotensin-converting enzyme (ACE) inhibitor moexipril and the calcium antagonist nitrendipine in postmenopausal women with mild to moderate hypertension. Methods: After a 4-week placebo run-in period, 93 postmenopausal women (age range 44–70 years) with primary hypertension were randomized to receive moexipril 15 mg once daily or nitrendipine 20 mg once daily for 8 weeks. The mean sitting systolic (SSBP) and sitting diastolic blood pressures (SDBP) at baseline were 161.3/103.0 mmHg in the moexipril group, and 162.2/102.3 mmHg in the nitrendipine group. Results: After the 8 weeks of treatment, the SSBP/SDBP reductions were −21.2/−15.2 mmHg in the moexipril group and −18.2/−13.6 mmHg in the nitrendipine group. Blood pressure responses were adequate in 82.2% of the moexipril-treated patients and in 80.9% in the nitrendipine-treated group. Adverse events were more frequent with nitrendipine than with moexipril. The most common adverse events in the nitrendipine group were headache (23.4%), flushing (21.3%) and ankle oedema (14.9%). In the moexipril group the most common adverse event was cough (8.9%). Conclusion: The results of the study suggest that moexipril and nitrendipine are equieffective in the given dosages. In the patient population of postmenopausal women, the ACE inhibitor moexipril appears to have an advantage over the calcium antagonist nitrendipine with regard to tolerability. [ABSTRACT FROM AUTHOR]

We have previously shown that transdermal nitroglycerin may induce an increase in the activity of the adrenergic and the renin-angiotensin-aldosterone systems (SRAA) in patients with chronic stable angina pectoris (SA); when the activation of these systems is more pronounced, the antianginal effect of this drug seems to be reduced. The aim of this study was to evaluate the antianginal efficacy of transdermal nitroglycerin administration (TTS-NG 10 mg. 24 h) in combination with an ACE inhibitor without sulphydryl groups (BNZ, benazepril 10 mg b.i.d.) in respect to placebo, or to TTS-NG or BNZ administered as monotherapy. Twenty-four patients (21M, 3F) were admitted to this multicentre, randomized, double-blind, latin square, placebo-controlled study. Patients received all the treatments (placebo, TTS-NG, BNZ and BNZ+ TTS-NG) each for one week; at the end of each week patients performed two exercise testi 2 and 22 h post-dosing. Two hours post-dosing, exercise duration at 1 mm ST depression was significantly increased in respect to placebo during TTS-NG (P<0.05) and TTS-NG+BNZ (<0.05) treatments. Two hours post-dosing, exercise duration at peak exercise was also increased in respect to placebo during TTS-NG (<0.05) ana TTS-NG+BNZ (<0.05); 22 h post-dosing the increase in exercise duration was significant only during TTS-NG+BNZ treatment (<0.05) in respect to placebo, but not during TTS-NG given alone. Rate-pressure product at 1 mm ST depression was significantly increased 2 h post-dosing during TTS-NG treatment (P<005). In conclusion, these results suggest that ACE inhibitor administration given in combination with TTS-NG can induce a statistically significant increase in exercise duration in stable angina patients in respect of placebo, 22 h post-dosing. The clinical significance of this finding must be evaluated in further studies. [ABSTRACT FROM PUBLISHER]

The aim of this study was to evaluate the acute effects of transdermal nitroglycerin on the sympathetic and renin-angiotensin-aldosterone systems activity, in a group of patients with stable exercise induced angina pectoris. Eighteen outpatients (15M, 3F, age range 47–65 years) were included in this double-blind, randomized, crossover trial comparing the antianginal effects of a transdermal system delivering 20mg. day of nitroglycerin to an identical placebo. Plasma renin activity, plasma aldosterone and catecholamine concentrations were measured in resting basal conditions and at 4.8.24, and 32 h post-dosing. Patients were subdivided in two groups according to the increase in exercise duration after patch application greater than 30% (responders, n=8) and less or equal to 30% (non-responders, n=10) in respect to placebo. In responders plasma norepinephrine was slightly increased during transdermal nitroglycerin administration in comparison to placebo while no change was observed in plasma adrenaline and aldosterone concentrations and in plasma renin activity. In non-responders plasma norepinephrine levels significantly increased during nitroglycerin treatment in comparison with placebo. Multiple comparisons showed that this increase was significant at 4,8 and 24 h post-dosing. Plasma epinephrine and aldosterone concentrations and plasma renin activity were also increased after nitroglycerin administration. In the population as a whole, a significant inverse correlation was found between the percent increase in exercise duration (active drug vs placebo) and the absolute values of plasma norepinephrine and aldosterone, 4 h post-dosing. In conclusion, the results of this study show that transdermal nitroglycerin may induce an increase in the activity of adrenergic and renin-angiotensin-aldosterone systems in patients with stable exercise-induced angina pectoris. When activation of these systems is more pronounced, the antianginal effect of this treatment appears to be reduced. [ABSTRACT FROM PUBLISHER]

1 Upright tilting in normal volunteers caused increases in plasma active and total renin, angiotensin II and aldosterone; a slight but significant fall in inactive renin accompanied these changes. 2 The alterations in the renin-angiotensin-aldosterone system on tilting took up to 1 h upright to become fully established. 3 Large intravenous doses of propranolol or metoprolol attenuated, without abolishing, the rises in active renin, angiotensin II, and aldosterone; the attenuation was most evident soon after tilting and was largely overcome by 1 h upright. Inactive renin did not fall significantly after beta- adrenoceptor blockade. 4 Intravenous frusemide caused immediate rises in plasma active, total and inactive renin, angiotensin II, and aldosterone, which then declined over 2 h despite increasing cumulative sodium losses. 5 Intravenous propranolol or metoprolol attenuated, without abolishing, these early increases in the components of the renin-angiotensin-aldosterone system after frusemide. 6 Prior oral metoprolol or propranolol, while significantly slowing the heart, did not limit the early rise in plasma angiotensin II following intravenous frusemide. 7 Thus in contrast to previous workers, we did not find that propranolol eliminated the response of the renin-angiotensin system to upright tilting; in part this difference appeared to be due to the longer tilt we employed. 8 Also in contrast to earlier work, we found attenuation by both intravenous propranolol and metoprolol of the immediate rise in renin after intravenous frusemide. [ABSTRACT FROM AUTHOR]

1 Labetalol 100 mg was given intravenously to 27 patients with essential hypertension (12 males, 15 females; WHO I-II; age range 30-66 yr; on average, a significant reduction of blood pressure was observed within 5 min (P less than 0.001). Average heart rate was also reduced significantly (P less than 0.01). 2 In 18 patients haemodynamic measurements were performed (dye-dilution or thermodilution technique): blood pressure reduction was related to peripheral vasodilatation, as cardiac index remained unmodified. 3 The absolute and percentage decrease of blood pressure, heart rate and total peripheral resistance after labetalol 100 mg intravenously, was significantly greater in the patients with higher baseline plasma noradrenaline concentration values. 4 In 12 out of 27 patients labetalol was given orally for 2 months (dose range 300-1200 mg); the pattern of blood pressure and heart rate changes after oral therapy were comparable to those observed after acute administration of the drug. 5 The degree of blood pressure and heart rate reductions after oral labetalol was also significantly related to pretreatment basal noradrenaline concentration. [ABSTRACT FROM AUTHOR]