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Udgivelsesdato: 2010 AIMS: To assess the association between circulating levels of chromogranin A (CgA) and outcome in a large population of patients with chronic heart failure (HF). METHODS AND RESULTS: Plasma CgA levels were measured at randomization and after 3 months in 1233 patients (median age 68 years, 80% male) with chronic, stable HF from the GISSI-HF trial. Circulating CgA levels were associated with several established risk markers in HF, including increased age, diabetes, reduced renal function, and heart rate variability. During a median follow-up of 3.9 years, 333 patients (27%) died. By univariable analysis, plasma CgA levels at baseline were strongly associated with all-cause mortality during follow-up; 2nd vs. 1st tertile: HR 1.58 (1.17-2.11), P = 0.002; and 3rd vs. 1st tertile: HR 2.35 (1.78-3.10), P < 0.0001. After adjustment for established risk factors of mortality, this association was attenuated and no longer significant. Randomized treatments with n-3 polyunsaturated fatty acid or rosuvastatin did not significantly change plasma CgA concentration over 3 months. CONCLUSION: Measurement of circulating CgA levels in patients with chronic, stable HF does not provide incremental prognostic information to that obtained from physical examination, routine biochemical analysis, and contemporary HF biomarkers.

Background— Increased urinary excretion of albumin is an early sign of kidney damage and a risk factor for progressive cardiovascular and renal diseases and heart failure. There is, however, only limited information on the prevalence and prognostic role of urinary albumin excretion in patients with established chronic heart failure. Methods and Results— A total of 2131 patients enrolled in 76 sites participating in the GISSI-Heart Failure trial provided a first morning spot sample of urine at any of the clinical visits scheduled in the trial to calculate the urinary albumin-to-creatinine ratio. The relation between log-transformed urinary albumin-to-creatinine ratio and all-cause mortality (428 deaths, time from urine collection to event or censoring) was evaluated with Cox multivariable models adjusted for all significant risk factors at the time of urine collection, in the study population, and in patients without diabetes or hypertension. Almost 75% of the patients had normal urinary albumin excretion, but 19.9% had microalbuminuria (30 to 299 mg/g creatinine) and 5.4% had overt albuminuria (≥300 mg/g). There was a progressive, significant increase in the adjusted rate of mortality in the study population (hazard ratio, 1.12; 95% CI, 1.05 to 1.18 per 1-U increase of log(urinary albumin-to-creatinine ratio), P =0.0002) and in the subgroup of patients without diabetes or hypertension. Randomized treatments (n-3 polyunsaturated fatty acids or rosuvastatin) had no major impact on albumin excretion. Conclusions— Independently of diabetes, hypertension, or renal function, elevated albumin excretion is a powerful prognostic marker in patients with chronic heart failure.

Self-monitoring of blood pressure by patients at home (home blood pressure monitoring (HBPM)) is being increasingly used in many countries and is well accepted by hypertensive patients. Current hypertension guidelines have endorsed the use of HBPM in clinical practice as a useful adjunct to conventional office measurements. Recently, a detailed consensus document on HBPM was published by the European Society of Hypertension Working Group on Blood Pressure Monitoring. However, in daily practice, briefer documents summarizing the essential recommendations are needed. It is also accepted that the successful implementation of clinical guidelines in routine patient care is dependent on their acceptance by involvement of practising physicians. The present document, which provides concise and updated guidelines on the use of HBPM for practising physicians, was therefore prepared by including the comments and feedback of general practitioners.Journal of Human Hypertension advance online publication, 3 June 2010; doi:10.1038/jhh.2010.54. ispartof: Journal of Human Hypertension vol:24 issue:12 pages:779-785 ispartof: location:England status: published

Estimates of the prevalence of atrial fibrillation (AF) in heart failure (HF) originate from patients enrolled in clinical trials.To assess the prevalence and clinical correlates of AF among HF patients in everyday clinical practice from HF patients screened for the T-wave ALternans in Patients with Heart fAilure (ALPHA) study; to investigate the correlation between AF and functional status.Consecutive patients (N=3513) seen at nine Heart Failure Clinics were studied; 21.4% were in AF. AF prevalence was greater with increasing age (OR 1.04/year, p0.001) in non-ischaemic cardiomyopathy (OR 2.34, p0.001) and with increasing NYHA class (p0.0001). Multiple logistic regression predictors of AF were age70 years (OR 2.35), NYHA class II III or IV vs class I (OR 1.8, 4.4 and 3.1) and non-ischaemic cardiomyopathy (OR 3.2). A logistic model indicated that AF was associated with a 2.5 OR of being in NYHA class III-IV vs I-II while accounting for age, gender, left ventricular ejection fraction (LVEF), and aetiology of HF.The prevalence of AF in HF patients exceeds 20%, and increases with age and functional class. The presence of AF leads to a more severe NYHA class, indicating that AF contributes to the severity of heart failure.

Objectives In patients with abnormal left ventricular ejection fraction (LVEF) after acute myocardial infarction (AMI), cardiac rehabilitation with physical training prevents cardiac remodelling. To define the role of rehabilitation in the recovery of ventricular function in less severe cases, we studied its effects on more refined indexes of left ventricular function in uncomplicated, low-risk patients. Methods and results Fifty-five patients underwent percutaneous coronary revascularization after uncomplicated first AMI. Thirty-four started cardiac rehabilitation with counselling and physical training; 21 patients did not train, followed a counselling program and were taken as controls. Echocardiography was performed at baseline, after rehabilitation or counselling program and at six months follow-up. We measured: global strain (GS%) with speckle tracking analysis, E/e’ by tissue Doppler imaging (TDI), left ventricular elastance (K LV ) from the deceleration time (DT), LVEF, systolic and diastolic volumes, wall motion score index (WMSI). At baseline, groups had similar GS%, K LV , LVEF, DT, E/e’, systolic and diastolic volumes, WMSI. Rehabilitation increased peak VO 2 by 18% (P < 0.05) and improved GS%, K LV , LVEF, E/e’ and WMSI (P < 0.02) that were unchanged in controls. The improvement persisted at six months. Conclusions After a first uncomplicated AMI, abnormalities of left systolic and diastolic ventricular function may be present persisting over time despite a normal LVEF, which are fully reverted by cardiac rehabilitation.

Background Acute exposure to high‐altitude hypobaric hypoxia induces a blood pressure rise in hypertensive humans, both at rest and during exercise. It is unclear whether this phenomenon reflects specific blood pressure hyperreactivity or rather an upward shift of blood pressure levels. We aimed at evaluating the extent and rate of blood pressure rise during exercise in hypertensive subjects acutely exposed to high altitude, and how these alterations can be counterbalanced by antihypertensive treatment. Methods and Results Fifty‐five subjects with mild hypertension, double‐blindly randomized to placebo or to a fixed‐dose combination of an angiotensin‐receptor blocker (telmisartan 80 mg) and a calcium‐channel blocker (nifedipine slow release 30 mg), performed a cardiopulmonary exercise test at sea level and after the first night's stay at 3260 m altitude. High‐altitude exposure caused both an 8 mm Hg upward shift ( P P P P Conclusions In hypertensive subjects exposed to high altitude, we observed a hypoxia‐driven upward shift and steepening of the blood pressure response to exercise. The effect of the combination of telmisartan/nifedipine slow release outweighed these changes and was associated with better muscle oxygen delivery. Clinical Trial Registration URL : http://www.clinicaltrials.gov . Unique identifier: NCT 01830530.

Background: Hypertension and severe obstructive sleep apnea (OSA)may independently contribute to left ventricular diastolic dysfunction. However, scanty data is available on this issue in hypertensives withmild.moderate OSA. Methods and results:Weperformed polysomnography, echocardiography and 24 h ambulatory blood pressure monitoring in 115 treated essential hypertensives with suspicion of OSA. After exclusion of severe/treated OSA and/or cardiovascular disease patients, mild.moderate OSA (5 ≥ apnoea/hypopnoea index b 30 events·h-1) was diagnosed in 47.3% of the remaining 91 patients, while 52.7% were free of OSA. Transmitral early (E) and late (A) peak flow velocities were assessed in 69 patients, and mitral annular velocity (E′) in 53. Compared to non- OSA, mild.moderate OSA heart rate was higher (p =0.031) while E/A was lower (p = 0.001) without differences in 24 h mean systolic and diastolic blood pressures (125.36 ± 12.46/76.46 ± 6.97 vs 128.63 ± 11.50/77.70 ± 7.72 mm Hg, respectively, NS). Patients with E′ > 10 cm/s and E/A > 0.8 showed a lower mean SpO2 than subjects with normal diastolic function (p = 0.004; p > 0.001). In a logistic regression model age, mean SpO2, daytime heart rate and nocturnal diastolic blood pressure fall were associated with altered relaxation pattern, independently from BMI and gender. Conclusions: In controlled hypertensives mild.moderate OSA may be associated with early diastolic dysfunction, independently from age, gender andmean blood pressure and in the absence of concentric left ventricular hypertrophy. Moreover nocturnal hypoxia may be a key factor in determining early diastolic dysfunction, under the synergic effects of hypertension and mild.moderate OSA.

This randomized, double-blind, placebo-controlled study was designed to explore the effects of exposure to very high altitude hypoxia on vascular wall properties and to clarify the role of renin–angiotensin–aldosterone system inhibition on these vascular changes. Forty-seven healthy subjects were included in this study: 22 randomized to telmisartan (age, 40.3±10.8 years; 7 women) and 25 to placebo (age, 39.3±9.8 years; 7 women). Tests were performed at sea level, pre- and post-treatment, during acute exposure to 3400 and 5400-m altitude (Mt. Everest Base Camp), and after 2 weeks, at 5400 m. The effects of hypobaric hypoxia on mechanical properties of large arteries were assessed by applanation tonometry, measuring carotid–femoral pulse wave velocity, analyzing arterial pulse waveforms, and evaluating subendocardial oxygen supply/demand index. No differences in hemodynamic changes during acute and prolonged exposure to 5400-m altitude were found between telmisartan and placebo groups. Aortic pulse wave velocity significantly increased with altitude ( P P P P P Clinical Trial Registration— URL: https://www.clinicaltrialsregister.eu/ . Unique identifier: 2008-000540-14.

High-altitude tourism is increasingly frequent, involving also subjects with manifest or subclinical coronary artery disease. Little is known, however, on the effects of altitude exposure on factors affecting coronary perfusion. The aim of our study was to assess myocardial oxygen supply/demand ratio in healthy subjects during acute exposure at high altitude and to evaluate the effect of acetazolamide on this parameter. Forty-four subjects (21 men, age range: 24–59 years) were randomized to double-blind acetazolamide 250 mg bid or placebo. Subendocardial viability ratio and oxygen supply/demand ratio were estimated on carotid artery by means of a validated PulsePen tonometer, at sea level, before and after treatment, and after acute and more prolonged exposure to high altitude (4559 m). On arrival at high altitude, subendocardial viability ratio was reduced in both placebo (from 1.63±0.15 to 1.18±0.17; P P P P P P

Aims The aim is to investigate autonomic nervous system imbalance in hypertrophic cardiomyopathy (HCM) by combining echocardiographic morphological and functional parameters with the analysis of the autonomic responses to orthostatic stress. Methods A 10-min tilting test and a transthoracic echocardiogram focused on ventricular septal systolic (S wave) and diastolic function (isovolumic relaxation time) were performed. Low frequency on high frequency ratio (LF/HF) and RR variation (variation of beat to beat intervals) in response to passive orthostatism were used as measures of sympathetic reflex activation [delta LF/HF (D-LF/HF) and delta RR (DRR), respectively]. Brain natriuretic peptide was measured. Results A total of 50 HCM patients were categorized in two groups: D-LF/HF more than 0 (group 1, sympathetic response) and D-LF/HF 0 or less (group 2, parasympathetic response). Patients in group 2 had higher New York Heart Association class, a more frequent history of atrial fibrillation (38 versus 9% P = 0.04) or syncope (46 versus 12% P = 0.01) and an increased septal isovolumic relaxation time (122 versus 82 ms P = 0.02). The same categorization was made according to lowest quartile DRR (DRR at least 23 ms, group 1: sympathetic response; DRR less than 23 ms, group 2: parasympathetic response). In group 2, patients were older, with advanced New York Heart Association class and higher history of atrial fibrillation. Conclusions Autonomic response to passive orthostatism in HCM appears correlated with specific functional features of the hypertrophic heart. Altered neural afferent traffic from the localized area of segmental hypertrophy resulted in autonomic changes with a blunted sympathetic response, and an inappropriate vagal activation, especially in patients with history of atrial fibrillation or syncope.

Background: Little is known about the effects of cardiovascular drugs at high altitude. Objective: To assess 24-h blood pressure (BP) and heart rate (HR) during short-term altitude exposure in healthy normotensive persons treated with carvedilol or nebivolol. Methods: Participants were randomized in double-blind to placebo, nebivolol 5 mg once daily or carvedilol 25 mg b.i.d. Tests were performed at sea level (baseline and after 2 weeks treatment) and on second to third day at altitude (Monte Rosa, 4559 m), still on treatment. Data collection included conventional BP, 24-h ambulatory BP monitoring (ABPM), oxygen saturation (SpO2), Lake Louise Score and adverse symptoms score. Results: Twenty-four participants had complete data (36.4 ± 12.8 years, 14 men). Both beta-blockers reduced 24-h BP at sea level. At altitude 24-h BP increased in all groups, mainly due to increased night-time BP. Twenty-four-hour SBP at altitude was lower with carvedilol (116.4 ± 2.1 mmHg) than with placebo (125.8 ± 2.2 mmHg; P < 0.05) and intermediate with nebivolol (120.7 ± 2.1 mmHg; NS vs. others). Rate of nondipping increased at altitude and was lower with nebivolol than with placebo (33 vs. 71%; P = 0.065). Side effects score was higher with carvedilol than with placebo (P = 0.04), and intermediate with nebivolol. SpO2 at altitude was higher with placebo (86.1 ± 1.2%) than with nebivolol (81.7 ± 1.1%; P = 0.07) or carvedilol (81.1 ± 1.1%; P = 0.04). Conclusions: Both carvedilol and nebivolol partly counteract the increase in BP at altitude in healthy normotensive individuals but are associated with a lower SpO2. Carvedilol seems more potent in this regard, whereas nebivolol more effectively prevents the shift to a nondipping BP profile and is better tolerated. © 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins.

In the 1930–1940s Levy and coworkers administered low oxygen tension (thus simulating exposure to an altitude of about 5000 m) while monitoring ECG, in order to demonstrate coronary inadequacy resulting from imbalance between myocardial oxygen supply and demand in hypoxic conditions...

AimsIt is unknown whether subclinical high-altitude pulmonary oedema reduces spontaneously after prolonged altitude exposure. Continuous positive airway pressure (CPAP) removes extravascular lung fluids and improves haemoglobin oxygen saturation in acute cardiogenic oedema. We evaluated the presence of pulmonary extravascular fluid increase by assessing CPAP effects on haemoglobin oxygen saturation under acute and prolonged altitude exposure.Methods and resultsWe applied 7 cm H2O CPAP for 30 min to healthy individuals after acute (Capanna Margherita, CM, 4559 m, 2 days permanence, and

Aims Previous studies investigating the effect of hypoxia on left ventricle focused on its global function, an approach that may not detect a selective dysfunction of subendocardial layers that are most sensitive to an inadequate oxygen supply. In the HIGHCARE study, aimed at exploring the effects of high altitude hypoxia on multiple biological variables and their modulation by an angiotensin receptor blocker, we addressed the effects of hypobaric hypoxia on both systolic and diastolic left ventricular geometry and function, focusing on echocardiographic assessment of left ventricle twist to indirectly examine subendocardial left ventricular systolic function. Methods and results In 39 healthy subjects, physiological and echocardiographic variables, including left ventricular twist and a simplified torsion-to-shortening ratio (sTSR), were recorded at sea level, at 3400 m, and at 5400 m altitude (Mount Everest base camp). Both left ventricular twist and sTSR were greater at 5400 m than at sea level (12.6° vs. 9.6° and 0.285 vs. 0.202, P < 0.05 for both), were linearly related to the reduction in arterial oxygen partial pressure ( P < 0.01 for both), and were associated with significant changes in LV dimensions and contractility. No effects of angiotensin receptor blockade were observed on these variables throughout the study. Conclusion Our study, for the first time, demonstrates an increase in left ventricular twist at high altitude in healthy subjects exposed to high altitude hypoxia, suggesting the occurrence of subendocardial systolic dysfunction in such condition.

Blood pressure increases during acute exposure to high altitude in healthy humans. However, little is known on altitude effects in hypertensive subjects or on the treatment efficacy in this condition. Objectives of High Altitude Cardiovascular Research (HIGHCARE)–Andes Lowlanders Study were to investigate the effects of acute high-altitude exposure on 24-hour ambulatory blood pressure in hypertensive subjects and to assess antihypertensive treatment efficacy in this setting. One hundred untreated subjects with mild hypertension (screening blood pressure, 144.1±9.8 mm Hg systolic, 92.0±7.5 mm Hg diastolic) were randomized to double-blind placebo or to telmisartan 80 mg+modified release nifedipine 30 mg combination. Twenty-four–hour ambulatory blood pressure monitoring was performed off-treatment, after 6 weeks of treatment at sea level, on treatment during acute exposure to high altitude (3260 m) and immediately after return to sea level. Eighty-nine patients completed the study (age, 56.4±17.6 years; 52 men/37 women; body mass index, 28.2±3.5 kg/m 2 ). Twenty-four–hour systolic blood pressure increased at high altitude in both groups (placebo, 11.0±9 mm Hg; P P P Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT01830530.

Arrhythmogenic Cardiomyopathy is a complex clinical entity, sometimes difficult to diagnose. Three main different patterns of disease expression characterize clinically this hereditary heart muscle disease: the “classic” right ventricular form (ARVC), the “left dominant” subtype (LDAC), with primary left ventricular involvement, and the “biventricular” variant, defined by parallel involvement of both ventricles. We report on a case of a 51 years old man with a strong family history of juvenile sudden cardiac death of supposed ischaemic origin and personal history of ventricular arrhythmias and supposed myocarditis. We demonstrate how an accurate anamnesis plus correct interpretation of traditional non invasive tests followed by more sophisticate new non invasive tests such as cardiac magnetic resonance and genetic testing allowed to reach the correct diagnosis.

Acute exposure to high altitude induces a blood pressure (BP) rise in healthy humans [(1)][1]. Arterial hypertension is associated both with enhanced BP response to exercise and with increased sympathetic discharge in hypoxic conditions [(2,3)][2], which may increase the risk of adverse consequences

Aim Many hypertensive subjects travel to high altitudes, but little is known on ambulatory blood pressure (ABP) changes and antihypertensive drugs' efficacy under acute and prolonged exposure to hypobaric hypoxia. In particular, the efficacy of angiotensin receptor blockers in this condition is unknown. This may be clinically relevant considering that renin–angiotensin system activity changes at altitude. The HIGHCARE-HIMALAYA study assessed changes in 24 h ABP under acute and prolonged exposure to increasing altitude and blood pressure-lowering efficacy and safety of an angiotensin receptor blockade in this setting. Methods and results Forty-seven healthy, normotensive lowlanders were randomized to telmisartan 80 mg or placebo in a double-blind, parallel group trial. Conventional and Ambulatory BPs were measured at baseline and on treatment: after 8 weeks at sea level, and under acute exposure to 3400 and 5400 m altitude, the latter upon arrival and after 12 days (Mt. Everest base camp). Blood samples were collected for plasma catecholamines, renin, angiotensin, and aldosterone. In both groups, exposure to increasing altitude was associated with: (i) significant progressive increases in conventional and 24 h blood pressure, persisting throughout the exposure to 5400 m; (ii) increased plasma noradrenaline and suppressed renin–angiotensin–aldosterone system. Telmisartan lowered 24 h ABP at the sea level and at 3400 m (between-group difference 4.0 mmHg, 95% CI: 2.2–9.5 mmHg), but not at 5400 m. Conclusion Ambulatory blood pressure increases progressively with increasing altitude, remaining elevated after 3 weeks. An angiotensin receptor blockade maintains blood pressure-lowering efficacy at 3400 m but not at 5400 m.

AimsWe assessed the haemodynamic changes induced by exposure to high altitude hypoxia and the effects on them of acetazolamide, a drug prescribed to prevent and treat mountain sickness.Methods and resultsIn 42 subjects (21 males, age 36.8 ± 8.9 years) randomized to double blind acetazolamide 250 mg b.i.d. or placebo, pulse wave velocity and pulse wave parameters were assessed (PulsePen) at baseline; after 2-day treatment at sea level; within 6 h and on 3rd day of exposure to high altitude. Exposure to high altitude significantly increased diastolic (P < 0.005) and mean blood pressure (BP) (P < 0.05, after prolonged exposure) in placebo but not in the acetazolamide group. Therefore, subjects on acetazolamide showed significantly lower values of diastolic (P < 0.005) and mean BP (P < 0.05) at altitude. Furthermore, they also showed significantly lower values of systolic BP (P < 0.05). Pulse wave velocity did not change at high altitude, while the augmentation index, normalized for a theoretical heart rate of 75 b.p.m., significantly increased (P < 0.05) under placebo, but not under acetazolamide. In a multivariate model, unadjusted augmentation index at high altitude was not affected by BP changes, while significant determinants were heart rate and gender.ConclusionAcute exposure to high altitude induced a rise in brachial BP and changes in pulse waveform-derived parameters, independent from changes in mean BP and partly counteracted by treatment with acetazolamide. The impact of acetazolamide on the haemodynamic alterations induced by hypobaric hypoxia may be considered among the beneficial effects of this drug in subjects prone to mountain sickness.Clinical Trial Registration: EudraCT Number: 2010-019986-27

SUMMARY High-altitude exposure is characterized by the appearance of periodic breathing during sleep. Only limited evidence is available, however, on the presence of gender-related differences in this breathing pattern. In 37 healthy subjects, 23 male and 14 female, we performed nocturnal cardio-respiratory monitoring in the following conditions: (1) sea level; (2) first/second night at an altitude of 3400 m; (3) first/second night at an altitude of 5400 m and after a 10 day sojourn at 5400 m. At sea level, a normal breathing pattern was observed in all subjects throughout the night. At 3400 m the apnea–hypopnea index was 40.3 ± 33.0 in males (central apneas 77.6%, central hypopneas 22.4%) and 2.4 ± 2.8 in females (central apneas 58.2%, central hypopneas 41.8%; P

Slow deep breathing improves blood oxygenation (Sp(O2)) and affects hemodynamics in hypoxic patients. We investigated the ventilatory and hemodynamic effects of slow deep breathing in normal subjects at high altitude. We collected data in healthy lowlanders staying either at 4559 m for 2-3 days (Study A; N = 39) or at 5400 m for 12-16 days (Study B; N = 28). Study variables, including Sp(O2) and systemic and pulmonary arterial pressure, were assessed before, during and after 15 minutes of breathing at 6 breaths/min. At the end of slow breathing, an increase in Sp(O2) (Study A: from 80.2±7.7% to 89.5±8.2%; Study B: from 81.0±4.2% to 88.6±4.5; both p

Purpose: Low birth weight and accelerated postnatal growth appear to play a significant role in the pathogenesis of hypertension and cardiovascular disease in adulthood. The aim of the present study was to characterize the factors determining pulse wave velocity (PWV) in teenagers and, in particular, to verify the relationship with birth weight, postnatal growth, timing of adiposity rebound, lifestyle, and hemodynamic parameters. Methods: Carotid-femoral and carotid-radial pulse wave velocities of 558 healthy teenagers (age range: 16.2–19.9 years) were determined by means of a PulsePen tonometer. Birth weight and gestational age were obtained from obstetrical records, and data regarding postnatal growth were obtained from pediatric clinical records. Results: No change in aortic PWV was found in association with birth weight, postnatal growth, and timing of adiposity rebound. However, the study showed a strong association between accelerated growth from 0 to 12 months and carotid-radial PWV (trend: p .02). Subjects with birth weight values 2,500 g showed higher values of upper limb PWV (p .05) and higher values of diastolic and mean arterial pressure (p .05). Stepwise regression analysis revealed that mean arterial pressure, age, and height were the main independent factors determining aortic PWV in this young population. Conclusions: These results suggest that there is no linear correlation between birth weight and hemodynamic parameters in teenagers; however, subjects characterized by very low birth weight and accelerated postnatal weight gain appear to demonstrate increased upper limb PWV and diastolic and mean arterial pressure values. 2012 Society for Adolescent Health and Medicine. All rights reserved.

Purpose: Acute mountain sickness (AMS) is a neurological disorder that may be unpredictably experienced by subjects ascending at a high altitude. The aim of the present study was to develop a predictive index, measured at an intermediate altitude, to predict the onset of AMS at a higher altitude. Methods: In the first part, 47 subjects were investigated and blood withdrawals were performed before ascent, at an intermediate altitude (3440 m), and after acute and chronic exposition to high altitude (Mount Everest Base Camp, 5400 m (MEBC1 and MEBC2)). Parameters independently associated to the Lake Louise scoring (LLS) system, including the self-reported and the clinical sections, and coefficients estimated from the model obtained through stepwise regression analysis were used to create a predictive index. The possibility of the index, measured after an overnight stay at intermediate altitude (Gnifetti hut, 3647 m), to predict AMS (defined as headache and LLS≥ 4) at final altitude (Capanna Margherita, 4559 m), was then investigated in a prospective study performed on 44 subjects in the Italian Alps. Results: During the expedition to MEBC, oxygen saturation, hematocrit, day of expedition, and maximum velocity of clot formation were selected as independently associated with LLS and were included in the predictive index. In the Italian Alps, subjects with a predictive index value≥ 5.92 at an intermediate altitude had an odds ratio of 8.1 (95% confidence limits = 1.7-38.6, sensitivity = 85%, specificity = 59%) for developing AMS within 48 h of reaching high altitude. Conclusion: In conclusion, a predictive index combining clinical and hematological parameters measured at an intermediate step on the way to the top may provide information on impending AMS. © 2011 by the American College of Sports Medicine.

BACKGROUND We analyzed the inodilator properties of levosimendan in patients with chronic heart failure and severe functional mitral regurgitation. METHODS We studied 20 patients under optimal treatment and in stable clinical condition (New York Heart Association 3.19 + or - 0.66; 70 + or - 7 years). Levosimendan was infused as a bolus (12 microg/kg in 10 min) followed by a 24-h infusion (0.1-0.2 microg/kg per min). Before and after infusion, Doppler echocardiography, brain natriuretic peptide determination and noninvasive hemodynamic monitoring with bioimpedance cardiography were performed. RESULTS Levosimendan improved left ventricular ejection fraction (ejection fraction 31 + or - 4 from 27 + or - 4, P < 0.05), decreased brain natriuretic peptide (333 + or - 139 from 629 + or - 63 pg/ml, P < 0.01), reduced mitral valve effective regurgitant orifice area to 27 + or - 5 from 36 + or - 7 mm (P < 0.01) and the velocity of displacement of mitral annulus [ratio between E and E' waves on Doppler and tissue Doppler (E/E') from 22.7 + or - 1.6 to 13.1 + or - 0.6, P < 0.01]. Noninvasive hemodynamic monitoring showed increased acceleration index (a marker of inotropism), and reduced peripheral resistances and thoracic fluid content (P < 0.01). After 4 weeks of washout, some of these effects were still evident. CONCLUSION In patients with chronic heart failure and functional mitral regurgitation, levosimendan acutely improved systolic and diastolic function, reduced mitral regurgitation and modulated neurohormonal activation, with a tendency for these changes to persist over a short-term follow-up.

Objective: To investigate the possibility that statins reduce blood pressure as well as cholesterol concentrations through clinic and 24 hour ambulatory blood pressure monitoring. Design: Randomised placebo controlled double blind trial. Setting: 13 hospitals in Italy Participants: 508 patients with mild hypertension and hypercholesterolaemia, aged 45 to 70 years. Intervention: Participants were randomised to antihypertensive treatment (hydrochlorothiazide 25 mg once daily or fosinopril 20 mg once daily) with or without the addition of a statin (pravastatin 40 mg once daily). Main outcome measures: Clinic and ambulatory blood pressure measured every year throughout an average 2. 6 year treatment period. Results: Both the group receiving antihypertensive treatment without pravastatin (n=254) (with little change in total cholesterol) and the group receiving antihypertensive treatment with pravastatin (n=253) (with marked and sustained reduction in total cholesterol and low density lipoprotein cholesterol) had a clear cut sustained reduction in clinic measured systolic and diastolic blood pressure as well as in 24 hour, and day and night, systolic and diastolic blood pressure. Pravastatin performed slightly worse than placebo, and between group differences did not exceed 1.9 (95% confidence interval -0.6 to 4.3, P=0.13) mm Hg throughout the treatment period. This was also the case when participants who remained on monotherapy with hydrochlorothiazide or fosinopril throughout the study were considered separately. Conclusions: Administration of a statin in hypertensive patients in whom blood pressure is effectively reduced by concomitant antihypertensive treatment does not have an additional blood pressure lowering effect. Trial registration: BRISQUI-*IV-2004-001 (registered at Osservatorio Nazionale sulla Sperimentazione Clinica dei Medicinali - National Monitoring Centre on Clinical Research with Medicines).

Information on arterial properties from home blood pressure monitoring: work still in progress

Summary ofmain advantages and limitations three different techniques for arterial stiffness evaluation Device Advantages LimitationsComplior The delay in pulse transit time between twoarteries sites is taken simultaneously usinga ‘foot to foot’ waveform method Operator’s skill dependency Numerous data on the prognostic value ofcf-PWV so obtained are available Carotid tonometry is difficult Necessity to undress and expose the groin Possibility of technical errors in obese patients Uncertainty and approximation in measurement of distance betweenthe two arterial sites Theoretical risk of carotid plaque rupture by probe (never reported) Patients with atrial fibrillation cannot be evaluated Unable to allow PWA Underestimation of elevated PWV by built-in algorithmSphygmoCor PWA is available allowing assessment ofaugmentation index and central BP througha transfer function application Operator’s skill dependency Numerous data on the prognostic value ofthe parameters so obtained are available Carotid tonometry is difficult Necessity to undress and expose the groin Possibility of technical errors in obese patients Uncertainty and approximation in measurement of distance betweenthe two arterial sites Theoretical risk of carotid plaque rupture by probe (never reported) Patients with atrial fibrillation cannot be evaluated Debate regarding the validity of the generic transfer function used Need of a precise BP calibration for PWA, currently not available The PWV transit time delay is calculated using reference ECG signalsobtained at different times, respectively, for carotid and femoral pulsewaveforms sequentially recordedArteriograph The technique only needs access to thepatient’s upper arm (no need to undress) Scarce data on its validation and on the prognostic value of parametersso obtained are available It is based on an easy methodology (largelyoperator-independent method) Patients with atrial fibrillation or marked bradycardia cannot be evaluated It is a time-saving method. This fast assessmentof arterial stiffness parameters is particularly suitableto population studies Higher reproducibility of parameters, as comparedwith the other two methods Potentially adaptable to ambulatory arterial stiffnessassessmentBP, blood pressure; cf-PWV, carotid–femoral pulse wave velocity; PWA, pulse wave analysis.

This document summarizes the available evidence and provides recommendations on the use of home blood pressure monitoring in clinical practice and in research. It updates the previous recommendations on the same topic issued in year 2000. The main topics addressed include the methodology of home blood pressure monitoring, its diagnostic and therapeutic thresholds, its clinical applications in hypertension, with specific reference to special populations, and its applications in research. The final section deals with the problems related to the implementation of these recommendations in clinical practice. ispartof: Journal of Hypertension vol:26 issue:8 pages:1505-1530 ispartof: location:Netherlands status: published

BACKGROUND: At sea level, ventilation kinetics are characterized during a ramp exercise by three progressively steeper slopes, the first from the beginning of exercise to anaerobic threshold, the second from anaerobic threshold to respiratory compensation point, and the third from respiratory compensation point to peak exercise. In the second ventilation phase, body CO2 stores are used to buffer acidosis owing to lactate production; it has been suggested that this extra CO2 production drives the ventilation increase. At high altitude, ventilation increases owing to hypoxia. We hypothesize that ventilation increase reduces body CO2 stores affecting ventilation kinetics during exercise. DESIGN: In eight healthy participants, we studied the ventilation kinetics during an exercise performed at sea level and at high altitude (4559 m). METHODS: We used 30 W/2 min step incremental protocol both at sea level and high altitude. Tests were done on a cyclo-ergometer with breath-by-breath ventilation and inspiratory and expiratory gas measurements. We evaluated cardiopulmonary data at anaerobic threshold, respiratory compensation point, peak exercise and the VE/VCO2 slope. RESULTS: At high altitude: (a) peak VO2 decreased from 2595±705 to 1745±545 ml/min (P