Duplicated left pulmonary artery: an unknown disease? Three case reports and review of the literature.

We report three cases of an abnormal finding of duplicated left pulmonary artery: two of these occurring in children with Kabuki syndrome and configuring the setting of a pseudo-pulmonary sling without any clinical or cardiac cross-sectional evidence of tracheal compression. The other case instead represents duplicated left pulmonary artery with pulmonary sling caused by the retro-tracheal course of the lower left pulmonary artery associated with "Christmas Tree" arrangement of the tracheo-bronchial system. In both patients with pseudo-pulmonary sling and Kabuki syndrome, the abnormal finding was incidental during echocardiographic examination and neither of the patients required surgical repair for the condition. To the best of our knowledge, they represent the third and fourth cases in which such an anomaly of the pulmonary artery branches not forming a sling is seen in association with Kabuki syndrome. Another case represents our second experience and the second case reported in literature with duplicated left pulmonary artery in the setting of a complex tracheal anatomy. In this symptomatic patient, surgical repair of atrial septal defect and relief of the vascular ring were indicated, and the surgical repair was performed successfully at the age of 3 years.

Corneal anesthesia following application of 0.4% oxybuprocaine hydrochloride ophthalmic solution to normal feline eyes.

OBJECTIVE: To evaluate the loss and recovery of corneal sensitivity after instillation of 0.4% oxybuprocaine hydrochloride solution in the normal feline eye. ANIMAL STUDIED: Eighteen European shorthair cats free of ocular disease PROCEDURES: Baseline corneal touch threshold (CTT) readings were obtained bilaterally with a Cochet-Bonnet aesthesiometer prior to treatment. Subsequently, each cat received a single drop of 0.4% oxybuprocaine ophthalmic solution in the right eye and one drop of sterile 0.9% NaCl in the left eye to serve as control. The corneal touch threshold (CTT) of both eyes was then measured 1 min after drug administration and every 5 min for 60 min. The potential for ocular irritation following oxybuprocaine application was also evaluated. RESULTS: Baseline CTT readings were not significantly different (P > 0.05) between the control and oxybuprocaine-treated eyes with values of 1.75 ± 0.31 cm and 1.75 ± 0.30 cm, respectively. In control eyes, mean CTT did not significantly change (P > 0.05) during the study period. By contrast, after oxybuprocaine application mean CTT was significantly reduced from baseline (P < 0.05) for 45 min. Maximal corneal anesthesia, with a CTT value of 0, was achieved at 1 and 5 min in all treated eyes. A markedly reduced mean CTT of 0.14 ± 0.23 cm was still present at 20 min. Age and gender did not significantly affect corneal anesthesia. No clinically relevant ocular side effects occurred during the observation period. CONCLUSION: This is the first study that provides objective information on the depth and duration of corneal anesthesia following instillation of oxybuprocaine in healthy feline eyes.

Sudden arrhythmic death syndrome: diagnostic yield of comprehensive clinical evaluation of pediatric first-degree relatives.

AIMS: Sudden arrhythmic death syndrome (SADS) is most often caused by heritable cardiac diseases. Studies in adults have identified evidence of inherited cardiovascular diseases in up to 53% of families, but data on the prevalence of familial disease in children are scarce. The aim of this study was to evaluate the yield of clinical screening in pediatric first-degree relatives of victims of SADS using a systematic and comprehensive protocol. METHODS: Patients referred for family screening after sudden cardiac death (SCD) of a family member were, retrospectively, enrolled into the study. Systematic evaluation of the children included clinical examination, family history, electrocardiogram (ECG), echocardiogram, 24-hour tape, and signal-averaged ECG. Older patients also underwent exercise testing, cardiac magnetic resonance imaging, and ajmaline provocation testing. RESULTS: A total of 90 children from 52 consecutive families were included in the study. An inherited cardiac disease was identified in seven first-degree children from seven (13.5%) families (five children were diagnosed with Brugada syndrome, one with long QT syndrome, and one with catecholaminergic polymorphic ventricular tachycardia). Two further children had late potentials on signal-averaged ECGs with no other abnormalities. CONCLUSIONS: These data show a high prevalence of inherited heart disease in pediatric first-degree relatives of SADS victims. The results highlight the importance of a systematic, comprehensive approach and ongoing screening of pediatric family members.

Self-reported weight and height: implications for left ventricular hypertrophy detection. An Italian multi-center study.

We examined the difference between self-reported and measured body size values and their impact on detection of left ventricular hypertrophy (LVH) by echocardiographic LV mass indexation. A total of 1963 subjects referred by their practitioners for routine echocardiographic examination to nine outpatient echocardiographic laboratories across Italy were included in the study. Left ventricular hypertrophy was defined according to two gender- specific criteria as: A) Left ventricular mass (LVM) index ≥49 g/h(2.7) in men and ≥45 g/h(2.7) in women; B) LVM index ≥125 g/m(2) in men and ≥110 g/m(2) in women. Prevalence of LVH was calculated by indexing LVM to both self-reported and measured anthropometric values. In the whole population, LVH tended to be underestimated by self-reported values by 5.4% according to criterion A (48.5% vs. 53.9%, p < 0.001) and by 1.2% according to criterion B (29.6% vs. 30.8%, p < 0.01); similar findings were observed in the hypertensive subgroup encompassing one-half of the sample. Underestimation of LVH was more pronounced in older patients than in younger patients: 8.6% vs. 3.2% (p < 0.001) by criterion A, 3.1% vs. 0.1% (p < 0.001) by criterion B, in women than in men (8.6% vs. 3.3% (p < 0.001) by criterion A and 1.8% vs. 0.5% (p < 0.01) by criterion B. In a sample of outpatients attending echocardiographic laboratories, LVH is misclassified when left ventricular mass is normalized to self-reported weight and height. The error is related to the clinical characteristics of patients and is more pronounced when LVM is normalized to height(2.7).

Impaired midwall mechanics and biventricular hypertrophy in essential hypertension.

OBJECTIVE: Impaired left ventricular (LV) mechanics in human hypertension are strongly related to LV hypertrophy (LVH). In the present study, we investigated the relationship between LV mid-wall fractional shortening (MWS) and biventricular hypertrophy in uncomplicated essential hypertensives. METHODS: A total of 328 hypertensive patients categorized in tertiles of MWS were considered for the analysis. All patients underwent routine and standardized echocardiographic examinations. Biventricular hypertrophy was defined by anterior right ventricular (RV) wall thickness >or=3.1 mm/m(2) in men and >or=3.0 mm/m(2) in women, combined with LV mass index (LVMI) >or=49 g/m(2.7) in men and 45 g/m(2.7) in women. RESULTS: Biventricular hypertrophy was found in 21% of the study population. In the lowest MWS tertile, the likelihood of biventricular hypertrophy was 1.4- and 1.9-fold greater (p<0.05) than in the intermediate and highest one, respectively; this was not the case for isolated LVH or RV hypertrophy (RVH). In a multivariate analysis, MWS was significantly associated with LV mass index (beta=-0.181, p=0.003) and RV wall thickness (beta=-0.171, p50.01). CONCLUSION: In systemic hypertension, a decrease in LV systolic performance may be related not only to LVH, but to the global cardiac involvement occurring in biventricular hypertrophy.

Left ventricular hypertrophy detection and body mass index in essential hypertension.

BACKGROUND AND AIM: Weight and height are two major determinants of left ventricular mass (LVM); the anthropometric parameter to which LVM should be normalized remains, however, debated. In a population of hypertensives, we compared the prevalence of left ventricular hypertrophy (LVH) defined by two indexation criteria of LVM in different subgroups of body mass index (BMI). METHODS: A total of 4468 essential hypertensives included in the Evaluation of Target Organ Damage in Hypertension (ETODH), were divided in four groups according to BMI thresholds: lean (BMI<20 kg/m(2), 4.5%), normal (20-24.9 kg/m(2), 36.5%), overweight (25-29.9 kg/m(2), 41.9%) and obese (≥ 30 kg/m(2), 17.1%). All patients underwent quantitative echocardiography; LVH was defined by two criteria of LVM indexation: (A) ≥ 116 g/m(2) in men and ≥ 96 g/m(2) in women; (B) ≥ 49 g/m(2.7) in men and ≥ 45 g/m(2.7) in women. RESULTS: Overall, 44.9% of the patients were found to have LVH by criterion A, 48.2% by criterion B and 37.0% by both criteria. Prevalence rates of LVH in the four BMI groups were 34.3%, 40.5%, 47.3%, 53.9% by criterion A, 19.8%, 37.0%, 53.6%, 69.7% by criterion B, and 14.2%, 30.9%, 41.5%, 47.8% by both criteria, respectively (p at least <0.05 for all). CONCLUSIONS: Our findings show that LVH prevalence in both overweight and obese hypertensives is higher when LVM is normalized to height(2.7) compared with body surface area (BSA), whereas the opposite trend occurs in normal weight/lean hypertensives. Thus, the risk related to LVH is underestimated when the LVH/height(2.7) criterion is applied to lean/normal weight individuals and the LVH/BSA criterion in overweight/obese individuals.

Left and right ventricular structural changes in obese hypertensives.

AIM: Obesity is known to be independently related to left ventricular (LV) hypertrophy (LVH); however, in human hypertension the association of obesity with right ventricular hypertrophy (RVH) is still unsettled. We investigated the relationship of obesity with RVH and biventricular hypertrophy in essential hypertension. METHODS: A cohort of untreated and treated uncomplicated essential hypertensives consecutively attending a hospital outpatient hypertension clinic, categorized in three groups according to body mass index (BMI) thresholds (<25, 25-29.9 and > or =30 kg/m2) was considered for the present analysis. RVH was defined by an anterior RV wall thickness equal or higher than 3.1/3.0 mm/m2 in men and women, respectively, and LVH by LV mass index (LVMI) equal or higher than 51 and 47 g/m(2.7) in men and women, respectively. RESULTS: A total of 124 patients (37.6%) had normal BMI, 151 patients (45.7%) were overweight and 55 (16.7%) obese. Prevalence rates of biventricular hypertrophy (i.e. LVMI>51 and 47 g/m(2.7) and RVWT>3.1 and 3.0 mm) in the three groups were 7.3%, 21.2% and 32.7%, respectively. In a multivariate analysis, BMI (OR=3.58, 95% CI 1.82-7.03, p=0.0002), was the most important correlate of biventricular hypertrophy. CONCLUSIONS: Our findings extend previous data on the impact of obesity on cardiac structure by showing that this phenotype is strongly associated with biventricular hypertrophy.

Studies on left ventricular hypertrophy regression in arterial hypertension: a clear message for the clinician?

BACKGROUND: Evidence-based medicine should provide clear and unbiased information to clinicians. We conducted an analysis on published randomized trials evaluating the effects of antihypertensive therapy on left ventricular (LV) morphology assessed by echocardiography to investigate (i) the consistency of criteria used for definition of LV hypertrophy (LVH) and (ii) the consistency of the way LVH regression and blood pressure (BP) control were reported. METHODS: Studies identified by a PubMed search were eligible for inclusion in the analysis, if they fulfilled the following criteria: (i) publication in a peer-reviewed journal within the last 12 years; (ii) double blind, randomized, controlled, parallel-group design; (iii) numerosity of at least 50 adult hypertensive subjects; (iv) follow-up duration of at least 6 months; (v) comparison between single-drugs or association regimens; (vi) LV mass (LVM) or wall thickness measured by echocardiography. RESULTS: Thirty-nine trials, including 9,162 hypertensive subjects of both genders in 78 active treatment arms or in 6 placebo arms were identified. Definition of LVH was provided by 34 studies (87.1%) according to 19 different criteria. All trials evaluated LVH regression as the absolute or relative changes of continuous variables such as LVM index (LVMI) or LV wall thickness. Data concerning prevalence rates of LVM normalization were reported in 12 studies (30.7%). The percentage of patients reaching BP target (<140/90 mm Hg) was reported in 11 studies (28.2%). CONCLUSIONS: Our findings indicate that (i) definition of hypertensive LVH phenotype is extremely variable, and (ii) no precise information on LVH regression rates or changes in LV geometrical patterns, as well as on target BP, is provided by the majority of papers.

Metabolic syndrome and multiple organ damage in essential hypertension.

AIM: We investigated the prevalence of the metabolic syndrome (MS) in hypertensive patients categorized according to the number of markers of organ damage (OD) in order to assess the value of a systematic search for cardiac and extra-cardiac OD in the MS setting. METHODS: A total of 3119 untreated and treated essential hypertensives included in the Evaluation of Target Organ Damage in Hypertension (ETODH), an observational registry of hypertension-related OD, were considered for this analysis. All patients underwent extensive investigation for left ventricular hypertrophy (LVH) or LV concentric remodeling (cardiac OD), carotid plaques and/or intima-media thickening (vascular OD) and microalbuminuria (MA) and/or increased serum creatinine (renal OD). Subjects were classified as: positive for none (group 0), one (group I), two (group II) or three markers (group III) of OD. RESULTS: MS prevalence rates progressively rose across the groups stratified according to the OD score, reaching a 2.3-fold increase in group III compared with their MS counterparts in group 0. The distribution of subjects with and without the MS across the groups was 15% vs 29% (group 0), 32% vs 38% (group I), 39% vs 26% (group II) and 14% vs 7% (group III), respectively. Thus, subjects having two or three markers of OD were 53% among those with MS and 33% (p<0.01) among those without it. CONCLUSION: Our findings indicate a strong association between the MS and OD by showing that a clustering of two or three markers of OD is the prevalent cardiovascular phenotype in MS hypertensives referred to a specialist center and call for a systematic evaluation of cardiac and extracardiac OD in this setting.

Alpha-Lipoic Acid and Antioxidant Diet Help to Improve Endothelial Dysfunction in Adolescents with Type 1 Diabetes: A Pilot Trial.

After evaluating the prevalence of early endothelial dysfunction, as measured by means of reactive hyperemia in adolescents with type 1 diabetes, we started a 6-month, double-blind, randomized trial to test the efficacy of an antioxidant diet (± alpha-lipoic acid supplementation) to improve endothelial dysfunction. Seventy-one children and adolescents, ages 17 ± 3.9 yrs, with type 1 diabetes since 9.5 ± 5.3 yrs, using intensified insulin therapy, were randomized into 3 arms: (a) antioxidant diet 10.000 ORAC + alpha-lipoic acid; (b) antioxidant diet 10.000 ORAC + placebo; (c) controls. BMI, blood pressure, fasting lipid profile, HbA1c, insulin requirement, dietary habits, and body composition were determined in each patient. An antioxidant diet significantly improved endothelial dysfunction when supplemented with alpha-lipoic acid, unlike diet with placebo or controls. A significant reduction in bolus insulin was also observed. We speculate that alpha-lipoic acid might have an antioxidant effect in pediatric diabetes patients by reducing insulin.

Serotonin reuptake inhibitors in pregnancy: can genes help us in predicting neonatal adverse outcome?

Lots has been written on use of SSRI during pregnancy and possible short and long term negative outcomes on neonates. the literature so far has described a various field of peripartum illness related to SSRI exposure during foetal life, such as increased incidence of low birth weight, respiratory distress, persistent pulmonary hypertension, poor feeding, and neurobehavioural disease. We know that different degrees of outcomes are possible, and not all the newborns exposed to SSRIs during pregnancy definitely will develop a negative outcome. So far, still little is known about the possible etiologic mechanism that could not only explain the adverse neonatal effects but also the degree of clinical involvement and presentation in the early period after birth. Pharmacogenetics and moreover pharmacogenomics, the study of specific genetic variations and their effect on drug response, are not widespread. This review describes possible relationship between SSRIs pharmacogenetics and different neonatal outcomes and summarizes the current pharmacogenetic inquiries in relation to maternal-foetal environment.

Nocturnal nondipping and left ventricular hypertrophy in hypertension: an updated review.

The classification of hypertensive subjects according to circadian blood pressure (BP) variations (i.e., dipping vs nondipping) is a useful means for reliable individual risk stratification and effective therapeutic decision-making. Increasing evidence, although not univocal, suggests that a reduced nocturnal BP fall relates to an excess of cardiovascular complications. The association between nondipping status with left ventricular hypertrophy (LVH) and its therapeutic implications are still debated; in this article we examined the studies published in the last decade on this controversial issue. The studies identified by a PubMed search were eligible for the analysis if they fulfilled the following criteria: full articles in English, published from 1 January 2000 to 31 December 2009, and inclusion of adult or elderly subjects. According to these criteria, 26 studies encompassing 3877 participants have been selected. A total of 17 studies for a total of 2497 subjects were positive for a link between nondipping and LVH, whereas the remaining nine studies were negative. Notably, three studies that accurately defined the nondipping status on the basis of two consistent ambulatory blood pressure monitoring sessions over a short time interval showed a significant association of this pattern with LVH; this suggests that a persisting nondipping pattern is associated with a more pronounced cardiac involvement. Preliminary data support the view that nondipping may be reverted to dipping by chronotherapy and by diuretics in salt-sensitive patients. Whether restoring the normal nocturnal BP dip in hypertensives with LVH regresses cardiac damage at present remains an untested hypothesis.

Left ventricular geometry, ambulatory blood pressure and extra-cardiac organ damage in untreated essential hypertension.

BACKGROUND AND AIM: Limited information is available on the association between left ventricular (LV) geometric patterns defined according to updated criteria and blood pressure (BP) levels and extra-cardiac organ damage (OD) in human hypertension. Thus, in untreated essential hypertensives we assessed the relationship between LV geometry, ambulatory BP and markers of vascular and renal OD. METHODS: A total of 669 hypertensives were categorized in four groups according to LV geometric patterns defined by two sets of sex-specific criteria (i.e. LV mass indexed to body surface area and height) and by the relative wall thickness (RWT) partition value of 0.42. Ambulatory BP variables were derived from two 24-h monitoring sessions performed within 4 weeks. RESULTS: Lower clinic and ambulatory BP values were associated with normal LV geometry, intermediate values with either LV concentric remodelling or eccentric LV hypertrophy (LVH) and higher values with concentric LVH, regardless of the criteria used to categorize these cardiac phenotypes. A decrease in nocturnal BP dip occurred from normal LV geometry to concentric LVH and this was associated with a parallel increase in the prevalence of carotid and renal OD, which was highest in concentric LVH. In a multivariate analysis age (beta=0.204, P<0.0001), followed by LDL cholesterol (beta=0.113, P=0.004), and night-time BP (beta=0.101, P=0.009) turned out to be the best independent correlates of RWT. CONCLUSION: These findings indicate that LV geometric patterns, regardless of categorization criteria, reflect different degrees of BP load and subclinical extra-cardiac alterations and may be regarded, in addition to absolute values of LV mass, as a reliable marker of cardiovascular (CV) risk.

Retinal changes and cardiac remodelling in systemic hypertension.

The clinical value of left ventricular hypertrophy (LVH), a cardinal manifestation of hypertensive organ damage, in predicting cardiovascular (CV) events, independently of blood pressure (BP) and other accompanying risk factors, has been widely documented and its role in CV stratification indisputability recognized. Although the examination of the fundus oculi provides a unique opportunity to evaluate retinal microvascular abnormalities, which may mirror systemic arteriolar damage due to high BP, no consistent evidence exists, on the prognostic value of mild degrees of retinopathy, encompassing the vast majority of uncomplicated hypertensive subjects. Personal and literature data indicate that: (1) there is a tight association between advanced retinopathy and LVH suggesting the existence of a parallel involvement of retinal tree and cardiac damage in severe untreated or poorly controlled hypertension; (2) in contrast, a firm conclusion about the relationship between early or nonspecific retinal changes (narrowing or arteriovenous crossing) and cardiac damage is not allowed by the majority of the studies; (3) future investigations, based on computer-assisted methods, are further required to document the relation between initial retinal changes with organ damage and more importantly to test their predictive value for clinical outcomes.

Effects of antihypertensive drugs on carotid intima-media thickness: Focus on angiotensin II receptor blockers. A review of randomized, controlled trials.

Carotid intima-media thickness (IMT) and plaques have been shown to have a strong continuous relationship with cardiovascular (CV) morbidity and mortality; therefore, carotid atherosclerosis, as assessed by ultrasonography, can be regarded as a reliable surrogate end-point for therapeutic interventions. In this survey, we report the results of 16 double blind, randomized, controlled studies comparing: 1) antihypertensive drugs versus placebo/no treatment (five trials including 3,215 patients); 2) different active antihypertensive drug regimens (five trials including 4,662 patients); 3) angiotensin-II receptor blockers (ARBs) versus other antihypertensive agents (six trials including 841 patients). Our main findings can be summarized as follows: I) Long-term antihypertensive treatment has a blunting effect on carotid IMT progression, regardless of types of drugs. II) Calcium-channel blockers (CCBs) are more effective than other antihypertensive drugs including diuretics, beta-blockers, and angiotensin converting-enzyme (ACE)-inhibitors in this blunting effect; III) the effect of ARBs compared to other antihypertensive regimens (mostly based on atenolol) on carotid atherosclerosis progression needs to be further elucidated, as a protective effect was demonstrated by some, but not all studies examined. Thus, further studies are needed to clarify the role of ARBs in this therapeutic area.

Is retinal arteriolar-venular ratio associated with cardiac and extracardiac organ damage in essential hypertension?

AIM: Whether retinal microvascular disease is associated with markers of cardiac and extracardiac organ damage in human hypertension is still unclear. We examined the relationship between retinal arteriolar-venular ratio (AVR) and left ventricular hypertrophy, carotid atherosclerosis and microalbuminuria in essential hypertension. METHODS: A total of 386 untreated and treated uncomplicated essential hypertensive individuals (mean age 56 +/- 13 years) consecutively attending our hospital outpatient hypertension clinic were considered for the analysis. All individuals underwent extensive clinical and laboratory investigations, including retinal AVR evaluation by a fully automated computer-assisted method, echocardiography and carotid ultrasonography. RESULTS: Mean retinal AVR was 0.790 +/- 0.079 (range 0.530-0.990). In univariate analyses, AVR showed a significant inverse association with left ventricular mass index (r = -0.15, P = 0.002) and carotid intima-media thickness (IMT) (r = -0.12, P = 0.02); no relationship with microalbuminuria was found. Overall, left ventricular mass index and carotid IMT as well as microalbuminuria, either as continuous or categorical variables, did not show significant differences across AVR quartiles. Moreover, a multivariate analysis failed to demonstrate independent correlations of carotid IMT and left ventricular mass index (P = 0.06 for both) with AVR. Finally, when patients were categorized according to the presence or absence of organ damage, with or without left ventricular hypertrophy (0.783 +/- 0.077 vs. 0.795 +/- 0.081), carotid plaques (0.789 +/- 0.079 vs. 0.791 +/- 0.079), carotid IMT (0.791 +/- 0.077 vs. 0.788 +/- 0.082) or microalbuminuria (0.791 +/- 0.080 vs. 0.777 +/- 0.073), no significant intergroup differences in AVR values were found. CONCLUSION: Our findings provide further evidence that retinal AVR is of limited value in identifying hypertensive patients at high cardiovascular risk related to cardiac and extracardiac organ damage.

Improving cardiovascular risk stratification in essential hypertensive patients by indexing left ventricular mass to height(2.7).

AIM: Clinical abnormalities associated with left ventricular hypertrophy (LVH) only defined by left ventricular mass (LVM) indexed to height(2.7) are still undefined. We investigated the prevalence, clinical correlates and extracardiac organ damage of such a cardiac phenotype in essential hypertensive patients. METHODS: Subclinical organ damage was searched in 3719 untreated and treated hypertensive patients. LVH was defined by two sets of sex-specific criteria, namely, LVM indexed to height(2.7) (left ventricular mass index >49/45 g/m in men and women, respectively) and LVM indexed to body surface area (BSA; left ventricular mass index >125/110 g/m in men and women, respectively). Patients were categorized into three groups, according to the absence of LVH by both criteria (n = 1912, group I), presence of LVH by the height(2.7) criterion only (n = 784, group II) and presence of LVH by both criteria (n = 997, group III). A fourth group (n = 26, <1%), positive for LVH only by the BSA criterion, was excluded from the analysis as being too small. RESULTS: Group II included a higher number of female, obese patients and individuals with metabolic syndrome than the other groups. Moreover, in group II, absolute LVM values and the extent of extracardiac organ damage, as assessed by carotid intima-media thickness, carotid plaques, microalbuminuria and retinal changes were intermediate between group I and III. CONCLUSION: Our data indicate that a consistent portion of essential hypertensive patients are positive for LVH by the criterion of LVM indexed to height(2.7), but not to BSA; this population is characterized by an unhealthy metabolic profile as well as by the presence of extracardiac organ damage. They also suggest that, in order to improve cardiovascular stratification, LVM should be routinely indexed to both BSA and height(2.7) and patients categorized according to the consistency of both criteria.

Prevalence and clinical correlates of right ventricular hypertrophy in essential hypertension.

AIM: Right ventricular hypertrophy (RVH) has been reported to be a component of cardiac damage in systemic hypertension; this evidence, however, is based on small studies and major determinants of biventricular hypertrophy are still undefined. Thus, the prevalence and clinical correlates of RVH have been investigated in essential hypertension. METHODS: A total of 330 untreated and treated uncomplicated essential hypertensives consecutively attending a hospital out-patient hypertension clinic were considered for the analysis. All individuals underwent a quantitative echocardiographic examination as well as extensive clinical and laboratory investigations. RVH was defined by an anterior RV wall thickness equal or higher than 3.1/3.0 mm/m2 in men and women, respectively, and left ventricular hypertrophy (LVH) by LV mass index equal or higher than 51/47g/m2.7 in men and women, respectively. RESULTS: Overall, 114 (34.5%) patients fulfilled the criteria for LVH and 111 (33.6%) for RVH; normal cardiac morphology was observed in 164 patients (49.6%), isolated RVH in 52 (15.7%), isolated LVH in 55 (16.6%) and bi-ventricular hypertrophy in 59 (17.8%). In a logistic regression analysis, modifiable risk factors such as abdominal obesity (OR 3.41, CI 1.73-6.74, P = 0.0004), LV mid-wall fractional shortening (OR 2.48, CI 1.26-4.85, P = 0.008), fasting blood glucose (OR 2.47, CI 1.25-4.89, P = 0.009) and systolic blood pressure (OR 2.39, CI 1.19-4.82, P = 0.014) were the major independent correlates of biventricular hypertrophy. CONCLUSION: RVH is commonly found in systemic hypertension and is associated with LVH (i.e., biventricular hypertrophy) in approximately one-fifth of the patients seen in a specialist setting. The clinical correlates of biventricular hypertrophy suggest that this phenotype is associated with a profile of very high cardiovascular risk.

Body mass index, nocturnal fall in blood pressure and organ damage in untreated essential hypertensive patients.

AIM: We sought to investigate the relationship between body mass index (BMI) and parameters derived from 48-h ambulatory blood pressure monitoring (ABPM) as well as organ damage in human hypertension. METHODS: A total of 658 consecutive outpatients with grade 1 and 2 hypertension, never treated with antihypertensive medications underwent the following procedures: (i) routine examination, (ii) 24-h urine collection for microalbuminuria, (iii) ABPM over two 24-h periods within 4 weeks, (iv) echocardiography and (v) carotid ultrasonography. Each patient was classified as lean (BMI<25 kg/m2) or overweight/obese (> or =25 kg/m2) and according to the consistency of the dipping or nondipping status in the first and second ABPM period, as dipper (DD), nondipper and variable dipper. RESULTS: Mean 48-h, daytime and nighttime systolic BP or diastolic BP were superimposable in the lean (n=314) and overweight (n=344) group. Overweight patients had a reduced nocturnal BP drop compared with their lean counterparts; the prevalence of DD pattern, indeed, was 15% lower in the overweight group as a whole, with a 17% difference in men and 13% in women. The prevalence of left ventricular hypertrophy was higher in overweight than in lean patients (31.8 vs. 15.9% in men and 48.7 vs. 15.6% in women, P<0.01); this more pronounced cardiac involvement was associated with structural carotid alterations. CONCLUSION: This study, the first to investigate the relationship between BMI and nocturnal BP patterns as assessed by two ABPM sessions, shows that overweight hypertensive patients are more likely to have a reduced nocturnal fall in BP and a greater cardiac and extracardiac organ damage as compared with their lean counterparts despite a similar overall BP load.