No abstract

The authors evaluated the retrieval power of PubMed "Clinical Queries," narrow search string, about therapy in comparison with a modified search string to avoid possible retrieval bias. PubMed search strategy was compared to a slightly modified string that included the Britannic English term "randomised." The authors tested the two strings joined onto each of four terms concerning topics of broad interest: hypertension, hepatitis, diabetes, and heart failure. In particular, precision was computed for not-indexed citations. The added word "randomised" improved total citation retrieval in any case. Total retrieval gain for not-indexed citations ranged from 11.1% to 21.4%. A significant number of Randomized Controlled Trial(s) (RCT)s (9.1-18.2%) was retrieved for each of the selected topics. They were often recently published RCTs. The authors think that correction of the Clinical Queries filter (when they focus on therapy and use narrow searches) is necessary to avoid biased search results with loss of relevant and up-to-date scientifically sound information.

BackgroundNitric oxide (NO) synthesized by endothelial nitric oxide synthase (eNOS) plays an important role in regulation of endothelial function and in the control of blood pressure. However, the results from some studies on the association between three clinically relevant eNOS gene polymorphisms (G894T, T786C and intron 4b/a) and essential hypertension are unclear. We designed a case-control study to evaluate the influence of eNOS polymorphisms on target organ damage in 127 hypertensives and 67 normotensives. Clinical evaluation, biochemical parameters, Urinary Albumin Excretion (UAE) and echocardiogram were performed to characterize target organ damage. eNOS polymorphism were recognized by PCR method.ResultsThe distribution of eNOS genotypes was similar in hypertensives and normotensives but 4aa was present in the 2.5% of hypertensives and completely absent in normotensives. Subjects with 4bb, G894T, and T786C genotypes showed an increased prevalence of target organ damage. Moreover prevalence of G894T and introne 4 variants was significantly higher in hypertensives than in normotensives both with cardiovascular damage. Logistic regression analysis didn't show any association between eNOS polymorphisms, Body Mass Index (BMI), hypertension, gender and cardiovascular damage. Only the age (OR 1.11; IC 95% 1.06–1.18) was predictive of cardiovascular damage in our population.ConclusionOur results seem to indicate a lack of association with eNOS variants and cardiovascular damage onset.

Our data suggest that TGFbeta1 levels are positively associated with BMI, MBP and UAE in hypertensive subjects. This also indicates that TGFbeta1 overproduction might be considered a pathophysiology mechanism of progressive renal function impairment in obese hypertensives.

Despite the fact that it is known that hypertension may be associated to early atherosclerosis manifestations, few data are to date available on the relationship between early carotid abnormalities and left ventricular diastolic dysfunction. To address this issue, 142 hypertensive patients (64 females and 78 males) younger than 55 years, at the first diagnosis of mild-tomoderate essential hypertension (WHO/ISH criteria), were selected from a database consisting of 3541 subjects referred to ultrasound cardiovascular laboratory in the last 5 years. Carotid intima-media thickness (IMT) was detected by high-resolution vascular ultrasound and left ventricular structure and function by the use of Doppler echocardiography. According to carotid IMT values, all patients were subgrouped into two groups consisting of 89 (62.6%) pts with IMT X1 mm (A) and 53 (37.4%) pts with IMT o1 mm (B). Our results show that isovolumic relaxation time (IVRT), deceleration time of E velocity (EDT) and left ventricular relative wall thickness (LV-RWT) were significantly (Po0.05) higher in group A (IVRT 112 7 8.9 ms; EDT 288 7 21.8 ms; LV-RWT 0.40 7 0.08) than in group B (IVRT 92.3 7 4.6 ms; EDT 203.3 7 27.01 ms; LV-RWT 0.37 7 0.06). Moreover, the prevalence of left ventricular hypertrophy (LVH) was significantly (Po0.01) higher in group A (30/89; 33.7%) than in group B (8/53; 15%). A positive correlation (Po0.001) between IMT, EDT and IVRT was found only in hypertensives without LVH. These results are consistent with the indication that IMT evaluation has to be recommended both in hypertensive patients with LVH and in those without LVH, but with left ventricular diastolic dysfunction. This approach might improve the prognostic stratification of hypertensive subjects and it might be suitable to recognize the subset of patients at a higher risk of cardiovascular disease or events early.

The Gerbode defect is characterized by a perimembranous ventricular septal defect (VSD) between the left ventricle and the right atrium. It is a rare defect representing less than 1 % of congenital cardiac defects [1]. Acquired cases have been described, most often due to endocarditis, but also secondary to valvular surgery, thoracic trauma and ischemic heart disease. Frank Gerbode was the first surgeon to report a successful series of patients who underwent surgery for left ventricular to right atrium shunt in 1958 [2].Gerbode has described two types of defect:-Type A: In this form, the concurrent presence of a perimembranous VSD plus the tricuspid valve defect are visible. The shunt starts from the left ventricle to the right ventricle and through the tricuspid valve into the right atrium. This is referred to as an indirect left ventricle-right atrium shunt. -Type B: This form is characterized by a left ventricle to the right atrium shunt.This rare form of interventricular septal defect should be suspected during the performance of an echocardiogram, when there is an unusually dilatated right atrium, and when, in the presence of an interventricular septal defect, high velocity flows or aliasing are absent in the right ventricle (mainly in inflow tract) [3]. A particular feature of the Gerbode defect is the high Doppler gradient of the shunt, due to the higher pressure gap between the left ventricle and the right atrium rather than left ventricleright ventricle (especially in the presence of pulmonary hypertension).We report the case of a 48-year-old woman admitted to our division because of mild exertional dyspnoea. Her clinical history included a previous diagnosis of a perimembranous VSD, in adolescence. Physical examination was unremarkable except for a 3/6 Levine pansystolic murmur heard at the left sternal border. The echocardiogram detected only a mild right atrium enlargement. The presence of a perimembranous ventricular septal was initially confirmed, but a careful color Doppler flow mapping analysis did not show high velocity flows in the right ventricle inflow during systole although high velocity flows were well present in the right atrium. How was it possible? Why were high velocity flows present only in the right atrium? This finding might suggest the presence of a tricuspid regurgitation and pulmonary hypertension defect (jet velocity 4.87 m/s, 95 mmHg gradient estimated). Doubts about the previous diagnosis were raised. For this reason a color Doppler analysis, frame by frame, was performed. Surprisingly, the short axis projection showed a sudden 90°turn of the jet from the left ventricle to the right atrium concurrent with the closure of the septal leaflet of the tricuspid valve (Fig. 1). The jet continued its course depicting the atrial surface of the tricuspid valve. The subcostal views of the right ventricle confirmed our analysis. A small thickening and abnormal insertion of the basal portion of the septal tricuspid leaflet were also present. These images were consistent with a left to righ...

This study has been designed to evaluate the relationship among transforming growth factor b1 (TGFb1) and some measurements of diastolic function in a population of hypertensive subjects with normal left ventricular ejection fraction. We studied 67 hypertensive outpatients who according to their BMI levels were subdivided into three groups: lean (L), overweight (OW) and obese (OB) hypertensives (HT). Circulating TGFb1 and M-and B-mode echocardiography was determined. All hypertensives were further subgrouped, according to European Society of Cardiology Guidelines, into two subsets of patients with normal diastolic function or with diastolic dysfunction. Prevalence of left ventricular hypertrophy (LVH) was determined in all the groups. TGFb1, left ventricular mass (LVM), LVM/h 2.7 , E-wave deceleration time and isovolumic relaxation time (IVRT) were significantly (Po0.005) higher and E/A velocity ratio was significantly (Po0.05) lower in OW-HT and OB-HT than in L-HT. Prevalence of LVH was significantly higher (Po0.03) in group OB-HT than in L-HT. TGFb1 (Po0.004), LVM/h 2.7 (Po0.001) and prevalence of LVH were (Po0.01) significantly higher in hypertensives with diastolic dysfunction than hypertensives with normal diastolic function. TGFb1 levels were positively correlated with BMI (r ¼ 0.60; Po0.0001), LVM/h 2.7 (r ¼ 0.28; Po0.03), IVRT (r ¼ 0.30; Po0.02) and negatively with E/A ratio (r ¼ À0.38; Po0.002) in all HT. Multiple regression analysis indicated that TGFb1, BMI and IVRT were independently related to E/A ratio explaining 71% of its variability (r ¼ 0.84; Po0.0001). This relationship was independent of LVH, age and HR suggesting that TGFb1 overproduction may be considered a pathophysiological mechanism in the development of left ventricular filling abnormalities in obesity-associated hypertension.

The effects of 24 weeks losartan and ramipril treatment, both alone and in combination, on left ventricular mass (LVM), circulating transforming growth factor b1 (TGFb1), procollagen type I (PIP) and III (PIIIP), have been evaluated in hypertensive (HT) patients. A total of 57 HT with stage 1 and 2 essential hypertension were included. After 4 weeks run in, a randomized doubleblind, three arms, double dummy, independent trial was used. All HT patients were randomly allocated to three treatment arms consisting of losartan (50 mg/daily), ramipril (5 mg/ daily) and combined (losartan 50 mg/ daily þ ramipril 5 mg/daily) for 24 weeks. TGFb1, PIP and PIIIP, LVM, LVM/h 2.7 and other echocardiographic measurements, blood urea nitrogen, creatinine and clearance and potassium were determined after run in and after 24 weeks. All groups were comparable for gender, age, body mass index, blood pressure and LVM. The prevalence of baseline left ventricular hypertrophy (LVH) was not significantly different among three groups. At the end of treatment, a significant (Po0.05) reduction in systolic blood pressure (SBP), diastolic blood pressure (DBP), mean blood pressure (MBP), TGFb1, PIP, PIIIP, LVM and LVM/h 2.7 was observed in all groups. The absolute and percent reduction in TGFb1 and LVM/h 2.7 were significantly higher in combined than losartan or ramipril groups and also in HT patients with LVH. No significant change in absolute and percent reduction of SBP, DBP and MBP were found. Our data indicate an additional cardioprotective effect of dual blockade of renin-angiotensin in HT patients.