The "Blood pressure levels, clinical features and markers of subclinical cardiovascular Damage of Asthma patients" (BADA) study is aimed at defining the cardiovascular risk profile and the markers of subclinical and clinical vascular and cardiac damage in asthmatic patients. Very few studies have assessed asthmatic patients without concomitant heart disease through a transthoracic echocardiogram. The goal of the present study is to investigate the prevalence of morphology and/or function changes in the cardiac chambers of a sample of 86 patients with chronic asthma, referred to the dedicated outpatient unit of the Division of Respiratory Diseases of the AOUP "P. Giaccone" of the University of Palermo, and the results obtained were compared with those of a control group without respiratory or cardiovascular diseases. Patients with asthma showed a marked and widespread involvement of the four cardiac chambers compared with the controls: enlargement of the two atria, greater left ventricular remodeling with interventricular septal thickening, increased indexed left ventricular mass with a significantly greater percentage of patients with overt left ventricular hypertrophy, worse left ventricular diastolic function proven by the significant difference in the E/A ratio, and worse right ventricular systolic function with global right ventricular dysfunction estimated by the Myocardial Performance Index (Tei Index). Multivariate regression analysis, after adjustment for essential hypertension, hypertension severity, diabetes, Body Mass Index, and creatinine clearance, seems to indicate that the indexed left ventricular mass, right atrial volume, and right ventricular Tei index (but not left ventricular hypertrophy) correlate significantly with asthma, severe asthma, and FEV1 (and to a lesser extent with asthma duration). No correlation is apparent between inhaled therapy (ICS, SABA) and myocardial involvement. These results seem to confirm that a more in-depth cardiovascular evaluation in patients with chronic respiratory disease allows the identification of unrecognized cardiovascular involvement. A transthoracic echocardiogram performed in asthmatic patients without clinically overt signs or symptoms of cardiovascular impairment has identified some features indicative of an early subclinical cardiac impairment not found in the control group. These findings, considering also the higher frequency of hypertension in the asthma group, deserve further validation in the future.
Objective: Several epidemiological studies suggest that the preservation of the physiological circadian rhythm of blood pressure or its disruption affects the extent of the organ damage developed by the patient. If we classify the circadian rhythm of blood pressure into four nocturnal profiles, significant differences emerge in terms of organ damage burden and prognosis: reverse dippers have the worst prognosis while dippers and mild dippers fall into an intermediate risk range. The risk profile of extreme dippers is still debated, and the available data are very conflicting and inconclusive. Starting from this gap of knowledge, we aimed to evaluate, retrospectively, in a cohort of hypertensive subjects, the degree of cardiac involvement in relation to the different nocturnal blood pressure profiles. Methods: We retrospectively evaluated 900 patients with essential hypertension, of whom 510 met our study criteria. We graded the 510 patients in relation to the percentage of reduction in mean systolic blood pressure (SBP) at night-time compared with day-time, considering this as a continuous variable, and then compared the extreme quintiles with each other and with the middle quintile (considered as reference). Results: Patients with less (or no) reduction in nocturnal SBP (reverse dipper) showed a higher level of organ damage and comorbidities. With regard to echocardiographic indexes, patients with maximum nocturnal pressure reduction (extreme dipper) showed a lower level of remodeling and/or impairment of E/e' ratio, Right Atrium Area, Basal Right Ventricular Diameter, Inferior Vena Cava Average Diameter, and Tricuspidal Anular Plane Systolic Excursion compared also with hypertensive patients with a physiological nocturnal pressure reduction, even after correction for the main confounders. Conclusions: These data suggest that extreme dippers may constitute the subgroup of hypertensive patients with the lowest 24-h pressure load and, therefore, less cardiac remodeling.
Background: It has been reported that changes in cardiac structure and ventricular function associated with obesity have to be attributable to hemodynamic and non-hemodynamic alterations. Accordingly, the aim of this was to evaluate left ventricular hypertrophy (LVH) prevalence and its effect on left ventricular systolic and diastolic function in a cohort of obese patients.Materials and Methods: LV internal diameter (LVID), left ventricular mass (LVM) and LVM/height2.7(LVMI), relative wall thickness (RWT), LV ejection fraction (LVEF), E/A ratio, isovolumic relaxation time, deceleration time of E velocity by echocardiography and pulsed-wave Doppler and total circulating adiponectin (ADPN) by radioimmunoassay were measured in 319 obese subjects with and without LVH.Results: Increased values of BMI, WHR, SBP, DBP, MBP LVID, LVM, LVMI, IVST (p < .001), increased prevalence of subjects with LVEF< 50%,(p < .001), central fat distribution (p < .001), hypertension (p < .001), diabetes (p < .001), metabolic syndrome (p < .02), and reduced value of ADPN (p < .0001) and LVEF (p < .001) were detected in LVH obese subjects than controls without LVH. No significant differences in diastolic parameters were observed between the two groups. LVEF correlated directly with ADPN (p < .0001) and inversely with age (p < .01), BMI (p < .01), WHR (p < .001), MBP (p < .01) MetS (p < .02) and LVMI (p < .001). WHR, MBP, LVMI and ADPN were independently associated with LVEF.Conclusions: In conclusion, our data indicate that obese subjects with LVH might be considered a distinct phenotype of obesity, characterised by LVH, increased prevalence of cardiometabolic comorbidities, central fat distribution, hypoadiponectinemia and early left ventricular systolic dysfunction.
Background: Different studies have indicated that thiazide diuretics can increase the risk of developing type 2 diabetes (T2D). Therefore, in this study, we investigated whether switching from hydrochlorothiazide (HCTZ) to amlodipine resulted in ameliorating different cardiovascular and metabolic measures in hypertensive patients with or without T2D. Methods: This study [Diuretics and Diabetes Control (DiaDiC)] was a 6-week, single-blind, single-center randomized controlled trial. The first 20 normal glucose-tolerant, 20 prediabetic, and 20 T2D consecutive patients were randomized to continue the previous antihypertensive treatment with HCTZ (12.5-25 mg/day) or to switch from HCTZ to amlodipine (2.5-10 mg/day). The primary endpoints were the absolute change in 7-day continuous subcutaneous glucose monitoring (CSGM) glycemia, serum uric acid concentrations, and endothelial function [measured as flow-mediated dilation (FMD)]. Other secondary endpoints were investigated, including changes in glycated hemoglobin (HbA1c), glycemic variability from 7-day CSGM, and the estimated glomerular filtration rate (eGFR). Results: Amlodipine treatment was associated with a significant reduction in HbA1c (P = 0.03) for both 7-day CSGM glycemia (P = 0.01) and glycemic variability (coefficient of variability %: HCTZ +3%, amlodipine -2.8%), and a reduction in uric acid concentrations (P < 0.001), especially in participants with T2D or prediabetes. Following amlodipine treatment, a significant increase in both eGFR (P = 0.01) and FMD (P = 0.02) was also observed. Conclusions: This study demonstrates that the replacement of HCTZ with amlodipine has several metabolic and cardiovascular beneficial effects. However, further intervention studies are necessary to confirm the clinical effects of thiazides, especially in diabetic people and in those at risk of diabetes.
"Tocilizumab therapy for unresponsive pulmonary arterial hypertension in a patient with Takayasu arteritis." Scandinavian Journal of Rheumatology, 45(3), pp. 251–252
Cirrhotic heart has been traditionally considered protected from cardiovascular disease, even if a large amount of literature has recently shown that patients affected by chronic liver disease are exposed to cardiovascular events, as well. Since the first recognition of cardiac involvement in cirrhosis, all published studies explain that decompensated cirrhotic patients suffer from haemodynamic changes, currently known as hyperdynamic syndrome, which finally lead to cirrhotic cardiomyopathy. This is defined by the presence of a subclinical systolic dysfunction unmasked under stress conditions, impaired diastolic function and electrophysiological abnormalities, in the absence of any known cardiac disease. In this review, we will discuss the clinical and diagnostic features of this condition, the prevalence of associated comorbidities, echocardiographic, electrocardiographic and cardiac magnetic resonance hallmarks and the possible diagnostic role of serum biomarkers.
A 59-year-old nursing home patient with Down syndrome was brought to the internal medicine department of our hospital due to fever, cough without expectorate, and dyspnea. A thoracic computed tomography revealed the presence of bilateral basal parenchymal opacities. Her condition deteriorated after admission and troponin reached a peak serum concentration of 16.9 ng/mL. The patient was in cardiogenic shock. In addition to fluid resuscitation, vaso-active amine infusion was administered to achieve hemodynamic stabilization. The differential diagnosis investigated possible pulmonary embolism, myocardial infarction, and myocarditis. Furthermore, a second transthoracic echocardiogram suggested Tako-Tsubo syndrome. This is a septic patient. The purpose of this manuscript is to review studies which formerly examined the possible association between high levels of troponin and mortality to see if it can be considered a positive predictive factor of fatal prognosis as the case of thrombocytopenia, already a positive independent predictive factor of multiple organ failure syndrome, and generally to characterize risk profile in a septic patient.
Background & Aims: Non-alcoholic fatty liver disease (NAFLD) has been associated with increased cardiovascular risk, including coronary artery disease and cardiac dysfunction. In addition, recent evidence highlighted the possible role of epicardial fat as a new cardiometabolic risk factor. We tested the correlation between epicardial fat, alterations in cardiac geometry and function, and severity of liver damage, in patients with biopsy-proven NAFLD.Methods: The anthropometric, biochemical and metabolic features were recorded in 147 consecutive biopsy-proven NAFLD cases (Kleiner score). Epicardial fat thickness was measured by echocardiography.Results: Epicardial fat was higher in patients with severe vs. milder fibrosis (8.5 +/- 3.0 vs. 7.2 +/- 2.3 mm; p = 0.006); this association was maintained at multivariate logistic regression analysis (OR 1.22, 95% C.I. 1.01-1.47; p = 0.04) after correction for gender, age > 50 years, visceral obesity, IFG/diabetes, non-alcoholic steatohepatitis and severe steatosis. Of note, 37.1% of patients with epicardial fat > 7 mm (median value) had severe liver fibrosis, compared to 18.3% of the cases with lower epicardial fat (p = 0.01). As for echocardiographic indices, after adjusting for cardiometabolic confounders, diastolic posterior-wall thickness (p = 0.01), left ventricular mass (p = 0.03), relative wall thickness (p = 0.02), and left atrial volume (0.04), as well as ejection fraction (p = 0.004), lower lateral TDI e' (p = 0.009), E/A ratio (0.04) (cardiac geometry alterations and diastolic dysfunction) were linked to severe liver fibrosis.Conclusions: In patients with NAFLD, a higher epicardial fat thickness is associated with the severity of liver fibrosis, in keeping with a possible pathogenic role of ectopic fat depots in whole body organ damage. In addition, morphological and functional cardiac alterations are more pronounced according to the severity of fibrosis. Further studies are needed to validate our results. (C) 2014 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
SIMI 2013 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 ventricle‐ right ventricle (especially in the presence of pulmonary hypertension).
In recent years, there has been a growing interest about complementary and alternative medicine (CAM), and the use of CAM interventions has become more common among people. For these reasons, health professionals must be able to effectively manage information in this field of knowledge according to an evidence-based point of view. This study assessed the anatomy of the available information about CAMs using PubMed, to give practical instructions to manage information in this field. We also analyzed the anatomy of information according to each alternative medicine branch, narrow and broad search methods, subset filters for indexed-for-Medline and non-indexed citations, and different publication types including randomized controlled trials (RCTs) and meta-analyses. Our results demonstrated that the use of CAMs subset (supplied by PubMed search engine) leads to a great number of citations determining an information overload. Our data reveal that it would be more useful to search for the CAM separately, identifying specific items and study design. Moreover, we found the largest number of randomized clinical trials and meta-analyses related to herbal medicine and acupuncture, neither RCTs nor meta-analyses were available for bach and flower remedies, auriculoacupuncture, iridology, and pranotherapy. For the first time, our study gives a comprehensive view of the anatomy of information regarding CAMs and each branch of them. We suggest a methodological approach to face with searching information about this emerging issue from an evidence-based point of view. Finally, our data pointed out some "grey zones" since neither RCTs nor meta-analyses were available for some CAMs.
The online version of the original article can be found underdoi:10.1007s11739-011-0523-9.C. Argano (&) E. La RoccaUnit of Internal Medicine, San Raffaele-G.Giglio Hospital,Contrada Pietrapollastra, Cefalu` (Palermo), Italye-mail: chargano@yahoo.itD. Colomba T. Di ChiaraBioMedical Department of Internal Medicine and Specialty(DiBiMIS), University of Palermo, Palermo, Italy
Our study was designed to optimize the search strategies based on the work of Haynes et al. for detecting randomized controlled trials (RCTs) through PubMed. In particular, we aimed to improve precision for broad and narrow searches on interventional studies. We used in addition to the string suggested by the Hedge Team the following: {NOT ((animals [mh] NOT humans [mh]) OR (review [pt] OR meta-analysis [pt]))} and tested its effectiveness. The search was carried out on a year's worth of articles from the PubMed database. We analyzed 35,590 bibliographic citations about four relevant major topics in internal medicine (hypertension, diabetes, heart failure, and hepatitis). Precision, percentage gain between the Hedge Team search strategies and the new one were computed and reported in the text. Moreover, a pooled analysis was carried out in terms of absolute precision difference. We observed better precision for both broad and narrow searches. However, effective gain resulted only for broad searches. In this case, bibliographic citation recall effectively reduced (−24 to −35 % retrieved citation with a gain of 32–54 %) without loss of information. The search strategy improved broad searches regarding each of the four considered topics. We think this new search strategy, based on a previous work of the Hedge team, could be a step forward and can save some time by researchers.
No data exist about the possibility that vertebral fracture in PMR patients could be independent of steroid therapy. For this reason, we aimed to investigate this topic by a case cohort study with a 1-year follow-up for each patient. We selected ten consecutive patients who experienced vertebral fractures (VF-group) during the first month of 1-year follow-up period and without any other significant associated condition. As a control group we studied ten control patients, without vertebral fractures and with a follow-up of 1 year, randomly selected among a larger group of patients affected by polymyalgia rheumatica. The following data were analysed: eritrosedimention rate (ESR), visual analogical scale score (VAS), methyprednisolone daily dosage. Each patient had been monthly evaluated by the aforementioned clinical and laboratoristic parameters during the 1-year follow-up period. The VF-group resulted with a higher and statistically significant median corticosteroid 12-month total dosage [mean 3,480 mg (95%CI 2,805–3,030) vs. 2,760 mg (2,666.25–3,247.5)]. The VF-group had statistically significant higher ESR and VAS AUC when compared to control group (median ESR AUC, 484.75 vs. 288.25; P = 0.0001; median VAS AUC, 70.75 vs. 43.5 P < 0.0001); ESR at the baseline (cut-off >80 mm) showed a specificity of 90% (95%CI 56–100) and sensitivity of 70% (95%CI 35–93). VAS difference from first to second month (cut-off ≤3) showed a specificity of 90% (95%CI 56–100) and sensitivity of 80% (95% CI 44–97). Our results point out that vertebral fracture might be predicted from commonly used laboratory (ESR) and clinical (VAS) findings.
The distribution of the T29C TGFβ1 gene polymorphism was analyzed in 198 hypertensives with left ventricular hypertrophy (LVH) and in 235 hypertensives without LVH. Circulating TGFβ1 levels, procollagen type III levels, microalbuminuria, and left ventricular geometry and function were evaluated in all the hypertensives with LVH subgrouped according to T29C TGFβ1 gene polymorphism. Circulating TGFβ1 was evaluated by ELISA technique, procollagen type III by a specific radioimmunoassay, microalbuminuria by radioimmunoassay, and left ventricular geometry and function by echocardiography. All groups were comparable for gender, age, and sex. Regarding T29C TGFβ1 gene polymorphism, prevalence of TC or CC genotypes was significantly (P < .05) higher in hypertensives with LVH than hypertensives without LVH TC and CC LVH hypertensives were characterized by a higher prevalence of subjects with microalbuminuria (P < .05 TC and CC versus TT), by increased levels of TGFβ1, procollagen type III, urinary albumin excretion, LVM, LVM/h(2.7), and lower values of left ventricular ejection fraction (P < .05 TC and CC versus TT). Our data suggest that T29C TGFβ1 gene polymorphism was associated with clinical characteristics adequate to recognize a subset of LVH hypertensives with a higher severity of hypertension.
The distribution of the T29C TGFβ1 gene polymorphism was analyzed in 198 hypertensives with left ventricular hypertrophy (LVH) and in 235 hypertensives without LVH. Circulating TGFβ1 levels procollagen type III levels, microalbuminuria and left ventricular geometry and function were evaluated in all the hypertensives with LVH subgrouped according to T29C TGFβ1 gene polymorphism. Circulating TGFβ1 was evaluated by ELISA technique, procollagen type III by a specific radioimmunoassay, microalbuminuria by radioimmuno-assay, left ventricular geometry and function by echocardiography. All groups were comparable for gender, age and sex. Regarding T29C TGFβ1 gene polymorphism, prevalence of TC or CC genotypes was significantly (p < 0.05) higher in hypertensives with LVH than hypertensives without LVH. TC and CC LVH hypertensives were characterized by a higher prevalence of subjects with microalbuminuria (p < 0.05 TC and CC vs TT), by increased levels of TGFâ1, procollagen type III, urinary albumin excretion, LVM, LVM/h2.7 and by lower values of left ventricular ejection fraction (p < 0.05 TC and CC vs TT). Our data suggest that T29C TGFβ1 gene polymorphism was associated with clinical characteristics adequate to recognize a subset of LVH hypertensives with a higher severity of hypertension.
We enrolled nine consecutive patients affected by newly diagnosed polymyalgia rheumatica and decompensated diabetes mellitus. All patients were treated with etanercept (25 mg twice weekly) and prednisone and were followed up to 1 year. At the sixth-month follow-up, etanercept and prednisone were withdrawn. Patients were seen at regular intervals (days 0, 30, 60, 90, 150, 180) and the following variables determined: erythrocytes sedimentation rate, C-reactive protein, fasting serum glucose, pain measured by visual analog scale, and the Health Assessment Questionnaire. Our results indicate that etanercept might have some steroid-sparing effects, but controlled investigations are needed to support etanercept use in clinical practice for this kind of patients.
Abstract Background Nitric 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. Results The 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. Conclusion Our results seem to indicate a lack of association with eNOS variants and cardiovascular damage onset.
AND trial (Title/Abstract))). Obviously, clini- cians using the PubMed Clinical Queries may be unaware of the PubMed search engine technical approach even whether they can remain unaware of what the PubMed search engine is doing. We demonstrated substantial mild retrieval bias of PubMed Clinical Queries filter focusing on therapy (narrow search) that can miss up-to-date scientifically information on treatments. This bias occurs because the search string does not consider the Britannic English variant of the term randomized (i.e., randomised). We suggested a slight change in the original search string by the addition of the term randomised as follows: (randomized controlled trial (Publication Type) OR ((randomized (Title/Abstract) OR randomised (Title/ Abstract)) AND controlled (Title/Abstract) AND trial
Distribution of T29C TGF beta 1 gene polymorphism was analysed in 260 hypertensive and 134 normotensive subjects. Circulating TGF beta 1 and procollagen type III levels, microalbuminuria, left ventricular geometry and function were evaluated in all the hypertensives subgrouped according to T29C TGF beta 1 gene polymorphism. Circulating TGF beta 1 by ELISA technique, procollagen type III by a specific radioimmunoassay, microalbuminuria by radioimmunoassay, left ventricular geometry and function by echocardiography were determined. All groups were comparable for gender, age and sex. Regarding T29C TGF beta 1 gene polymorphism, prevalence of TC or CC genotypes was significantly (p < 0.05) higher in hypertensives than normotensives. TC and CC hypertensives were characterized by a higher prevalence of subjects with microalbuminuria (p < 0.001 TC vs TT; p < 0.05 CC vs TT), left ventricular hypertrophy (p < 0.01 TC and CC vs TT), and by increased levels of procollagen type III (p < 0.05 TC and CC vs TT). TC hypertensives were also characterized by a significant increase (p < 0.05) of LVM and LVM/h(2.7) and of urinary albumin excretion (p < 0.05) values than those detectable in TT hypertensives. Our data suggest that T29C TGF beta 1 gene polymorphism was associated to clinical characteristics suitable to recognize hypertensives with a higher severity of hypertension.