AIMS:The purpose of the study was to examine the association between visceral adiposity form of non-alcoholic fatty liver and coronary artery disease severity and also to investigate the relationship between the epicardial adipose tissue thickness and non-alcoholic fatty liver disease with clinical and anthropometric measurements.MATERIALS AND METHODS:This study included 105 patients (mean age of patients were 57 ± 11, 82 of them male) who were hospitalized for coronary angiography because of chest pain. Nonalcoholic fatty liver disease was investigated by using ultrasonography. Thickness of the epicardial adipose tissue was measured by transthorasic echocardiography to right ventricular free wall adjacent to the parasternal long and short axis images. Gensini score was used for the severity of coronary artery disease.RESULTS:In patients with non-alcoholic fatty liver disease, right ventricular free wall epicardial adipose tissue thickness average of parasternal long and short axis were thicker than those who do not have non alcholic fatty liver disease (0,90 ± 0,19 cm; 0.58 ± 0.18 cm, p<0.001). Also, in patients with severe coronary artery disease, right ventricular free wall parasternal long and short axis average thickness of epicardial fat tissue was thicker than those of patients without severe coronary stenosis (0.86 ± 0.21 cm; 0,66 ± 0.26 cm, p=0.001). For predictability of coronary artery disease, Receiver Operating Characteristic analysis of the area under the curve was found to be 0.60 (50.2 to 74.7, 95% Confidence Limits).CONCLUSIONS:Not only the fatty tissue which surrounds the heart effects the coronary arteries but also other visceral organs adiposity effects the coronary arteries atherosclerotic process.

Aim: The most important adverse event of anthracyclines is cardiotoxicity and can limit the use of them. Spironolactone is an aldosterone antagonist and has antifibrotic and antioxidant effects. In the present study, we aimed to investigate the effects of spironolactone in the prevention of the cardiotoxic effects of the anthracycline. Materials and methods: A total of 83 female patients who diagnosed with breast cancer and planned anthracycline including chemotherapy regimen were enrolled in to the study. Study population were randomized as spironolactone and control group. Twenty five mg/day spironolactone was administrated to the patients in spironolactone group. Results: LVEF decreased from 67.0±6.1 to 65.7±7.4 (p=0.094) in the spironolactone group, while from 67.7±6.3 to 53.6±6.8 in control group (p<0.001). Diastolic functional class was prevented in spironolactone group (p=0.247). In the control group, however, diastolic functional class was deteriorated (p<0.001). Mitral inflow E wave/lateral wall e' wave ratio which is one of the most important sign of the diastolic functions was significantly increased in the control group while prevented in the spironolactone group. ![Figure][1] Figure 1 Conclusions: Prophylactic administration of spironolactone 25 mg/day prevents the left ventricular systolic and diastolic functions in patients who administrated anthracyclines. [1]: pending:yes

AIM:The serotonin levels in thrombocytes are decreased in hypertensive patients. The aim of our study was to investigate the relationship between serotonin levels and insufficient nocturnal blood pressure (BP) decrease (non-dipper) in hypertensive patients. PATIENTS AND METHODS:Fifty-six hypertensive patients and 27 healthy control subjects were included in the study. Of the hypertensive patients, 28 were classified as dippers and 28 as non-dippers based on nocturnal BP drops of >10 mmHg and <10 mmHg, respectively. Thrombocyte serotonin levels, serum uric acid, and C-reactive protein (CRP), and urinary albumin/creatinine ratios were analysed. Thrombocyte serotonin levels were measured using an enzyme immunoassay. RESULTS:The thrombocyte serotonin level was 378.9 +/- 69.5 ng/10(9) platelet in the non-dipper group, 424.7 +/- 58.6 ng/10(9) platelet in the dipper group, and 518.1 +/- 35.9 ng/10(9) platelet in the control group. Serotonin levels in the non-dipper group were significantly lower than in the dipper group. Serotonin levels negatively correlated with blood pressure (r = -0.6, p<0.001). CRP concentration in the non-dipper group was higher than in the dipper (4.8 +/- 1.4 vs 3.6 +/- 1.6, p<0.01) and control (2.4 +/- 0.9, p<0.001) groups, and microalbuminuria was significantly higher in the non-dipper group compared with dipper (24.9 +/- 8.6 vs 13.4 +/- 8.8, p<0.001) and control (9.6 +/- 4.8, p<0.001) groups. Serotonin level was negatively correlated with microalbuminuria (p<0.001, r = -0.3), uric acid (p<0.01, r = -0.3), and CRP (p<0.01, r = -0.35). CONCLUSION:In non-dipper hypertensive patients, thrombocyte serotonin levels were significantly lower than in dipper and control groups. Serotonin levels may be related to insufficient nocturnal blood pressure decrease in hypertensive patients.

Sitosterolemia is a disease characterized by an intestinal hyperabsorption of plant sterols and cholesterol. Affected individuals have mutations in both alleles of either ABCG5 or ABCG8 genes, leading to a total loss of one of the proteins and subsequent functional deficiency. We here report a Mexican family with clinical and biochemical features of sitosterolemia carrying 2 new mutations of the ABCG5 gene. Concentrations of sitosterol, campesterol, and cholesterol were found to be higher for the index case (a 10-year-old girl) than for her also affected sibling (64.1 vs 19 mg/dL, 32 vs 12.1 mg/dL, and cholesterol 295 vs 235 mg/dL, respectively). Both individuals showed 2 new ABCG5 gene mutations identified by sequencing, which is concordant with their biochemical diagnosis of sitosterolemia. The first mutation was a c.144 -1G>A transition that disrupts the intron 1 splicing acceptor site. The second mutation is the deletion c.1523 delC, which occurred in exon 11, causing an amino acid change at codon 510 (p.His510Thr) and a stop codon at codon 511 (p.Leu511X). The father is heterozygote for the mutation c.144 -1G>A, whereas the mother is heterozygote for the mutation c.1523 delC. In conclusion, we here report the first case of a Mexican family with sitosterolemia carrying two new ABCG5 gene mutations.

Aortic stenosis is the most common type of valve disease in the adults. Until recently its treatment was an exclusive domain of cardiac surgery. At the same time the aortic valve replacement (SAVR) was not indicated in about 1/3 of the patients, though the prognosis of conservatively treated patients is very unfavourable with one-year mortality rate of 50%. These facts were the main reasons for starting a new interventional era of the aortic valve disease therapy in 2002 and from 2007 two types of valves fixed in stents have been commercially available.In the early phase the transcatheter aortic valve implantation (TAVI) was used just in patients with contraindication to SAVR or with high perioperative risk after surgery. Before applying this therapy to less risky patients some problems have to be solved: 1. clinical impact of the relatively high rate of paravalvular leaks and 2. long-term function of the implanted valve in follow-up exceeding 5 years.In the Czech Republic the first TAVI was performed in Prague, IKEM in December 2008. During a short period of time the TAVI programme was initiated also in other complex cardiovascular centres in Hradec Kralove, Brno, Prague—FN Kralovske Vinohrady and Trinec. Including the later starting centres (Usti n. Labem, Olomouc, Ceske Budejovice and other three centres in Prague—Nemocnice na Homolce, FN Motol and VFN) there is a total of 11 centres providing the TAVI at present. All centres except one (FN Motol) are part of the Czech TAVI Registry that was developed with the support of the Czech Society of Cardiology and started on 1 September, 2010. In general and more theoretically there are two parts of the Registry: 1. “Retrospective” including all the TAVI procedures from the beginning of the TAVI programme in the Czech Republic that was terminated on June 30, 2011 and 2. “Prospective” that has been following. Institute of Biostatistics and Analyses of Masaryk University takes care of the online and anonymized database.The results of the national Czech TAVI Registry should help to answer the clinical relevant questions mentioned above.

BackgroundB-type natriuretic peptide (BNP) is secreted from the ventricles in response to volume expansion and pressure overload. We aimed to investigate plasma BNP levels in inferior myocardial infarction (MI) with and without right ventricular MI (RVMI). MethodsWe enrolled 49 patients (mean age: 60±10 years, 45 males) who were admitted with first acute inferior MI. Sixteen patients (mean age: 58±10 years, 15 males) had also RVMI. The BNP levels were measured at admission. All patients underwent echocardiographic examination in the first day of hospitalization. Receiver-operating characteristic curve was obtained for prediction of inferior MI with RVMI. ResultsInferior MI with RVMI had lower RV fractional area change (36±14% vs. 48±15%, P=0.03) and right ventricle lateral annulus S velocity (10.6±1.9 m/s, 12.2±2.6 m/s, P=0.02). The BNP levels were higher in inferior MI with RVMI than isolated inferior MI (75±44 pg/ml vs. 32±24 pg/ml, P=0.001). On the basis of the receiver-operating characteristic analysis, the cutoff value of BNP concentration >46 pg/ml provided the best discrimination of patients with and without RVMI (sensitivity 76%, specificity 88%) with positive and negative predictive values of 92 and 63%, respectively. ConclusionPlasma BNP levels are higher in inferior MI with RVMI than isolated inferior MI. RV involvement may be suspected when BNP levels are higher than 46 pg/ml in inferior MI.

OBJECTIVES The aim of this study was to determine the protective effect of carvedilol in anthracycline (ANT)-induced cardiomyopathy (CMP). BACKGROUND Despite its broad effectiveness, ANT therapy is associated with ANT-induced CMP. Recent animal studies and experimental observations showed that carvedilol prevented development of CMP due to chemotherapeutics. However, there is no placebo-controlled clinical trial concerning prophylactic carvedilol use in preventing ANT-induced CMP. METHODS Patients in whom ANT therapy was planned were randomized to administration of carvedilol or placebo. We enrolled 25 patients in carvedilol and control groups. In the carvedilol group, 12.5 mg once-daily oral carvedilol was given during 6 months. The patients were evaluated with echocardiography before and after chemotherapy. Left ventricular ejection fraction (EF) and systolic and diastolic diameters were calculated. RESULTS At the end of 6 months of follow-up, 1 patient in the carvedilol group and 4 in the control group had died. Control EF was below 50% in 1 patient in the carvedilol group and in 5 in the control group. The mean EF of the carvedilol group was similar at baseline and control echocardiography (70.5 vs. 69.7, respectively; p 0.3), but in the control group the mean EF at control echocardiography was significantly lower (68.9 vs. 52.3; p 0.001). Both systolic and diastolic diameters were significantly increased compared with basal measures in the control group. In Doppler study, whereas E velocities in the carvedilol group decreased, E velocities and E/A ratios were significantly reduced in the control group. CONCLUSIONS Prophylactic use of carvedilol in patients receiving ANT may protect both systolic and diastolic functions of the left ventricle. (J Am Coll Cardiol 2006;48:2258–62) © 2006 by ublished by Elsevier Inc. doi:10.1016/j.jacc.2006.07.052

In several epidemiological studies, it was suggested that a high titer of cytomegalo-virus (CMV) antibody meant CMV reactivation, and that this condition was a determinant of coronary artery disease (CAD). The purpose of this study was to investigate both the prevalence of the CMV infections in our study population and whether high CMV sero-positivity is a determinant of CAD. Blood samples from 179 (58 female, 121 male) individuals being evaluated for CAD suspicion by coronary angiography were tested for CMV seropositivity and CRP levels. Fifty-six patients had normal coronary arteries and 123 patients had CAD. Six patients did not have anti-CMV antibodies and 87 of the 173 seropositive patients had high levels of anti-CMV antibodies (> or = 8 U/mL). High CMV seropositivity (> or = 8 U/mL) was a significant CAD determinant even after adjustment for traditional CAD risk factors (odds ratio [OR] = 2.1 P = 0.04, respectively). The results indicate that the prevalence of high CMV seropositivity is an independent predictor of CAD in our study population and that our study population with CAD had a high rate of CMV infection.