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Chronic inflammatory diseases are associated with increases in cardiovascular diseases (CVD) and subclinical atherosclerosis as well as early-stage endothelial dysfunction screening using the FMD method (Flow Mediated Dilation). This phenomenon, referred to as accelerated pathological remodeling of arterial wall, could be attributed to traditional risk factors associated with atherosclerosis. Several new non-invasive techniques have been used to study arterial wall's structural and functional alterations. These techniques (based of Radio Frequency, RF) allow for an assessment of artery age through calculations of intima-media thickness (RF- QIMT), pulse wave rate (RF- QAS) and endothelial dysfunction degree (FMD). The inflammatory and autoimmune diseases should now be considered as new cardiovascular risk factors, result of the major consequences of oxidative stress and RAS (Renin Angiotensin System) imbalance associated with the deleterious effect of known risk factors that lead to the alteration of the arterial wall. Inflammation plays a key role in all stages of the formation of vascular lesions maintained and exacerbated by the risk factors. The consequence of chronic inflammation is endothelial dysfunction that sets in and we can define it as an integrated marker of the damage to arterial walls by classic risk factors. The atherosclerosis, which develops among these patients, is the main cause for cardiovascular morbi-mortality and uncontrolled chronic biological inflammation, which quickly favors endothelial dysfunction. These inflammatory and autoimmune diseases should now be considered as new cardiovascular risk factors.

Xavier Castellon, Vera BogdanovaDepartment of Cardiology, Private Hospital Athis Mons, Paris, FranceAbstract: Atherosclerosis is a leading cause of cardiovascular death due to the increasing prevalence of the disease and the impact of risk factors such as diabetes, obesity or smoking. Sudden cardiac death is the primary consequence of coronary artery disease in 50% of men and 64% of women. Currently the only available strategy to reduce mortality in the at-risk population is primary prevention; the target population must receive screening for atherosclerosis. The value of screening for subclinical atherosclerosis is still relevant, it has become standard clinical practice with the emergence of new noninvasive techniques (radio frequency [RF] measurement of intima-media thickness [RFQIMT] and arterial stiffness [RFQAS], and flow-mediated vasodilatation [FMV]), which have been used by our team since 2007 and are based on detection marker integrators which reflect the deleterious effect of risk factors on arterial remodeling before the onset of clinical events. These techniques allow the study of values according to age and diagnosis of the pathological value, the thickness of the intima media (RFQIMT), the speed of the pulse wave (RFQAS), and the degree of endothelial dysfunction (FMV). This screening is justified in asymptomatic patients with cardiovascular risk factors (hypertension, diabetes, obesity, dyslipidemia, and tobacco smoking). Studies conducted by RF coupled with two-dimensional echo since 2007 have led to a more detailed analysis of the state of the arterial wall. The various examinations allow an assessment of the degree of subclinical atherosclerosis and its impact on arterial remodeling and endothelial function. The use of noninvasive imaging in screening and early detection of subclinical atherosclerosis is reliable and reproducible and allows us to assess the susceptibility of our patients with risk factors and ensures better monitoring of atherosclerosis, thus reducing the occurrence of cardiovascular events in the long term.Keywords: radio frequency, RF QIMT, RF QAS, FMV, arterial age, velocimetry, MRI

Pronostic of cardiogenic shock (CS) is severe and mortality is still more than 50%.Aim of the studyProspective study of patients consecutively hospitalized for a first CS due to cardiomyopathy (CM) with LV dysfunction and a 18-month period of follow-up.Inclusion criteriaCS is defined by systolic BP 8% (n=11), HBP (n=7), tabacco (n=9), dyslipidemia (n=8). Upon admission NT proBNP value was 5025ng/mL and 1730ng/ml 8 weeks later. The mean LVEF was initially 23±8% and 39,5±13,7% at the end of the follow up. The duration of hospitalisation was 12±15 days.initial 6 mois 18 moisNYHA IV Stage (%) 100 20 18LBBB(%) 46Creatininemia (umol/l) 150±100 130±50 127±42LVEF% 24±9% 30±8% 39,5± 13,7LVEDD (mm) 64±9 62±10 61± 20,3SPAP (mmHg) 50±14 49±10 30±9,4NT pro BNP (ng/ml) 5025±8200 3800±6200 1730±4200At the end of the follow up, in 6 patients heart failure symptoms decreased and 3 patients normalized their LVEF. 3 patients alone had a βblocker treatment, 2 resynchronisations, and with DAI for 1 patient and 2 transplantations. 3 patients died due to cardiogenic complications (all with an ischemic cardiomyopathy) and 7 patients had iterative hospitalisation for heart failure.ConclusionThe pronostic of cardiogenic shock without acute coronary syndrome is better with the improvement of therapeutic methods but, in this study the severity was important: death = 12.5%, morbidity = 31.2%.

Background Oxidative stress (OS) implication is paramount in pathology: ischemia reperfusion sequence (acute coronary syndrome, cardiac surgery, transplantation). Involvement of OS in heart failure (HF) is less known but is increased in the failing heart, and this might contribute to the pathogenesis of myocardial remodeling and HF. Aim Prospective study to identify OS in plasma from patients with a cardiogenic shock and to evaluate the role of etiologies of cardiomyopathy: ischemia or no. Methods Consecutive patients hospitalized in the cardiology unit with a first cardiogenic shock that complicated an idiopathic or ischemic dilated cardiomyopathy (DCM) with left ventricular (LV) dysfunction. Exclusion criteria: known cardiomyopathy, acute coronary syndrome, septic or anaphylactic or hypovolemic shock, treatment with angiotensin converting enzyme inhibitors (ACEI) or angiotensin II antagonists (AA II). OS was evaluated in blood samples at the admission (T0) and one month later: thiobarbituric acid-reactive substances (TBARS), total antioxidant status (TAS), protein carbonyls (PC) and LDL oxidized; superoxide dismutase (SOD), glutathione peroxidase(GSH and GSSG/GSH) and catalase activities; plasma α tocopherol, vitamin A and β carotene. Results 23 consecutive patients (90% men), mean age 59±11y. Follow-up of 15 months. The aetiologies of CMD were ischemic (n=6), idiopathic (n=15), toxic (n=1) or restrictive (n=1). The mean LV ejection fraction was 23.3±8%. The NT-proBNP level was 9600±2000ng/ml. To 1 MONTH NORMAL VALUE PC (μmol/g prot) 0.16 (0.05-0.41) 0.14 (0.07-0.29) TBARS (nmol/gHb) 2.2 (1.3-17.3) 2.5 (1.1-6.5) 0.7-1.6 LDLox (UI/L) 48 (20-83) 49 (26-98) 16-18 GSH (μmol/g Hb) 2.1 (0.8-3.1) 2.2 (1.7-4) 3.3-6.9 GSSG/GSH 0.19 (0.09-0.93) 0.13 (0.07-0.29) Acute heart failure was associated with an increased OS. OS was more important in patients with arrhythmia. Conclusion Acute heart failure increased the level of oxygen free radicals. We hypothetized that modifications of OS could be implied in arrhythmias and complications of acute heart failure.

Oxidative stress (OS) is a keystone in the pathology of the ischemia reperfusion sequence (acute coronary syndromes, cardiac surgery, transplantation). In heart failure, the implication of OS is less understood. This study was intended to evaluate OS in acute heart failure. Criteria for inclusion were consecutive patients hospitalized in our cardiology department for a first pulmonary edema that revealed a dilated cardiomyopathy (DCM). Exclusion criteria included known cardiomyopathy, smoker, acute coronary syndrome, and treatment with angiotensin converting enzyme inhibitors (ACEI) or angiotensin II receptor blockers (ARAII). OS was evaluated in blood samples: thiobarbituric acid-reactive substances (TBARS), total antioxidant status (TAS), plasma alpha-tocopherol, vitamin A, and beta-carotene. Standard biochemical parameters including CRP, fibrinogen, lipid, and creatinine were assayed. Ten patients (80% men, mean age 55.3 +/- 7.9 years) were included and followed during a 6 month period. The etiologies of DCM were alcohol (n = 3), anti-cancer drugs (n = 2), valvulopathies (n = 2), or idiopathic (n = 3). In acute heart failure, TBARS were elevated (1.69 micromol/L; normal value 0.6-4.2 micromol/L) and TAS status was decreased (0.96 mmol/L; normal value 1.3-1.9 pmol/L). OS was more important when patients had atrial or ventricular arrhythmia. Nevertheless, liposoluble antioxidant parameters (beta-carotene, vitamin A, alpha-tocopherol) had a usual value. At the term of the follow-up, patients returned to a stable condition, OS markers revealed normal values, and every Holter ECG showed no supraventricular or ventricular arrhythmias. In acute heart failure, oxygen-free radicals are increased. We thus hypothetized that a modification in OS could be responsible for arrhythmias and complications of acute heart failure.

The mouse PancChip, a microarray developed for studying endocrine pancreatic development and diabetes, represents over 13,000 cDNAs. After computationally assigning the cDNAs on the array to known genes, manual curation of the remaining sequences identified 211 novel transcripts. In microarray experiments, we found that 196 of these transcripts were expressed in total pancreas and/or pancreatic islets. Of 50 randomly selected clones from these 196 transcripts, 92% were confirmed as expressed by qRT-PCR. We evaluated the coding potential of the novel transcripts and found that 74% of the clones had low coding potential. Since the transcripts may be partial mRNAs, we examined their translated proteins for transmembrane or signal peptide domains and found that about 40 proteins had one of these predicted domains. Interestingly, when we investigated the novel transcripts for their overlap with noncoding microRNAs, we found that 1 of the novel transcripts overlapped a known microRNA gene.

Objective Evaluation by radio frequency in real-time, the quality of arterial rigidity in patients with cardiovascular risk factors. Method 3 measurements each carotid artery to determined coefficients, parameters rigidity, velocity of wave of pulse according by age. Quality of the rigidity of the arterial wall is measured from the velocity of the wave of pulse (PWV), variation of arterial diameter blood pressure on level of humeral artery, with measures of rigidity parameters. Results 2 carotid axes: 200 patients, 3 groups (age 30–69) according by age, sex, race 2 groups: white race, dyslipidemia, type II diabetes, smoking: according by sex. 1 group: 60 M, white race, the 2 group: 40 F (white race), 3 group 50 patients (hypertension, overweight) according to the sex and race; in 2 sub-groups: group A 25 M (20 white race, 5 black) group B 25 F white race. Brachial blood pressure calculated to obtain the velocity of the wave of pulse, coefficients of arterial rigidity, local pressure. The pathological wave of pulse >13 m/s, coefficients of rigidity: >11, β > 20. In the 2 groups (10% men, 8% women) had pathological >11, β>20 and velocity propagation of PWV >13 m/s. In 3 group 20% M, 12% F with hypertension, pathological rigidity, local pressure systolic increased despite the treatment. Conclusion QAS non invasive mesure of arterial rigidity on carotid, independent marker, in patients with cardiovascular risk factors, study the local and central blood pressure hypertensive patients to better control a pharmacological therapy. QAS by radiofrequency calculation of arterial rigidity on carotid level, parameters of rigidity, and velocity of propagation of wave of pulse, the local and central pressure of the studied artery. In 1 and 2 group, patients with nicotinic intoxication and risk factors, in 3 group (hypertension, overweight) not find pathological data neither differences according to the sex and the race among all hypertensive patients. 2 patients of race black, 5 of the sub-group (hypertension) with pathological coefficient > 11. QAS calculation of arterial rigidity, RF: radio frequency, PWV (wave velocity pulse), β: stiffness parameters.