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International audience; Background and aims: High-density lipoprotein (HDL) particles play atheroprotective roles by their ability to efflux cholesterol from foam cells and to protect low-density lipoproteins (LDLs) from oxidative damage in the arterial intima. We hypothesized that antioxidative properties of HDLs can be attenuated in the oxygen-rich prooxidative arterial environment, contributing to the development of atherosclerosis. To evaluate this hypothesis, we compared antioxidative activity of HDLs from arterial and venous plasmas.Methods and results: Arterial and venous blood samples were simultaneously obtained from 16 patients (age 68 ± 10 years; 75% males) presenting with ischemic or valvular heart disease. Major HDL subfractions and total HDLs were isolated by density gradient ultracentrifugation and their chemical composition and the capacity to protect LDLs from in vitro oxidation were evaluated. HDL-cholesterol, triglycerides and apolipoprotein (apo) B-100 levels were slightly but significantly reduced by -4 to -8% (p < 0.01) in the arterial vs. venous samples. Total mass of HDL subpopulations was similar and HDL subpopulations did not reveal marked compositional differences between the arterial and venous circulation. Potent antioxidative activity of the small, dense HDL3c subpopulation was significantly reduced in the particles of arterial origin vs. their counterparts from venous plasma (increase of +21% in the propagation rate of LDL oxidation, p < 0.05). Interestingly, antioxidative properties of venous HDLs were enhanced in statin-treated patients relative to untreated subjects.Conclusion: Antioxidative properties of small, dense HDLs from arterial plasma are attenuated as compared to the particles of venous origin, consistent with the development of atherosclerosis in the arterial wall.

Migration of a bullet to a distant part of the body after a gunshot is rarely observed in the clinical setting; migration to the heart is even rarer. There are usually no clear symptoms or signs from migration of a bullet. The case of a 28-year-old man with an intracardiac bullet migration 2 months after a gunshot wound to the right abdomen is presented. We propose that the bullet migrated along the vena cava to the right ventricle. Interventional radiology with a percutaneous transjugular extraction was used to recover this intracardiac projectile.

The report describes a case of mixed hyperlipoproteinemia in a 64-year-old patient presenting a serum hypertriglyceridemia at 25 mmol/L and hypercholesterolemia at 15.75 mmol/L, giant xanthomas and symptomatic atherosclerotic disease.

The aim was to determine (a) Ala-16Val-SOD2 dimorphisms; (b) allelic frequency and phenotype of a common Pro-Leu polymorphism in GPx1, in a cohort of patients with a cardiogenic shock (CS) due to dilated cardiomyopathy without acute coronary syndrome. Consecutive patients with de novo CS that worsened a dilated (DCM) or ischemic (ICM) cardiomyopathy. Congenital heart disease, pacemaker and other shock aetiologies were excluded. To determine oxidative stress (OS), this study evaluated lipid peroxidation, protein oxidation and erythrocyte GPx, SOD and catalase activities. Ala16Val-SOD2 (dbSNP: rs4880) and Pro198Leu-GPx1 (dbSNP: rs1050450) polymorphisms were studied by allelic discrimination using fluorogenic probes and the 5'nuclease (TaqMan) assay. Twenty-four patients (with ICM (n = 8) or DCM (n = 16), age = 57.5 ± 10.7 years, LVEF = 25.3 ± 8.5%, NT-proBNP levels = 8540 ± 1703 ng/L) were included during a 15 month follow-up. OS parameters were significantly higher in patients than in controls. Distribution of MnSOD genotypes was 47% Val/Val-variant, 29.5% Ala/Val and 23.5% Ala/Ala-variants. Severity of CS was more important in patients with Val/Val-variant and can be put in parallel with NT-proBNP levels (Val/Val-variant: 11 310 ± 3875 ng/L vs Ala/Ala-variant: 6486 ± 1375 ng/L and Ala/Val-variant: 6004 ± 2228 ng/L; p0.05) and hemodynamic support duration (144.6 vs Ala/Val-variant: 108.8 h and Ala/Ala-variant: 52.5 h; p0.05) with a positive correlation (Spearman rho = 0.72, p0.05). Moreover, Val/Val-variant significantly influenced the mortality (Spearman rho = 0.67, p0.05), but not the morbidity (p = 0.3). Distribution of GPx genotypes was 64% Pro/Pro, 18% Pro/Leu and 18% Leu/Leu. GPx-variants influenced neither GPx activities nor cardiac events. In conclusion, CS was associated with markers of increased OS. GPx polymorphism did not influence the GPx activity. Only the Val-encoding MnSOD allele was significantly correlated with the severity and prognosis of CS.

Several factors are known to limit cardiac transplantation, such as number of donors, quality of cardiac graft preservation, and ischemia-reperfusion injury. Some mechanisms of reperfusion injury are now recognized; they include oxygen free radical (OFR), white blood cells activation, changes in calcium influx, alteration of microvascular blood flow, and sympathetic activation. The goal of this study was to assess the effects of two types of cardioplegia with long-term storage, either static or continuous perfusion, in 30 isolated sheep hearts as a model for heart transplantation. We examined myocardial function, histology, ischemic damage, and markers of oxidative stress. Two types of cardioplegia and storage conditions using a Langendorff reperfusion were studied in a combined approach: crystalloid (CP) [groups I and III] or cold oxygenated autologous blood (BC) [groups II and IV], immediate storage during 8h in profound hypothermia (groups I and II), or reperfused with crystalloid (group III), or blood cardioplegia (group IV). All perfusate samples were drawn from the coronary sinus. Lactate levels increased progressively in groups I, II, and IV, but not in group III, as no significant elevation was shown [90 min: 13.6 ± 1.7 versus 5.2 ± 1.0 mmol/L (P

Les patients obeses ont une prevalence elevee de pathologies cardiaques et pulmonaires, qui peuvent etre connues ou meconnues, lors de la prise en charge pour chirurgie de l’obesite. Le but de cette etude a ete d’evaluer la pertinence des explorations cardiaques et pulmonaires, effectuees en routine, avant une intervention bariatrique par pose d’anneau gastrique. Nous avons etudie une population composee de 67 femmes et de dix hommes, âges de 39 ± 10 ans (m ± SD), avec un indice de masse corporelle de 43 ± 10 kg/m 2 (m ± SD). Tous les patients, candidats a une chirurgie de l’obesite ont eu : un electrocardiogramme (ECG), une echocardiographie cardiaque, un test de somnolence d’Epworth, une polysomnographie, une spirometrie, des gaz du sang, et une radiographie de thorax. L’ECG a montre des anomalies de la conduction ou de la repolarisation chez 48 patients (62 %). L’allongement de l’intervalle QT a ete constate chez 13 patients (17 %), mais n’a ete responsable d’aucune contre-indication a une chirurgie de l’obesite. Les tests d’effort etaient negatifs chez 56 patients (73 %) et ont ete ininterpretables chez les 21 autres (27 %), les epreuves etant sous-maximales. L’echocardiographie a montre une hypertrophie de la paroi du ventricule gauche anterieure chez 47 patients (61 %). Cela n’a pas modifie les indications operatoires. La polysomnographie a revele un syndrome d’apnee-hypopnee obstructive du sommeil (SAOS) chez 31 patients (40 %), conduisant a un traitement par ventilation sous pression positive continue (VPPC) chez 17 patients (22 %). L’echelle de somnolence d’Epworth etait pathologique chez seulement 17 patients (22%). Dix patients (13%) ont presente des radiographies de thorax avec des alterations mineures. La spirometrie a montre un syndrome obstructif chez 13 patients (17 %) et un syndrome restrictif chez cinq patients (6 %). Une hypoxemie inferieure a 80 mmHg a ete observee chez 21 patients (27 %), et une hypercapnie superieure a 45 mmHg a ete observee chez six patients (8 %), sans aucune consequence sur la gestion de la periode perioperatoire. Les explorations cardiorespiratoires preoperatoires peuvent etre divisees en trois groupes : le premier, celui des explorations non informatives, comprenant le test d’effort et l’echelle de somnolence d’Epworth ; le deuxieme, celui des explorations informatives, comprenant la radiographie de thorax, l’ECG, l’echographie cardiaque, la spirometrie, les gaz du sang ; est a part, la polysomnographie, qui est informative et pertinente, car elle peut entrainer une modification de la prise en charge pre et postoperatoire.

Morbidly obese patients have a high prevalence of known and unknown cardiopulmonary diseases. The aim of this study was to assess the value of cardiopulmonary tests routinely performed before bariatric surgery.The population studied included 67 women and 10 men, aged 39 +/- 10 years, with a body mass index of 43 +/- 4 kg/m2. All patients, candidates for laparoscopic gastric banding, underwent after clinical evaluation: resting electrocardiography (ECG), Doppler-echocardiography, exercise stress testing, Epworth Sleepness Scale, and polysomnography, spirometry, blood gases, and chest x-ray.The ECG demonstrated conduction or ST-T wave abnormalities in 48 patients (62%). Prolongation of the QT interval10% was found in 13 patients (17%). Stress tests were negative in 56 patients (73%) and were not interpretable in the remaining 21 patients (27%). Doppler-echocardiography showed hypertrophy of the left ventricular posterior wall in 47 patients (61%) without any consequences on perioperative management. Polysomnography showed an obstructive sleep apnea-hypopnea syndrome (OSAHS) in 31 patients (40%), leading to preoperative continuous positive airway pressure (CPAP) treatment in 17 patients (22%). Nevertheless, the Epworth Sleepness Scale was pathological in only 17 patients (22%). Ten patients (13%) presented minor chest x-ray alterations. Spirometry demonstrated an obstructive respiratory syndrome in 13 patients (17%) and a restrictive syndrome in five patients (6%). Hypoxemia80 mmHg was observed in 21 patients (27%) and hypercapnia45 mmHg in six patients (8%), without any consequences on the management of the perioperative period.We recommend the preoperative assessment by clinical evaluation, ECG, and polysomnography. For patients with cardiac or pulmonary histories and/or ECG abnormalities, we recommend echocardiography, spirometry, and blood gases.

This study aimed at evaluating OS in an amyotrophic quadricipital syndrome with cardiac impairment in a family of 80 members with a mutation in lamin A/C gene. Twelve patients had cardiac involvement (5 cardiac and skeletal muscles impairment). OS was evaluated in blood samples (thiobarbituric acid-reactive substances (TBARS), carbonylated proteins (PCO)) 6 "affected patients" with phenotypic and genotypic abnormalities without heart failure and 3 "healthy carrier" patients. OS was higher in affected patients than in healthy, as shown by the higher TBARS and PCO values. Patients with cardiac and peripheral myopathy exhibited a higher OS than patients with only cardiac disease (TBARS: 1.73 +/- 0.05 vs. 1.51 +/- 0.04 mmol/l (p = 0.051), PCO: 2.73 +/- 0.34 vs. 0.90 +/- 0.10 nmol/mg protein (p = 0.47)), and with healthy carriers patients (TBARS: 1.73 +/- 0.05 vs. 1.16 +/- 0.14 mmol/l (p = 0.05), PCO: 2.73 +/- 0.34 vs. 0.90 +/- 0.20 nmol/mg protein (p = 0.47)). OS may thus contribute to the degenerative process of this laminopathy. ROS production occurs, prior to heart failure symptoms. We suggest that the extent activation may also promote the variable phenotypic expression of the disease.

This study reports a family affected by a new phenotype associated with dilated cardiomyopathy and quadriceps myopathy. 1 Methods: 29 family members underwent a physical and neurological examination, including an electromyogram and biopsy of muscle abnormalities. A cardiac examination was performed in all subjects. 2 Results: The family pedigree (n=72) demonstrated that transmission was autosomal dominant. Eleven subjects had cardiac involvement, only four had quadriceps muscle involvement. Cardiac impairment preceded neurological involvement. The mean age for neurological involvement was 44±0.8 years (range 43–45) and cardiac involvement was 37±7.9 years (range: 24–45). Cardiac involvement consisted of: hypokinetic dilated cardiomyopathy (64%); atrial fibrillation (100%); ventricular arrhythmias (64%); impaired conduction with bundle branch or complete atrio ventricular block (73%). Four patients required pacemakers and anti arrhythmic therapies. Four patients died: two of refractory heart failure and two of sudden death; two patients were resuscitated following cardiac arrest. Three patients required a prophylactic implantable cardiac defibrillator (ICD). Muscle morphological abnormalities were characterized by a variable number of fibers with rimmed vacuoles. The quadriceps deteriorated progressively without impairment of other muscles. Genotypic study showed a lamin A/C gene mutation. 3 Conclusions: This family was affected by a new phenotype composed of an autosomal dominant severe dilated cardiomyopathy with conduction defects or arrhythmias and quadriceps myopathy. Cardiac abnormalities preceded neuromuscular disorders and defined the prognosis of this disease.

Resume Introduction La radiotherapie mediastinale a bouleverse le pronostic de nombre de neoplasies, en particulier les cancers du sein et les lymphomes. Cependant, avec l’augmentation de la survie, des effets secondaires sont apparus parmi lesquels les complications cardiaques, souvent tardives. Observation Il s’agit d’un patient atteint d’une maladie de Hodgkin et traite par radiotherapie. Celle-ci s’est compliquee de troubles conductifs et d’une pericardite chronique, exsudative puis constrictive, 28 ans apres la radiotherapie. Commentaires Comme en temoignent les donnees de la litterature, les complications cardiaques de la radiotherapie peuvent se succeder. Une surveillance attentive et prolongee pour une prise en charge therapeutique adaptee est necessaire.

Heritable dilated cardiomyopathy is a genetically highly heterogeneous disease. To date 17 different chromosomal loci have been described for autosomal dominant forms of dilated cardiomyopathy with or without additional clinical manifestations. Among the 10 mutated genes associated with dilated cardiomyopathy, the lamin A/C (LMNA) gene has been reported in forms associated with conduction-system disease with or without skeletal muscle myopathy. For the first time, we report here a French family affected with a new phenotype composed of an autosomal dominant severe dilated cardiomyopathy with conduction defects or atrial/ventricular arrhythmias, and a specific quadriceps muscle myopathy. In all previously reported cases with both cardiac and neuromuscular involvement, neuromuscular disorders preceded cardiac abnormalities. The screening of the coding sequence of the LMNA gene on all family members was performed and we identified a missense mutation (R377H) in the lamin A/C gene that cosegregated with the disease in the family. Cell transfection experiments showed that the R377H mutation leads to mislocalization of both lamin and emerin. These results were obtained in both muscular (C2C12) and non-muscular cells (COS-7). This new phenotype points out the wide spectrum of neuromuscular and cardiac manifestations associated with lamin A/C mutations, with the functional consequence of this mutation seemingly associated with a disorganization of the lamina.

In December 2009, a 79-year-old white man was admitted to the Department of Cardiology for a moderate dyspnea (New York Heart Association II) with breath. His past medical history included a cardiac surgery with double coronary arteries bypass grafting in 1996 and thyroid cancer treated with surgery and radiotherapy. On admission, the physical examination revealed regular heart sounds at 60 bpm, and blood pressure was 100/60 mm Hg. No cardiac murmur was heard. Chest x-ray showed a mild cardiomegaly with a retrocardiac mass without pulmonary edema or pleural effusion. The left ventricular (LV) ejection fraction on echocardiography was at 67%. No LV hypertrophy and no LV dilation (LV end-diastolic diameter, 46 mm; index LV end-diastolic diameter, 40 mm/m2 …

A 75-year-old man was admitted to our department with a severe condition and a large tumefaction at the level of xiphoid region ( Panel A ). Seven years earlier he underwent a coronary artery bypass for left anterior descending artery revascularization using the left internal thoracic artery without closure of the …

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.

The spectrum of cardiac side-effects of cancer chemotherapy has expanded with the development of combination, adjuvant and targeted chemotherapies. Their administration in multiple regimens has increased greatly, including in older patients and in patients with cardiovascular and/or coronary artery disease (CAD). Cardiac toxicity of anthracyclines involves oxidative stress and apoptosis. Early detection combines 2D-echocardiography and/or radionuclide angiography and recent methods such as tissue Doppler imaging, strain rate echocardiography and sampling of serial troponin and/or NT-proBNP levels. Dexrazoxane has proven effective in the prevention of dose-related toxicity in children and adults. High doses of the alkylating drugs cyclophosphamide and ifosfamide may result in a reversible heart failure and in life-threatening arrhythmias. Myocardial ischemia induced by the antimetabolites 5-fluorouracil and capecitabine impacts prognosis of patients with prior CAD. Severe arrhythmias may complicate administration of microtubule inhibitors. Targeted therapies with the antibody-based tyrosine kinases (TK) inhibitors trastuzumab and, to a lesser extent, alemtuzumab induce heart failure or asymptomatic LV dysfunction in 1-4% and 10%, respectively. Cetuximab and rituximab induce hypotension, whereas bevacizumab may promote severe hypertension and venous thromboembolism. Small molecule TK inhibitors may also elicit LV dysfunction, in only few patients treated with imatinib mesylate, but in a substantially higher proportion of those receiving the multitargeted TK inhibitor sunitinib or the recently approved drugs erlotinib, lapatinib and dasatinib. Management of patients at increased cardiovascular risk associated with advancing age, previous CAD or targeted therapies may be optimized by referral to a cardiologist in a cross-specialty teamwork.

A 47-year-old woman with a history of blood transfusion-acquired hepatitis C was treated with interferon- α when she developed fever, arthralgia, erythema nodosum, dyspnea, and diffuse alveolitis. The diagnosis of IFN- α -induced sarcoidosis was retained. The patient’s clinical status rapidly improved after IFN- α discontinuation, with complete resolution of signs and symptoms. Admission and follow-up assessment of peripheral blood CD4 + T cells showed a transient activation process that peaked at 1 to 3 months after onset of symptoms and discontinuation of IFN- α . It was marked by a mild increase in activated cells (expressing R-IL2 and HLADR), and a markedly reduced percentage of CD4 T cells expressing the costimulation molecule CD28, ie, an expansion of the CD4 + CD28 negative subset that is associated with proinflammatory and tissue damaging properties. This activation process also improved over time, but more slowly than clinical symptoms.

After more than two decades of AIDS epidemic, the spectrum of HIV-associated vascular diseases has mainly evolved from infectious and inflammatory vasculitides to premature atherosclerosis, its related contributing conditions (metabolic syndrome, dyslipidemia, insulin resistance syndrome) and complications (acute coronary and cerebrovascular syndromes). Today, as the AIDS epidemic further progress worldwide and as the life expectancy of HIV-infected patients treated with effective antiviral regimens has dramatically increased, more than 10% of patients experience cardiovascular manifestations. The complex interplay between viral infection, inflammatory and cytokines pathways, protease inhibitors-induced hyperlipidemia and direct effects on endothelial cells has not, by far, been integrated in a single comprehensive pathogenesis network. However, recognition of its main components has resulted in a broader appreciation of cardiovascular risk and risk factors in HIV-infected/treated patients. Cardiovascular prevention is required in more than one half of HIV-infected/treated patients to achieve a reliable effectiveness of modern antiretroviral therapy. As the prognosis of HIV patients improves continuously, this rate is also likely to increase in the future.

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.

Xenotransplantation (XT) reveals a growing interest for the treatment of cardiomyopathy. The major barrier is an acute vascular rejection due to an acute humoral rejection. This pathogenesis is a difficult issue and in order to elaborate means for its prevention, we analysed the implication of oxidative stress (OS) on hearts from mini-pigs followed by reperfusion with either autologous or human blood in an attempt to simulate xenotransplantation. About 14 hearts were studied after a Langendorff blood reperfusion: allografts with autologous blood (n = 7) or xenografts with human blood (n = 7). Blood samples were drawn from the coronary sinus to assess ischemia and OS. In xenografts, arrhythmias occurred more frequently (p0.01, left ventricular systolic pressure decreased more significantly (p0.05), thiobarbituric acid-reactive substances concentrations increased at 30 min (0.7 +/- 0.1 vs. 2.4 +/- 0.3 mmol/l; p0.05) while vitamin A levels decreased (p0.05). XT was associated with a significant increase in ischemic injury and OS production. OS might play an eminent role in hyperacute humoral rejection.

Among the multiple cardiac manifestations occurring in HIV-infected patients, cardiomyopathy is one of the most challenging. Its incidence has only slightly decreased since the introduction of highly active antiretroviral therapy (HAART). Also, its pathogenesis remains relatively unclear. Although several studies demonstrated the presence of HIV genome in the heart of patients, more recent developments found that viral infection plays an indirect role only, as well as they recognized the contribution of proinflammatory cytokines in the progression of the disease. Experimental studies on animals and cultured myocytes have established the signalling pathway triggered by proinflammatory cytokines in heart failure and cardiomyopathy. Tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1) and IL-6 promote expression of inducible nitric oxide synthase (iNOS) in cardiomyocytes through activation of p38 mitogen-activated protein kinase (p38 MAPK) and nuclear factor kappaB (NFkappaB). TNF-alpha and high concentrations of NO also induce cardiomyocyte apoptosis by TNF type 1 receptor activation. This biological framework, which is also involved in progression of cardiomyopathy in humans, is more pronounced in HIV-infected patients, in whom proinflammatory cytokines TNF-alpha, IL-1 and IL-6 are increased, resulting in an enhanced expression of cardiac iNOS, especially in patients with a low CD4 T cell count. This may account for the worse outcome of heart failure in HIV-infected patients. However, there are only few data today to support future therapeutic implications of cytokines antagonism in treatment of HIV-infected patients with cardiomyopathy. Whether modulation of TNF production or selective inhibition of p38 MAPK pathway could be useful approaches remains uncertain.

Although early cardiopulmonary resuscitation (CPR) is associated with increased survival of sudden cardiac arrest victims, it may also result in miscellaneous injuries. A 25-year-old inebriated man rescued from drowning in a swimming pool was apnoeic and pulseless after being pulled out of the water. Successful CPR was provided by untrained bystanders, including abdominal thrusts thought to remove water from the airways and chest compressions to provide haemodynamic support. As the patient progressively improved during his subsequent hospital stay, he complained of right upper abdominal and thoracic pain. A computed tomographic scan showed a 11 cm subcapsular haematoma contiguous to the right hepatic lobe. A favourable outcome was obtained after conservative, non-operative treatment. Subcapsular haematoma of the liver is a potentially life threatening complication that warrants consideration in survivors of cardiac arrest who have received closed chest compression and/or abdominal thrusts.

Mediastinal irradiation treatment has drastically improved the prognosis for several neoplasms, mostly particularly breast cancer and lymphoma. Nonetheless, the increase in survival is accompanied by side effects, including cardiac complications that often appear much later.This patient with Hodgkin disease received radiation therapy. Complications developed 28 years later and included conduction disorders and chronic pericarditis, first exudative and then constrictive.As the literature shows, different cardiac complications of radiation therapy can follow one another. Attentive long-term monitoring is necessary for appropriate treatment.

Many others cancer agents can lead to cardiovascular toxicity apart from anthracyclines, 5-fluorouracil, trastuzumab and ionizing radiations. Paclitaxel, high-dose cyclophosphamide and ifosfamide, mitomycin and irinotecan cardiotoxicity is unusual but for certain. Hormonal therapy is extensively used in breast and prostate cancers. Thromboembolic and cardiovascular events are increased by estrogens, synthetic progestatives and tamoxifene. Because of major toxicities related to intravenous interleukin-2, subcutaneous interleukin-2 regimens have been developed, allowing an improvement of cardiovascular tolerability. Interferon is less frequently associated with cardiotoxicity. Before treatment initiation, risk factors favouring cardiac toxicity should be evaluated. These risk factors can be related to the cancer agent, to the patient or to the tumour. Uncommon toxic events in general population can be more frequent in high risk patients. Therapeutic option can be influenced by these uncommon toxic events in high risk patients.

Carcinoma of the breast is relatively rare among men, accounting for less than 1% of all malignancies. An increased risk has been associated with benign breast diseases, such as gynecomastia, Klinefelter's syndrome, testicular disorders, exogenous estrogen use, radiation, or a family history of male or female breast cancer. To date, hypogonadotrophic hypogonadism has never been associated with male breast cancer. We report here the first case of breast cancer coexisting with Kallmann's syndrome in a 66-year-old man.

Transient reproducible complete infrahisian atrioventricular block occurred after endocavitary cardioversion of ventricular tachycardia and ventricular fibrillation by an automatic implantable cardiac defibrillator in a patient with left bundle branch block and baseline borderline H-V interval. Six months later, a permanent complete atrioventricular block occurred after repetitive endocavitary shocks. Several hypothetical mechanisms may explain this infrahisian atrioventricular block a "fatigue" phenomenon of the His-Purkinje system, vagally mediated atrioventricular block, and/or ablation of the His conduction system. The last seems to be the most probable, which would justify implantation of an automatic implantable cardiac defibrillator with backup pacing in all patients, especially in the presence of bundle branch block.

We report a cardiac complication in a patient treated with regular doses of venlafaxine. A 49-year-old man with prior normal cardiac function and stable chronic hepatitis C was treated for a major depressive disorder with usual doses of venlafaxine during an 8-month period until the occurrence of a cardiogenic shock in a context of dilated cardiomyopathy. Three months after withdrawal of the drug, the left ventricular ejection fraction returned to normal values. Cardiomyopathy is a rare complication with high doses of venlafaxine that was not previously reported in patients free of prior cardiac disease and cardiomyopathy and treated with usual doses (initially 150 mg daily; after 3 months, 75 mg daily). An objective assessment revealed that venlafaxine was probably implied in the subsequent development of cardiomyopathy when considering the Naranjo Probability Scale. Physicians who usually prescribe venlafaxine have to be briefed on such potential cardiac adverse effects even with usual doses.

BackgroundCoronary artery disease (CAD) can be associated with aortic stenosis (AS). Conventional coronary angiography (CCA) is the best method for ruling out significant CAD when surgery is planned. However, significant percentage of patients had normal coronary arteries. New non invasive methods are needed to select patients undergo CCA and reduce risks of this invasive exam.Lipoprotein-associated phospholipase A2 (Lp-PLA2) is an inflammatory biomarker secreted in the atherosclerotic plaque. The main objective of this study is to compare Lp-PLA2 with CCA in AS-patients prior to aortic valve surgery and to evaluate Lp-PLA2 as an independent predictor of associated CAD.Methods and Results285 patients with AS and/or CAD were included into 3 groups: “CAD-Group”: stable CAD; “AS-Group”: AS and normal coronary arteries and “AS-CAD-Group”: AS and stable CAD associated. Lp- PLA2 mass concentration was assessed in serum with a Plac®-test turbidimetric immunoassay. Normal Lp-PLA2 values of the lipids laboratory were specifically obtained from 61 healthy Caucasian volunteers.In healthy controls, Lp-PLA2 was 163±43μg/L. Lp-PLA2 was significantly higher in patients than in controls (219.2±49.1 vs 163.0±43.0μg/L; p=0.01) and was significantly higher in the AS-CAD group (246±51μg/L, p

BackgroundVascular inflammation increased in HFand produced pro-inflammatory cytokines, activation of complement and adhesion molecules that sustain inflammatory state. Lipoprotein-associated phospholipase A2 (Lp-PLA2) hydrolyze phospholipids and is a marker of inflammation that plays a critical role in atherogenesis and endothelial dysfunction.AimsIn this study, we evaluated (1) predictive value of Lp-PLA2 in patients with de novo cardiogenic shock (CS) without acute coronary syndrome (ACS), (2) evolution of this biomarker when cardiac function improved upon cardiac treatment during a 30±3 month follow-up.MethodsInclusion criteria for patients: CS defined by systolic BP