Antiatherogenic properties of high-density lipoproteins from arterial plasma are attenuated as compared to their counterparts of venous origin.

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.

Safe right bundle branch block pattern during permanent right ventricular pacing: a case report.

We present the case of a 72-year-old male who underwent a permanent transvenous DDD pacemaker implantation for symptomatic complete heart block. The postoperative surface electrocardiogram (ECG) revealed a right bundle branch block (RBBB) pacing pattern with transition in lead V3 and left bundle branch block (LBBB) in D1, suggesting a malpositioned ventricular lead in the left heart. Malposition of a lead was ruled out by chest X-ray and echocardiogram confirming apical right ventricular pacing. After a literature review, a surface ECG maneuver, by placing leads V1 and V2 one intercostal space lower, restored the usual patterns of paced LBBB pattern. We discuss the literature concerning safe-paced RBBB.

Oxidative stress implication after prolonged storage donor heart with blood versus crystalloid cardioplegia and reperfusion versus static storage.

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<0.01)]. Arrhythmias were more frequent when using BC (n=5) than CP (n=0). For plasma thiobarbituric acid-reactive substances (TBARS) levels a significant difference was found between group III and the other groups since 15 to 90 min (P<0.05). Vitamin E concentration decreased significantly from 5 min for groups II and IV, 15 min for group I, and 30 min for group III, with a significant difference between groups II and IV (P<0.05) but not between groups I and III. CP followed by a reperfusion with the same solution showed a significantly lower ischemic injury and OFR production, less frequent ventricular arrhythmias while stable hemodynamic parameters carried on. However, this protocol did not act on the early postoperative contractile function.

Cardiogenic shock associated with reversible dilated cardiomyopathy during therapy with regular doses of venlafaxine.

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.

T cells subtypes in a patient with interferon-alpha induced sarcoidosis.

A 47-year-old woman with a history of blood transfusion-acquired hepatitis C was treated with interferon-alpha when she developed fever, arthralgia, erythema nodosum, dyspnea, and diffuse alveolitis. The diagnosis of IFN-alpha-induced sarcoidosis was retained. The patient's clinical status rapidly improved after IFN-alpha 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-alpha. 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 CD4CD28 negative subset that is associated with proinflammatory and tissue damaging properties. This activation process also improved over time, but more slowly than clinical symptoms.

Preoperative cardiac and pulmonary assessment in bariatric surgery.

BACKGROUND: 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. METHODS: 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. RESULTS: The ECG demonstrated conduction or ST-T wave abnormalities in 48 patients (62%). Prolongation of the QT interval >10% 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%). Hypoxemia <80 mmHg was observed in 21 patients (27%) and hypercapnia >45 mmHg in six patients (8%), without any consequences on the management of the perioperative period. CONCLUSION: 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.

Oxidative stress in patients with 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.

Percutaneous Transjugular Extraction of Venous Bullet Embolism to the Right Ventricle.

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.

Oxidative stress implication in a new ex-vivo cardiac concordant xenotransplantation model.

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 (p < 0.01, left ventricular systolic pressure decreased more significantly (p < 0.05), thiobarbituric acid-reactive substances concentrations increased at 30 min (0.7 +/- 0.1 vs. 2.4 +/- 0.3 mmol/l; p < 0.05) while vitamin A levels decreased (p < 0.05). XT was associated with a significant increase in ischemic injury and OS production. OS might play an eminent role in hyperacute humoral rejection.

Subcapsular liver haematoma after cardiopulmonary resuscitation by untrained personnel.

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.

Severe dilated cardiomyopathy and quadriceps myopathy due to lamin A/C gene mutation: a phenotypic study.

UNLABELLED: This study reports a family affected by a new phenotype associated with dilated cardiomyopathy and quadriceps myopathy. 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. 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. 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.

Celiprolol-induced lupus-like syndrome.

Systemic lupus erythematosus can be idiopathic or drug-induced. Although a number of beta-blockers have been reported to induce a lupus-like syndrome, to the best of our knowledge, no such case has been described following celiprolol therapy. We diagnosed a lupus-like syndrome in a 67-year-old female patient who developed febrile polyarthritis, percarditis, antinuclear and anti-histone antibodies after taking celiprolol for 2 years. Despite drug withdrawal, prolonged corticotherapy was needed to obtain clinical and biological remission.

[Late cardiac complications of radiation therapy]. / Complications cardiaques tardives de la radiothérapie.

INTRODUCTION: 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. CASE: 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. COMMENTS: As the literature shows, different cardiac complications of radiation therapy can follow one another. Attentive long-term monitoring is necessary for appropriate treatment.

Giant xanthomas associated with severe mixed dyslipidemia and arteriosclerotic vascular disease: A case report.

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.

Functional consequences of an LMNA mutation associated with a new cardiac and non-cardiac phenotype.

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.

Transient neurological disorders during a simulated ascent of Mount Everest.

BACKGROUND: Transient neurological disorders are often observed at high altitude but are poorly documented under field conditions. The mechanism usually invoked is a hypocapnic vasoconstriction due to severe hypoxic hyperventilation. During a simulated ascent of Mount Everest in a hypobaric chamber by eight volunteer alpinists (Operation Everest III, Comex '97), three subjects presented neurological symptoms. We report here on the clinical observations and testing to detect mechanisms in addition to hypocapnic vasoconstriction. METHODS: The experiment was designed to investigate factors limiting physiological performance at altitude and the pathophysiology of acute mountain sickness. A retrospective analysis was made comparing the three cases of transient neurological disorder at high altitude (TNDHA) with the five subjects who had no neurological symptoms. RESULTS: Analysis of clinical and blood parameters showed no difference between cases and controls. The cases showed no neurological sequelae following the experiment and were normal on cardiac imaging. However, one case had a history of migraine in his youth, leading us to hypothesize that segmental vasoconstriction was a factor. In another case, gas bubbles were detected in the pulmonary artery by transthoracic echocardiography when he was symptomatic, suggesting that gas emboli may have played a role. All three cases shared a possible triggering factor in that each experienced hyperventilation alternating with straining against a closed glottis shortly before the onset of symptoms. CONCLUSION: Mechanisms other than hypocapnic vasoconstriction in hypoxia may be causal factors of TNDHA. The existence of triggering factors and evidence of a possible embolic mechanism should be further explored.

Cardiac side-effects of cancer chemotherapy.

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.

HIV-associated vascular diseases: structural and functional changes, clinical implications.

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 progresses 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.