ST2 as a predictor of late ventricular remodeling after myocardial infarction.

Out of 163 STEMI patients, 33 presented left ventricular remodeling (LVR) as assessed by multiple cardiac magnetic resonance (CMR) scans. LVR patients were identified as EarlyLVR (LVR occurring between baseline and 3 months) or LateLVR (LVR occurring between 3 months and one year), and matched to non-remodeler patients in term of age, gender, anterior infarction, baseline LV ejection fraction and infarct size. ST2 and NT-proBNP were measured at baseline and 3 months. Systolic wall stress (SWS) was calculated by CMR. At baseline, mean levels of ST2, NT-proBNP and SWS were 67.1 ±â€¯54.1 ng/mL, 1529 ±â€¯1702 ng/L and 17.9 ±â€¯7.1 103 N·m-2, respectively, and did not differ among the groups. At 3 months, EarlyLVR patients presented significant higher ST2, NT-proBNP and SWS (31.6 ±â€¯12.7 ng/mL, 1142 ±â€¯1069 ng/L, 25.5 ±â€¯9.7 103 N·m-2), compared to the corresponding non-remodelers (20.5 ±â€¯8.6 ng/mL, 397 ±â€¯273 ng/L, 18 ±â€¯7.3 103 N·m-2; with p = 0.017, 0.040, and 0.036, respectively). LateLVR patients presented higher ST2 at 3 months than their non-remodelers (33.6 ±â€¯15.9 versus 23.66 ±â€¯8.7 ng/mL, p = 0.046), while NT-proBNP and SWS were not different between groups at both timepoints.

Fondaparinux upregulates thrombomodulin and the endothelial protein C receptor during early-stage reperfusion in a rat model of myocardial infarction.

INTRODUCTION: Fondaparinux (FDX) was demonstrated to be cardioprotective in a rat model of myocardial ischemia reperfusion. In this model, FDX reduced infarct size after 2h of reperfusion, involving the activation of the survivor activating factor enhancement (SAFE) pathway as early as 30min post-reperfusion. Our aim was to study if this cardioprotection could be explained by anti-inflammatory mechanisms and a protective effect on vessels. METHODS: Wistar male rats were subjected to 40minutes (min) of myocardial ischemia, followed by 30min or 2h of reperfusion. Rats were randomized into four groups: control 30min (n=7), FDX 30min (n=7), control 2h (n=7), and FDX 2h (n=7). The FDX groups received 10mg/kg injection of FDX 10min prior to initiating reperfusion. We studied: 1) mRNA expression of endothelial markers, such as thrombomodulin (TM), endothelial protein C receptor (EPCR), and tissue factor (TF) and 2) proteic expression of ICAM-1, NF-κB, IκB, and JNK. Leukocyte infiltration was assessed by histochemistry. We also evaluated TM and EPCR mRNA expression in a model of isolated rat mesenteric arteries incubated with FDX. RESULTS: FDX upregulated the expression of TM and EPCR mRNA in the models of myocardial infarction and isolated mesenteric arteries. No difference was observed between the treated and control groups regarding the expression of pro-inflammatory signaling proteins, adhesion molecules, and leukocyte infiltration after 2h of reperfusion. CONCLUSION: The cardioprotective effect of FDX at early-stage reperfusion could be related to vascular protection, yet not to an anti-inflammatory effect.

No post-conditioning in the human heart with thrombolysis in myocardial infarction flow 2-3 on admission.

AIMS: Proof-of-concept evidence suggests that mechanical ischaemic post-conditioning (PostC) reduces infarct size when applied immediately after culprit coronary artery re-opening in ST-elevation myocardial infarction (STEMI) patients with thrombolysis in myocardial infarction 0-1 (TIMI 0-1) flow grade at admission. Whether PostC might also be protective in patients with a TIMI 2-3 flow grade on admission (corresponding to a delayed application of the post-conditioning algorithm) remains undetermined. METHODS AND RESULTS: In this multi-centre, randomized, single-blinded, controlled study, STEMI patients with a 2-3 TIMI coronary flow grade at admission underwent direct stenting of the culprit lesion, followed (PostC group) or not (control group) by four cycles of (1 min inflation/1 min deflation) of the angioplasty balloon to trigger post-conditioning. Infarct size was assessed both by cardiac magnetic resonance at Day 5 (primary endpoint) and cardiac enzymes release (secondary endpoint). Ninety-nine patients were prospectively enrolled. Baseline characteristics were comparable between control and PostC groups. Despite comparable size of area at risk (AAR) (38 ± 12 vs. 38 ± 13% of the LV circumference, respectively, P = 0.89) and similar time from onset to intervention (249 ± 148 vs. 263 ± 209 min, respectively, P = 0.93) in the two groups, PostC did not significantly reduce cardiac magnetic resonance infarct size (23 ± 17 and 21 ± 18 g in the treated vs. control group, respectively, P = 0.64). Similar results were found when using creatine kinase and troponin I release, even after adjustment for the size of the AAR. CONCLUSION: This study shows that infarct size reduction by mechanical ischaemic PostC is lost when applied to patients with a TIMI 2-3 flow grade at admission. This indicates that the timing of the protective intervention with respect to the onset of reperfusion is a key factor for preventing lethal reperfusion injury in STEMI patients. CLINICAL TRIAL NUMBER: NCT01483755.

Chronic erythropoietin treatment decreases post-infarct myocardial damage in rats without venous thrombogenic effect.

OBJECTIVES: Whereas administration of erythropoietin (EPO) acutely after myocardial infarction (MI) reduces infarct size and chronic EPO therapy attenuates post-MI remodeling, the safety of chronic EPO therapy following MI is unknown. Therefore, we examined the thrombogenic effects of a chronic EPO therapy after MI. METHODS: Rats underwent coronary occlusion followed by reperfusion. They were assigned to one of the following groups: EPO-A, single injection of EPO 5,000 U/kg at the time of reperfusion; EPO-C, injection of EPO 5,000 U/kg at the time of reperfusion followed by 300 U/kg/week; PBS-C, injection of vehicle only. After eight weeks of treatment they were exposed to a validated prethrombotic test based on partial stenosis of the inferior vena cava. RESULTS: As compared to the rats receiving vehicle only, the rats treated with EPO exhibited a significant reduction in MI size (28.7 +/- 2.1% and 25.8 +/- 1.9 vs. 39.8 +/- 3.0% in EPO-A, EPO-C and PBS-C, respectively; p < 0.05). Whereas the hematocrit was significantly increased in EPO-C (59.7 +/- 2.0% vs. 44.7 +/- 0.9% in EPO-A, p < 0.001), the proportion of rats in which a thrombus occurred was similar in all groups (p = 0.52). CONCLUSION: Chronic EPO therapy added to the single high dose of EPO injected acutely did not induce venous pro-thrombotic effect in rats.

Enhanced activity of the myocardial Na+/H+ exchanger contributes to left ventricular hypertrophy in the Goto-Kakizaki rat model of type 2 diabetes: critical role of Akt.

AIMS/HYPOTHESIS: Diabetes mellitus is a strong risk factor for the development of heart failure, and left ventricular (LV) hypertrophy has been detected in a significant proportion of diabetic patients. Because several studies have suggested that the Na(+)/H(+) exchanger (NHE1) plays a part in the molecular mechanisms involved in cardiac hypertrophy, we investigated its activity and its role in LV myocytes from the Goto-Kakizaki (GK) rat model of type 2 diabetes. MATERIALS AND METHODS: Fluorometric measurements were used to assess sarcolemmal NHE1 activity in isolated myocytes. NHE1 levels and the possible molecular pathways driving and/or related to NHE1 activity were investigated in relation to the diabetic LV phenotype. RESULTS: Enhanced NHE1 activity was associated with LV myocyte hypertrophy. This occurred in the absence of any change in NHE1 protein levels; however, activation of several molecular pathways related to NHE1 activity was demonstrated. Thus, phosphorylation of the extracellular signal-regulated protein kinase (Erk), of the protein kinase Akt (also known as protein kinase B) and of the Ca(2+)/calmodulin-dependent kinase II was increased in GK LV myocytes. Intracellular Ca(2+) levels were also increased. Chronic treatment (10-12 weeks) with the NHE1 inhibitor cariporide normalised NHE1 activity, decreased [Formula: see text] levels and reduced LV myocyte hypertrophy. Moreover, among the various activated pathways, cariporide treatment markedly reduced Akt activity only. CONCLUSIONS/INTERPRETATION: These findings indicate that activation of the Akt pathway represents a likely mechanism mediating the hypertrophic effect of increased NHE1 activity in the GK model of type 2 diabetes.

[Long term evolution of chronic constrictive pericarditis. A study of 56 patients]. / Evolution a long terme des péricardites constrictives chroniques. A propos de 56 patients.

OBJECTIVE AND METHOD: We retrospectively analysed 56 consecutive patients with a confirmed diagnosis of chronic constrictive pericarditis over a period of 23 years. The objective was to analyse the evolution of the annual frequency of constrictive pericarditis, its aetiology and to define the prognostic factors for mortality. RESULTS: The annual frequency of constrictive pericarditis has not diminished over the 23 years of this study, remaining at 2.4 cases per year. Cases with a tuberculous origin have diminished progressively, being replaced by complications of cardiac surgery and mediastinal radiotherapy. Pericardectomy was performed in 41 patients and the average follow up was 9.5 +/- 8.6 years. By the end of the study, 34 patients had died (61.8%), 18 from a cardiovascular cause (38.3%). The independent predictive factors for overall mortality were a history of mediastinal radiotherapy, the age, and plasma sodium level. Only the presence of first degree atrio-ventricular block was an independent predictive factor for cardiovascular mortality. In the pericardectomy group, 24 patients died (60%). A history of mediastinal radiotherapy and the presence of pre-operative hyponatraemia were independent predictive factors for overall mortality. CONCLUSION: Constrictive pericarditis remains a serious pathology. Pericardectomy allows a clear functional improvement, but following pericardectomy more than 60% of patients will die within 10 years of the diagnosis being made.

[Hopes for gene therapy for cardiac failure]. / Espoirs de la thérapie génique dans l'insuffisance cardiaque.

Although the drug therapies developed over the last decades have improved the prognosis of congestive cardiac failure, the condition remains a principal cause of mortality and hospital admission in the industrialised world. The hopes for gene therapy in cardiac failure are based on the possibility of acting on the underlying physiopathological mechanisms by the transfer of genetic material to the failing myocardium. A number of experimental studies targeting the regulation of the calcium ATPase of the sarcoplasmic reticulum, the pathways of beta-adrenergic desensibilisation and the pathways of apoptosis reported encouraging results. Although improvements in the efficacy and safety of techniques of vector construction and methods of delivery to the myocardium incite a certain optimism, the clinical benefits of gene therapy in cardiac failure have yet to be demonstrated.

[Acute coronary syndromes and myocardial perfusion. Cardiac magnetic resonance imaging and ultrafast CT]. / Syndromes coronaires aigus et perfusion myocardique. Les acquis de l'IRM cardiaque, les perspectives du scanner multibarrettes.

Imaging myocardial perfusion is essential in the management of acute coronary syndromes without ST elevation (ACS ST-) confirming the diagnosis of coronary lesions and quantifying the myocardial ischaemia, an important factor in the stratification of coronary risk. In ACS ST-, perfusion imaging allows evaluation of myocardial viability, diagnosis of residual ischaemia and also the detection of no-reflow phenomena after reperfusion procedures. Although myocardial scintigraphy is the reference method in clinical practice, it has many limitations such as its spatial resolution, its irradiation, its attenuation artefacts, and also the fact that it does not visualise the coronary arteries. This has led to the rapid development of two new non-invasive imaging techniques: cardiac MRI and ultrafast CT. The major advantage of MRI is the possibility of associating analysis of myocardial perfusion with that of cardiac muscle function by investigating right and left ventricular function at rest and during myocardial ischaemia stress tests and by analysis of myocardial viability. More recently, ultrafast CT has been clinically validated for coronary imaging. However, analysis of myocardial perfusion and ventricular function by CT scan is still only at the research stage.

[Intra-aortic balloon pumping and variations in flow in the dilated coronary artery in acute myocardial infarction]. / Contrepulsion intra-aortique et variation du flux de l'artère coronaire dilatée à la phase aiguë de l'infarctus du myocarde.

The object of this study of acute anterior myocardial infarction uncomplicated by cardiogenic shock, a context in which the role of intra-aortic balloon pumping (IABP) remains controversial, was to analyse the effects of IABP on coronary flow in the culprit artery. Twenty-one patients admitted for angioplasty in the acute phase of anterior myocardial infarction were included. The IABP was performed in 6 patients (Group 1) because of clinical signs of cardiac failure. Fifteen patients (Group 2) had no signs of cardiac failure. Coronary flow velocity was recorded by a Doppler catheter after successful angioplasty. The following parameters were analysed: average peak velocity (APV), average diastolic peak velocity (ADPV), average systolic peak velocity (ASPV), diastolic to systolic velocity ratio (DSVR) and maximum peak velocity (MPV). Intra-aortic balloon pumping was associated with an increase in the diastolic indices (APV 17.9 +/- 3.5 vs 14.9 +/- 3.6 cm/s; p < 0.05; ADPV 27.6 +/- 5.2 vs 19.7 +/- 4.7 cm/s; p < 0.05), and a decrease in the systolic index ASVP (3.8 +/- 1.3 vs 7.6 +/- 2.6 cm/s; p < 0.05). The diastolic indices recorded with IABP did not change in Group 2. The velocity spectra changed with the appearance of abnormalities usually described in the presence of microcirculatory abnormalities ("no reflex" phenomenon): decrease in anterograde systolic flow, rapid deceleration of diastolic velocities with appearance of a retrograde systolic flow. The authors conclude that IABP increases diastolic velocities of coronary flow in the acute phase of revascularised anterior myocardial infarction complicated by left ventricular failure but does not seem to be accompanied by improved myocardial perfusion.

[Loffler's fibroblastic endocarditis. A report of a case complicating toxocarosis]. / Endocardite fibroblastique de Löffler. A propos d'un cas compliquant une toxocarose.

The authors report a case of Löffler's fibroblastic endocarditis complicating a toxocarosis infection. Parasitic infestation with toxocara canis is usually asymptomatic, but this was a very rare observation of cerebral involvement associated with symptomatic Löffler's endocarditis. This is an unusual form of restrictive cardiac disease constantly accompanied by prolonged hypereosinophilia. In addition to the classical signs of cardiac failure, an acute febrile illness imitating a connective tissue disease may be observed. Echocardiography helps diagnosis by showing endomyocardial fibrosis and adherent thrombosis at one or both ventricular apices. The management of cardiac failure should include, whenever possible, radical treatment of the hypereosinophilia. At an advanced stage, surgical endocardial decortication is the only means of improving symptoms and the prognosis of these patients.

Discovery of a parachute mitral valve complex (Shone's anomaly) in an adult.

Parachute mitral valve complex is an unusual congenital anomaly described by Shone et al. It is characterized by a parachute deformity of the mitral valve associated with additional forms of left heart anomalies, such as aortic valvular stenosis and coarctation of the aorta. Fewer than 50 cases of Shone's complex have been reported in the literature, and it has only been observed in children. We report the case of a 33-year-old man who was referred to our department because of atrial fibrillation. Echocardiographic evaluation and aortogram evidenced a Shone's complex, including a parachute mitral valve anomaly, an aortic bicuspid valvular anomaly, and a coarctation of the aorta.

[Emergency coronary angioplasty following treatment with 5-fluorouracil]. / Angioplastie coronaire en urgence au décours d'une cure de 5-fluoro-uracile.

INTRODUCTION: The incidence of cardiac toxicity due to 5-fluorouracil (5-FU) ranges from 1.2 to 18%. Most complications occur at the time of the first cure. Their mechanisms have not yet been clearly defined. EXEGESIS: The authors report a case of unstable angina induced by 5-FU. A coronary angioplasty was performed on a previously ignored coronary lesion. CONCLUSION: Recent studies support the hypothesis that 5-FU has endothelial toxicity resulting in thrombogenic effect and release of vasoactive substances. Unstable angina pectoris would be related to plaque rupture caused by 5-FU. Patients with previous history of coronary disease are at significantly increased risk for 5-FU-induced cardiotoxicity. They probably would benefit from continuous electrocardiographic monitoring. Rechallenge with 5-FU after cardiotoxicity problems should include only those patients for whom there is no alternative treatment.

[Malignant non-Hodgkin's lymphoma presenting with arrhythmia and conduction defects. Report of 2 cases]. / Troubles du rythme et de la conduction révélateurs d'une localisation cardiaque de lymphome malin non hodgkinien. A propos de 2 cas.

Primary cardiac lymphoma is very rare. Secondary localisations are more common, observed in 15 to 30% of autopsy series. Clinical symptoms of cardiac involvement are rare, explaining the usual post-mortem diagnosis. The presentation of cardiac involvement by arrhythmias and conduction defects is very uncommon. The authors report two cases, the first of a 35 year old man in whom primary cardiac lymphoma presented with ventricular tachycardia complicated secondarily by complete atrioventricular block (AVB) with pseudo-inferior wall infarction. The second case was a 37 year old man with a cutaneous T cell lymphoma in whom complete AVB was the first sign of a secondary cardiac localisation of his disease. The finding of cardiac lymphoma should lead to aggressive chemotherapy as soon as possible.

[Variations of coronary blood flow measured by intracoronary doppler in the acute phase of myocardial infarction before and after revascularization by angioplasty]. / Variations du flux sanguin coronaire mesuré par doppler intracoronaire à la phase aiguë de l'infarctus du myocarde avant et après revascularisation par angioplastie.

The authors studied the changes in coronary blood flow before, during and after reperfusion by angioplasty of the disease coronary vessel responsible for myocardial infarction using intracoronary Doppler. Forty patients aged 60.2 +/- 15.4 years, admitted for primary myocardial infarction (inferior: 22, anterior: 18) were included. Before reperfusion, the peak velocity of the collateral coronary circulation was 14.8 +/- 8.1 cm/s. The flow was bidirectional, mainly retrograde (N = 32), negative (N = 1) or positive (N = 5). The five Rentrop 0 patients had velocities similar to Rentrop 1, 2 or 3 patients (Rentrop 0: 14.9 +/- 6.4 cm/s; Rentrop 1: 12.3 +/- 9.9 cm/s; Rentrop 2: 15.2 +/- 8.2 cm/s; Rentrop 3: 17.5 +/- 6.3 cm/s). Patients with TIMI 3 reperfusion flow had the highest APV Doppler velocities (average peak velocities during the cardiac cycle) (APV TIMI 3 = 20.2 cm/s versus APV TIMI 1 and 2 = 10.9 cm/s, p = 0.05). After angioplasty, the APV was 18.7 +/- 10.4 cm/s (p < 0.001). Diastolic flow was dominant. Seventeen patients had retrograde systolic flow, 12 had minimal systolic flow and 17 had a steep diastolic deceleration slope. Intracoronary Doppler demonstrates the wide range of coronary flow in TIMI 3 flow patients, both from the morphological and the quantitative points of view, which seems to be independent of the presence of residual stenosis and could be related to abnormalities of the microcirculation. This could allow identification of a subgroup of patients at high risk and candidates for a complementary therapeutic intervention (intra-aortic balloon pumping...).

[Fistulas after Lewis-Santy's operations. Diagnosis, treatment, prevention]. / Les fistules après interventions de Lewis-Santy. Diagnostic, traitement, prévention.

Fistulas of the anastomosis is the most severe complication after the Lewis-Santy operation. Over the last 10 years, we have performed 227 such operations for cancer of the oesophagus and have observed 16 fistulizations (7%). The aim of this study was to analyze the clinical manifestations and laboratory findings in these cases of fistulization as a function of the site of the plasty, the treatment and the results. We attempted to determine factors which could lead to means of preventing this complication. The fistula occurred at the oeso-gastric anastomosis in 11 cases (4.8%), at the apex of the gastric tube in 2 and on the line of gastric tubulization in 3. A comparison between patients with fistulas (group 1) and those without (group 2) showed that 19% of the patients in group 1 were over 70 years of age versus 9% in group 2 (NS). Three of the 16 patients (19%) with fistula had cirrhosis due to ethylism versus 2 of the 211 patients in group 2 (p < 0.001). Six patients among the 58 with palliative with a fistula (6%) (NS). Thoracic drainage was sufficient in 11 patients and surgical treatment was not required. In 5 reoperation (thoracotomy 4, cervicotomy 1) was necessary due to an intrapleural abscess. After 227 Lewis-Santy operations, 11 patients died during hospitalization (4.8%, 4 of which were complicated with fistula (1.7% of the operated patients and 25% of the patients with fistulas). The frequency of fistulizations after Lewis-Santy operation has decreasing (8%) and the gravity has improved (3 out of 4 were cured).(ABSTRACT TRUNCATED AT 250 WORDS)

[Four cases of tracheoesophageal fistula associated with prolonged ventilation]. / Quatre cas de fistules oeso-trachéales au cours de la ventilation prolongée.

On the basis of four cases of oesophago-tracheal fistulae developing in ventilated patients, the authors describe the pathogenesis of these lesions, related to circulatory disturbances in the tracheal mucosa in contact with the balloon of the balloon of the tracheal tube. The spontaneous course is rapidly fatal and the results of surgical treatment remain disappointing. Prevention of these lesions is essential but difficult. It is based above all on the use of "large volume and low pressure" balloons, with periodic exsufflation. The diagnosis of these lesions must be make early and is base upon the development of tracheal dilatation, even minimal and seen radiologically by the appearance of the tube balloon. Such a finding should lead to endoscopic exploration of the tranchea and oesophagus, in order that treatment may be strated rapidly.