In pulmonary arterial hypertension (PAH), the raise of vascular resistance lead to right ventricular dysfunction, fluid retention and death. In this setting, we evaluated the determinants of moderate ...renal dysfunction and its impact on mortality.
38 consecutive PAH patients were prospectively enrolled. Right ventricular dysfunction was assessed by echocardiography using two-dimensional strain, tissue Doppler imaging and tricuspid annular displacement (TAPSE). Right-sided catheterism, 6-minute walking distance and biological sampling was performed within 48 hours. Moderate Renal dysfunction was defined by a creatinine clearance below 60
ml/min.
In the overall cohort, renal dysfunction was associated with decreased cardiac output, SVO 2, TAPSE, haemoglobin levels, 6 min walking distance and increased BNP levels. By univariate analysis, predictors of mortality were TAPSE < 15
mm (OR: 10.25 95% CI 1.06–29.44; p
=
0.028), BMI < 25
kg/m
2 (OR: 5.00 95% CI 1.04–23.84; p
=
0.043) and renal dysfunction (OR: 9.43 95% CI 1.96–45.29; p
=
0.005). By multivariate analysis, renal dysfunction remains the sole independent predictor of mortality at one year follow-up (OR: 5.597 95% CI 1.064–29.441; p
=
0.042).
Moderate renal dysfunction is a powerfull marker of prognosis in PAH.
Cardiac resynchronisation therapy (CRT) has been shown to improve clinical status in heart failure patients. Some patients treated by CRT fail to respond to the treatment. Predisposing factors for ...non-response should be investigated to optimize patient selection.
The purpose of the study was to evaluate before device implantation and 3, 6 and 12 month after, echocardiographic and biological parameters with respect to CRT response.
Thirty two patients with heart failure (72% of men; age 66
±
10 years; 59% non-ischaemic cardiomyopathy; NYHA III–IV; left ventricular ejection fraction (LVEF) 22.7
±
6.7%; QRS width 146
±
26
ms) were implanted with CRT device and followed during twelve month. Responders (R) were defined as patients with improvement of one or more NYHA functional class, with a significant improvement in quality of life and without episode nor hospitalization for heart failure during follow-up.
34% of the patients constitute the non-responder group (NR). No difference between R and NR was observed in LVEF, QRS width, NYHA, cardiovascular risk factors nor drug medication. Non-ischaemic dilated cardiomyopathy was significantly more present in R (71% vs 27%; p
=
0.03). Before CRT, NR had more important left ventricular end-diatolic diameter, left ventricular end-systolic diameter and more elevated left pressions. Atrioventricular dyssynchrony was significantly more observed in R (66% vs 9%; p
=
0.006) so as intraventricular dyssynchrony (95% vs 27%; p
=
0.001).BNP is significantly more elevated in NR (602
±
385 vs 320
±
361; p
=
0.03) before CRT.After 3 and 6 month, a significant decrease in left ventricular end-diatolic and end-systolic diameters, LVEF and normalisation of left and right pressions occur in R. Likewise, BNP levels were lower in R.
NR patients have before implantation a more severe cardiomyopathy. At follow-up, left ventricular remodelling could only be observed in R patients. These data suggest that cardiac CRT should not be proposed too late so that left ventricular remodelling could be expected.
The peroxisome proliferator-activated receptor alpha (PPARalpha) plays an important role in the metabolism of lipoproteins and fatty acids, and seems to protect against the development of ...atherosclerosis. To evaluate the possible protective role of PPARalpha on cardiovascular function, the effect of the PPARalpha agonist, fenofibrate was assessed with respect to ischaemia/reperfusion injury and endothelial function in mice.
Fenofibrate treatment reduces myocardial infarction size and improves post-ischaemic contractile dysfunction. Hearts from PPARalpha null mice exhibit increased susceptibility to ischaemic damages and were refractory to protection by fenofibrate treatment suggesting that the beneficial effects of fenofibrate were mediated via PPARalpha. Furthermore, fenofibrate improves endothelium- and nitric oxide-mediated vasodilatation in aorta and mesenteric vascular bed. A decreased inhibitory effect of reactive oxygen species in the vessel wall accounts for enhanced endothelial vasodilatation. However, the latter cannot be explained by an increase in nitric oxide synthase expression nor by an increase sensitivity of the arteries to nitric oxide.
Altogether the present data suggest that fenofibrate exerts cardioprotective effect against ischaemia and improves nitric oxide-mediated response probably by enhancing antioxidant capacity of the vessel wall. These data underscore new therapeutic perspectives for PPARalpha agonists in ischaemic myocardial injury and in cardiovascular diseases associated with endothelial dysfunction.
In atrial fibrillation (AF), the reasons why most of the thrombi form in the left atrium are mainly unknown. In the vasculature, endothelial damage together with platelet activation and inflammation ...contribute to initiation of blood coagulation and thrombus growth.
The purpose of this study was to investigate whether atrial-specific differences in endothelial damage, leukocyte activation, platelet stimulation occur in patients with AF.
Twenty patients (15 men, 5 women; age 55
±
8 years, 15 paroxystic AF, 5 persistent AF) with AF undergoing ablation were investigated. Blood samples from the left and right atrium were obtained at the start of the procedure. Procoagulant microparticles (MPs), reliable markers of vascular damage were measured by capture assays. Their procoagulant abilities were quantified by functional prothrombinase assay and their cellular origin were determined (endothelium, platelet, leukocyte). In addition, platelet reactivity was evaluated by whole blood flow cytometry for expression of platelet Pselectin (CD62P), active glycoprotein IIbIIIa receptor (PAC-1). Platelet aggregation was evaluated using Arachidonic acid (AA), ADP, TRAP and collageninduced whole blood aggregometry.
No atrial-specific differences in the levels of total procoagulant MP, leukocyte-derived-MP and platelet-derived MP could be evidenced. Conversely, endothelial-derived MPs (CD105+) were slightly elevated in the right atrium (RA 0.96
±
0.53 vs. LA 0.80
±
0.45
nm PhtdSer Eq.; p
=
0.041). Likewise, collagen-induced platelet aggregation was evidenced in the right atrium (Collagen 1
mg/l RA: 48
±
33% vs LA 37
±
29%; p 0.035; collagen 2,5
mg/l RA: 76
±
25% vs LA: 60
±
29%; p
=
0.001).
In patients with AF, endothelial damage and collageninduced platelet aggregation appear slightly more pronounced in the right atrium. Our data did not substantiate the view that chamber specific enhanced thrombogenic status could be a reliable explanation for the increased propensity for thrombus formation observed in the left atrium in AF patients.
In atrial fibrillation (AF), the reasons why most of the thrombi form in the left atrium are mainly unknown. In the vasculature, endothelial damage together with platelet activation and inflammation ...contribute to initiation of blood coagulation and thrombus growth.
The purpose of this study was to investigate whether atrial-specific differences in endothelial damage, leukocyte activation, platelet stimulation occur in patients with AF.
Twenty patients (15 men, 5 women; age 55
±
8 years, 15 paroxystic AF, 5 persistent AF) with AF undergoing ablation were investigated. Blood samples from the left and right atrium were obtained at the start of the procedure. Procoagulant microparticles (MPs), reliable markers of vascular damage were measured by capture assays. Their procoagulant abilities were quantified by functional prothrombinase assay and their cellular origin were determined (endothelium, platelet, leukocyte). In addition, platelet reactivity was evaluated by whole blood flow cytometry for expression of platelet Pselectin (CD62P), active glycoprotein IIbIIIa receptor (PAC-1). Platelet aggregation was evaluated using Arachidonic acid (AA), ADP, TRAP and collageninduced whole blood aggregometry.
No atrial-specific differences in the levels of total procoagulant MP, leukocyte-derived-MP and platelet-derived MP could be evidenced. Conversely, endothelial-derived MPs (CD105+) were slightly elevated in the right atrium (RA 0.96
±
0.53 vs. LA 0.80
±
0.45
nm PhtdSer Eq.; p
=
0.041). Likewise, collagen-induced platelet aggregation was evidenced in the right atrium (Collagen 1
mg/l RA: 48
±
33% vs LA 37
±
29%; p 0.035; collagen 2,5
mg/l RA: 76
±
25% vs LA: 60
±
29%; p
=
0.001).
In patients with AF, endothelial damage and collageninduced platelet aggregation appear slightly more pronounced in the right atrium. Our data did not substantiate the view that chamber specific enhanced thrombogenic status could be a reliable explanation for the increased propensity for thrombus formation observed in the left atrium in AF patients.
The implantation of pace maker or defibrillator expose to the risk of infection of these devices. The use of antimicrobial prophylaxis before implantation is not clearly recommended, because there ...are only few studies that establish its benefit.
We conducted a retrospective case control study between 2004 and 2007, to determine the risk factor associated with infection, especially if the administration of an antimicrobial prophylaxis is associated with decrease of devices infection. Inclusion criteria were following: presence of wound inflammation, or device externalisation, and Klug's modified Dukes criteria for endocarditis. All micro-organisms results from deep wound sample or blood culture.
979 patients had a non valvular cardiac device during the study period. 34 of them developed infectious complication (incidence 3.5%) : 19 local infections, and 15 endocarditis. 70 patients constituted the age and sex matched control population. Staphylococcus was isolated in 88% of the cases. 27% of them were S. aureus. 53% of Staphylococcus were resistant to meticillin. The risk factors associated with infection were following : number of surgical interventions related to the cardiac devices (p
<
0.001), early wound inflammation or hematoma (p
<
0.001), INR or partial thromboplastin time ratio > 1.5 the day of implantation, fever before implantation (p< 0.001), more infections after defibrillator implantation vs pace maker (p
=
0.03) and absence of antibioprohylaxis (p
=
0.03). Antibioprophyxis were in majority of case intra venous cephalosporin (16/17).
Antibioprophylaxis and surveillance of anticoagulation could be helpful to prevent infection after cardiac devices implantation; prospective studies could be interesting to confirm these results.
Table. Risk factors for cardiac device infection
Risk factors for infection
p
Number of surgical operation related to cardiac device
p<0.001
Early wound inflammation or hematoma
p<0.001
INR or partial thromboplastin time ratio > 1.5
p<0.015
Fever before implantation
p<0.001
Defibrillator implantation versus pacemaker
p=0.03
Absence of antibioprophylaxis
p<0.03
BACKGROUNDThe presence of a dilated coronary sinus (CS) assessed by transthoracic echocardiography (TTE) is highly suggestive of inferior or superior vena cava (SVC) anomalies, in the absence of a ...shunt. The most frequent finding is the persistence of a left superior vena cava (LSVC): well-known feature to electrophysiologists. Abnormal inferior vena cava (IVC) drainage is another cause of CS dilatation. CASE SUMMARYAn 83-year-old woman presented with heart failure symptoms, atrial fibrillation with rapid ventricular rate, and a dilated CS assessed by TTE. Atrioventricular (AV) node ablation was considered given the poor efficacy of a rate control strategy. Cardiac computed tomography (CT) revealed a double SVC with an LSVC draining directly into the dilated CS. Single-lead pacemaker implantation was performed using a right-sided vascular access with no technical difficulties. An aborted AV node ablation procedure was due to the impossibility of getting to the right atrium. Fluoroscopy and CT imaging at second look analysis confirmed the diagnosis of an abnormal IVC with an agenesia of its supra-hepatic segment directly drained into the CS. DISCUSSIONOur clinical case illustrates an unusual and rare double venous abnormality: both LSVC and IVC directly drained into the CS and were responsible for its massive dilatation.
New transvenous devices using cryoenergy have been recently introduced to perform pulmonary vein isolation (PVI) for the treatment of atrial fibrillation (AF). Experimental data suggested that ...cryoenergy (CRYO) produced less endothelial disruption and platelet activation than radiofrequency energy (RF) offering safety benefits. We aimed to compare both systems with regards to safety in patients by measuring for the first time sensitive laboratory markers of cell damage. platelet activation and inflammation after a PVI using either one of those energies.
Sixty patients with symptomatic drug-resistant AF referred for PVI (56
±
9 years of age, 48 males. 38 with paroxysmal and 22 with persistent AF) were randomly assigned to undergo the ablation procedure using either an open irrigated tip RF catheter (Thermocool®. Biosense Webster) or a cryoballoon catheter (Arctic front®. Medtronic). Systemic markers of cell damage (procoagulant microparticles MPs of various cellular origin, troponin T, CK and CK-MB). platelet activation (ADP-induced light transmittance aggregation LTA, expression of the platelet surface proteins P-selectin pSEL and activated GPIIb/IIIa PAC-1) and inflammatory response (hs-CRP) were determined frequently before and 4, 24 and 48 hours after the procedure.
Procedure time was significantly shorter in patients treated with the cryoballoon (177
±
30
min versus 200
±
46
min. p
=
0.028), but there were no differences in fluoroscopic time, clinical event rate and success rate. Post-procedural increases of MPs Troponin T and hs-CRP were observed but there were no consistent differences in parameters used for comparative laboratory safety assessment of the ablation systems using either cryoenergy or radiofrequency energy.
Neither systematic sensitive markers of cell damage, of platelet activation nor of inflammatory response could detect any difference in the safety profile between cryoenergy and RF energy used for transseptal PVI in patients with AF.
Abdominal obesity and metabolic syndrome are important risk factors of atherothrombosis. In obesity, metabolic and inflammatory-mediated tissular injury could contribute to enhanced shedding of ...procoagulant microparticles (MPs). At sites of endothelium injury, the swift recruitment of procoagulant-MPs enables the initiation of blood coagulation and thrombus growth.
In obese female, we sought to evaluate the impact of vey low caloric diet (VLCD) on procoagulant MPs levels, fibrinolytic status, inflammation and endothelium damage.
Circulating biomarkers of vascular damage, fibrinolytic status, platelet activation, inflammation were measured before, 30 and 90 days after VLCD. Microparticles were measured by flow cytometry and capture assays. Their procoagulant abilities were quantified by functional prothrombinase assay and their cellular origin were determined (endothelium, platelet, leukocyte, lymphocyte and erythrocyte phenotypes).
24 obese females (39
±
10 yr) were prospectively enrolled. At baseline, higher PAI-l or platelet-derived procoagulant MPs levels were respectively evidenced in patients with metabolic syndrome or insulin resistance (HOMA>2.4). Procoagulant leukocytes-derived MPs were associated with waist circumference at baseline (r
=
0.534: p
=
0.010) and at 90 days follow-up (r
=
0.487; p
=
0.021). At 90 days, weight reduction (−9.8%) was associated with a lowering of blood pressure, improvement of metabolic parameters and a significant reduction of PAI-1 (−38%), procoagulant platelet-derived MPs (−43%) and leptin (−32%) levels.
In obese female, very low caloric diet enables an overall improvement of the haemostatic balance characterized by the reduction of PAI-levels, a fibrinolysis inhibitor, diminished platelet release of procoagulant MPs and reduction of leptin levels, an adipocyte-derived cytokine.
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