Comparison of Enoxaparin and Unfractionated Heparin on Thrombin Generation in Acute Coronary Syndromes without ST-Segment Elevation

SummaryRecent clinical trials have demonstrated a better ability of low-molecular-weight heparin, compared to unfractionated heparin, in reducing ischemic cardiac events in patients with acute coronary syndromes without ST-segment elevation. No data are available concerning the in-vivo comparison of enoxaparin and unfractionated heparin on thrombin generation in patients with unstable angina or non-Q-wave myocardial infarction. We measured the plasma levels of prothrombin fragment 1+2 (a marker of prothrombin activation) and thrombin/anti-thrombin complex (a marker of thrombin generation) in 45 patients with non ST-elevation acute coronary syndromes who were randomized to receive enoxaparin, 3000 IU anti-Xa as an i. v. bolus, followed by 70 IU anti-Xa/Kg every 8 h for 3 days (23 pts, Group 1) or a bolus of 100 IU/kg of unfractionated heparin followed by infusion for 3 days titrated to maintain the aPTT between 70 and 90 s (22 pts, Group 2). Plasma levels of prothrombin fragment 1+2 reduced significantly at 3rd h of treatment in both groups (–42% in Group 1 and –45% in Group 2), reached the lowest plasma concentration at the 24th h and exhibited a slight increase at the 72nd h; no differences were observed between the two groups at any time points. Plasma thrombin/antithrombin complex levels had a similar behaviour: reduced markedly in both groups at the 3rd h (–52% in Group 1 and –46% in Group 2), remained lower during the first two days and slightly rose at 72nd h. No differences between the two groups in plasma levels of this marker were apparent during drug infusion. In Group 1 the aPTT did not show significant changes; in Group 2 the mean value of aPTT doubled the basal value at any time point of determination. Both enoxaparin and unfractionated heparin produced a marked and similar reduction of thrombin generation. Other unknown mechanisms might explain the different clinical effects of the two heparins.</jats:p

Circulatory response to fluid overload removal by extracorporeal ultrafiltration in refractory congestive heart failure

AbstractOBJECTIVESThe goal of this study was to investigate the hemodynamic and circulatory adjustments to extracorporeal ultrafiltration (UF) in refractory congestive heart failure (rCHF).BACKGROUNDIn rCHF, UF allows clinical improvement and restores diuretic efficacy. However, in the course of a UF session, patients are exposed to rapid variations of body fluid composition so that, as fluid is withdrawn from the intravascular compartment, hypotension or even shock could occur.METHODSIn 24 patients with rCHF undergoing UF, we measured, after every liter of plasma water removed, hemodynamics, blood gas analysis (in both systemic and pulmonary arteries), plasma volume changes (PV) and plasma refilling rate (PRR). The PV and PRR were calculated by considering hematocrit and ultrafiltrate volume.RESULTSIn all patients, UF was performed safely, without side effects or hemodynamic instability (ultrafiltrate = 4,880 ± 896 ml). Mean right atrial, pulmonary artery and wedge pressures progressively reduced during the procedure. Cardiac output increased at the end of the procedure and, to a greater extent, 24 h later, in relation to the increase of stroke volume. Heart rate and systemic vascular resistance did not increase, and other peripheral biochemical parameters did not worsen during UF. Intravascular volume remained stable throughout the entire duration of the procedure, indicating that a proportional volume of fluid was refilled from the congested parenchyma.CONCLUSIONSIn patients with rCHF, subtraction of plasma water by UF is associated with hemodynamic improvement. Fluid refilling from the overhydrated interstitium is the major compensatory mechanism for intravascular fluid removal, and hypotension does not occur when plasma refilling rate is adequate to prevent hypovolemia

Bloody tricuspid stenosis: case report of an uncommon cause of haemoptysis

Abstract Background Haemoptysis is usually caused by pulmonary and infectious diseases. In few cases, it has a cardiac cause, such as pulmonary embolism or mitral valve stenosis. Haemoptysis may be an uncommon symptom of prosthetic valve dysfunction, being related to elevated right heart pressures. Case summary A 22-year-old woman from sub-Saharan Africa known for a triple valve replacement was hospitalized for dyspnoea and haemoptysis. A careful clinical evaluation excluded the most common causes of haemoptysis. Transthoracic echocardiogram showed normal biventricular function, normally functioning mechanical prosthetic aortic and mitral valves, and the biological tricuspid prosthesis showed an increased transvalvular gradient. Contrast chest computed tomography scan excluded pulmonary embolism and mechanical valve obstruction, but revealed marked systemic venous hypertension. Right heart catheterization confirmed increased right heart pressures and severe bioprosthetic tricuspid valve stenosis. The patient underwent a successful percutaneous tricuspid valve-in-valve replacement, with complete resolution of symptoms. Discussion The increase in venous pressures due to bioprosthetic tricuspid stenosis caused veno-venous shunts: blood from the lower body was drained into the superior vena cava via the azygos vein. Increased pressure in the latter affected pressure in bronchial veins and arteries, leading to haemoptysis. Cardiac surgical reinterventions are associated with worse outcomes and higher mortality rates. Management of a degenerated prosthetic tricuspid valve is challenging and requires a multidisciplinary assessment. Transcatheter tricuspid valve replacement is becoming a feasible option in patients with prosthetic dysfunction. Based on evidence to date, tricuspid valve-in-valve replacement appears to be a safe, feasible, and effective alternative in selected young patients. </jats:sec