Myocardial infarct heterogeneity assessment by late gadolinium enhancement cardiovascular magnetic resonance imaging shows predictive value for ventricular arrhythmia development after acute myocardial infarction.

Aims: The aim of this study was to assess the association between the proportions of penumbra-visualized by late gadolinium enhanced cardiovascular magnetic resonance imaging (LGE-CMR)-after acute myocardial infarction (AMI) and the prevalence of ventricular tachycardia (VT).

Methods: One-hundred and sixty-two AMI patients, successfully, treated by primary percutaneous coronary intervention (PCI) underwent LGE-CMR after a median of 3 days (3-4) and 24-h Holter monitoring after 1 month. With LGE-CMR, the total amount of enhanced myocardium was quantified and divided into an infarct core (>50% of maximal signal intensity) and penumbra (25-50% of maximal signal intensity).

Measurement of collagen- and serotonin-induced platelet aggregation in whole blood.

Upon erosion and rupture of an atherosclerotic plaque, collagen and serotonin (5-hydroxytyramine [5-HT]) induce a process of simultaneous platelet aggregation and vasoconstriction. Simultaneous inhibition of these pathophysiological processes, attainable by 5-HT inhibition, is a potential drug target and could offer an attractive treatment modality. The availability of a reliable and accurate test to measure inhibition of 5-HT-induced platelet aggregation would facilitate the rational development of such new compounds.

Clinically important interaction between tedisamil and verapamil.

Tedisamil, a class III antiarrhythmic drug, is a P-glycoprotein substrate. Tedisamil treatment may implicate coadministration with class IV antiarrhythmics such as verapamil, a P-glycoprotein inhibitor. Pharmacokinetic and pharmacodynamic interactions between tedisamil and verapamil were evaluated in a double-blind, crossover study.

Central nervous system effects of moxonidine experimental sustained release formulation in patients with mild to moderate essential hypertension.

Objectives: The primary aim was to demonstrate that moxonidine, given in an experimental sustained release (SR) formulation, had no clinically relevant central nervous system (CNS) effects after 4 weeks of treatment. A clinically relevant CNS effect was predefined as more than 45 degrees s-1 reduction in saccadic peak velocity (SPV), corresponding to the effects of one night's sleep deprivation.

Methods: In a randomized, double-blind fashion, 35 patients with mild to moderate essential hypertension received placebo run-in medication for 2 weeks, followed by 4 weeks' moxonidine sustained release (1.

Endothelial binding of recombinant tissue plasminogen activator: quantification in vivo using a recirculatory model.

Binding of tissue plasminogen activator (t-PA) to the endothelium may be important in the prevention of thrombus formation. The aim was to develop a method to quantify endothelial binding in vivo. Nine healthy male volunteers received a 40 min continuous infusion with low dose recombinant t-PA (3.

Local tissue factor pathway inhibitor release in the human forearm.

Nineteen healthy men received unilateral brachial artery infusions of either unfractioned heparin (0.3-100 IU/min), saline or the endothelium-dependent vasodilators substance P (2-8 pmol/min) and bradykinin (100-1000 pmol/min), and the endothelium-independent vasodilator sodium nitroprusside (2-8 micro g/min). Heparin caused a dose-dependent increase in plasma TFPI concentrations in both arms (ANOVA, p <0.

Quantification of heparin-induced TFPI release: a maximum release at low heparin dose.

Aims: Heparin releases tissue factor pathway inhibitor (TFPI) from the endothelium and this release may decrease after repeated high dose heparin administration. The primary aim was to investigate and quantify this phenomenon during a short low dose heparin infusion. Also, the effects of heparin on tissue plasminogen activator (t-PA) were studied.