Enhanced postmyocardial infarction fibrosis via stimulation of the transforming growth factor-beta-Smad2 signaling pathway: role of transient receptor potential vanilloid type 1 channels.

Objective: To test the hypothesis that the transient receptor potential vanilloid type 1 (TRPV1) channels modulate postmyocardial infarction (MI) fibrosis and matrix formation via the transforming growth factor-beta-Smad signaling pathway to conserve cardiac function and geometrical regeneration.

Background: Several lines of evidence indicate that activation of TRPV1 expressed in afferent nerve fibers innervating the heart may preserve cardiac function after MI. However, the underlying mechanisms of TRPV1-mediated protection are largely unknown.

Transient receptor potential vanilloid gene deletion exacerbates inflammation and atypical cardiac remodeling after myocardial infarction.

The transient receptor potential vanilloid (TRPV1) channels expressed in sensory afferent fibers innervating the heart may be activated by protons or endovanilloids released during myocardial ischemia (MI), leading to angina. Although our previous in vitro data indicate that TRPV1 activation may preserve cardiac function after ischemia-reperfusion injury, the underlying mechanisms are largely unknown. To test the hypothesis that TRPV1 modulates inflammatory and early remodeling processes to prevent cardiac functional deterioration after myocardial infarction, TRPV1-null mutant (TRPV1(-/-)) and wild-type (WT) mice were subjected to left anterior descending coronary ligation or sham operation.

Atheromatous plaque cap thickness can be determined by quantitative color analysis during angioscopy: implications for identifying the vulnerable plaque.

Background: Coronary angioscopy in acute myocardial infarction has frequently revealed disrupted yellow lesions. Furthermore, postmortem studies have demonstrated that these lesions have thin collagenous caps with underlying lipid-rich cores.

Hypothesis: We hypothesized that the yellow color is due to visualization of reflected light from the lipid-rich yellow core through a thin fibrous cap.

Laser-light scattering, a new method for continuous monitoring of platelet activation in circulating fluid.

We evaluated a novel technique of laser-light scattering (LLS) to detect platelet-volume changes continuously, reflecting platelet aggregation in circulating fluid. Carotid arteries from 20 dogs were mounted in a dual perfusion chamber. Balloon angioplasty (BA) was performed and arteries perfused with platelet-rich plasma (PRP).

Long balloon angioplasty with focal stenting for the treatment of diffuse coronary artery disease.

The objective of this study was to evaluate the efficacy of treating long coronary lesions (> 30 mm) with either a 40 or a 60 mm long Scimed Cobra balloon followed by focal (contingency) stenting of areas with suboptimal results. Diffuse lesion length is a morphological characteristic associated with a poorer clinical outcome after balloon angioplasty with or without stenting. Patients were enrolled in a prospective randomized fashion to have initial PTCA with either a 40 or a 60 mm long balloon followed by focal stenting in areas with suboptimal results.

Thrombostatin, a bradykinin metabolite, reduces platelet activation in a model of arterial wall injury.

Objective: Thrombin activates platelets and contributes to the occlusion of arteries following thrombolytic therapy or angioplasty. Thrombostatin (RPPGF), the angiotensin converting enzyme degradation product of bradykinin, inhibits alpha-thrombin induced platelet activation. We hypothesized that thrombostatin prevents platelet aggregation and adhesion after balloon angioplasty (BA).