Incidence and Significance of Spontaneous ST Segment Re-elevation After Reperfused Anterior Acute Myocardial Infarction - Relationship With Infarct Size, Adverse Remodeling, and Events at 1 Year.

Background: Up to 25% of patients with ST elevation myocardial infarction (STEMI) have ST segment re-elevation after initial regression post-reperfusion and there are few data regarding its prognostic significance.

Methods and results: A standard 12-lead electrocardiogram (ECG) was recorded in 662 patients with anterior STEMI referred for primary percutaneous coronary intervention (PPCI). ECGs were recorded 60-90 min after PPCI and at discharge.

Rationale and design of the Cyclosporine to ImpRove Clinical oUtcome in ST-elevation myocardial infarction patients (the CIRCUS trial).

Background: Both acute myocardial ischemia and reperfusion contribute to cardiomyocyte death in ST-elevation myocardial infarction (STEMI). The final infarct size is the principal determinant of subsequent clinical outcome in STEMI patients. In a proof-of-concept phase II trial, the administration of cyclosporine prior to primary percutaneous coronary intervention (PPCI) has been associated with a reduction of infarct size in STEMI patients.

Prehospital abciximab in ST-segment elevation myocardial infarction: results of the randomized, double-blind MISTRAL study.

Background: The value of prehospital initiation of glycoprotein IIb/IIIa inhibitors remains a controversial issue. We sought to investigate whether in-ambulance initiation of abciximab in patients with ST-segment elevation myocardial infarction (STEMI) improves ST-segment elevation resolution (STR) after primary percutaneous coronary intervention (PCI).

Methods And Results: MISTRAL (Myocardial Infarction with ST-elevation Treated by Primary Percutaneous Intervention Facilitated by Early Reopro Administration in Alsace) is a prospective, randomized, double-blind study.

Long-term benefit of intracardiac delivery of autologous granulocyte-colony-stimulating factor-mobilized blood CD34+ cells containing cardiac progenitors on regional heart structure and function after myocardial infarct.

Background Aims: Starting from experimental data proposing hematopoietic stem cells as candidates for cardiac repair, we postulated that human peripheral blood (PB) CD34+ cells mobilized by hematopoietic growth-factor (G-CSF) would contain cell subpopulations capable of regenerating post-ischemic myocardial damages.

Methods: In a phase I clinical assay enrolling seven patients with acute myocardial infarct, we directly delivered to the injured myocardium autologous PB CD34+ cells previously mobilized by G-CSF, collected by leukapheresis and purified by immunoselection. In parallel, we looked for the eventual presence of cardiomyocytic and endothelial progenitor cells in leukapheresis products of these patients and controls, using flow cytometry, reverse transcription-quantitative (RTQ)-polymerase chain reaction (PCR), cell cultures and immunofluorescence analyzes.

Clopidogrel 150 mg/day to overcome low responsiveness in patients undergoing elective percutaneous coronary intervention: results from the VASP-02 (Vasodilator-Stimulated Phosphoprotein-02) randomized study.

Objectives: We investigated whether maintenance therapy with clopidogrel 150 mg/day produces greater platelet inhibition than the standard 75-mg/day dose and whether the higher maintenance dose increases platelet inhibition in low responders to clopidogrel 75 mg/day.

Background: Patients show interindividual variability in their platelet response to clopidogrel. Low responders could potentially obtain greater clinical benefit from greater doses of clopidogrel.

Reperfusion injury in acute myocardial infarction: from bench to cath lab. Part II: Clinical issues and therapeutic options.

Two forms of reperfusion injury can occur in patients with ST-segment elevation acute myocardial infarction who are undergoing primary angioplasty: no-reflow phenomenon and reperfusion syndrome. No-reflow, defined as low or no distal perfusion despite removal of epicardial occlusion, can be detected by angiographic flow, myocardial blush grade and contrast echocardiography. Reperfusion syndrome involves haemodynamic and rhythmic disturbances, but an overall paradoxical ST-segment increase.

Reperfusion injury in acute myocardial infarction. From bench to cath lab. Part I: Basic considerations.

Early reperfusion during evolving myocardial infarction is essential for saving myocardium and patients' lives. Nevertheless, lethal reperfusion injury can occur, limiting myocardial salvage. Numerous experimental studies have proved the deleterious effects of reoxygenating endothelial cells and cardiomyocytes.

Effect of cyclosporine on reperfusion injury in acute myocardial infarction.

Background: Experimental evidence suggests that cyclosporine, which inhibits the opening of mitochondrial permeability-transition pores, attenuates lethal myocardial injury that occurs at the time of reperfusion. In this pilot trial, we sought to determine whether the administration of cyclosporine at the time of percutaneous coronary intervention (PCI) would limit the size of the infarct during acute myocardial infarction.

Methods: We randomly assigned 58 patients who presented with acute ST-elevation myocardial infarction to receive either an intravenous bolus of 2.

[Postinfarction management].

Postinfarction management of patients must be individualized. The essential prognostic factor is the ejection fraction, measured at one month. The four basic drugs to be used in combination are antithrombotics, beta-blockers, converting enzyme inhibitors and statins.

Prognostic value of C-reactive protein and cardiac troponin I in primary percutaneous interventions for ST-elevation myocardial infarction.

Background: The rise in cardiac troponin I after ST-elevation myocardial infarction treated by primary percutaneous coronary interventions (PCIs) is predictive of infarct size and left ventricular ejection fraction (LVEF). However, the comparative value of C-reactive protein (CRP) and troponin I for infarct size evaluation and the respective relationships between these biomarkers and mortality have not been investigated.

Methods: We studied 87 patients who underwent primary PCI for ST-elevation myocardial infarction.

Evaluation of the effect of oral verapamil on clinical outcome and angiographic restenosis after percutaneous coronary intervention: the randomized, double-blind, placebo-controlled, multicenter Verapamil Slow-Release for Prevention of Cardiovascular Events After Angioplasty (VESPA) Trial.

Objectives: We investigated the effect of oral verapamil on clinical outcome and angiographic restenosis after percutaneous coronary intervention (PCI).

Background: Thus far, there is no established systemic pharmacologic approach for the prevention of restenosis after PCIs. Five small studies reported encouraging results for calcium channel blockers.

Incomplete resolution of ST-segment elevation is a marker of transient microcirculatory dysfunction after stenting for acute myocardial infarction.

Background: Incomplete ST-segment resolution (STR) after successful primary angioplasty for acute myocardial infarction (AMI) is associated with a poor prognosis. We used intracoronary Doppler velocimetry to investigate whether incomplete STR after primary angioplasty is a marker of severe microcirculatory dysfunction.

Methods And Results: Fifty patients with < or =12-hour AMI underwent successful primary angioplasty and systematic stenting with a Doppler guidewire.

Troponin I concentrations following primary percutaneous coronary intervention predict large infarct size and left ventricular dysfunction in patients with ST-segment elevation acute myocardial infarction.

The aim of this study was to investigate the ability of troponin I (cTnI) levels to predict myocardial infarction size in patients with ST-segment elevation acute myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI). In 87 patients with STEMI undergoing primary PCI, serial plasma concentrations of cTnI and alpha-hydroxybutyrate deshydrogenase (HBDH) were measured before PCI and over the following 72 h. Enzymatic infarct size was estimated by the cumulative release of HBDH during the 72 h following PCI (QHBDH72).