[Coronary thrombosis: Physiopathology and treatment in the era of tailored medicine]. / Thrombose coronaire : physiopathologie et traitement à l'ère de la médecine personnalisée.

Coronary thrombosis remains the leading cause for cardiovascular death in France. Great advances have been made in the knowledge of the basic mechanism involved in coronary thrombogenesis and in antithrombotic treatments. They have led to substantial survival benefit after myocardial infarction and enabled development of tailored therapeutic strategies, especially for high-risk patients. Direct oral anticoagulants have now entered the game for secondary prevention after coronary thrombosis.

The association of the coronary thrombus burden with all-cause mortality and major cardiac events in ST-segment elevation myocardial infarction patients treated with tirofiban.

BACKGROUND: The aim of this study was to investigate the association of the coronary thrombus burden with all-cause mortality and major adverse cardiac events (MACE) in ST-segment elevation myocardial infarction (STEMI) patients treated with 'in-cath lab' (downstream) high-dose bolus tirofiban. METHODS: This study included 2452 patients with STEMI treated with a primary percutaneous coronary intervention. All glycoprotein IIb/IIIa receptor inhibitor (GPI) (tirofiban) infusions were started in the catheterization laboratory according to the coronary thrombus burden; tirofiban was not administered to patients who did not have coronary thrombus burden. All patients with small, moderate, or large thrombus burden received tirofiban therapy. The primary study endpoint was the incidence of all-cause mortality. The secondary study endpoints were major bleeding and MACE, which included all-cause death, nonfatal acute coronary syndrome, and target lesion revascularization. RESULTS: The patients were followed up for a mean period of 28.3±10.4 months. The groups showed similar in-hospital and long-term event rates (MACE, major bleeding, and all-cause mortality). The 3-year Kaplan-Meier overall survivals for no thrombus, small thrombus, moderate thrombus, and large thrombus were 91.9, 92.6, 92.3, and 89.5%, respectively. CONCLUSION: Despite the fact that the large coronary thrombus was found to be a predictor of MACE and mortality in many previous studies, we found that the large thrombus was not associated with MACE or in-hospital mortality or long-term mortality. This can be an effect of downstream GPI therapy. We suggest the use of downstream GPI therapy for STEMI patients with large coronary thrombus without an increased risk of bleeding.

Contrasting effects of a dietary copper deficiency in male and female mice.

Female rats are protected from the lethal effects of a dietary copper (Cu) deficiency, but female mice fed a Cu-deficient diet develop atrial thromboses and die. To further investigate the effect of sex on Cu status in mice (n = 16), male and female adult Swiss-Webster mice were fed Cu-supplemented (8.4 mg Cu/kg) or Cu-deficient (0.3 mg Cu/kg) diets with deionized water for 43-49 days. Six female mice, but only one male mouse, fed the Cu-deficient diet died during the experiment. Both male and female mice fed the Cu-deficient diet exhibited typical features of deficiency. The severity of anemia and the values observed for several indicators of Cu status (plasma ceruloplasmin [EC 1.16.3.1.] and erythrocyte copper-zinc superoxide dismutase [EC 1.15.1.1.] activities, cardiac Cu) were similar in both male and female Cu-deficient mice. However, cardiac enlargement (0.97 vs 0.73 g/100 g body wt, P < 0.05), cardiac edema (79.9% vs 78.2% cardiac water, P < 0.05) and depletion of renal Cu (10.4 vs 12.5 micrograms/g dry weight, P < 0.05) were more severe in female compared with male, Cu-deficient mice. Furthermore, although hepatic Cu was significantly (P < 0.05) lower in female Cu-deficient compared with Cu-supplemented mice, it was not significantly decreased by deficiency in male mice. These data indicate that the female mice experienced a more extreme form of Cu deficiency than the males.

Reduction in infarct size and enhanced recovery of systolic function after coronary thrombolysis with tissue-type plasminogen activator combined with beta-adrenergic blockade with metoprolol.

The effect of beta-adrenergic blockade on the salvage and functional recovery of reperfused myocardium was investigated in anesthetized dogs. Immediately after thrombotic occlusion of the left anterior descending coronary artery, the cardioselective beta-blocking agent metoprolol was given intravenously at a dose of 0.5 mg/kg infused over 10 min. One hour after the onset of occlusion, recanalization was initiated by intravenous infusion of recombinant human tissue-type plasminogen activator (rt-PA, 10 micrograms/kg/min for 30 min). Anatomic infarct size expressed as percent of the left ventricular mass (I/LV), global ejection fraction, and mean systolic shortening of the segmental radii (SS) of the infarcted area were measured either after 24 hr or 1 week in six groups of six dogs each: group I (rt-PA + metoprolol, evaluated at 24 hr), group II (rt-PA + metoprolol, evaluated at 1 week, group III (rt-PA alone, evaluated at 24 hr), group IV (rt-PA alone, evaluated at 1 week), group V (persistent occlusion, evaluated at 24 hr), and group VI (persistent occlusion, evaluated at 1 week). The smallest infarcts were found in reperfused dogs given metoprolol, but the differences from dogs receiving rt-PA alone were not statistically significant (I/LV, expressed as mean +/- SEM: 5.5 +/- 0.9% in group I, 6.7 +/- 1.9% in group II, 15.4 +/- 5.0% in group III, 11.4 +/- 3.5% in group IV, 23.6 +/- 2.5% in group V, and 26.9 +/- 2.3% in group VI).(ABSTRACT TRUNCATED AT 250 WORDS)