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Giuseppe Patti

Publications and source records attributed to Giuseppe Patti.

At least 19 recordsLinked to original sources
PubMed2006

Simvastatin reduces CD40 expression in an experimental model of early arterialization of saphenous vein graft.

BACKGROUND: Saphenous vein graft (VG) failure occurs more frequently compared with arterial grafts, and graft thrombosis represents the main cause of early occlusion. Because CD40-CD40L pathway CD40 represents a culprit link between local inflammation and coagulation cascade, we investigate the role of CD40 and its soluble ligand (sCD40L) in the immediate in vitro response of VG to arterial pressures, and the potential effects of Simvastatin (Merck Sharp&Dohme, White-house Station, NJ) supplementation. METHODS: Samples of saphenous vein and of internal mammary artery (IMA) were obtained from sixteen patients without history of statin therapy. Segments underwent pulsatile pressure distension and culture with or without supplementation of Simvastatin. CD40 and sCD40L were assessed in tissue lysate and in culture supernatant, respectively. sCD40L serum concentrations were also measured. RESULTS: During the course of the experiment, the CD40 expression was significantly lower in IMA samples compared with both distended and not distended VG. Pressure distension up-regulated the production of CD40 in VG segments after 24 and 48 h. Statin supplementation significantly reduced the expression of CD40 in both venous (P < 0.001) and arterial samples (P < 0.001). This effect of Simvastatin was not affected by the treatment with L-NAME, but it was reversed by the addition of mevalonic acid. Mean sCD40L content in culture supernatants increased over time, suggesting that not only platelets but also the vessel wall is a source of CD40 and sCD40L. CONCLUSIONS: Simvastatin treatment modulates endothelial CD40-sCD40L in both venous and arterial grafts, and therefore may represent a useful tool in the pharmacological prevention of graft failure.

Aged↗
PubMed2006

Protection from procedural myocardial injury by atorvastatin is associated with lower levels of adhesion molecules after percutaneous coronary intervention: results from the ARMYDA-CAMs (Atorvastatin for Reduction of MYocardial Damage during Angioplasty-Cell Adhesion Molecules) substudy.

OBJECTIVES: The goal of this work was to investigate whether protection from myocardial injury during percutaneous coronary intervention (PCI) by atorvastatin is related to reduction of endothelial inflammatory response. BACKGROUND: In the randomized ARMYDA (Atorvastatin for Reduction of MYocardial Damage during Angioplasty) trial, 7-day pre-treatment with atorvastatin before PCI significantly reduced procedural myocardial injury; mechanisms underlying this effect are not characterized. METHODS: In a planned subanalysis of the ARMYDA trial, a subgroup of 76 patients was blind-tested for measurement of plasma levels of vascular cell adhesion molecule-1 (VCAM-1), intercellular cell adhesion molecule-1 (ICAM-1), and E-selectin: 38 patients belonged to atorvastatin (40 mg/day) and 38 to the placebo arm. Adhesion molecules were evaluated 7 days before intervention, immediately before PCI, and after 8 and 24 h. RESULTS: Reduction of procedural myocardial injury after statin pre-treatment was also confirmed in this subgroup. Intercellular cell adhesion molecule-1, E-selectin, and VCAM-1 levels were not different at randomization and before intervention in either arm. At 8 h, increase of ICAM-1 levels was similar in the 2 arms, whereas 24-h levels were significantly lower in the atorvastatin versus placebo group (282 +/- 56 vs. 325 +/- 70 ng/ml; p = 0.007). Attenuation of E-selectin elevation occurred at 8 h in the atorvastatin group (50 +/- 8 vs. 59 +/- 13 ng/ml; p = 0.002) and became even more significant at 24 h (57 +/- 9 vs. 73 +/- 18 ng/ml; p = 0.0008). Vascular cell adhesion molecule-1 levels were not different at any time point in the 2 arms. CONCLUSIONS: In patients undergoing PCI, reduction of procedural myocardial injury after 7-day pre-treatment with atorvastatin is paralleled by concomitant attenuation of post-procedural increase of ICAM-1 and E-selectin levels; thus, reduction of endothelial inflammatory response may explain this protective effect of statins.

Angina Pectoris↗
PubMed2006

Randomized trial of atorvastatin for reduction of postoperative atrial fibrillation in patients undergoing cardiac surgery: results of the ARMYDA-3 (Atorvastatin for Reduction of MYocardial Dysrhythmia After cardiac surgery) study.

BACKGROUND: Atrial fibrillation (AF) after cardiac surgery is associated with increased risk of complications, length of stay, and cost of care. Observational evidence suggests that patients who have undergone previous statin therapy have a lower incidence of postoperative AF. We tested this observation in a randomized, controlled trial. METHODS AND RESULTS: Two hundred patients undergoing elective cardiac surgery with cardiopulmonary bypass, without previous statin treatment or history of AF, were enrolled. Patients were randomized to atorvastatin (40 mg/d, n=101) or placebo (n=99) starting 7 days before operation. The primary end point was incidence of postoperative AF; secondary end points were length of stay, 30-day major adverse cardiac and cerebrovascular events, and postoperative C-reactive protein (CRP) variations. Atorvastatin significantly reduced the incidence of AF versus placebo (35% versus 57%, P=0.003). Accordingly, length of stay was longer in the placebo versus atorvastatin arm (6.9+/-1.4 versus 6.3+/-1.2 days, P=0.001). Peak CRP levels were lower in patients without AF (P=0.01), irrespective of randomization assignment. Multivariable analysis showed that atorvastatin treatment conferred a 61% reduction in risk of AF (odds ratio 0.39, 95% confidence interval 0.18 to 0.85, P=0.017), whereas high postoperative CRP levels were associated with increased risk (odds ratio 2.0, 95% confidence interval 1.2 to 7.0, P=0.01). The incidence of major adverse cardiac and cerebrovascular events at 30 days was similar in the 2 arms. CONCLUSIONS: Treatment with atorvastatin 40 mg/d, initiated 7 days before surgery, significantly reduces the incidence of postoperative AF after elective cardiac surgery with cardiopulmonary bypass and shortens hospital stay. These results may influence practice patterns with regard to adjuvant pharmacological therapy before cardiac surgery.

Aged↗
PubMed2006

Virulent strains of Helicobacter pylori and vascular diseases: a meta-analysis.

BACKGROUND: Cytotoxin-associated gene A (CagA)-positive strains of Helicobacter pylori are an etiological factor for peptic ulcer and gastric cancer. Studies on the role of these virulent strains in vascular diseases yield conflicting results. METHODS: We searched the MEDLINE database for relevant studies. Meta-analysis was performed using the random effects method. RESULTS: We found 10 retrospective case-control studies (with 1527 case patients and 1661 control subjects) and 3 prospective cohort studies (with 701 case patients and 1439 control subjects) on CagA status and ischemic heart disease and 4 retrospective case-control studies (with 513 case patients and 590 control subjects) on CagA status and cerebral ischemia. In the case-control studies, an association of ischemic heart disease with CagA-positive strains (OR 1.87, 95% CI 1.46-2.40) but no significant association with CagA-negative strains (OR 1.15, 95% CI 0.83-1.60) has been found; in the 3 prospective studies, association with ischemic heart disease was weaker but still significant (OR 1.26, 95% CI 1.05-1.51). In the 4 case-control studies, CagA-positive strains were significantly associated with cerebral ischemia (OR 2.43, 95% CI 1.89-3.13), again with no association for CagA-negative strains. CONCLUSIONS: We found a small but significant association between vascular diseases and virulent CagA-positive strains of H. pylori. The lack of association with CagA-negative strains further supports the hypothesis of an independent relationship between virulent strains of H. pylori and vascular diseases. The magnitude of the association with cerebral ischemia needs to be confirmed by prospective studies.

Antigens, Bacterial↗
PubMed2006

Effects of atorvastatin on systemic inflammatory response after coronary bypass surgery.

OBJECTIVES: Systemic inflammatory response occurs frequently after coronary artery bypass surgery, and it is strongly correlated with the risk of postoperative morbidity and mortality. Recent studies demonstrate that treatment with statin is associated with a significant and marked decrease in inflammation-associated variables such as the C-reactive protein, cytokines, and adhesion molecules. Therefore, we investigated the effects of preoperative atorvastatin treatment on systemic inflammatory response and perioperative morbidity after cardiopulmonary bypass. DESIGN: Double-blinded, placebo-controlled, randomized study. SETTING: University hospital. PATIENTS: Forty patients were randomized to treatment with atorvastatin (20 mg/day, group A, n=20) or placebo (group B, n=20) 3 wks before surgery. INTERVENTIONS: Three-week treatment by atorvastatin 20 mg/day. MEASUREMENT AND MAIN RESULTS: Postoperative serum levels of both interleukin-6 and interleukin-8 increased significantly over baseline, but the peak levels observed 4 hrs postoperatively were significantly lower in the atorvastatin group. In the same fashion, CD11b expression on neutrophils was significantly lower in the statin group at 4 and 24 hrs postoperatively. Finally, neutrophil-endothelial adhesion was significantly reduced in the statin patients compared with controls. The operation time, blood loss, need for inotropic support, intubation time, and length of intensive care unit or hospital stay did not differ significantly between the two groups. The systemic inflammatory response syndrome score on postoperative days 1 and 2 was comparable in both groups. CONCLUSIONS: Pretreatment with atorvastatin significantly reduces cytokine release and neutrophil adhesion to the venous endothelium in patients undergoing coronary artery bypass grafting with cardiopulmonary bypass.

Aged↗
PubMed2006

Prevention of myocardial damage during coronary intervention.

Myocardial injury during coronary intervention occurs in 10-40% of cases and is often characterized by a slight increase of markers of myocardial necrosis, without symptoms, electrocardiographic changes or impairment of cardiac function. However, even small increases of creatine kinase-MB levels are expression of a true and detectable infarction, and may be associated with higher follow-up mortality. The cause of CK-MB elevation in case of procedural complications (dissection, transient vessel closure, no reflow, side branch occlusion etc.) is obvious; however, most cases of minor CK-MB elevation occur in patients with uncomplicated procedure with excellent final angiographic results. It has been suggested that the main mechanism explaining occurrence of myocardial necrosis during otherwise successful coronary interventions may be distal microembolization of plaque components, an enhanced inflammatory state or due to total plaque burden and/or to plaque instability. Different treatments have been proposed to prevent myocardial injury during coronary intervention, including nitrate infusion, intracoronary beta-blockers, adenosine, clopidogrel and IIb/IIIa inhibitors, but none of those (apart from the use of IIb/IIIa inhibitors) has been routinely introduced in clinical practice. We performed the ARMYDA (Atorvastatin for Reduction of MYocardial Damage during Angioplasty) trial, i.e. the first prospective, randomised, placebo controlled study to evaluate effects of 7 days of pre-treatment with a fixed dose of atorvastatin (40 mg/day) on post-procedural release of markers of myocardial damage in patients with stable angina undergoing percutaneous intervention. In this study therapy with atorvastatin has been associated with 80% risk reduction on the occurrence of peri-procedural myocardial infarction, as well as with significant reduction of post-intervention peak levels of all markers of myocardial damage. The mechanisms underlying the beneficial effects of atorvastatin may be an inflammatory action reducing myocardial necrosis due to microembolization, an improvement of endothelial function on microcirculation, and direct protection of myocardium.

Aged↗
PubMed2005

Effects of atorvastatin on arterial endothelial function in coronary bypass surgery.

OBJECTIVE: Endothelial dysfunction represents a critical early component of organ injury following cardiopulmonary bypass. Recent studies demonstrate that the treatment with atorvastatin is associated with a significant improvement of endothelial function independently of its efficacy on cholesterol levels. Therefore, we investigated the effects of preoperative atorvastatin treatment on endothelium function after coronary surgery. METHODS: Forty patients undergoing coronary surgery were randomized to treatment with atorvastatin (20 mg/die; N=20) or placebo (N=20) 3 weeks before surgery. Twenty normal patients served as control group. The flow-mediated dilations (FMD) of the brachial artery after both reactive hyperemia (endothelium dependent) and nitroglycerin administration (endothelium independent) were evaluated at baseline, at 48 h, and 5 days postoperatively. RESULTS: At baseline, the endothelium-dependent FMD was significantly attenuated in coronary versus normal patients (normal 10.3+/-1.8% vs coronary 4.1+/-1.6%, p<0.01). At 48 h postoperatively all patients exhibited a reduced FMD compared with baseline values: the endothelium-dependent dilatation showed a drop of 60.1+15% in the patients of the placebo group compared with 45.8+16.6% (p<0.05) those in the atorvastatin group. At the univariate analysis, no significant correlation was found between serum levels of either total cholesterol or HDL cholesterol and FMD. The nitroglycerin-induced dilation was not significantly influenced by extracorporeal circulation as well as by atorvastatin treatment. CONCLUSIONS: The endothelial dysfunction following cardiopulmonary bypass is improved by the treatment with atorvastatin, by a mechanism unrelated to the drug efficacy of controlling serum cholesterol levels.

Adult↗
PubMed2005

Randomized trial of high loading dose of clopidogrel for reduction of periprocedural myocardial infarction in patients undergoing coronary intervention: results from the ARMYDA-2 (Antiplatelet therapy for Reduction of MYocardial Damage during Angioplasty) study.

BACKGROUND: Aggressive platelet inhibition is crucial to reduce myocardial injury and early cardiac events after coronary intervention. Although observational data have suggested that pretreatment with a high loading dose of clopidogrel may be more effective than a conventional dose, this hypothesis has never been tested in a randomized trial. METHODS AND RESULTS: A total of 255 patients scheduled to undergo percutaneous coronary intervention were randomized to a 600-mg (n=126) or 300-mg (n=129) loading regimen of clopidogrel given 4 to 8 hours before the procedure. Creatine kinase MB, troponin I, and myoglobin levels were measured at baseline and at 8 and 24 hours after intervention. The primary end point was the 30-day occurrence of death, myocardial infarction (MI), or target vessel revascularization. The primary end point occurred in 4% of patients in the high loading dose versus 12% of those in the conventional loading dose group (P=0.041) and was due entirely to periprocedural MI. Peak values of all markers were significantly lower in patients treated with the 600-mg regimen (P< or =0.038). Safety end points were similar in the 2 arms. At multivariable analysis, the high loading regimen was associated with a 50% risk reduction of MI (OR 0.48, 95% CI 0.15 to 0.97, P=0.044). An incremental benefit was observed in patients randomized to the 600-mg dose who were receiving statins, with an 80% risk reduction. CONCLUSIONS: Pretreatment with a 600-mg loading dose of clopidogrel 4 to 8 hours before the procedure is safe and, as compared with the conventional 300-mg dose, significantly reduced periprocedural MI in patients undergoing percutaneous coronary intervention. These results may influence practice patterns with regard to antiplatelet therapy before percutaneous revascularization.

Aged↗
PubMed2005

Effect of dexamethasone-eluting stents on systemic inflammatory response in patients with unstable angina pectoris or recent myocardial infarction undergoing percutaneous coronary intervention.

The effect of treatment with steroid-eluting stents on systemic inflammatory response was investigated in patients with unstable angina pectoris or recent myocardial infarction who underwent percutaneous intervention. Compared with controls, dexamethasone-eluting stents significantly reduced C-reactive protein peak levels 48 hours after the procedure; this effect persisted for 7 days and was particularly evident in patients with elevated (>/=3 mg/L) preprocedural C-reactive protein values. Patients receiving a dexamethasone-eluting stent had lower adverse events during follow-up.

Angina Pectoris↗
PubMed2005

Impaired flow-mediated dilation and risk of restenosis in patients undergoing coronary stent implantation.

BACKGROUND: Impaired endothelial function is a key event in the atherosclerosis process and predicts future cardiovascular events in subjects with and without coronary artery disease (CAD). We performed the first prospective study evaluating whether early measurement of brachial artery endothelium-dependent dilation (flow-mediated dilation [FMD]) after coronary stenting could predict occurrence of in-stent-restenosis. METHODS AND RESULTS: The study population included 136 patients with single-vessel CAD undergoing percutaneous coronary intervention (PCI) with stenting and at least 6 months of follow-up. All patients underwent ultrasound detection of brachial artery reactivity 30 days after PCI; FMD was investigated before and after 5 minutes of occlusion of the brachial artery, and nitroglycerin-mediated dilation was investigated before and after administration of sublingual nitrates. Clinical in-stent restenosis was demonstrated in 20 patients (15%), whereas 116 patients (85%) remained free of signs or symptoms of recurrent ischemia. FMD was significantly impaired in patients with restenosis versus those without restenosis (percent diameter variation 4.6+/-5.8% versus 9.5+/-6.6%, P=0.002); moreover, 4% of patients with FMD > or =7% (median value) developed in-stent restenosis versus 28% of those with FMD <7% (P=0.0001). On multivariate analysis, FMD was the strongest predictor of restenosis (OR 4.5, 95% CI 2.4 to 12.0); conversely, nitroglycerin-mediated dilation did not independently predict the risk of restenosis (OR 2.4, 95% CI 0.8 to 6.3). CONCLUSIONS: This is the first prospective study indicating that impaired FMD independently predicts occurrence of in-stent restenosis in patients undergoing PCI. Early evaluation of endothelial function after stenting may represent a useful screening tool to stratify patients according to future risk of restenosis.

Aged↗
PubMed2005

Interleukin-1 receptor antagonist levels correlate with extent of myocardial loss in patients with acute myocardial infarction.

BACKGROUND: Interleukin-1 receptor antagonist (IL-1Ra) levels are elevated early in patients with acute myocardial infarction (MI) and often precede release of markers of necrosis; however, IL-1Ra levels did not correlate previously with infarct size and prognosis in such patients. HYPOTHESIS: The goal of our study was to evaluate prospectively the correlation between IL-1Ra levels upon emergency department (ED) presentation and the extent of myocardial necrosis and prognosis in patients with ST-segment elevation MI. METHODS: Levels of IL-1Ra were measured upon ED presentation in 44 consecutive patients (40 men, aged 55 +/- 10 years). Peak values of creatine kinase (CK) and CK-MB were determined during hospitalization, and left ventricular ejection fraction (LVEF) was evaluated by echocardiography before discharge. All patients were followed prospectively and underwent clinical and echocardiographic assessment at 42 +/- 3 months after the infarction. RESULTS: Levels of IL-1Ra upon ED presentation correlated directly with CK (p = 0.002) and CK-MB (p = 0.01) peak levels and correlated inversely with LVEF before discharge (p = 0.009). Patients with in-hospital adverse events had significantly higher IL-1Ra levels upon ED admission (n = 10,2620 +/- 4706 pg/ml) than those without events (n = 34,598 +/- 457 pg/ml) (p = 0.015). CONCLUSIONS: In patients with MI, levels of IL-1Ra upon ED presentation correlated significantly with the extent of myocardial necrosis, as measured by cardiac enzymes peak and reduction of LVEF, and are predictive of in-hospital events. Results of this study may influence early therapeutic approach in patients with acute MI.

Adult↗
PubMed2005

Dexamethasone-eluting stents and plasma concentrations of adhesion molecules in patients with unstable coronary syndromes: results of the historically controlled SESAME study.

BACKGROUND: Plasma concentrations of intercellular adhesion molecule-1 [ICAM-1], vascular cell adhesion molecule-1 [VCAM-1], and E-selectin may increase after percutaneous coronary intervention (PCI). OBJECTIVE: The aim of this study was to assess whether anti-inflammatory treatment with steroid-eluting stents influenced concentrations of adhesion molecules after PCI in patients with unstable coronary syndromes. METHODS: Consecutive patients with unstable coronary syndromes who were prospectively assigned to undergo implantation of a dexamethasone-eluting stent were compared with a control group of consecutive historical patients who received a similar non-drugeluting stent in the period immediately preceding availability of the steroid-eluting stents. Circulating concentrations of adhesion molecules were measured before the procedure and at 6 and 24 hours after implantation. RESULTS: The study included 50 patients who received the dexamethasone-eluting stent (41 men, 9 women; mean [SD] age, 60 [9] years) and 50 historical controls who received the non-drug-eluting stent (40 men, 10 women; mean age, 63 [11] years). Baseline values for the adhesion molecules were similar in the 2 groups: in patients who received the dexamethasone-eluting stent, mean (SD) values were 210 (41) ng/mL for ICAM-1, 637 (119) ng/mL for VCAM-1, and 46 (9) ng/mL for E-selectin; in the control group, the corresponding values were 218 (42), 618 (140), and 43 (10) ng/mL. Circulating concentrations at 24 hours were significantly lower in patients receiving the drug-eluting stent compared with controls for both ICAM-1 (279 [49] vs 338 [60] ng/mL, respectively; P = 0.001) and VCAM-1 (772 [163] vs 896 [207] ng/mL; P = 0.004). There was no significant between-group difference in E-selectin concentrations at 24 hours (60 [10] vs 56 [11] ng/mL). CONCLUSION: In this study, dexamethasone-eluting stents reduced plasma concentrations of ICAM-1 and VCAM-1 after PCI in patients with unstable coronary syndromes compared with historical controls.

Analysis of Variance↗
PubMed2005

[Prevention of periprocedural myocardial damage in patients undergoing percutaneous coronary intervention].

Myocardial injury during coronary intervention occurs in 10-40% of cases and is often characterized by a slight increase in the markers of myocardial necrosis, without symptoms, electrocardiographic changes or impairment of cardiac function. However, even small increases in creatine kinase (CK)-MB levels are an expression of a true and detectable infarction and may be associated with a higher follow-up mortality. The cause of CK-MB elevation in case of procedural complications is obvious; however, most cases of minor CK-MB elevation occur in patients with uncomplicated procedures with excellent final angiographic results. It has been suggested that the main mechanism explaining the occurrence of myocardial necrosis during otherwise successful coronary intervention may be distal microembolization of plaque components, an enhanced inflammatory state or total plaque burden and/or instability. Different treatments have been proposed to prevent myocardial injury during coronary intervention, including nitrate infusion, intracoronary beta-blockers, adenosine and IIb/IIa inhibitors, but none of these (apart from the use of IIb/IIIa inhibitors) have been routinely introduced into clinical practice. Previous observational studies suggested a beneficial effect of pre-treatment with statins in this setting; the ARMYDA (Atorvastatin for Reduction of Myocardial Damage During Angioplasty) trial is the first prospective, randomized, placebo-controlled study, evaluating the effects of 7-day therapy with 40 mg/day of atorvastatin on post-procedural release of markers of myocardial damage in patients with stable angina undergoing percutaneous intervention. In this study therapy with atorvastatin was associated with an 80% risk reduction in the occurrence of periprocedural myocardial infarction, as well as with a significant reduction in post-intervention peak levels of all markers of myocardial damage. The mechanisms underlying the beneficial effects of atorvastatin may be an inflammatory action reducing myocardial injury necrosis due to microembolization, an improvement in endothelial function on microcirculation, and direct myocardial protection.

Actuarial Analysis↗
PubMed2005

[The role of endothelial dysfunction in the pathogenesis and in clinical practice of atherosclerosis. Current evidences].

Endothelium is not a mere monolayer of cells separating flowing blood and vascular wall, but plays a key role in maintenance of vascular homeostasis. Nitric oxide is the principal mediator of endothelial function; it is a potent vasodilator, it inhibits platelet aggregation, vascular smooth muscle cell migration and proliferation, and monocytes adhesion. Cardiovascular risk factors promote development of endothelial dysfunction, characterized by impairment of endothelium-dependent vasodilation (EDV) and by pro-coagulant/pro-inflammatory endothelial activities. The assessment of EDV is a common parameter for testing endothelial function. EDV in the coronary arteries is angiographically evaluated by measurement of the vessel response to endothelial agonists, such as acetylcholine. A non-invasive technique for the detection of EDV employs the ultrasound evaluation of flow-mediated dilation (FMD) of the brachial artery following reactive hyperemia. A close relation between FMD and coronary vasomotor response to acetylcholine has been demonstrated. Endothelial dysfunction in the coronary circulation may precede development of angiographically evident coronary atherosclerosis; endothelial dysfunction has been also associated with a higher prevalence of coronary artery disease and resulted predictive of future cardiovascular events; recently, it has been associated with a higher risk of restenosis after coronary stent implantation. Endothelial dysfunction is actually considered a reversible phenomenon; drug therapies with ACE-inhibitors, angiotensin receptor blockers, statins, antioxidants agents have shown a beneficial effect on endothelial function.

Atherosclerosis↗
PubMed2004

Randomized trial of atorvastatin for reduction of myocardial damage during coronary intervention: results from the ARMYDA (Atorvastatin for Reduction of MYocardial Damage during Angioplasty) study.

BACKGROUND: Small myocardial infarctions after percutaneous coronary intervention have been associated with higher risk of cardiac events during follow-up. Observational studies have suggested that statins may lower the risk of procedural myocardial injury. The aim of our study was to confirm this hypothesis in a randomized study. METHODS AND RESULTS: One hundred fifty-three patients with chronic stable angina without previous statin treatment were enrolled in the study. Patients scheduled for elective coronary intervention were randomized to atorvastatin (40 mg/d, n=76) or placebo (n=77) 7 days before the procedure. Creatine kinase-MB, troponin I, and myoglobin levels were measured at baseline and at 8 and 24 hours after the procedure. Detection of markers of myocardial injury above the upper normal limit was significantly lower in the statin group versus the placebo group: 12% versus 35% for creatine kinase-MB (P=0.001), 20% versus 48% for troponin I (P=0.0004), and 22% versus 51% for myoglobin (P=0.0005). Myocardial infarction by creatine kinase-MB determination was detected after coronary intervention in 5% of patients in the statin group and in 18% of those in the placebo group (P=0.025). Postprocedural peak levels of creatine kinase-MB (2.9+/-3 versus 7.5+/-18 ng/mL, P=0.007), troponin I (0.09+/-0.2 versus 0.47+/-1.3 ng/mL, P=0.0008), and myoglobin (58+/-36 versus 81+/-49 ng/mL, P=0.0002) were also significantly lower in the statin than in the placebo group. CONCLUSIONS: Pretreatment with atorvastatin 40 mg/d for 7 days significantly reduces procedural myocardial injury in elective coronary intervention. These results may influence practice patterns with regard to adjuvant pharmacological therapy before percutaneous revascularization.

Aged↗
PubMed2004

Early interleukin-1 receptor antagonist elevation in patients with acute myocardial infarction.

OBJECTIVES: We sought to evaluate interleukin-1 receptor antagonist (IL-1Ra) levels in patients with ST-segment elevation acute myocardial infarction (AMI) upon emergency department (ED) admission in order to assess the sensitivity of such a determination by comparison with common markers of myocardial necrosis. BACKGROUND: Inflammatory markers are elevated in patients with unstable coronary syndromes, but IL-1Ra levels during the early phases of AMI have not been previously investigated. METHODS: Levels of IL-1Ra were measured in 44 consecutive patients with AMI and compared with creatine kinase (CK), CK-MB, troponin I, myoglobin, and C-reactive protein (CRP). RESULTS: Upon admission, 82% of patients had elevated (>230 pg/ml) IL-1Ra levels, compared with 41% of patients with raised CK (p = 0.001), CK-MB (45%, p = 0.002), troponin I (57%, p = 0.027), myoglobin (48%, p = 0.004), and CRP (57%, p = 0.019) levels. The IL-1Ra values were significantly higher in patients with heralded AMI than in those without pre-infarction angina (671 vs. 320 pg/ml, p = 0.013). The sensitivity of IL-1Ra determination increased to 86% when chest pain duration was < or =3 h and to 91% if heralded infarction occurred. CONCLUSIONS: Our study indicates that, unlike markers of necrosis, an increase of IL-1Ra levels occurs early in patients with AMI, is more significant in those with heralded infarction and symptom onset < or =3 h, and precedes the release of markers of necrosis. Thus, IL-1Ra determination may be an important early adjuvant toward the diagnosis of AMI in the ED.

Adult↗