PubMed Health⌕ Search

Biomedical subjects

Vincenzo Pasceri

Publications and source records attributed to Vincenzo Pasceri.

At least 19 recordsLinked to original sources
PubMed2006

Cumulative exercise-induced left ventricular systolic and diastolic dysfunction in hypertrophic cardiomyopathy.

The phenomenon of cumulative exercise-induced left ventricular function impairment was studied in 40 patients with non-obstructive hypertrophic cardiomyopathy with resting normal left ventricular function and no increase in ejection fraction on exercise. All patients underwent two symptom-limited exercise tests one-hour apart. Cumulative myocardial dysfunction was seen in 13 patients (group I) but not in the remaining 27 patients (group II). During follow-up, group I showed more commonly than group II a deterioration in symptoms (67% vs 22%, P=0.025) and left ventricular function (50% vs 9%, P=0.019). In conclusion, cumulative exercise-induced myocardial dysfunction can occur in hypertrophic cardiomyopathy and may be associated with clinical deterioration and worse outcome.

Adult↗
PubMed2006

Safety and efficacy of short-term celecoxib before elective percutaneous coronary intervention for stable angina pectoris.

Fifty patients with stable angina pectoris entered a randomized, double-blind study and were assigned to receive celecoxib (200 mg 2 times daily) or placebo 7 days before percutaneous coronary intervention (PCI). Results showed that detection of markers of myocardial injury above the upper normal limit was significantly lower in the celecoxib than in the placebo group: 12% versus 35% for creatine kinase-MB (CK-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 CK-MB determination was less commonly seen after PCI in the celecoxib than in the placebo group (5% vs 18%, p = 0.025). Postprocedural peak levels of CK-MB (2.9 +/- 18 vs 7.5 +/- 18 ng/ml, p = 0.0002) were also significantly lower in the celecoxib than in the placebo group. No significant side effect was reported by the 2 groups of patients. In conclusion, pretreatment with celecoxib 200 mg 2 times daily for 7 days significantly decreased procedural myocardial injury in elective PCI. These findings indicate that the antiphlogistic action of cyclo-oxygenase-2 inhibition may provide a friendly protection to ischemic cardiomyocytes.

Angina Pectoris↗
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

Frequency and clinical correlates of changes in Thrombolysis In Myocardial Infarction risk score during observation period at emergency department in "low-risk" patients with acute chest pain.

Among 4,333 patients who were triaged in the emergency department (ED) over a 1-year period in 2003 because of acute chest pain, 1,747 (40%) were stratified as "low risk" on the basis of a Thrombolysis In Myocardial Infarction (TIMI) risk score of 0 to 2. Results showed that, during ED stay, TIMI risk score increased to > or =3 in 63% of patients and that such patients were more likely to be diabetic, hypertensive, hyperlipidemic, and smokers, and to have had previous myocardial infarction or revascularization. Patients with changes in TIMI risk score were admitted more often to the hospital, whereas more patients with unchanged TIMI risk score were discharged home directly from the ED. In conclusion, TIMI risk score may change soon after arrival to the ED in 50% of patients with acute chest pain who are initially triaged as low risk. Changes in TIMI risk score are more common in patients with multiple risk factors and/or previous diagnosis of coronary artery disease. Serial, frequent assessments of TIMI score during the ED observation period are mandatory, particularly in these subsets of patients.

Biomarkers↗
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

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↗
PubMed2006

Very late thrombosis after sirolimus-eluting stent implantation.

Drug-eluting stents are widely used to prevent restenosis after coronary angioplasty. We here report a case of stent thrombosis within a sirolimus-eluting stent occurring two years after stent implantation, while the patient was on chronic aspirin therapy. The patient presented with acute ST-elevation myocardial infarction and pulmonary oedema; stent thrombosis was successfully treated with coronary angioplasty and deployment of a new coronary stent. This case suggests that long-term follow-up is needed in clinical studies on drug-eluting stents.

Aged↗
PubMed2005

Effects of reperfusion obtained two to six months after acute myocardial infarction on myocardial electrical stabilization in patients with an occluded infarct-related coronary artery.

To assess the changes in electrical stability markers in patients with previous myocardial infarction after very late reopening of the infarct-related artery, we studied QT dispersion, corrected-QT dispersion, and late potentials before and 1, 3, and 6 months after an attempt at late percutaneous coronary intervention (PCI) in 31 consecutive patients with single-vessel disease (infarct-related artery occlusion or subocclusion) diagnosed > or = 4 weeks after the ST-elevation myocardial infarction. Patients underwent PCI 3.9 +/- 2 months after ST-elevation myocardial infarction. PCI was successful in 24 patients (group A) and unsuccessful in 7 (group B). The 2 groups were similar in clinical and angiographic characteristics, as well as the prevalence of basal late potentials, average QT dispersion, and corrected-QT dispersion. One month after PCI, the successful reperfusion group had a significant 67% decrease in the prevalence of late potentials and average QT dispersion and corrected QT dispersion (51 +/- 9 vs 72 +/- 11 ms, p <0.00001, and 51 +/- 10 vs 76 +/- 15 ms, p <0.00001, respectively). These benefits remained stable at 3 and 6 months after PCI. Conversely, the unsuccessful group did not show any improvement in electrical stability markers after PCI failed. Thus, reperfusion obtained very late after ST-elevation myocardial infarction confers significant electrical stabilization that may contribute to a better outcome in patients with patent infarct-related arteries.

Aged↗
PubMed2005

Effects of the nitric oxide donor nitroprusside on no-reflow phenomenon during coronary interventions for acute myocardial infarction.

We tested the effects of the nitric oxide donor nitroprusside as treatment for no reflow in 23 consecutive patients who underwent coronary angioplasty for acute myocardial infarction. No reflow was defined as a decrease of >/=1 Thrombolysis In Myocardial Infarction (TIMI) trial flow grade occurring after successful initial coronary recanalization. Nitroprusside induced a significant improvement in coronary flow, with an increase in TIMI flow grade from 1.5 +/- 0.8 to 2.9 +/- 0.3 (p <0.0001) and in TIMI frame count from 46 +/- 25 to 16 +/- 5 (p <0.0001). There were no significant adverse effects apart from transient hypotension. Intracoronary nitroprusside should be considered as a treatment of no reflow occurring in acute myocardial infarction.

Angioplasty, Balloon, Coronary↗
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↗