TL;DR: In patients who presented with an acute coronary syndrome and underwent percutaneous coronary intervention, major adverse cardiovascular events occurring during follow-up were equally attributable to recurrence at the site of culprit lesions and to nonculprit lesions.
Abstract: A b s t r ac t Background Atherosclerotic plaques that lead to acute coronary syndromes often occur at sites of angiographically mild coronary-artery stenosis. Lesion-related risk factors for such events are poorly understood. Methods In a prospective study, 697 patients with acute coronary syndromes underwent three-vessel coronary angiography and gray-scale and radiofrequency intravascular ultrasonographic imaging after percutaneous coronary intervention. Subsequent major adverse cardiovascular events (death from cardiac causes, cardiac arrest, myocardial infarction, or rehospitalization due to unstable or progressive angina) were adjudicated to be related to either originally treated (culprit) lesions or untreated (nonculprit) lesions. The median follow-up period was 3.4 years. Results The 3-year cumulative rate of major adverse cardiovascular events was 20.4%. Events were adjudicated to be related to culprit lesions in 12.9% of patients and to nonculprit lesions in 11.6%. Most nonculprit lesions responsible for follow-up events were angiographically mild at baseline (mean [±SD] diameter stenosis, 32.3±20.6%). However, on multivariate analysis, nonculprit lesions associated with recurrent events were more likely than those not associated with recurrent events to be characterized by a plaque burden of 70% or greater (hazard ratio, 5.03; 95% confidence interval [CI], 2.51 to 10.11; P<0.001) or a minimal luminal area of 4.0 mm 2 or less (hazard ratio, 3.21; 95% CI, 1.61 to 6.42; P = 0.001) or to be classified on the basis of radiofrequency intravascular ultrasonography as thin-cap fibroatheromas (hazard ratio, 3.35; 95% CI, 1.77 to 6.36; P<0.001). Conclusions In patients who presented with an acute coronary syndrome and underwent percutaneous coronary intervention, major adverse cardiovascular events occurring during follow-up were equally attributable to recurrence at the site of culprit lesions and to nonculprit lesions. Although nonculprit lesions that were responsible for unanticipated events were frequently angiographically mild, most were thin-cap fibroatheromas or were characterized by a large plaque burden, a small luminal area, or some combination of these characteristics, as determined by gray-scale and radiofrequency intravascular ultrasonography. (Funded by Abbott Vascular and Volcano; ClinicalTrials.gov number, NCT00180466.)
TL;DR: Vessel healing at the culprit site in AMI patients treated with DES is substantially delayed compared with the culprit sites in patients receiving DES for stable angina, emphasizing the importance of underlying plaque morphology in the arterial response to DES.
Abstract: Background— The long-term safety of drug-eluting stents (DES) for acute myocardial infarction (AMI) remains uncertain. Using autopsy data, we evaluated the pathological responses of the stented segment in patients treated with DES for AMI and compared with patients with stable angina. Methods and Results— From the CVPath Registry of 138 DES autopsies, we identified 25 patients who presented with AMI and had an underlying necrotic core with a ruptured fibrous cap. Twenty-six patients who had stable angina with thick-cap fibroatheroma treated by DES were selected as controls. Histomorphometric analysis was performed in patients with >30-day stent duration. We compared the response to stenting at the culprit site in these 2 groups and to nonculprit sites within each stent. Late stent thrombosis was significantly less frequent in stable (11%) than in AMI (41%; P=0.04) patients. Although neointimal thickness in the AMI culprit site was significantly less (median, 0.04 mm; interquartile range [IQR], 0.02 to 0.0...
TL;DR: Arteriographically apparent intraluminal thrombus and improvement of the culprit lesion with either of these regimens were only moderately frequent in patients with unstable angina or non-Q wave myocardial infarction, and in two prospectively defined subgroups.
Abstract: BACKGROUND The early effects of tissue-type plasminogen activator (t-PA) on the "culprit" coronary lesion in patients presenting with unstable angina or non-Q wave myocardial infarction were determined by quantitative arteriography.
METHODS AND RESULTS Of 391 such patients, 306 satisfied clinical and arteriographic requirements for eligibility and received a 90-minute front-loaded infusion of t-PA (0.8 mg/kg i.v.; maximum, 80 mg) or placebo plus conventional antianginal therapy. All patients received full heparinization and a follow-up arteriogram 18-48 hours after treatment. A non-Q wave myocardial infarction (MI) was diagnosed in 97 patients (32%) after entry. In the entire patient population, among t-PA- and placebo-treated patients, respectively, 25% versus 19% (p = 0.25) of all culprit lesions achieved the primary study end point, measurable improvement (by > or = 10% reduction of stenosis or two Thrombolysis in Myocardial Infarction [TIMI] flow grades) at follow-up. Substantial improvement (by > or = 20% reduction of stenosis or two TIMI grades) was seen with t-PA in 15% of all culprit lesions versus 5% with placebo (p < 0.003). Arteriographically apparent thrombus was present at baseline in the culprit lesion of 107 patients (35%). Substantial improvement was more frequent with t-PA among lesions containing apparent thrombus (in 36% with t-PA versus 15% with placebo; p < 0.01), as it was among patients evolving a non-Q wave MI (33% versus 8%; p < 0.005). By multivariate analysis, the significant, independent predictors of substantial improvement include apparent thrombus (p = 0.0001), non-Q wave MI (p = 0.003), and t-PA use (p = 0.01). Both non-Q wave MI status and thrombus had been specified a priori as important variables.
CONCLUSIONS Arteriographically apparent intraluminal thrombus and improvement of the culprit lesion with either of these regimens were only moderately frequent in patients with unstable angina or non-Q wave MI. Substantial improvement of culprit lesions was more frequent with t-PA than with placebo overall and in two prospectively defined subgroups. The clinical relevance of these observations is being tested in the larger, ongoing clinical TIMI IIIB study.
TL;DR: In this paper, the authors investigated whether percutaneous coronary intervention (PCI) should be confined to the culprit or also nonculprit vessels and whether it should take place during primary PCI or staged procedures.
TL;DR: The findings support the American College of Cardiology/American Heart Association (ACC/AHA) recommendation that culprit vessel PCI be used for STEMI patients with multivessel disease at the time of the index PCI when patients are not hemodynamically compromised.
Abstract: Objectives The purpose of this study was to examine the differences in in-hospital and longer-term mortality for ST-segment elevation myocardial infarction (STEMI) patients with multivessel disease as a function of whether they underwent single-vessel (culprit vessel) percutaneous coronary interventions (PCIs) or multivessel PCI. Background The optimal treatment of patients with STEMI and multivessel disease is of continuing interest in the era of drug-eluting stents. Methods STEMI patients with multivessel disease undergoing PCIs in New York between January 1, 2003, and June 30, 2006, were subdivided into those who underwent culprit vessel PCI and those who underwent multivessel PCI during the index procedure, during the index admission, or staged within 60 days of the index admission. Patients were propensity-matched and mortality rates were calculated at 12, 24, and 42 months. Results A total of 3,521 patients (87.5%) underwent culprit vessel PCI during the index procedure. A total of 259 of them underwent staged PCI during the index admission and 538 patients underwent staged PCI within 60 days of the index procedure. For patients without hemodynamic compromise, culprit vessel PCI during the index procedure was associated with lower in-hospital mortality than multivessel PCI during the index procedure (0.9% vs. 2.4%, p = 0.04). Patients undergoing staged multivessel PCI within 60 days after the index procedure had a significantly lower 12-month mortality rate than patients undergoing culprit vessel PCI only (1.3% vs. 3.3%, p = 0.04). Conclusions Our findings support the American College of Cardiology/American Heart Association (ACC/AHA) recommendation that culprit vessel PCI be used for STEMI patients with multivessel disease at the time of the index PCI when patients are not hemodynamically compromised. However, staged PCI within 60 days after the index procedure, including during the index admission, is associated with risk-adjusted mortality rates that are comparable with the rate for culprit vessel PCI alone.