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Objectives: To determine whether staged percutaneous coronary intervention (PCI) within the same hospitalization as primary PCI is safe., Background: In ST-segment elevation myocardial infarction (STEMI) patients with multivessel disease undergoing primary PCI, staged non-culprit vessel PCI at a separate session is recommended., Methods: We conducted a retrospective analysis of 282 consecutive STEMI patients with multivessel disease who underwent primary PCI followed by staged PCI of the non-culprit vessel. Patients were categorized into staged PCI in the same hospitalization (n=184) and staged PCI at a separate hospitalization within 8 weeks of primary PCI (n=98)., Results: Baseline characteristics, presentation of STEMI, and procedural characteristics were similar in both groups. Contrast amount was higher in the separate hospitalization group for both index (175 vs. 153 ml, p=0.011) and staged (144 vs. 120 ml, p=0.004) procedures. More staged left main PCI was performed in the separate hospitalization group (3.9 vs. 0.3%, p=0.008). Angiographic success of staged PCI was similar in both groups, with similar rates of vascular complications and major bleeding. Following staged PCI, in-hospital major adverse cardiac events (3.3 vs. 1.0%, p=0.43) and mortality (2.7 vs. 0%, p=0.17) were similar in both groups., Conclusions: Our study supports the safety and feasibility of staged PCI within the same hospitalization as primary PCI, achieving similar procedural success and in-hospital outcomes as staged PCI at a separate hospitalization. Higher contrast amount used during primary PCI and presence of left main lesion in non-culprit vessels may influence the decision to stage the PCI at a separate hospitalization., (Copyright © 2013. Published by Elsevier Inc.)

Background: The adjunctive use of eptifibatide in patients undergoing primary percutaneous coronary intervention (PCI) for ST-elevation myocardial infarction (STEMI) remains controversial. We therefore set out to determine the safety and efficacy of eptifibatide in this population., Methods: The study comprised 857 consecutive patients who underwent primary PCI for STEMI at the Washington Hospital Center. Three hundred eighteen patients also received adjunctive therapy with eptifibatide. Patients who had received thrombolysis prior to undergoing cardiac catheterization were excluded. The primary end-point was all-cause mortality and the composite of all-cause mortality or Q-wave MI. The primary safety end-point was the rate of thrombolysis in myocardial infarction (TIMI) major bleeding., Results: The eptifibatide group was younger, had a higher body mass index, and a lower proportion of patients with systemic hypertension, diabetes mellitus, previous history of ischemic heart disease, coronary revascularization, and congestive heart failure. This cohort also used bivalirudin less often (23.3% vs. 72%; P < 0.001). Following multivariable analysis, the eptifibatide group had a significantly lower rate of all-cause mortality (hazard ratio 0.55; 95% confidence interval 0.34-0.89; P = 0.01) and the composite of all-cause mortality or Q-wave MI (hazard ratio 0.59; 95% confidence interval 0.37-0.95; P = 0.03) at 6 months. The rate of TIMI major bleeding was similar in both groups (hazard ratio 0.54; 95% confidence interval 0.25-1.17; P = 0.12)., Conclusion: The adjunctive use of eptifibatide in patients presenting with STEMI may be associated with improved clinical outcomes. (J Interven Cardiol 2011;24:351-356)., (©2011, Wiley Periodicals, Inc.)

Objectives: We sought to describe characteristics of patients presenting with an acute MI from a SVG culprit, compared with a native culprit., Background: Percutaneous coronary intervention (PCI) of saphenous vein grafts (SVG) results in worse outcomes than native vessel PCI, but outcomes of such patients with acute myocardial infarction (MI) setting are not well-described., Methods: Patients presenting with ST-elevation or non-ST-elevation MI undergoing PCI from 2000 to 2010 were retrospectively analyzed to identify the culprit as a SVG vs. native vessel. Multiple linear regression was used to identify predictors of peak troponin-I level. Cox proportional hazards regression was used to identify predictors of 30-day mortality and 1-year major adverse cardiac events (MACE)., Results: 192 patients underwent PCI for a SVG culprit, compared with 4,001 with a native culprit. After multivariable adjustment, SVG culprit remained significantly associated with lower levels of the logarithm of the peak troponin (β = -0.17, SE = 0.07, P = 0.02). The likelihood of MACE was higher in SVG vs. native culprits in patients with small to modest troponin elevations. Patients with a SVG culprit also suffered higher unadjusted rates of mortality at 30 days (14.3% vs. 8.4%, P = 0.03) and MACE at 1 year (36.8% vs. 24.5%, P = 0.005); a modest effect upon mortality and MACE remained after multivariable adjustment., Conclusion: Even minimal elevations of troponin in patients with a SVG culprit may portend a poorer prognosis than in patients with a native culprit. The risk of PCI in this setting is driven by mortality and arises from both substantial comorbidities and the SVG itself., (Copyright © 2011 Wiley-Liss, Inc.)

Objectives: Previous studies have found an apparent paradox in smokers: acute phase outcomes after an acute myocardial infarction are superior to those of nonsmokers. Furthermore, it is reported that smoking has an impact on the metabolism of clopidogrel. This study aimed to examine whether this paradoxical finding exists in patients who undergo drug-eluting stent implantation and are treated with clopidogrel., Methods: From April 2003 to June 2010, 1424 consecutive patients with acute myocardial infarction who underwent primary or rescue percutaneous coronary intervention with drug-eluting stent and clopidogrel were enrolled. They were divided into three groups: current smokers (n = 486); previous smokers (n = 349); and nonsmokers (n = 589). The primary end point was a composite of 30-day, all-cause death, nonfatal myocardial infarction, or definite stent thrombosis., Results: Compared with nonsmokers, current smokers were younger (P < 0.001) and more often men (P < 0.001). They had larger myocardial infarctions than did nonsmokers [maximum troponin I, 8.9 (2.4, 38.4) vs. 6.8 (1.4, 30.1) ng/ml, P = 0.01]. Current smokers less frequently met the primary end point than did nonsmokers (2.9 vs. 6.1%, P = 0.01). However, after adjustment for baseline and angiographic characteristics, the beneficial effect of smoking was no longer seen (odds ratio 1.35, confidence interval: 0.53-3.44, P = 0.5)., Conclusion: A beneficial effect of smoking ('smoker's paradox') in the unadjusted primary end point continues to be present; however, after adjustment for differences in baseline characteristics, no benefit was detectable.

Previous studies have documented disparities in both access to invasive cardiovascular procedures and outcomes in patients with Medicaid, Medicare, or no insurance. Outcomes by insurance have yet not been examined in a percutaneous coronary intervention (PCI) population. Data from patients undergoing PCI from June 2000 to June 2009 were retrospectively analyzed. Insurance was categorized as private, Medicare, Medicaid, and uninsured, according to the primary insurance at discharge. The outcome variable of interest was major adverse cardiac events (a composite of death, Q-wave myocardial infarction, and target vessel revascularization) at 1 year. Multivariable Cox regression analysis was stratified according to age <65 and ≥65 years. Of the 13,573 patients who had undergone PCI, 6,653 (49.0%) had private insurance, 6,150 (45.3%) had Medicare, 486 (3.6%) had Medicaid, and 284 (2.1%) were uninsured. Of the patients <65 years old, Medicaid (hazard ratio [HR] 1.59, 95% confidence interval [CI] 1.04 to 2.43), Medicare (HR 2.18, 95% CI 1.58 to 2.99), and no insurance (HR 2.41, 95% CI 1.36 to 4.27) were associated with greater rates of adjusted major adverse cardiac events at 1 year compared with private insurance. Of the patients ≥65 years old, only Medicaid (HR 3.07, 95% CI 1.09 to 8.61) was associated with a greater rate of adjusted major adverse cardiac events at 1 year. In conclusion, patients with government-sponsored insurance and no insurance have worse cardiovascular outcomes than patients with private insurance after PCI at 1 year. This implies that the provision of health insurance alone might not have a dramatic effect on cardiovascular outcomes after PCI., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Gastrointestinal bleeding (GIB) complicating percutaneous coronary intervention (PCI) results in high mortality, but clinical factors associated with and long-term outcomes of GIB are poorly understood. We sought to examine clinical and procedural factors associated with GIB complicating PCI. We also examined the impact of GIB on 30-day mortality and 1-year major adverse cardiac events (MACEs). Patients undergoing PCI from January 2000 to January 2010 were retrospectively analyzed for the occurrence of in-hospital GIB. Multivariable logistic regression and Cox proportional hazards regression were used to identify predictors of in-hospital GIB and 30-day mortality. Landmark analysis of patients surviving to hospital discharge was performed to assess the impact of GIB on 1-year MACEs. Of 20,621 patients who underwent PCI, 147 (0.72%) who developed in-hospital GIB were identified. Variables associated with increased risk of GIB included older age, shock, acute myocardial infarction, chronic renal insufficiency, lower baseline hematocrit, and glycoprotein IIb/IIIa inhibitors; bivalirudin decreased the risk. Unadjusted 30-day mortality rate of patients with GIB was 20.5% compared to 2.4% of patients without GIB. After multivariable adjustment, GIB and shock (and an interaction between the 2) were the most important correlates of 30-day mortality. In the population surviving to discharge, however, GIB was not associated with adjusted mortality or MACEs. In conclusion, GIB complicating PCI has a dramatic impact on 30-day mortality, and bivalirudin was associated with lower rates of GIB., (Copyright © 2010 Elsevier Inc. All rights reserved.)

Several reports have alluded to the adverse effect of chronic obstructive pulmonary disease (COPD) on long-term prognosis of patients with myocardial infarction (MI). Little information is available, however, regarding the effects of a decrease in cardiopulmonary reserve imposed by COPD on in-hospital outcome of acute MI. This study aimed to evaluate the impact of COPD on acute-phase outcome of patients with acute MI. From a cohort of 3,249 consecutive patients with ST-elevation MI who underwent primary or rescue percutaneous coronary intervention, 365 patients were identified as having coexistent COPD. Their clinical presentation and in-hospital outcome were compared to those of 2,884 patients without COPD. The primary end point was a composite of in-hospital death or cardiogenic shock on presentation. Patients with COPD were older (p <0.001), more often women (p <0.001), and smokers (p <0.001). They had higher prevalence of chronic renal insufficiency (p <0.001), systemic hypertension (p = 0.001), and diabetes mellitus (p = 0.01). Patients with COPD had higher rates of the composite end point of death or cardiogenic shock (p <0.0001). After multivariate analysis, COPD remained a strong independent predictor of the composite end point of death or cardiogenic shock (p = 0.008). In conclusion, COPD is a very strong predictor of hemodynamic compromise resulting in death or cardiogenic shock in patients presenting with ST-elevation MI. This observation suggests that hemodynamic and pulmonary consequences of COPD decrease the capacity of the circulatory system to adjust to the effects of acute MI. Recognition of the potential for combined therapy is vital., (Copyright (c) 2010 Elsevier Inc. All rights reserved.)

Aims: We investigated the incidence, predictors, and prognostic impact of a decline in platelet count (DPC) in patients treated by percutaneous coronary intervention (PCI)., Methods and Results: A total of 10 146 consecutive patients treated by PCI from 2003 to 2006 were included. According to the magnitude of the DPC, the population was divided into four groups: no DPC (<10%), minor DPC (10-24%), moderate DPC (25-49%), and severe DPC (>or=50%). The primary haemorrhagic endpoint was a composite of post-procedure surgical repair major bleeding. The primary ischaemic endpoint was 30-day all-cause mortality-non-fatal myocardial infarction. Among the total population, 36% had a DPC <10%, 47.7% had a DPC of 10-24%, 14% had a DPC of 25-49%, and 2.3% had a DPC >or=50%. On multivariate analysis, moderate and severe DPC were independent predictive factors of the ischaemic outcome. Two procedural practices were identified that, if modified, might reduce the incidence of acquired thrombocytopaenia. Both the intraprocedural use of heparin (as opposed to bivalirudin) and of low molecular weight contrast material were independently associated with severe acquired thrombocytopaenia., Conclusion: Moderate and severe DPC are independent predictors of adverse bleeding and ischaemic outcomes in PCI. Adoption of intraprocedural anticoagulant other than heparin and avoidance of a low molecular weight contrast agent could potentially decrease the occurrence of severe acquired thrombocytopaenia.

Patients with diabetes mellitus (DM) are at a greater risk of mortality and cardiovascular events after percutaneous coronary intervention than those without DM. We aimed to determine whether differences exist in the long-term mortality of patients with versus without DM who present with acute myocardial infarction and receive drug-eluting stents. Data were collected on 161 patients with and 395 without DM referred for primary percutaneous coronary intervention for acute myocardial infarction and treated with drug-eluting stents. The patients with cardiac arrest or cardiogenic shock were excluded. The 1-year major cardiac event (MACE) rates, defined as death, Q-wave myocardial infarction, or target lesion revascularization, were compared between the 2 groups. The patients with DM were sicker at baseline. The MACE rates at 1 year were significantly increased in those with DM compared to those without DM. This was primarily driven by all-cause mortality. No differences in Q-wave myocardial infarction, target lesion revascularization, stent thrombosis, type of drug-eluting stents used, or procedure-related renal failure were seen. No differences were found in death or MACE rates at 1 year after adjusting for age, gender, race, systemic hypertension, peripheral artery disease, and a history of chronic renal failure between the 2 groups (weighted log-rank statistic, p = 0.37 and p = 0.37, respectively). In patients presenting with acute myocardial infarction, those with DM were sicker than those without DM. In conclusion, after correction for co-morbid conditions, no difference was seen in the 1-year MACE or death rates between those with and without DM who presented with acute myocardial infarction and were treated with drug-eluting stents., (Copyright 2010 Elsevier Inc. All rights reserved.)

Objectives: The aim of this study was to examine the utility of routine intravascular ultrasound (IVUS) guidance in patients with acute myocardial infarction (MI) undergoing percutaneous coronary intervention (PCI) with stent implantation., Background: Stent thrombosis (ST) is a serious complication of PCI with stent implantation for patients presenting with acute MI. Mechanical factors such as incomplete stent expansion and smaller stent diameters are known to correlate with ST and restenosis. IVUS guidance for stent deployment is reported to reduce these events in stable patients., Methods: We analyzed a cohort of 905 consecutive patients who underwent primary PCI for acute MI and were discharged alive. The clinical outcomes of 382 patients who underwent IVUS-guided PCI were compared to those of 523 patients who did not. Patients who presented with cardiogenic shock and rescue PCI were excluded. The primary composite endpoint of death, MI, and target lesion revascularization at 1-year follow-up was systematically indexed and a propensity score was performed with regard to the use of IVUS-guided PCI., Results: Patients undergoing IVUS-guided PCI were older, more diabetic and hypertensive, but presented with less history of previous MI. The severity of coronary artery disease was balanced between both groups. The number of treated lesions and stents used was higher in the IVUS-guided group, with a longer procedural duration. The overall rates of the composite primary outcome were similar (14.5% vs. 14.3%, P = 0.94) as were the rates of definite and probable stent thrombosis at 1 year (2.1% vs. 2.1%, P = 0.99) in the IVUS-guided and no-IVUS groups, respectively. After multivariate and propensity score adjustment, IVUS guidance was not an independent predictor for the primary endpoint., Conclusion: This study does not support the routine use of IVUS guidance for stent deployment in patients who present with acute MI and undergo primary PCI., (Copyright 2009 Wiley-Liss, Inc.)

Drug-eluting stents (DES) have been shown to markedly reduce the need for repeat revascularization compared to bare-metal stents in patients with stable coronary artery disease. The benefit of DES in patients with acute coronary syndromes (ACS) is unclear. This analysis was undertaken to determine if DES have similar advantages over bare-metal stents in patients with ACS. A cohort of 3,771 patients underwent percutaneous coronary intervention with stent implantation in native coronary arteries. Patients presenting for primary angioplasty or rescue angioplasty were excluded. Patients were classified as having stable or unstable symptoms on presentation and then further divided by stent type, DES or bare-metal stent. Although there was a difference in efficacy, with fewer major adverse cardiac events after DES implantation for the stable patients at 1 year (8.2% vs 13.2%, p = 0.008), this benefit was not found in patients with ACS (11.2% vs 12.0%, p = 0.6). A reduced need for repeat revascularization of the initially treated artery accounted for this difference (5.6% vs 11.4%, p <0.001). Stent thrombosis by 1 year was equally rare with each stent type. In conclusion, the reduction in the need for repeat revascularization associated with DES appears to be limited to patients who present with stable angina pectoris. This observation may reflect the more frequent presence of vulnerable plaques in patients with ACS.

Background: In patients receiving primary percutaneous coronary intervention for ST elevation myocardial infarction (STEMI), bivalirudin with provisional glycoprotein (GP) IIb/IIIa inhibitors has been demonstrated to be noninferior to heparin plus systematic GP IIb/IIIa inhibitors in preventing recurrent ischemic events with improved safety in terms of bleeding. However, no study has been performed comparing head-to-head bivalirudin with heparin without GP IIb/IIIa inhibitor infusion in STEMI patients., Methods: We retrospectively studied 899 consecutive patients who presented with STEMI treated by primary angioplasty within 12 h after symptoms. Among them, 566 received bivalirudin and 333 received unfractionated heparin. Their in-hospital outcome in terms of efficacy and safety was assessed using rates of major adverse cardiac events (MACE) and major bleeding, respectively. Clinical, angiographic and procedural characteristics were well matched between the two groups., Results: Patients in the heparin group more frequently required intra-aortic balloon pumping (6.6% vs. 3.6%, P=.037). Regarding the safety end point, the MACE rate, including death, ischemic stroke and urgent repeated revascularization, was low and similar in both groups (2.7% bivalirudin vs. 1.2% heparin, P=.15). The rate of major bleeding, including major hematoma, gastrointestinal bleeding and hematocrit drop >15% during hospitalization, was high and identical in the two groups (4.1% bivalirudin vs. 4.2% heparin, P=.92)., Conclusion: This study suggests that bivalirudin and heparin present similar safety and efficacy profiles when used without GP IIb/IIIa inhibitor infusion during primary angioplasty.

Background: Recent data suggest a clinical benefit with the systematic use of thrombus aspiration (TA) for the treatment of ST-elevation myocardial infarction (STEMI). Nevertheless, the impact of TA as a treatment strategy for stent thrombosis (ST) is unknown. This study aimed to analyze the impact of TA use for the treatment of ST on patient outcomes., Methods: From 2003 to 2008, 91 consecutive patients who presented with a definite ST were included in this analysis. We compared procedural success rates and the incidence of the composite criteria death-recurrent MI-recurrent ST at 30 days in patients who were treated with TA (TA group, n = 36) versus those who were not (No-TA group, n = 55)., Results: Baseline characteristics were similar between the two groups except for the body mass index: 26.2 +/- 5.4 vs. 29.3 +/- 6.2 in the TA and No- TA groups, respectively (p = 0.028). ST presented more likely as STEMI in the TA group: 86.1% vs. 67.3% (p = 0.043). Except for TA use, there was no difference in the treatment therapeutics between groups, including for glycoprotein IIb/IIIa inhibitors. The rate of procedural success was higher in the TA group than in the No-TA group: 88.9% vs. 70.9% (p = 0.043). The incidence of the endpoint of death-recurrent MI-recurrent ST was significantly lower in the TA group: 22.2% vs. 47.2% (p = 0.026). By multivariate analysis, TA use was independently associated with a decrease in the composite criteria (HR = 0.45, p = 0.039)., Conclusion: This study suggests that TA use for ST treatment permits an improvement in patient outcomes at 30 days with a significant decrease in the incidence of the composite criteria death-recurrent MI-recurrent ST. Further prospective studies are needed, however, to definitively address the benefit of TA use in this particular setting.

Background: In the recently published universal definition of myocardial infarction (MI), a troponin elevation above 3x above the 99th percentile of normal after percutaneous coronary intervention (PCI) is a procedure-related (type 4a) MI. Although troponin rise is common after saphenous vein graft (SVG) PCI, its prognostic value remains undetermined. We aimed to investigate the prognostic value of the universal definition of PCI-related MI in SVG interventions., Methods: A cohort of 589 unselected consecutives patients with normal preprocedural troponin Ic undergoing isolated SVG PCI with drug-eluting stent implantation was included. Patients were divided into 2 groups according to the peak troponin value post PCI: those with MI defined as a peak troponin value above 3x the 99th percentile of normal post-PCI (MI group, n = 166) and those without (no MI group, n = 423). The primary end point was the rate of major adverse cardiac events including death, MI, and target vessel revascularization at 1-year follow-up., Results: Baseline characteristics were similar between the 2 groups. In the MI group, patients had more complex angiographic features (type C lesions: 44.7 vs 34.8%; P = .006). The rate of direct stenting and distal protection use were similar in the 2 groups (MI vs no MI: 29.2 vs 28.7%; P = .9 and 32 vs 37.5%; P = .24, respectively). Patients in the MI group had a worse inhospital course but a similar 1-year rate of major adverse cardiac events (22.3 vs 19.1%; P = .39)., Conclusion: Procedure-related MI after PCI, as defined by the universal definition, is associated with an adverse inhospital course but may not predict long-term outcome in SVG PCI.

Despite improving strategies for control of risk factors, progression of atherosclerosis may lead to recurrent cardiac events related to a lesion other than that treated with initial percutaneous coronary intervention (PCI) after ST-elevation myocardial infarction (STEMI). Of 1,007 consecutive patients undergoing primary or rescue PCI for STEMI, 897 who were discharged alive were followed for up to 3 years. Those who underwent nontarget lesion revascularization (non-TLR) were compared with those who did not. Those who underwent a second procedure were followed for an additional 1 year. Altogether, 94 patients (10.5%) required a non-TLR. The median time from the first to the second PCI was 396 days (interquartile range 131 to 533). Subsequent PCI was required for non-STEMI in 46.1% and STEMI in 9.7% of cases. Independent predictors of need for non-TLR were diabetes mellitus, history of coronary bypass surgery, or peripheral vascular disease. By 1 year after the second PCI, 9 patients (9.6%) died, 4 (4.3%) had sustained MI, and 4 (4.3%) had TLR. One of these major adverse events had occurred in 17 (18%). In conclusion, after STEMI, nearly 10% of patients will develop an event that requires subsequent PCI to an unrelated lesion. Patients with diabetes mellitus, history of coronary bypass surgery, or peripheral vascular disease are at increased risk for this event. Aggressive preventive and medical management should be applied to this population for prevention of these subsequent events.

The risk of late thrombotic events and the need for prolonged dual antiplatelet therapy detract from the clinical advantage offered by drug-eluting stents (DESs). Short-term studies have shown premature clopidogrel cessation to be a strong predictor of stent thrombosis (ST) after DES implantation. Data pertaining to the utility of clopidogrel therapy and its optimal duration to prevent late ST remain limited. The study population consisted of 2,889 patients who underwent unrestricted intracoronary DES implantation from April 2003 to January 2007 for whom clopidogrel compliance data were available. Definite ST proved by angiography or autopsy within 12 months of the index procedure occurred in 61 patients. Comparisons of clinical and procedural characteristics in addition to outcomes (death and Q-wave myocardial infarction) were made between the ST and no-ST (2,828 patients) groups. Clopidogrel compliance was assessed at all follow-up time points. For patients in the ST group, clopidogrel compliance status for the remaining study period was defined as that at the time of ST. Logistic regression analysis was performed at 30 days, 6 months, and 12 months to identify independent predictors of cumulative ST. Patients with ST were more likely to have previous congestive heart failure and worse left ventricular ejection fraction. ST was associated with significantly higher mortality at 12 months (23.5% vs 3.2%, p <0.001). Clopidogrel compliance was 80.2% in the overall population and 73.8% in patients presenting with ST (82.6% in patients presenting with early ST and 43.8% in those with late ST). By logistic regression analysis, clopidogrel cessation was an independent predictor of cumulative ST at 30 days and 6 months but not at 12 months. In conclusion, high rates of clopidogrel compliance can be achieved in contemporary practice. Clopidogrel cessation by 12 months is no longer predictive of ST, thus suggesting the optimal duration of therapy for the prevention of ST to be 6 to 12 months.

We conducted a genome-wide association study testing single nucleotide polymorphisms (SNPs) and copy number variants (CNVs) for association with early-onset myocardial infarction in 2,967 cases and 3,075 controls. We carried out replication in an independent sample with an effective sample size of up to 19,492. SNPs at nine loci reached genome-wide significance: three are newly identified (21q22 near MRPS6-SLC5A3-KCNE2, 6p24 in PHACTR1 and 2q33 in WDR12) and six replicated prior observations (9p21, 1p13 near CELSR2-PSRC1-SORT1, 10q11 near CXCL12, 1q41 in MIA3, 19p13 near LDLR and 1p32 near PCSK9). We tested 554 common copy number polymorphisms (>1% allele frequency) and none met the pre-specified threshold for replication (P < 10(-3)). We identified 8,065 rare CNVs but did not detect a greater CNV burden in cases compared to controls, in genes compared to the genome as a whole, or at any individual locus. SNPs at nine loci were reproducibly associated with myocardial infarction, but tests of common and rare CNVs failed to identify additional associations with myocardial infarction risk.

Conflicting data exist regarding an advantage of drug-eluting stents (DES) over bare metal stents (BMS) in catheter-based treatment of saphenous vein graft (SVG) stenoses. This study was undertaken to compare the efficacy of these modalities in that lesion subset. The DES group consisted of 138 cases with 183 lesions (sirolimus-eluting stents, n = 117; paclitaxel-eluting stents, n = 66) and the BMS group consisted of 344 cases with 478 lesions that were followed to 1 year. We examined a composite end point that comprised death, Q-wave myocardial infarction, and target lesion revascularization. More BMS were deployed per patient (p <0.001) and the diameters of BMS deployed was significantly greater (p <0.001). Peak postprocedure values of creatine kinase-MB (p = 0.003) and troponin I (p = 0.05) were higher in BMS. At 1 year there was no significant superiority of DES over BMS with regard to hard end points (death and Q-wave myocardial infarction). In conclusion, this study indicates that both DES and BMS for SVG disease provide acceptably safe and efficacious results, but unlike the case in native coronary arteries, DES use does not reduce the frequency of the need for repeat revascularization.

In patients undergoing percutaneous coronary intervention (PCI), clinical trials have demonstrated that the use of bivalirudin with provisional glycoprotein IIb/IIIa inhibitors is not inferior to heparin with systematic glycoprotein IIb/IIIa inhibitors on major adverse cardiac events and is associated with lower rates of bleeding in various clinical settings. Patients with cardiogenic shock (CS), however, have been excluded from all pivotal trials. A retrospective analysis of 86 consecutive patients undergoing PCI for acute myocardial infarction complicated by CS in our center from April 2003 to September 2007 was performed. In-hospital death, major adverse cardiac events, and bleeding rates were compared in 37 patients who received bivalirudin with or without glycoprotein IIb/IIIa inhibitors and 49 patients who were treated with heparin and glycoprotein IIb/IIIa inhibitors as anticoagulation management. Baseline demographic, clinical, and biological characteristics were similar in the 2 groups. The in-hospital death rate was significantly lower in the bivalirudin group (5.4 vs 32.7%, p = 0.002). There were no differences in the rate of major hematoma between the bivalirudin group and the heparin group (3 vs 2.6%, p = 0.46). In conclusion, bivalirudin with provisional use of glycoprotein IIb/IIIa inhibitors appears to be a safe and effective anticoagualtion strategy in patients undergoing primary PCI for acute myocardial infarction complicated by CS.

Routine aspiration thrombectomy (AT) in percutaneous coronary intervention for patients with ST-segment elevation myocardial infarction (STEMI) has not proved effective in randomized trials. However, in patients undergoing primary percutaneous coronary intervention with severely reduced flow or visible thrombus, AT remains an intuitively attractive option. The use of adjunctive AT in a high-risk cohort of 158 consecutive patients with STEMI and Thrombolysis In Myocardial Infarction (TIMI) 0 to 1 flow or visible thrombus on baseline angiography was examined. Of these, 80 patients underwent AT as an adjunct to primary percutaneous coronary intervention, and 78 underwent percutaneous coronary intervention without AT (non-AT). TIMI 3 flow rates, residual thrombus after percutaneous coronary intervention, and major adverse cardiac events (mortality and nonfatal Q-wave myocardial infarction) at 30 days, 6 months, and 1 year were compared. Baseline characteristics were similar between groups. The AT group more frequently achieved TIMI 3 flow after the intervention (91.3% AT vs 67.9% non-AT; p <0.001) and had less residual thrombus (7.5% AT vs 19.2% non-AT; p = 0.03). AT was associated with reduced major adverse cardiac events at 6 months (6.8% AT vs 24.0% non-AT; p = 0.004) and 1 year (16.6% AT vs 29.2% non-AT; p = 0.009), and decreased mortality rates in the AT group at 6 months (5.4% AT vs 21.3% non-AT; p = 0.004) and 1 year (7.7% AT vs 26.2% non-AT; p = 0.005). In conclusion, for patients with STEMI and TIMI 0 or 1 flow or visible thrombus on baseline angiography, AT was associated with increased TIMI 3 flow rates, decreased residual thrombus, and decreased clinical events, including mortality.

Background: Recent randomized trials have demonstrated conflicting results regarding the use of drug-eluting stents (DESs) as compared to bare metal stents (BMSs) in primary percutaneous coronary intervention (PCI). We compared outcomes among patients presenting with acute ST-elevation myocardial infarction (STEMI) who received DES with those who received BMS., Methods: In-hospital, 30-day, 6-month, and 1-year outcomes of a cohort of 122 patients who underwent primary or facilitated PCI and received a BMS were compared to 122 propensity-matched patients who received a DES. Seventy-two patients received sirolimus-eluting stents, and 50 received paclitaxel-eluting stents., Results: Baseline demographics were similar among groups. One-, 6-, and 12-month outcomes, including reinfarction, death, stent thrombosis, and target vessel revascularization (TVR), were similar among groups. At 1 year, all-cause mortality was 13.3% in the BMS group and 9.2% in the DES group [P=not significant (ns)], recurrent MI was 5.3% in the BMS group vs. 4.4% in the DES group (P=ns), and TVR was 7% in the BMS group vs. 8.7% in the DES group (P=ns)., Conclusions: Our data do not support the general use of DES in the setting of STEMI given similar cardiovascular outcomes among patients receiving BMS or DES, the need for long-term dual antiplatelet therapy with DES, and the possible repercussions of very late stent thrombosis.

Although drug-eluting stents reduce restenosis and target lesion revascularization compared with bare metal stents (BMSs), the specter of late stent thrombosis has curbed enthusiasm for the widespread use of drug-eluting stents. Alternatively, increasing BMS use would increase restenosis and potentially increase adverse events. The presentation and outcomes of BMS restenosis are controversial. We evaluated 2,539 patients with BMS restenosis referred for repeat revascularization. Major adverse cardiac events, including mortality and myocardial infarction (MI), were assessed at clinical presentation, 30 days, and 6 months. Patients with acute presentation (i.e., unstable angina requiring hospitalization or MI) were compared with patients with stable presentation. At presentation, 19.2% of patients were asymptomatic, 27.5% had exertional angina, 46.6% had unstable angina, and 6.7% had MI. Mortality and MI rates were 1.1% and 1.4%, respectively, at 30 days and 3.3% and 4.5%, respectively, at 6 months. Patients with acute coronary syndrome (ACS) and those without ACS had similarly low mortality rates at 30 days (1.2% ACS vs 1.0% non-ACS, p = 0.65) and 6 months (3.4% ACS vs 3.3% non-ACS, p = 0.93) and MI rates at 30 days (1.3% ACS vs 1.4% non-ACS, p = 0.87) and 6 months (4.7% ACS vs 4.3% non-ACS, p = 0.65). Combined major adverse cardiac events were similar at 30 days (2.5% vs 2.1%, p = 0.53) and 6 months (7.4% ACS vs 6.9%, non-ACS, p = 0.65). In conclusion, although BMS restenosis often manifests as an ACS, it is associated with a low incidence of 6-month major adverse cardiac events and does not predict a negative outcome.

High-density lipoprotein (HDL) cholesterol has protective cardiovascular effects. We investigated the effect of baseline HDL cholesterol on the outcomes of patients who underwent drug-eluting stent implantation for acute coronary syndrome. Since March 2003, 1,032 consecutive patients were, according to their baseline HDL cholesterol level, included in a low HDL cholesterol group (n = 550, <40 mg/dl in men, <45 mg/dl in women, mean 32 +/- 7) or a high HDL cholesterol group (n = 482, >40 mg/dl in men, >45 mg/dl in women, mean 55 +/- 19). End points were death, Q-wave myocardial infarction, target lesion revascularization, and a composite of major adverse cardiac events at 30 days and 1 year. We assessed the relation between HDL cholesterol and end points. Patients with low HDL cholesterol more often had diabetes, a higher body mass index, higher triglyceride levels, and lower total cholesterol levels. Low-density lipoprotein cholesterol and statin treatment (98% in the 2 groups) were comparable. Incidences of mortality and major adverse cardiac events at 30 days were higher in the low than in the high HDL cholesterol group (p <0.001 and p = 0.002, respectively; chi-square analysis). At 1 year, more deaths occurred in the low HDL cholesterol group (p <0.001; chi-square analysis), as did major adverse cardiac events (p <0.001; chi-square analysis). Multivariate analysis showed low HDL cholesterol at baseline (hazard ratio 2.61, 95% confidence interval 1.33 to 5.12) to be a key predictor of major adverse cardiac events and death (hazard ratio 3.33, 95% confidence interval 1.15 to 10.0) at 1 year. In conclusion, regardless of baseline low-density lipoprotein cholesterol levels and statin therapy, additional strategies to increase HDL cholesterol should be evaluated in patients with acute coronary syndrome.

Background: Bivalirudin is replacing heparin as the anticoagulant agent of choice for elective percutaneous coronary intervention (PCI). This study aimed to assess the safety and clinical outcomes of bivalirudin versus unfractionated heparin (UFH) in patients undergoing PCI for acute myocardial infarction (AMI)., Methods: A cohort of 672 consecutive patients presenting with AMI without prior thrombolytic therapy were treated with either bivalirudin (216 patients) or UFH (456 patients). Platelet glycoprotein IIb/IIIa inhibitors were administered at the operator's discretion. The in-hospital, 30-day, and 6-month outcomes of the two groups were compared., Results: Baseline clinical and angiographic characteristics were similar between the groups. In-hospital complications were similar, although there was a trend of a less major hematocrit drop in the bivalirudin group (0.9% vs. 3.1%, P=.09). All clinical outcomes were similar between the groups at 30-day and 6-month follow-ups. There was no statistical significance for acute thrombosis and subacute thrombosis between the groups, and there was no late thrombosis from either group. The event-free survival rate was similar between the groups (P=.41)., Conclusion: The use of bivalirudin in patients undergoing PCI after AMI is safe and feasible. Bivalirudin should be considered as an alternative anticoagulant agent during PCI to treat patients presenting with AMI.

Objectives: We aimed to compare clinical outcomes of octogenarians > or =80 years of age after coronary drug-eluting stent (DES) implantation., Background: Although octogenarians constitute a fast-growing portion of cardiovascular patients, they are not adequately represented in current clinical revascularization trials., Methods: We analyzed the data of 3,166 consecutive patients who underwent percutaneous coronary intervention (PCI) and DES implantation since March 2003. Periprocedural events, 1- and 6-month clinical outcomes were compared between octogenarians (n = 339) and patients <80 years of age (n = 2,827)., Results: Baseline characteristics revealed a higher prevalence of females (P < 0.001), Caucasians (P = 0.004), chronic renal failure (P < 0.001), heart failure (P < 0.001), number of diseased vessels (P = 0.009), and lower ejection fraction (P = 0.03) in octogenarians. Patients <80 years showed more positive family history (P < 0.001), hyperlipidemia (P = 0.006), smoking (P < 0.001), and obesity (P < 0.001). Clinical presentation and procedural success were similar in both groups as were death, myocardial infarction (MI), and repeat revascularization in-hospital. At 6 months, restenosis rates were low and comparable. In the subgroup of octogenarians who presented with acute coronary syndrome, mortality (15% vs. 3%, P < 0.001) and Q-wave MI occurred more often. Multivariate analysis revealed age >80 (P = 0.008), cardiogenic shock (P < 0.001), Q-wave MI at presentation (P = 0.003), and length of hospital stay (P = 0.003) to be independent predictors of mortality., Conclusions: PCI with DES in octogenarians results in a similar reduction of restenosis rates when compared to patients <80 years. Yet in octogenarians who presented with acute coronary syndrome, incidence of mortality and Q-wave MI at 6 months was higher as compared to younger patients., (Copyright 2006 Wiley-Liss, Inc.)

Objectives: The goal of this study was to use intravascular ultrasound (IVUS) to compare octogenarians versus patients <65 years of age with regard to culprit lesion morphology in acute myocardial infarction (MI)., Background: Although octogenarians represent the fastest-growing segment of our population and have a higher risk profile, they are underrepresented in therapeutic trials., Methods: Between 2002 and 2005, 42 octogenarians and 52 patients <65 years of age underwent pre-intervention IVUS within 2 days from onset of an MI. Qualitative and quantitative measurements were performed at the lesion site and at the proximal and distal references. Positive remodeling was defined as a remodeling index (lesion/mean reference arterial area) > or =1., Results: Elderly patients mostly (71%) presented with non-ST-segment elevation myocardial infarction (NSTEMI), whereas patients <65 years of age presented almost equally with ST-segment elevation myocardial infarction (STEMI) and NSTEMI (56% vs. 44%). The frequency of rupture/dissection was greater in the <65-year-old group (32% vs. 9%, p = 0.009), and culprit lesions contained more thrombus in this group (14% vs. 2%, p = 0.04). Conversely, in octogenarians, lesions were predominantly calcified (57% vs. 10%, p < 0.001) and longer (20.9 +/- 7.8 mm vs. 16.6 +/- 6.1 mm, p = 0.004) with less positive remodeling (19% vs. 56%, p < 0.001). On multivariant logistic regression analysis, age was the only independent predictor of calcified plaque (p = 0.02) and remodeling (p = 0.005)., Conclusions: Negative remodeling and calcified plaque with rare plaque ruptured were common in elderly people with acute MI. These findings may contribute to the difference in clinical presentation and may suggest a different pathophysiologic mechanism of MI in octogenarians.

Background: Metabolic syndrome (MS), the combination of hypertension, obesity, dyslipidemia, and insulin resistance, is a precursor of diabetes mellitus (DM) and highly prevalent among patients with acute myocardial infarction (AMI). Diabetes mellitus is associated with larger infarct size and worse outcomes after AMI. This study examined infarct size and short-term outcomes among nondiabetic patients with MS following contemporary treatment of AMI., Methods: Four hundred five consecutive patients with AMI treated with primary percutaneous coronary intervention were evaluated. Patients with diabetes (n=105) were excluded. Those with MS (n=167) included patients with three or more of the following criteria: hypertension, elevated fasting blood glucose, hypertriglyceridemia, low high-density lipoprotein, and obesity [body mass index (BMI)> or =30]. The control group (n=133) included patients without MS or DM., Results: Baseline characteristics were similar except for hypertension, BMI, and dyslipidemia, which by study design were higher in the MS group. The MS group had larger infarct size as determined by peak creatine kinase-MB (79.8+/-133.8 vs. 30.84+/-51.5, P<.001). Overall in-hospital complications were higher in patients with MS (21.1% vs. 9.2%, P=.003). Metabolic syndrome is associated with a 10-fold increased risk of acute renal failure after myocardial infarction (7.9% vs. 0.8%, P=.007)., Conclusion: Metabolic syndrome in nondiabetic patients with AMI is associated with larger infarct size, more in-hospital complications, and a marked increase of acute renal failure. Awareness of MS and preventative measures is crucial in this population to minimize infarct size and decrease morbidity after AMI.

The long-term outcome of patients who present with an identified plaque rupture in a nonflow-limiting lesion is not well known. We retrospectively studied 17 consecutive patients in whom intravascular ultrasound identified plaque rupture in nonflow-limiting lesions (minimum lumen area >4.0 mm2) that were not treated with coronary intervention. After a mean follow-up of 43 +/- 25 months, events related to those lesions were 1 death (6%) of undetermined cause (6%) that occurred after 69 months, no myocardial infarction, and 2 revascularizations (12%) that occurred at 3 and 67 months. Overall, the cumulative rate of cardiac events was 18%.

Sirolimus-eluting stents (SESs) are currently being used in patients undergoing percutaneous coronary intervention (PCI). SESs have not been evaluated in the treatment of acute myocardial infarction by primary angioplasty. We report our initial experience with SESs implanted during primary angioplasty. One hundred and three patients were treated within 12 hr after onset of acute myocardial infarction (AMI) with primary angioplasty and SES implantation. Those patients were compared to 504 patients treated with bare metal stents (BMSs). Angiographic success (TIMI flow grade 3 and residual stenosis < 50%) was completed in 98% of patients with SESs and no subacute stent thrombosis was reported. In-hospital outcomes were similar in the SES and BMS groups. At 6 months, major cardiac events were less frequent in the SES group than in the BMS group (9% vs. 24%, respectively; P < 0.001), driven by a lesser need for repeat revascularization with SESs (1% vs. 10.3% with BMSs; P = 0.014). Mortality at 6 months was 7% with SESs and 11% with BMSs (P = 0.14). SESs are safe and effective for the treatment of AMI by primary angioplasty. As compared to BMSs, SESs improve long-term outcome after AMI, mainly by reducing the need for repeat revascularization.

Background: Previous studies have reported diffuse destabilization of atherosclerotic plaques in acute myocardial infarction (AMI)., Methods and Results: We used intravascular ultrasound (IVUS) to assess 78 coronary arteries (38 infarct-related arteries [IRAs] with culprit and nonculprit lesions and 40 non-IRAs) from 38 consecutive AMI patients. IVUS analysis included qualitative and quantitative measurements of reference and lesion external elastic membrane (EEM), lumen, and plaque plus media (P&M) area. Positive remodeling was defined as lesion/mean reference EEM >1.0. Culprit lesions were identified by a combination of ECG, wall motion abnormalities (ventriculogram or echocardiogram), scintigraphic perfusion defects, and coronary angiogram. Culprit lesions contained more thrombus (23.7% versus 3.4% in nonculprit IRA plaques and 3.1% in non-IRA plaques; P=0.0011). Culprit lesions were predominantly hypoechoic (63.2% versus 37.9% of nonculprit IRA plaques and 28.1% of non-IRA plaques; P=0.0022). Culprit lesions were longer (17.5+/-10.1, 9.8+/-4.0, and 10.3+/-5.7 mm, respectively; P<0.0001), had larger EEM area (15.0+/-6.0, 11.5+/-5.7, and 12.6+/-5.6 mm2, respectively; P=0.0353) and P&M area (13.0+/-6.0, 7.5+/-3.7, 9.3+/-4.3 mm2, respectively; P<0.0001), smaller lumens (2.0+/-0.9, 4.1+/-3.1, and 3.4+/-2.5 mm2, respectively; P=0.0009), and more positive remodeling (79.4%, 59.0%, and 50.8%, respectively; P=0.0155). The frequency of plaque rupture/dissection was greater in culprit, nonculprit IRA, and non-IRA plaques in AMI patients than in a control group of chronic stable angina patients with multivessel IVUS imaging., Conclusions: Culprit plaques have more markers of instability (thrombus, positive remodeling, and large plaque mass); however, these markers of instability are not typically found elsewhere. This suggests that the vascular event in AMI patients is determined by local pre-event lesion morphologies.

Troponin I is a predictive marker of short- and intermediate-term adverse cardiac events in patients with acute coronary syndromes (ACS). These high-risk patients may benefit from early percutaneous coronary intervention. However, whether additional myocardial injury, defined as postprocedural troponin I elevation, may be associated with adverse short- and intermediate-term outcomes has not been fully explored. Accordingly, we studied 132 consecutive patients with non-ST-elevation ACS (62% with non-Q-wave myocardial infarction) and elevated troponin I levels at admission (>0.15 ng/ml) who underwent percutaneous coronary intervention > or =48 hours after admission. Troponin I levels were routinely measured at 6 and 18 to 24 hours after intervention and patients were stratified according to the presence or absence of troponin I re-elevation, defined as postprocedural troponin I levels >1 times the admission levels. In-hospital and cumulative 6-month clinical outcomes were compared between groups. Patients with troponin I re-elevation (n = 51) were older (68 +/- 13 vs 64 +/- 12 years, p = 0.05) and had experienced prior myocardial infarction more frequently (92.5 vs 82.1, p = 0.09), but otherwise had similar baseline clinical characteristics. Patients with troponin I re-elevation had significantly higher in-hospital mortality (9.8% vs 0%, p = 0.016) and a higher 6-month cumulative death rate (24% vs 3.7%, p = 0.001). There was a trend for an increased 6-month myocardial infarction rate in patients with troponin I re-elevation (13.7% vs 3.7%, p = 0.11) and target vessel revascularization was similar between groups (16.7% vs 17.4%, p = 0.92). By multivariate analysis, troponin I re-elevation (odds ratio [OR] 6.2, p = 0.011) and diabetes mellitus (OR 5.7, p = 0.014) were the strongest independent predictors for increased 6-month cumulative mortality, whereas creatine kinase MB-fraction re-elevation had no prognostic value. We conclude that troponin I re-elevation after percutaneous coronary intervention in high-risk patients with ACS is associated with a substantial increase in mortality and reduced event-free survival at 6-month follow-up.

Pre-intervention administration of abciximab in patients at "high risk" for coronary angioplasty has been shown to reduce acute and long-term cardiac outcomes. The role of intra-procedural ("rescue") administration of abciximab has not been fully elucidated. We assessed the clinical outcomes associated with rescue administration of abciximab during complex percutaneous coronary interventions. We studied in-hospital and long-term (1-year) outcomes (death, myocardial infarction and target lesion revascularization) of 298 consecutive patients (78% male; age, 62 +/- 11 years; 83% with acute coronary syndrome) treated with abciximab for thrombus-containing lesions, sub-optimal angioplasty results, procedural dissections or other complications. Stents were used in 73% of procedures. Procedural success was 97.0% and overall major in-hospital complication rate was 3.0% (death, 1.3%; Q-wave myocardial infarction, 0.7%; and emergent bypass surgery, 1.0%). Most frequent angiographic complications included visible thrombus (17%), dissections (17%), threatened closure (7%), and distal embolization (7%). In-hospital non-Q wave myocardial infarction (defined as CK-MB 5 times normal) occurred in 31.0%. Out-of-hospital to one-year events included death (1.7%), Q-wave myocardial infarction (2.7%), and target lesion revascularization (15.1%); cardiac event-free survival was 82.9%. We conclude that rescue administration of abciximab is associated with relatively low in-hospital complications and favorable long-term outcome in patients with sub-optimal angioplasty results and/or procedure-related complications, although peri-procedural non-Q wave myocardial infarction rate is high. A clinical and cost-effective comparison between provisional and rescue administration of abciximab may be warranted.

Objectives: To evaluate in-hospital and long-term clinical outcomes in a large consecutive series of patients undergoing percutaneous multivessel stent intervention., Background: High restenosis and recurrent angina rates have limited the clinical outcomes of multivessel coronary angioplasty before stents were available to improve angioplasty results., Methods: We evaluated in-hospital and long-term clinical outcomes (death, Q-wave myocardial infarction [MI], and repeat revascularization rates at one year) in 398 consecutive patients treated with coronary stents in two (94% of patients) or three native arteries, compared to 1,941 patients undergoing stenting procedure in a single coronary artery between January 1, 1994 and August 29, 1997., Results: Overall procedural success was obtained in 96% of patients with two- or three-vessel stenting and in 970% of patients with single-vessel stent intervention (p = 0.36). Procedural complications were also similar (3.8% for multivessel versus 2.9% for single vessel, p = 0.14). During follow up, target lesion revascularization was 15% in multivessel and 16% in single-vessel interventions (p = 0.38), and repeat revascularization (calculated per treated patient) was also similar for both groups (20% vs. 21%, p = 0.73). There was no difference in death (1.4% vs. 0.7%, p = 0.26), and Q-wave MI (1.2% vs. 0%, p = 0.02) was lower following multivessel interventions. Overall cardiac event-free survival was similar for both groups (p = 0.52)., Conclusions: Unlike previous conventional angioplasty experiences, multivessel stenting has (1) similar in-hospital procedural success and major complication rates and (2) similar long-term (one year) clinical outcomes compared with single-vessel stenting. Thus, stents may be a viable therapeutic strategy in carefully selected patients with multivessel coronary disease.

Initial experiences with coronary stents in acute coronary syndromes have suggested higher risk of ischemic complications and stent thrombosis. We evaluated in-hospital and 1-year clinical outcomes of coronary stent implantation in perimyocardial infarction (MI) syndromes. We studied 334 consecutive patients undergoing stent interventions in the first week after acute MI. Stenting was performed within 24 hours (n = 31), within 1 to 3 days (n = 95), and within 4 to 7 days (n = 208). Stents were used to improve angioplasty results and to treat dissections and abrupt/threatened closure. Postprocedure anticoagulation regimens were aspirin, ticlopidine, and low molecular weight heparin. Overall procedural success was achieved in 93% of patients. Major in-hospital complications included death (1.0%), recurrent Q-wave MI (0.6%), and emergent bypass surgery (3.0%). Stent thrombosis occurred in 0.6% of patients. At follow-up, cardiac event-free survival was 80%, mortality 2.2%, recurrent MI 3.5%, and target lesion revascularization 11%. We conclude that coronary stenting in periinfarction syndromes was effective in achieving sustained clinical benefit up to 1 year with low morbidity and mortality. Thus, stents seem to be a viable therapeutic strategy in patients sustaining perimyocardial infarction syndromes.

Emergency coronary artery bypass grafting is necessary in 2.7% to 13.5% of patients undergoing elective percutaneous transluminal coronary angioplasty. Myocardial infarction develops in 11% to 49% of these patients, with 18% to 46% of infarcts resulting in new Q waves. Since February 1987 a revised protocol for myocardial preservation has been used in 19 patients undergoing emergency bypass grafting for failed angioplasty. Cardioplegia is induced with a normothermic blood cardioplegic solution. Multiple maintenance doses of cold (4 degrees C) blood cardioplegic solution are then delivered through the aortic root and vein grafts. Before the aortic crossclamp is removed, normothermic reperfusion cardioplegic solution is delivered through the aortic root and vein grafts. This group was compared with all patients undergoing emergency bypass grafting for failed angioplasty before February 1987. These 45 patients received cold induction of cardioplegic solution, multiple maintenance doses of cold cardioplegic solution, and no reperfusion cardioplegic solution. The prevalence of myocardial infarction in the group receiving cold cardioplegic solution was 65% versus 26% in the group receiving normothermic cardioplegic solution (p less than 0.007). Multivariate analysis identified the use of the normothermic cardioplegia protocol (p less than 0.005), nontotal occlusion of the angioplasty vessel (p less than 0.03), and presence of collateral flow to the angioplasty vessel (p less than 0.04) as being independently associated with absence of myocardial infarction.

Successful intravenous thrombolytic therapy early in myocardial infraction has the potential to reduce patient mortality without the additional risk and cost of aggressive invasive therapy. Noninvasive detection of successful reperfusion using resolution of chest pain, ST-segment changes assessed on static electrocardiograms, arrhythmia evolution, early isoenzyme peaking or changes in ventricular perfusion or function has been hampered by poor sensitivity or specificity, or inability to provide timely information. A newly available portable programmable microprocessor-driven real-time 12-lead electrocardiographic monitor has been introduced that may address these limitations. A continuously updated precise digital record of ST-segment activity at the bedside provides valuable information both in monitoring patients during reperfusion therapy to determine the efficacy of such treatment and in the subsequent hours to signal threatened reocclusion. This report describes the salient features of the monitor and presents 4 distinct situations in which the monitor detected timely information regarding coronary patency after reperfusion.

Unlabelled: Patients undergoing coronary angioplasty have a 2% to 7% risk of requiring emergency coronary artery bypass graft surgery for impending infarction. These patients provide a unique model of early reperfusion because the exact time of compromise to blood flow and the composition of the reperfusion solution are known. However, the amount of myocardium salvaged is unknown. Between December 1981 and September 1985, 859 patients underwent coronary angioplasty. Forty-two patients had emergency surgery for objective evidence of impending infarction. Five patients died. Thirty-six patients were contacted for follow-up; 21 (58%) of 36 had a radionuclide ventriculogram performed at a mean of 39 +/- 13 months after surgery. These radionuclide studies were compared with the patient's preangioplasty contrast ventriculogram. One patient had a myocardial infarction 3 years after surgery. Eleven (55%) of the remaining 20 patients had a normal radionuclide ventriculogram at follow-up study (ejection fraction 65 +/- 9%). Five (25%) of the 20 patients had a depressed ejection fraction (46 +/- 4%) with wall motion abnormalities, but these were unchanged from the preangioplasty studies. Four patients (20%) had a significant decrease in ejection fraction over baseline (37 +/- 10%) with new wall motion abnormalities., In Conclusion: 1) there is an 80% chance that left ventricular function will be unchanged at 3 year follow-up study in patients surviving emergency bypass grafting for failed angioplasty; 2) these data suggest that early revascularization for impending infarction in this setting is associated with a good late outcome; and 3) this patient group offers a unique opportunity to study the effects of early reperfusion in a human model.

Maximal myocardial salvage appears to be related to the severity of residual coronary arterial stenosis after thrombolysis. The degree of residual infarct vessel stenosis was assessed in 119 consecutive patients with patent arteries who received streptokinase during acute myocardial infarction. After administration of streptokinase, 99 of 119 patients (83%) had a residual stenosis 70% or more in diameter. Assuming that a residual diameter stenosis of at least 70% is flow limiting, the feasibility for percutaneous transluminal coronary angioplasty (PTCA) was determined by the following criteria: length less than 10 mm, no significant distal narrowing or left main stenosis, and an adequate-sized distal artery. In 81 of 99 patients (82%), arterial anatomy was suitable for PTCA. Thus, after therapy with streptokinase for acute myocardial infarction, most patients have a significant infarct arterial residual stenosis and are candidates for PTCA.

Emergency cardiac catheterization and angiography in patients have resulted in an appreciation of the pathogenesis of AMI and the efficacy of thrombolytic therapy. Simple reperfusion of the infarcted myocardium, however, does not necessarily guarantee myocardial salvage, and preliminary studies have been somewhat confusing as to its beneficial effects. Metabolic support of the ventricle during early reperfusion may enhance left ventricular performance. Although the potential effects of thrombolytic therapy are still unclear, the routine administration of these agents has resulted in more frequent performance of early coronary angiography, with the result that appropriate therapeutic decisions can be made immediately regarding medical treatment, coronary angioplasty, or complete myocardial revascularization. In fact, in prolonged chest pain syndromes, emergency angiography may play a very important role in establishing appropriate initial therapy early in the course of hospitalization, potentially lowering mortality, morbidity, and cost. These issues will be answered ultimately only by carefully designed long-term randomized trials.

Continuous ST-segment Holter recordings were analyzed from 46 patients with acute myocardial infarction (AMI) receiving intracoronary streptokinase (SK) during the first 48 hours of hospitalization. Changes in ST deviation and the time periods of these changes were quantitated and correlated with angiographic evidence of reperfusion. Thirty-six patients had total occlusion of the infarct vessel and 10 had subtotal occlusion. Of the 36 vessels that were totally occluded, 19 were reperfused and 17 were not. In patients in whom reperfusion was successful, an ST steady state was achieved 55 +/- 32 minutes after SK administration. In patients in whom it was not successful, a steady state was achieved in 219 +/- 141 minutes (p less than 0.001). Achievement of steady state within 100 minutes after SK reperfusion indicated successful reperfusion with 89% sensitivity and 82% specificity. All patients with subtotal occlusion achieved an ST steady state before SK infusion. No patient with total occlusion achieved a steady state before SK. Achievement of ST steady state before SK infusion was 100% sensitive and 100% specific for subtotal occlusion at initial angiography. Continuous, quantitative ST-segment analysis is a sensitive and specific noninvasive technique for following coronary artery patency during AMI.

Although thrombolytic therapy can result in lysis of a coronary artery thrombus, salvage of myocardium as measured by enzymatic, electrocardiographic and regional wall motion evaluation has not been clearly documented. Many patients after successful reperfusion continue to experience recurrent chest pain. The presence of recurrent chest pain suggests salvaged myocardium. Controlled reocclusion of the infarct vessel with the use of coronary angioplasty may support evidence for myocardial salvage. Experience in 50 patients who underwent angioplasty was reviewed retrospectively. Sixteen of the 50 patients had electrocardiographic or clinical evidence of ischemia at the time of balloon inflation. Prospectively, all patients who underwent angioplasty after they had received streptokinase were evaluated, and 5 of 5 patients had chest pain and ST-segment elevation during balloon inflation. The development of ischemic changes during balloon catheter inflation suggests the presence of persistently viable, salvaged myocardium after successful thrombolysis.

Regional coronary blood flow was determined with the radioactive microsphere technique 10 an 70 minutes and 2 1/2 and 5 hours after abrupt occlusion of the left anterior descending coronary artery in 12 closed chest sedated dogs. In six dogs, nitroglycerin, 200 to 400 microng/min, was infused intravenously 10 to 70 minutes after occlusion. Methoxamine was administered to return blood pressure and heart rate to prenitroglycerin levels. Ten minutes after occlusion (before treatment) collateral flow values and ischemic zone endocardial/epicardial flow ratios were equivalent in untreated (0.11+/-0.03 ml/min per g; 0.31+/-0.05) and treated dogs (0.14+/-0.02 ml/min per g; 0.29+/-0.03). In untreated dogs, collateral flow did not change over 5 hours; the endocardial/epicardial flow ratio was decreased at 5 hours (0.21+/-0.05, P less than 0.05). In contrast, in treated dogs, collateral flow and the endocardial/epicardial flow ratio were increased at 70 minutes (0.27+/-0.04 ml/min per g, P less than 0.05; 0.53+/-0.10, P less than 0.05). Most importantly, collateral flow remained elevated 5 hours after occlusion (0.26+/-0.03 ml/min per g, P less than 0.05) although treatment was discontinued 70 minutes after occlusion. Hence, collateral flow was unchanged over 5 hours of occlusion in untreated dogs, but short-term treatment with nitroglycerin and methoxamine resulted in a sustained increase in collateral flow. These findings may be a result of stimulation by nitroglycerin and methoxamine of the spontaneous rate at which intrinsic collateral function increases after ischemia. Alternatively, nitroglycerin and methoxamine may maintain cell viability until collateral vessels develop spontaneously.

"Stunned" myocardium prevents the assessment of myocardial salvage after streptokinase. In order to unmask "stunning," we sought to evaluate left ventricular inotropic contractile reserve of patients after streptokinase. Radionuclide ventriculograms were obtained in 75 consecutive patients 2 weeks after myocardial infarction, at rest and during intravenous isoproterenol infusion. Resting and isoproterenol-stressed ejection fractions were compared in the patent and closed-infarct vessel groups. Although there was no difference in the resting ejection fractions between the patent group (0.48 +/- 0.02) and the closed group (0.48 +/- 0.02), isoproterenol increased the ejection fractions in the patent group (increase 0.14 +/- 0.01) significantly more than in the closed group (increase 0.06 +/- 0.01) (p less than 0.0001). Thus, despite identical resting ventricular function, the greater inotropic contractile reserve in the patent infarct vessel group suggests that restoration of blood flow in acute myocardial infarction salvages myocardium.