Early Invasive Strategy In Patients Research Articles

Subcutaneous enoxaparin with early invasive strategy in patients with acute coronary syndromes

Background Subcutaneous enoxaparin during at least 48 hours provides adequate anticoagulation and good clinical results in patients with non-ST–segment elevation acute coronary syndromes undergoing percutaneous coronary intervention (PCI). Methods In this nonrandomized retrospective study, we compared 347 patients with non-ST–segment elevation acute coronary syndromes who underwent rapid PCI after only 2 injections of subcutaneous enoxaparin (EI, n = 117) to those referred later to the catheterization laboratory with ≥3 injections (DI, n = 230). We measured anti-Xa at the time of PCI and evaluated bleeding and major ischemic events (death/myocardial infarction) at 30 days. Results Patients in the EI group more frequently received glycoprotein IIb/IIIa inhibitors and clopidogrel preceding PCI than did patients in the DI group (58.1% vs 31.7%, P < .0001 for glycoprotein IIb/IIIa inhibitors and 68.4% vs 40.4% for clopidogrel pretreatment, P < .0001, respectively). The anti-Xa activity measured at the time of catheterization (0.92 ± 0.04 U/mL vs 0.96 ± 0.02 U/mL, EI vs DI, P = .25) and the injection-to-catheterization times (5.6 ± 0.2 h vs 5.2 ± 0.1 h, EI vs DI, P = .17) were similar in both groups. The 30-day bleeding rates of 1.7% and 4.8% in the EI and DI strategies were found to be equivalent with a significant non-inferiority test for the EI strategy ( P < .05). There was a nonsignificant trend for less death or myocardial infarction at 30 days in the EI group compared to the DI group (4.3% vs 7.0%, non-inferiority test not significant). Conclusion A rapid invasive strategy with only 2 subcutaneous injections of enoxaparin provides similar levels of anticoagulation, and is associated with a favorable trend for ischemic events and with safety equivalent to a more prolonged “upstream” treatment with enoxaparin.

Comparison of positron emission tomography with the resting electrocardiogram for assessing viable myocardium in chronic ischemic cardiomyopathy involving the anterior left ventricular wall

patients with acute coronary syndromes. Am Heart J 2000;140:917–927. 3. Braunwald E. Unstable angina. A classification. Circulation 1989;80:410–414. 4. Morrow DA, Rifai N, Tanasijevic MJ, Wybenga DR, de Lemos JA, Antman EM. Clinical efficacy of three assays for cardiac troponin I for risk stratification in acute coronary syndromes: a Thrombolysis In Myocardial Infarction (TIMI) 11B Substudy. Clin Chem 2000;46:453–460. 5. Cole CR, Blackstone EH, Pashkow FJ, Snader CE, Lauer MS. Heart-rate recovery immediately after exercise as a predictor of mortality. N Engl J Med 1999;341:1351–1357. 6. Cannon CP, Weintraub WS, Demopoulos LA, Vicari R, Frey MJ, Lakkis N, Neumann FJ, Robertson DH, DeLucca PT, DiBattiste PM, Gibson CM, Braunwald E. Comparison of early invasive and conservative strategies in patients with unstable coronary syndromes treated with the glycoprotein IIb/IIIa inhibitor tirofiban. N Engl J Med 2001;344:1879–1887. 7. Anonymous. Randomised placebo-controlled trial of abciximab before and during coronary intervention in refractory unstable angina: the CAPTURE Study. Lancet 1997;349:1429–1435. 8. Kaul P, Fu Y, Chang WC, Harrington RA, Wagner GS, Goodman SG, Granger CB, Moliterno DJ, Van de Werf F, Califf RM, Topol EJ, Armstrong PW. Prognostic value of ST segment depression in acute coronary syndromes: insights from PARAGON-A applied to GUSTO-IIb. PARAGON-A and GUSTO IIb Investigators. Platelet IIb/IIIa Antagonism for the Reduction of Acute Global Organization Network. J Am Coll Cardiol 2001;38:64–71. 9. Abrahamsson P, Andersen K, Grip L, Wallentin L, Dellborg M. Early assessment of long-term risk with continuous ST-segment monitoring among patients with unstable coronary syndromes. Results from 1-year follow-up in the TRIM study. J Electrocardiol 2001;34:103–108. 10. Holmvang L, Andersen K, Dellborg M, Clemmensen P, Wagner G, Grande P, Abrahamsson P. Relative contributions of a single-admission 12-lead electrocardiogram and early 24-hour continuous electrocardiographic monitoring for early risk stratification in patients with unstable coronary artery disease. Am J Cardiol 1999;83:667–674. 11. Morrow DA, Cannon CP, Rifai N, Frey MJ, Vicari R, Lakkis N, Robertson DH, Hille DA, DeLucca PT, DiBattiste PM, et al, and the TACTICS-TIMI 18 Investigators. Ability of minor elevations of troponins I and T to predict benefit from an early invasive strategy in patients with unstable angina and non-ST elevation myocardial infarction: results from a randomized trial. JAMA 2001; 286:2405–2412.

Multimarker approach to risk stratification in non-ST elevation acute coronary syndromes: simultaneous assessment of troponin I, C-reactive protein, and B-type natriuretic peptide

The aim of this study was to compare a delayed and a very early invasive strategy in patients with non–ST-segment elevation acute coronary syndromes (NSTE-ACS) without pre-treatment.The optimal delay of the invasive strategy in patients with NSTE-ACS remains debated and has never been investigated in patients not pre-treated with P2Y12–adenosine diphosphate receptor antagonists.A prospective, open-label, randomized controlled trial was conducted. Altogether, 741 patients presenting with intermediate- or high-risk NSTE-ACS intended for an invasive strategy were included. The modified intention-to-treat analysis was composed of 709 patients after 32 withdrew consent. Patients were randomized 1:1 to the delayed invasive group (DG) (n = 363) with coronary angiography (CA) performed 12 to 72 h after randomization or the very early invasive group (EG) (n = 346) with CA within 2 h. No pre-treatment with a loading dose of a P2Y12–adenosine diphosphate receptor antagonist was allowed before CA. The primary endpoint was the composite of cardiovascular death and recurrent ischemic events at 1 month, as determined by a blinded adjudication committee.Most patients had high-risk NSTE-ACS in both groups (93% in the EG vs. 92.5% in the DG). The median time between randomization and CA was 0 h (interquartile range [IQR]: 0 to 1 h) in the EG group and 18 h (IQR: 11 to 23 h) in the DG. The primary endpoint rate was significantly lower in the EG (4.4% vs. 21.3% in the DG; hazard ratio: 0.20; 95% confidence interval: 0.11 to 0.34; p < 0.001), driven by a reduction in recurrent ischemic events (19.8% vs. 2.9%; p < 0.001). No difference was observed for cardiovascular death.Without pre-treatment, a very early invasive strategy was associated with a significant reduction in ischemic events at the time of percutaneous coronary intervention in patients with intermediate- and high-risk NSTE-ACS. (Early or Delayed Revascularization for Intermediate and High-Risk Non ST-Elevation Acute Coronary Syndromes; NCT02750579)

Platelet glycoprotein IIb/IIIa inhibitors: recognition of a two-edged sword?

Glycoprotein (GP) IIb/IIIa antagonists are potent inhibitors of platelet aggregation that provide marked protection from ischemic events in patients undergoing percutaneous coronary intervention (PCI).1,2⇓ Abciximab, the prototypic GP IIb/IIIa inhibitor, has been studied in >8000 patients undergoing elective or high-risk PCI.2,3,4⇓⇓ In these patients, it produces a consistent 35% to 56% reduction in ischemic end points at 30 days, with a significant 22% reduction in the risk of death, as shown in a combined analysis of long-term (3-year minimum) follow-up of the Evaluation of 7E3 for the Prevention of Ischemic Complications (EPIC), Evaluation in PTCA to Improve Long-term Outcome with abciximab GP IIb/IIIa blockade (EPILOG), and Evaluation of Platelet IIb/IIIa Inhibitor for Stenting (EPISTENT) trials.5 Similar results, albeit of a smaller magnitude, have been seen with the small-molecule antagonists tirofiban and eptifibatide, with a 16% to 35% reduction in ischemic events in patients undergoing PCI.1,6⇓ Attempts to expand the therapeutic indication of GP IIb/IIIa antagonists to other conditions associated with platelet-mediated thrombosis, however, have been less fruitful than expected. Instead of reducing major ischemic events, long-term oral GP IIb/IIIa inhibitor therapy7 has uniformly increased the fatality rate. Furthermore, the overall efficacy of a number of the intravenous antagonists in non–ST-segment elevation acute coronary syndromes (ACS), or in combination with thrombolysis in ST-segment elevation myocardial infarction (MI), has been less than anticipated.8 Of particular concern is the fact that there has been a paradoxical increase in adverse events in 2 of the trials of intravenous therapy in ACS.9,10⇓ Platelets are known to play an important role in the pathogenesis of ACS, yet the high levels of platelet inhibition attainable with GP IIb/IIIa antagonists have failed to dramatically improve clinical outcomes outside of PCI. In this article, we discuss these …

Outcome measurement: evaluating evidence for managing patients with acute coronary syndromes.

Evidence-based practice has been proposed as a means to improve the quality of care and decrease unwarranted variability in practice, but evaluating clinical trial data as evidence for practice is made more difficult because practice changes rapidly. This article reviews current clinical trial data on the management of patients with acute coronary syndromes, but the same principles can be used when evaluating alternative medicines. Current evidence supports risk stratification, early treatment with glycoprotein IIb/IIIa inhibitors, and an early invasive strategy in patients who are at intermediate to high risk. In addition, cholesterol-lowering statins should be initiated early in the patient's hospitalization.

Stent in acute non-Q wave myocardial infarction

Dear Editor, This is in reference to the case report “Stents in non-Q wave myocardial infarction” along with very informative discussion by Lt Col JS Duggal et al. Some important aspects though need to be highlighted. 1. Patients presenting with non-Q wave Myocardial Infarction (NQWMI) have a long term outcome, which is similar to that with a Q wave MI (QWMI), including the subset of patients who undergo coronary revascularisation (Fig 1). Thus, there has been extensive use of coronary arteriography (CAG) and revascularisation following NQWMI in an attempt to reduce subsequent morbidity and mortality. Fig. 1 The outcome alter angioplasty for recurrent ischemia after a Q wave or non-Q wave myocardial infarction is similar. Angioplasty was performed because of recurrent ischemia after a Q wave myocardial infarction (175 patients) or a non-Q wave infarction ... 2. Patients with mechanical complications, recurrent angina, electrical instability or congestive heart failure following NQWMI, have a very high risk of reinfarction and death. As a result, CAG followed by revascularisation is used extensively in these patients with complicated NQWMI. In uncomplicated NQWMI cases, routine CAG followed by PTCA of the culprit lesion performed days to weeks after acute NQWMI has become a standard practice at many centres. Only one trial, VANQWISH trial [1], which compared early and late coronary interventions in patients with NQWMI only, reveals that there is no evidence of benefit from an early invasive strategy in patients with uncomplicated NQWMI (Fig 2). Patients who do not have left ventricular (LV) dysfunction or inducible ischemia are at low risk of recurrent events and may well be harmed by unnecessary invasive procedures (Fig 3). Fig. 2 Conservative therapy is better after NQWMI Kaplan-Meier analysis demonstrates that, for patients with a non-Q wave myocardial infarction (NQWMI), a conservative strategy (catheterization and revascularization only for evidence of ischemia) results in ... Fig. 3 A conservatice management approach is effective for a non-Q wave myocardial infarction. Two studies have compared a conservative approach (medical therapy with catheterization and reascularization when clinically indicated) with an invasive approach (catheterization ... 3. Thus recommended approach to CAG and revascularization in patients of NQWMI based on those published by the ACC/AHA task force on practice guidelines (committee on coronary arteriography) [2] is as follows: Patients with cardiogenic shock should undergo immediate coronary angiography followed by PTCA or CABG if anatomy is suitable. Patients with mechanical complications, recurrent angina, electrical instability or CHF following NQWMI should also undergo prompt CAG followed by PTCA or CABG based upon anatomical considerations. Patients with uncomplicated NQWMI should have a non-invasive assessment of LV function and a physiologic evaluation for ischemia prior to discharge. Those with significant LV dysfunction or evidence of inducible ischemia should undergo CAG followed by revascularisation based upon anatomic considerations. There is no apparent benefit from an early invasive approach. The remaining patients are at low risk for recurrent events and should be treated medically. 4. As per recent ACC/AHA guidelines for treatment of patients with NQWMI, Diltiazem is recommended in patients only if there is no LV dysfunction or pulmonary congestion [2]. Also, short-term therapy with ACE inhibitors appears to be beneficial in NQWMI patients with anterior infarction and long-term treatment appears to be effective in those with reduced LV function [3]. 5. Stents in acute MI have come a long way. A large number of case reports and small series support a potential role for intra-coronary stents for acute Ml with success rate reported from 81 to 98%. Although primary stenting improves the short-term outcome of patients, long-term data are sparse. The American College of Cardiology experts consensus documents state that stenting is a promising approach to optimize the results of primary angioplasty for acute Ml and to treat complications [4]. Whether stenting should be used only to treat sub-optimal results or should be recommended as a primary therapy, is still uncertain.

Early angiography versus conservative treatment in patients with non–ST elevation acute myocardial infarction

OBJECTIVESTo compare short- and long-term outcome after early invasive or conservative strategies in the treatment of non-ST segment elevation acute myocardial infarction (AMI).BACKGROUNDIt is uncertain whether or not there is benefit from emergent invasive diagnosis and treatment of AMI in patients without ST segment elevation on the admission electrocardiogram (ECG).METHODSIn a cohort of 1,635 consecutive patients with AMI who presented to hospitals without ST segment elevation on their admission ECG, we compared treatments, hospital course and outcome in 308 patients who presented to hospitals whose initial strategy favored early angiography and appropriate intervention when indicated versus 1,327 similar patients who presented to hospitals that favor a more conservative initial approach.RESULTSAt baseline, patients admitted to hospitals favoring an early invasive strategy were younger, more predominately Caucasian and had less comorbidity. Early coronary angiography occurred in 58.8% versus 8% (p < 0.001), and early angioplasty was performed in 44.8% versus 6.1% (p < 0.001) in the two different cohorts. Patients treated in hospitals favoring the early invasive strategy had a lower 30-day (5.5% vs. 9.5%, p = 0.026) and four-year mortality (20% vs. 37%, p < 0.001). Multivariate analysis showed a trend towards lower hospital mortality (OR = 0.56, 95% CI: 0.29 to 1.09) and a significant lower long-term mortality (hazard ratio = 0.61, 95% CI: 0.47 to 0.80) in patients admitted to hospitals favoring an early invasive strategy.CONCLUSIONSThese data suggested that an early invasive strategy in patients with AMI and nondiagnostic ECG changes is associated with lower long-term mortality.