PubMed Health⌕ Search

Biomedical subjects

C B Granger

Publications and source records attributed to C B Granger.

At least 91 records · Page 5Linked to original sources
PubMed1998

Myonecrosis after revascularization procedures.

The detection of elevated cardiac enzyme levels and the occurrence of electrocardiographic (ECG) abnormalities after revascularization procedures have been the subject of recent controversy. This report represents an effort to achieve a consensus among a group of researchers with data on this subject. Creatine kinase (CK) or CK-MB isoenzyme (CK-MB) elevations occur in 5% to 30% of patients after a percutaneous intervention and commonly during coronary artery bypass graft surgery (CABG). Although Q wave formation is rare, other ECG changes are common. The rate of detection is highly dependent on the intensity of enzyme and ECG measurement. Because most events occur without the development of a Q wave, the ECG will not definitively diagnose them; even the ECG criteria for Q wave formation signifying an important clinical event have been variable. At least 10 studies evaluating > 10,000 patients undergoing percutaneous intervention have demonstrated that elevation of CK or CK-MB is associated not only with a higher mortality, but also with a higher risk of subsequent cardiac events and higher cost. Efforts to identify a specific cutoff value below which the prognosis is not impaired have not been successful. Rather, the risk of adverse outcomes increases with any elevation of CK or CK-MB and increases further in proportion to the level of intervention. This information complements similar previous data on CABG. Obtaining preprocedural and postprocedural ECGs and measurement of serial cardiac enzymes after revascularization are recommended. Patients with enzyme levels elevated more than threefold above the upper limit of normal or with ECG changes diagnostic for Q wave myocardial infarction (MI) should be treated as patients with an MI. Patients with more modest elevations should be observed carefully. Clinical trials should ensure systematic evaluation for myocardial necrosis, with attention paid to multivariable analysis of risk factors for poor long-term outcome, to determine the extent to which enzyme elevation is an independent risk factor after considering clinical history, coronary anatomy, left ventricular function and clinical evidence of ischemia. In addition, tracking of enzyme levels in clinical trials is needed to determine whether interventions that reduce periprocedural enzyme elevation also improve mortality.

Angioplasty, Balloon, Coronary↗
PubMed1998

Randomized comparison of direct thrombin inhibition versus heparin in conjunction with fibrinolytic therapy for acute myocardial infarction: results from the GUSTO-IIb Trial. Global Use of Strategies to Open Occluded Coronary Arteries in Acute Coronary Syndromes (GUSTO-IIb) Investigators.

OBJECTIVES: We sought to show that hirudin might interact differently with streptokinase (SK) and tissue-type plasminogen activator (t-PA), which could reduce the incidence of death or reinfarction at 30 days. BACKGROUND: In a large-scale trial of patients with acute coronary syndromes, hirudin provided modest benefit compared with heparin. However, the interaction with thrombolytic agents was not specifically assessed. METHODS: Patients with symptoms of acute myocardial infarction and electrocardiographic ST segment elevation were treated with thrombolytic therapy and randomly assigned to receive hirudin or heparin. RESULTS: A total of 2,274 patients received t-PA, and 1,015 received SK. Baseline characteristics were balanced by antithrombin assignment. Among SK-treated patients, death or reinfarction at 30 days occurred more often in those treated with adjunctive heparin (14.4%) rather than hirudin (8.6%, odds ratio [OR] 1.78, 95% confidence interval [CI] 1.20 to 2.66, p = 0.004). Among t-PA-treated patients, the rates were 10.9% with heparin and 10.3% with hirudin (OR 1.06, 95% CI 0.81 to 1.38, p = 0.68; for treatment heterogeneity: chi-square 4.20, degrees of freedom [df] 1, p = 0.04). After adjustment for baseline differences between thrombolytic groups, the rates were 9.1% for SK with hirudin, 10.3% for t-PA with hirudin, 10.5% for t-PA with heparin and 14.9% for SK with heparin (for treatment heterogeneity: chi-square 4.5, df 1, p = 0.03), suggesting that the beneficial treatment effect of hirudin was limited to the SK-treated patients. CONCLUSIONS: Hirudin interacts favorably with SK but not t-PA, highlighting the importance of thrombin activity after SK therapy and the potential for simulating the effects of a more potent fibrinolytic agent through direct antithrombin therapy.

Aged↗
PubMed1998

Atenolol use and clinical outcomes after thrombolysis for acute myocardial infarction: the GUSTO-I experience. Global Utilization of Streptokinase and TPA (alteplase) for Occluded Coronary Arteries.

OBJECTIVES: We assessed the use and effects of acute intravenous and later oral atenolol treatment in a prospectively planned post hoc analysis of the GUSTO-I dataset. BACKGROUND: Early intravenous beta blockade is generally recommended after myocardial infarction, especially for patients with tachycardia and/or hypertension and those without heart failure. METHODS: Besides one of four thrombolytic strategies, patients without hypotension, bradycardia or signs of heart failure were to receive atenolol 5 mg intravenously as soon as possible, another 5 mg intravenously 10 min later and 50 to 100 mg orally daily during hospitalization. We compared the 30-day mortality of patients given no atenolol (n=10,073), any atenolol (n=30,771), any intravenous atenolol (n=18,200), only oral atenolol (n=12,545) and both intravenous and oral drug (n=16,406), after controlling for baseline differences and for early deaths (before oral atenolol could be given). RESULTS: Patients given any atenolol had a lower baseline risk than those not given atenolol. Adjusted 30-day mortality was significantly lower in atenolol-treated patients, but patients treated with intravenous and oral atenolol treatment vs. oral treatment alone were more likely to die (odds ratio, 1.3; 95% confidence interval, 1.0 to 1.5; p=0.02). Subgroups had similar rates of stroke, intracranial hemorrhage and reinfarction, but intravenous atenolol use was associated with more heart failure, shock, recurrent ischemia and pacemaker use than oral atenolol use. CONCLUSIONS: Although atenolol appears to improve outcomes after thrombolysis for myocardial infarction, early intravenous atenolol seems of limited value. The best approach for most patients may be to begin oral atenolol once stable.

Administration, Oral↗
PubMed1998

Potential impact of evidence-based medicine in acute coronary syndromes: insights from GUSTO-IIb. Global Use of Strategies to Open Occluded Arteries in Acute Coronary Syndromes trial.

OBJECTIVES: The purpose of this study to determine whether use of cardiac medications reflects evidence-based recommendations for patients with non-ST elevation acute coronary syndromes. BACKGROUND: Agency for Health Care Policy and Research practice guidelines for unstable angina recommend the use of cardiac medications based on evidence from randomized trials. It is unknown whether practitioners in the U.S., Canada and Europe follow these recommendations in patients with non-ST elevation acute coronary syndromes. METHODS: We studied 7,743 patients with non-ST elevation acute coronary syndromes enrolled in the international Global Use of Strategies to Open Occluded Arteries in Acute Coronary Syndromes trial. The use of aspirin, beta-adrenergic blocking agents, angiotensin-converting enzyme inhibitors and calcium channel blocking agents was determined at discharge for all patients and "ideal" patients (those with indications and no contraindications). Using published estimates of relative mortality reductions with these drugs, we calculated the lives that could have been saved at 1 year if discharge medication use had better matched guideline recommendations. RESULTS: Overall, guideline adherence at discharge in "ideal" patients was 85.6% for aspirin, 59.1% for beta-blockers and 51.7% for angiotensin-converting enzyme inhibitors. Calcium channel blockers were given to 26.7% of patients with a contraindication to these drugs. These rates were similar across locations of enrollment. Women and older patients less often received aspirin when "ideal," and younger patients more often received calcium channel blockers when they were contraindicated. If medication use had been more evidence-based, 1-year mortality might have been reduced by a relative 22%. CONCLUSIONS: There is significant room for improvement in the use of recommended drugs in patients with non-ST elevation acute coronary syndromes. Medication use that more closely follows recommendations could reduce mortality in this population.

Adrenergic beta-Antagonists↗
PubMed1998

Relation between inhibition of platelet aggregation and clinical outcomes.

Despite a clinical trials experience in excess of 30,000 randomized patients, there is no definitive answer or agreement as to the relation between the level of inhibition of platelet aggregation and clinical outcome. Work with abciximab in the setting of percutaneous intervention would suggest that a level of platelet inhibition in excess of 80% provides the most favorable clinical benefit. Whether this applies to the small molecule inhibitors such as eptifibatide, tirofiban, and lamifiban is unknown and will require testing of the hypothesis in large-scale clinical trials. In the acute coronary syndromes, only the peptide and nonpeptide inhibitors have been studied independent of a need for percutaneous intervention. The level of platelet inhibition required to achieve maximal clinical benefit is unknown and awaits data from the large-scale unstable angina and myocardial infarction trials. Issues of combining heparin with GP IIb/IIIa inhibition and the platelet-altering effects of thrombolysis must be considered when examining what might be the optimal level of platelet inhibition that provides maximal efficacy while maintaining safety. Long-term therapy with the oral platelet inhibitors poses a particular challenge in determining an optimal level of treatment that renders clinical effectiveness while preserving safety. Large, ongoing clinical trials with these agents should provide insight into this question. Finally, given the complexity of using such potent therapies in any individual patient, there is a need for improved monitoring of the platelet inhibitory effect. Standard platelet aggregometry has its problems and limitations, as described, and is not a test that has wide-scale applicability. Whole blood aggregometry and other methods of rapidly assessing platelet function at the point of care have promise in this arena. In a clinical trial, such technology might allow better delineation of the population's pharmacodynamic response to an agent because it could be more widely applied and therefore more patients would be studied. In clinical practice, patients could be dosed individually so that a range of platelet inhibition could be achieved that was believed to provide optimal benefit and safety.

Biomarkers↗
PubMed1998

Heparin management in acute myocardial infarction (AMI).

Antithrombotic agents have been shown to be beneficial in the setting of acute coronary syndromes, and as an adjunct to thrombolysis for acute myocardial infarction (AMI). The optimal type and dosing of antithrombotic drug, however, remains elusive. Heparin, the agent most commonly used, has several limitations, the most important of which may be its inability to inhibit clot-bound thrombin. Newer, direct thrombin inhibitors (such as hirudin) provide potent and predictable thrombin inhibition and are able to inhibit clot-bound thrombin. Both heparin and hirudin can carry a substantial risk of haemorrhage, however, and thrombin activity is likely to rebound after discontinuation of either agent. Further, the relationships of antithrombotic/thrombolytic dosing, measures of anticoagulation (such as APTT), and clinical outcomes are not always clear. Nonetheless, from the data available from large, randomised trials, intravenous heparin should remain a standard adjunct to thrombolytic therapy for AMI.

Fibrinolytic Agents↗
PubMed1998

Thrombolysis-related intracranial hemorrhage: a radiographic analysis of 244 cases from the GUSTO-1 trial with clinical correlation. Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries.

BACKGROUND AND PURPOSE: Intracranial hemorrhage (ICH) is a serious complication of thrombolytic therapy. We systematically reviewed the radiographic features of 244 cases of symptomatic ICH complicating thrombolysis for acute myocardial infarction in the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO-1) trial, correlated these observations with clinical data, and speculated on hemorrhage pathogenesis. METHODS: CT scans from 244 patients suffering symptomatic ICH were systematically reviewed for selected radiographic features, including ICH type, location, hematoma characteristics, mass effect features, hydrocephalus, and preexisting lesions. Hematoma volume was estimated by computer-assisted volumetric analysis. Data from this analysis were correlated with clinical data including hypertension, anticoagulation, age, thrombolytic regimen, and ICH timing. RESULTS: Most hemorrhages were large (median [25th, 75th percentile] volume, 72 mL [39, 118]), solitary (66%), lobar (77%), confluent (80%), and intraparenchymal (82%) with a blood/fluid level (82%) and little edema (median [25th, 75th percentile] volume, 9 mL [5, 16]). Hydrocephalus (P<.001), any one mass effect feature (P<.001), intraventricular hemorrhage (P=.022), mottled hematoma appearance (P=.050), and hematoma blood/fluid level (P<.001) were associated with higher hemorrhage volume in the radiographic analysis, as were older age (P=.005), treatment with combined streptokinase and tissue plasminogen activator (P=.034), and hemorrhage onset 8 to 13 hours after treatment (P=.008) in the clinical analysis. Subdural hemorrhage was a high-volume subgroup whose risk increased with antecedent trauma (P=.026) or syncope (P=.006). Deep intraparenchymal hemorrhage was associated with hypertension (P=.016), and multifocal ICH occurred significantly earlier after treatment (P=.002). CONCLUSIONS: Although the majority of postthrombolytic ICH are large, solitary, and supratentorial, the spectrum is diverse. Features of mass effect reflected the large volumes, and hematoma characteristics of mottling and blood/fluid levels were frequent. Thrombolysis-related coagulopathy and age appear to be the most important identifiable factors in the genesis of postthrombolytic ICH, but the hemorrhage subtype seen may reflect an interaction with other factors such as hypertension, ICH timing, antecedent head trauma, and syncope.

Cerebral Hemorrhage↗
PubMed1998

Comparison of the ABC/2 estimation technique to computer-assisted volumetric analysis of intraparenchymal and subdural hematomas complicating the GUSTO-1 trial.

BACKGROUND AND PURPOSE: The volume of an intracerebral hemorrhage has been shown to be an important independent predictor of mortality in several reports. A technique for estimating hematoma volume, known as the ABC/2 method, has been proven a reliable, simple bedside technique for the volume measurement of intraparenchymal intracerebral hemorrhage. Subdural hematomas also carry a significant mortality risk but are more amenable to surgical evacuation. A reliable, simple bedside measurement of subdural hematoma volume may prove a valuable tool in prognostication and management of patients with this entity. METHODS: Computed tomographic (CT) brain scans of 244 patients suffering from intracranial hemorrhage in the GUSTO-1 trial were systematically reviewed. The volumes of 298 intraparenchymal hematomas were measured by the ABC/2 technique, and the volumes of 44 subdural hematomas were measured by an adaptation of this technique and compared to computer-assisted volumetric analysis. RESULTS: Excellent correlation between the techniques were achieved for both subdural (r=0.842; slope, 0.982) and intraparenchymal hematoma volume measurements (r=0.929; slope, 1.11). CONCLUSIONS: The ABC/2 method is a simple and accurate technique for the measurement of intraparenchymal hematoma volume, and a simple adaptation allows for a similarly accurate measurement of subdural hematoma volume as well.

Clinical Trials as Topic↗
PubMed1998

Converting i.v. nitroglycerin therapy to nitroglycerin ointment therapy: a comparison of two methods.

BACKGROUND: Methods of converting treatment with i.v. nitroglycerin to treatment with nitroglycerin ointment 2% vary greatly and may affect the length of time patients remain in the ICU, nursing time, and possible recurrent angina. To date, no randomized, controlled studies have evaluated the methods used for conversion. OBJECTIVE: To evaluate two methods of conversion. METHODS: Two hundred patients receiving i.v. nitroglycerin at doses of 10 to 100 micrograms/min were randomized to two methods of conversion: (1) Apply nitroglycerin ointment and stop i.v. nitroglycerin 30 minutes later. (2) Decrease the dose of i.v. nitroglycerin by 10 micrograms/min every 15 minutes, apply one half the dose of nitroglycerin ointment when the original i.v. dose has been decreased by one half, and apply the full dose of the ointment when the i.v. nitroglycerin is stopped. The primary end point was the time patients remained in the ICU after the conversion. Secondary end points included time to hospital discharge, estimate of nursing time, and selected clinical end points. Kaplan-Meier and Cox regression analyses were used to evaluate time patients remained in the ICU and nursing time. Clinical outcomes were analyzed by using a chi-square test. RESULTS: Use of the first method reduced median time before transfer from the ICU by 23 minutes and median nursing time by 45 minutes. Analysis of all clinical outcomes showed no differences between the two methods. CONCLUSIONS: Use of the first method was associated with a reduction in the time patients remained in the ICU before transfer to another unit and savings in nursing time, but the two methods did not differ according to clinical outcomes.

Administration, Cutaneous↗
PubMed1998

Cardiac troponin T and cardiac troponin I: relative values in short-term risk stratification of patients with acute coronary syndromes. GUSTO-IIa Investigators.

We compared cardiac troponins T (cTnT) and I (cTnI) collected within 3.5 h of ischemic symptoms for predicting clinical outcomes in 770 patients. cTnT (cutoff > 0.1 microgram/L) and cTnI (cutoff > 1.5 micrograms/L) were concordant (both positive or negative) in 90.4% of patients. Among discordant results, 66 were cTnT positive and cTnI negative vs 8 who showed the reverse (P < 0.001). Five cTnT-positive and cTnI-negative patients died within 30 days; none who were cTnT negative and cTnI positive died. cTnT showed a slightly greater association (chi 2 = 18.0, P < 0.001) with 30-day mortality than cTnI (chi 2 = 12.5, P = 0.002). The area of the ROC curve for predicting 30-day mortality was significantly larger (Z = 2.08; P = 0.0375) for cTnT, at 0.68 [95% confidence interval (CI) 0.60-0.75], compared with cTnI, at 0.64 (95% CI 0.56-0.72). When cTnI and the electrocardiogram (ECG) were put in a logistic multiple regression model, cTnT added significant information (chi 2 = 8.03, P = 0.045); however, cTnI did not add to a model containing cTnT and the ECG (chi 2 = 0.84, P = 0.657). cTnT provided more information than cTnI for predicting 30-day mortality early after presentation with acute coronary syndromes.

Aged↗
PubMed1997

End-systolic volume index at 90 to 180 minutes into reperfusion therapy for acute myocardial infarction is a strong predictor of early and late mortality. The Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO)-I Angiographic Investigators.

BACKGROUND: Left ventricular remodeling is an important sequela of myocardial infarction (MI). Although remodeling occurs soon after MI, the effect of early left ventricular dilatation on outcome is not established and may be useful for early risk stratification. We assessed whether end-systolic volume index (ESVI) at 90 to 180 minutes into thrombolytic therapy for MI is associated with adverse outcomes. METHODS AND RESULTS: In the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO)-I study, 41021 patients with evolving MI received one of four thrombolytic regimens. At 90 or 180 minutes into reperfusion therapy, 1300 patients underwent left ventriculography. ESVI was measured and correlated with adverse outcomes: 30-day and 1-year mortality and in-hospital congestive heart failure, shock, and reinfarction. Clinical variables were also tested in a stepwise logistic regression analysis to determine predictors of left ventricular dilatation. ESVI was directly related to all adverse outcomes with univariate analysis. ESVI of > or = 40 mL/m2 was independently associated with mortality (adjusted odds ratio [95% confidence interval]: 30-day, 3.4 [2.0 to 5.9]; 1-year, 4:1 [2.6 to 6.2], both P < .001). Male sex, prior angina or MI, weight of < 70 kg, heart rate of > or = 80 bpm, systolic blood pressure of < 110 mm.Hg, and anterior infarction were independent predictors of an ESVI of > or = 40 mL/m2. CONCLUSIONS: Left ventricular ESVI early into reperfusion therapy for MI strongly predicts adverse outcomes, including early and late mortality. The study establishes the role of very early left ventricular dilatation on outcome in MI and may be useful in identifying high-risk patients who might benefit from aggressive treatment, including the early use of ACE inhibitors.

Aged↗
PubMed1997

Adenosine for myocardial protection in acute myocardial infarction.

Although reperfusion therapy for acute myocardial infarction is known to reduce infarct size, improve left ventricular function, and reduce mortality, the full potential benefit may be limited by acceleration of damage resulting from reperfusion, or "reperfusion injury." Evidence of a variety of mechanisms of reperfusion injury has led to a wide range of proposed therapeutic interventions, including agents to prevent oxygen free radical damage, inhibit white blood cell function, reduce calcium influx, improve microvascular blood flow, inhibit sympathetic stimulation, and improve energy stores. A multitude of agents have been shown to limit infarct size in animals when administered before or during reperfusion. Unfortunately, most have been disappointing when tested clinically. Adenosine, a theoretically attractive agent for preventing reperfusion injury, has shown promise in small, clinical studies, and appears to be an endogenous substance involved in the protective effect of ischemic preconditioning. When studied in the setting of angioplasty for acute myocardial infarction, adenosine was associated with small infarct size and improved coronary flow. As myocardial preservation with reperfusion during bypass surgery shares pathophysiologic characteristics with the reperfused myocardium in acute infarction, early results of adenosine during bypass surgery presented at this symposium support the concept that adenosine may be beneficial. Two ongoing Phase II trials of adenosine in acute myocardial infarction-one with thrombolysis and one with direct angioplasty-will provide important information about the potential benefits of adenosine in the context of reperfusion.

Adenosine↗
PubMed1997

Incidence and predictors of bleeding after contemporary thrombolytic therapy for myocardial infarction. The Global Utilization of Streptokinase and Tissue Plasminogen activator for Occluded coronary arteries (GUSTO) I Investigators.

BACKGROUND: Although the benefit of thrombolytic therapy in reducing mortality in acute myocardial infarction is well established, the types of bleeding and risk factors for bleeding are less well described in large trials. METHODS AND RESULTS: We analyzed the baseline characteristics, outcomes, and incidence of bleeding by location, severity, and treatment assignment among 41,021 patients in the GUSTO-I trial of thrombolysis for acute myocardial infarction. Of the 40,903 patients for whom there were complete data, 1.2% suffered severe bleeding and 11.4% experienced moderate hemorrhage at a variety of sites. The most common sources of bleeding were procedure related. The thrombolytic regimen was strongly related to the incidence of bleeding; comparatively more bleeding was seen with the therapies of streptokinase plus intravenous heparin and the streptokinase and tissue plasminogen activator plus intravenous heparin combination. In multivariate analysis, the four most powerful independent predictors of hemorrhage were older age, lighter body weight, female sex, and African ancestry; they remained the most important predictors of bleeding when multivariate analysis was performed on patients who did not undergo invasive procedures. The presence of serious hemorrhage was associated with other undesirable outcomes (recurrent events, left ventricular dysfunction, arrhythmia, or stroke). CONCLUSIONS: Important predictors of bleeding in this population are increased age, lighter weight, female sex, African ancestry, and experiencing invasive procedures. Other nonhemorrhagic adverse clinical outcomes were associated with moderate and severe bleeding, which was in turn associated with increased length of hospital stay and mortality at 30 days.

Age Factors↗
PubMed1997

Thrombolysis and Q wave versus non-Q wave first acute myocardial infarction: a GUSTO-I substudy. Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Arteries Investigators.

OBJECTIVES: We assessed the outcomes of patients with a first myocardial infarction with ST segment elevation, with and without the development of abnormal Q waves after thrombolysis. BACKGROUND: Prethrombolytic era studies report conflicting short-versus long-term mortality in the overall non-Q wave population, probably related to its heterogeneity. METHODS: Patients with no electrocardiographic (ECG) confounding factors or evidence of previous infarction were included. Q wave infarction was defined as a Q wave duration > or = 30 ms in lead aVF; R wave > or = 40 ms in lead V1; any Q wave or R wave < or = 10 ms and < or = 0.1 mV in lead V2; or Q wave > or = 40 ms in at least two of the following leads: I, aVL, V4, V5 or V6. In-hospital clinical events and mortality at 30 days and 1 year were assessed. RESULTS: No Q waves developed in 4,601 (21.3%) of the 21,570 patients. This group comprised more women and had a lower Killip class, lower weight and less anterior baseline ST elevation. The non-Q wave group had less in-hospital cardiogenic shock (2.1% vs. 3.3%, p < 0.0001), less heart failure (8.5% vs. 13.9%, p < 0.0001) and a trend toward less stroke (0.7% vs. 1.0%, p = 0.07) but an increased use of angioplasty (28% vs. 24%, p = 0.0001). The unadjusted mortality rate in the non-Q wave group was lower at 30 days (0.9% vs. 1.8%, p = 0.0001) and 1 year (2.7% vs. 4.2%, p = 0.0001), as was the adjusted 30-day mortality rate (4.8% vs. 5.3%, p < 0.0001). CONCLUSIONS: Patients with no ECG confounding factors or evidence of previous infarction who do not develop Q waves after thrombolysis have a better 30-day and 1-year prognosis than patients with a Q wave infarction.

Aged↗
PubMed1997

TIMI grade 3 flow and reocclusion after intravenous thrombolytic therapy: a pooled analysis.

Early and sustained flow of grade 3 according to Thrombolysis in Myocardial infarction (TIMI) criteria and reocclusion rates are the key measures that define the physiologic efficacy of thrombolytic agents in the treatment of acute myocardial infarction. We performed a systematic overview of angiographic studies after intravenous thrombolysis with accelerated and standard-dose tissue-plasminogen activator (TPA), anisoylated plasminogen streptokinase activator complex (APSAC), and streptokinase. There were 5475 angiographic observations from 15 studies for TIMI flow analysis and 3147 angiographic observations from 27 studies for reocclusion. At 60 and 90 minutes, the rates of TIMI grade 3 flow were 57.1% and 63.2%, respectively, with accelerated TPA, 39.5% and 50.2% with standard-dose TPA, 40.2% and 50.1% with APSAC, and 31.5% at 90 minutes with streptokinase. Overall reocclusion with standard-dose TPA was 11.8% versus 6.0% for accelerated TPA, 4.2% for streptokinase, and 3.0% for APSAC. Although the incidence of TIMI grade 3 flow increased over time with all thrombolytic regimens, decreased patency was observed at 180 minutes with accelerated TPA. Still, accelerated TPA is the most effective agent to establish early (90-minute) TIMI grade 3 flow.

Anistreplase↗
PubMed1997

Influence of diabetes mellitus on clinical outcome in the thrombolytic era of acute myocardial infarction. GUSTO-I Investigators. Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries.

OBJECTIVES: This study was undertaken to define and better understand the characteristics and outcomes of patients with diabetes treated for acute myocardial infarction with contemporary thrombolysis. BACKGROUND: Although thrombolysis has substantially improved survival of patients with myocardial infarction, diabetes mellitus remains an independent predictor for a poor prognosis. METHODS: We characterized the contemporary relation between diabetes and outcome after myocardial infarction treated with thrombolytic agents from a large international cohort. Of 41,021 patients randomized to receive accelerated tissue-type plasminogen activator (t-PA), streptokinase or a combination of both agents in the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries study, there were 5,944 patients with diabetes and 34,888 patients without diabetes. RESULTS: Patients with diabetes were older and more likely to be female, to present with anterior wall infarction, to receive thrombolysis later and to have triple-vessel coronary artery disease. Mortality at 30 days was highest among diabetic patients treated with insulin (12.5%) compared with non-insulin-treated diabetic (9.7%) and nondiabetic (6.2%) patients (p < 0.001). Mortality was lowest among those with diabetes receiving accelerated t-PA, which is consistent with the results of the overall patient cohort. Although stroke occurred more frequently among diabetic (1.9%) than nondiabetic patients (1.4%, p < 0.001), there was no significant difference in the rates of intracranial hemorrhage. Cardiac failure, shock, atrioventricular block and atrial flutter/ fibrillation were more common among diabetic patients. The proportion of patients undergoing revascularization was similar between patients with and without diabetes, although diabetic patients were more likely to undergo coronary artery bypass graft surgery (10.4% vs. 8.3%). Diabetes remained an independent predictor for mortality at 1-year follow-up (14.5% vs. 8.9%, p < 0.001). CONCLUSIONS: Diabetes, alone and in association with its comorbidities, portends a substantially worse 30-day and 1-year prognosis for patients with myocardial infarction.

Aged↗