How should a patient presenting with unstable angina and a recent stroke be managed?
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Angina, Unstable↗
Biomedical subjects
E M Ohman
Publications and source records attributed to E M Ohman.
Significance of a coronary artery with thrombolysis in myocardial infarction grade 2 flow "patency" (outcome in the thrombolysis and angioplasty in myocardial infarction trials). Thrombolysis and Angioplasty in Myocardial Infarction Study Group.
To determine whether pharmacologic reperfusion to Thrombolysis in Myocardial Infarction (TIMI) grade 2 flow during acute myocardial infarction confers the same clinical benefit as restoration of TIMI 3 flow, in-hospital clinical and angiographic outcomes in 1,229 patients prospectively enrolled in the Thrombolysis and Angioplasty in Myocardial Infarction trials were analyzed. Patients were treated with intravenous tissue plasminogen activator or urokinase, or both. Angiography of the infarct-related artery 90 minutes after initiation of thrombolytic therapy demonstrated TIMI grades 0, 1, 2, or 3 flow in 20%, 7%, 17%, and 55% of vessels, respectively. Rescue or adjunctive coronary angioplasty was performed in 80%, 27%, and 16% of patients with TIMI 0/1, 2, or 3 flow, respectively. Predischarge angiography was performed in 963 patients. A significant gradient of increasing mortality was seen in patients with lower TIMI flow (4.3%, 6.1%, and 10.1% with TIMI 3, 2, and 0/1 flow, respectively, p = 0.002). The incidence of congestive heart failure and recurrent ischemia was significantly higher in patients with TIMI 2 than with TIMI 3 perfusion (26% vs 19% for heart failure, p = 0.03; 23% vs 17% for recurrent ischemia, p = 0.05). Acute left ventricular ejection fraction and infarct zone regional wall motion were also significantly improved in patients with TIMI 3 than with TIMI 2 flow, with trends toward better improvement in global and regional function in the TIMI 3 group. These findings were not affected by the use of acute coronary angioplasty.(ABSTRACT TRUNCATED AT 250 WORDS)
Angioplasty, Balloon, Coronary↗
Rebound increase in thrombin generation and activity after cessation of intravenous heparin in patients with acute coronary syndromes.
BACKGROUND: The abrupt cessation of heparin and other thrombin inhibitors when used to treat acute coronary syndromes has been accompanied by a clustering of thrombotic events. It is unknown whether these events are the result of inadequate antithrombin therapy or whether they represent a rebound increase in thrombin activity. This study was designed to determine whether there is a true rebound, as defined by an increase followed by a subsequent decrease, in thrombin activity after discontinuation of intravenous heparin therapy. METHODS AND RESULTS: Thirty-five patients with recent acute myocardial infarction or unstable angina who had received at least 48 hours of intravenous heparin were studied. Patients underwent ST-segment monitoring, and blood samples for determination of thrombin generation and activity were drawn at 0, 3, 6, 10, and 24 hours after heparin discontinuation. Median aPTT was 65 seconds before heparin discontinuation. Median fibrinopeptide A increased from 9.5 to 16.9 ng/mL at 3 hours (P < .0004) and returned to 10.5 by 24 hours. Prothrombin fragment 1.2 likewise transiently increased, from 0.34 to 0.51 nmol/L at 6 hours (P < .0002). Modified antithrombin III decreased over time (P < .002), and activated protein C increased from 2.3 to 4.5 ng/mL at 3 hours (P < .001). Although there were no clinical thrombotic events in the first 24 hours, 4 patients had evidence of ischemia by ST-segment monitoring at a median of 12 hours after heparin discontinuation. The degree of increase in fibrinopeptide A and prothrombin fragment 1.2 was not found to be associated with baseline diagnosis, duration of heparin therapy, baseline level of antithrombin III, or activated protein C. CONCLUSIONS: This study demonstrates a transient rebound increase in thrombin activity as well as in activated protein C upon abrupt discontinuation of intravenous heparin. Clinicians should be vigilant for associated thrombotic events. Further investigation of the significance, mechanism, and possible prevention of this rebound phenomenon is needed.
Aged↗
[Serum myoglobin as a non-invasive marker of coronary reperfusion after intravenous thrombolytic therapy in patients with acute myocardial infarction].
Non-invasive methods for evaluation of intravenous thrombolytic treatment in patients with acute myocardial infarction (AMI) are needed, since approximately 30% of the patients never obtain coronary reperfusion. These patients could be candidates for additional thrombolytic treatment or acute PTCA. This study included 63 AMI patients. Intravenous and/or intracoronary thrombolysis was given to 52 patients, and 11 patients received conservative treatment (placebo). Serum myoglobin was measured every 15 min. Acute coronary angiography showed a patent coronary artery in 49 patients ("Reperfusion" group), and 14 patients had no coronary reperfusion ("No-Reperfusion" group). Mean time to peak serum myoglobin was 149 (57-194) minutes in the "Reperfusion" group and 476 (330-660) minutes in the "No-Reperfusion" group, p < 0.0001. An observed peak serum myoglobin < 5 hrs. after initiation of intravenous thrombolysis would indicate coronary reperfusion with sensitivity = 0.94; specificity = 0.79; predictive values of positive and negative test: 0.94 and 0.79, respectively. It is concluded that an peak serum myoglobin < five hrs. after start of thrombolysis predicts reperfusion status with a high level of accuracy.
Adult↗
Characteristics and consequences of myocardial infarction after percutaneous coronary intervention: insights from the Coronary Angioplasty Versus Excisional Atherectomy Trial (CAVEAT).
OBJECTIVES: We examined the results of the Coronary Angioplasty Versus Excisional Atherectomy Trial (CAVEAT) to determine the characteristics and consequences of creatine kinase (CK) and creatine kinase, MB myocardial isoenzyme fraction (CK-MB) elevations after percutaneous coronary intervention. BACKGROUND: Enzyme elevations after interventional procedures have usually been thought to be without long-term clinical consequences. However, recent preliminary reports have suggested that there are important long-term clinical sequelae in patients with even mild enzyme elevations after coronary procedures. METHODS: Patients with new native lesions undergoing coronary intervention at 35 clinical sites were randomized to undergo percutaneous coronary angioplasty (n = 500) or directional coronary atherectomy (n = 512). Cardiac enzyme levels were measured 12 and 24 h after the interventional procedure and when clinically indicated for recurrent myocardial ischemia. Enzyme profiles were analyzed using a ratio that compared the peak enzyme level and the local laboratory upper limit of normal. Standard 12-lead electrocardiograms (ECGs) recorded before and after the procedure were interpreted by two independent readers who had no knowledge of the randomization data. Postprocedural myocardial infarction was defined as the appearance of new Q waves on the ECG, CK-MB levels three or more times the upper limit of normal or a total CK concentration two or more times the upper limit of normal when CK-MB levels were unavailable. Regression models were used to evaluate the predictive significance of a postintervention myocardial infarction with respect to clinical outcomes at 30 days and 1 year. RESULTS: There were 78 myocardial infarctions in the atherectomy group and 34 in the angioplasty group (15.2% vs. 6.8%, p = 0.001). Patients with a myocardial infarction more often had a repeat intervention or emergency coronary artery bypass surgery. Hospital length of stay was increased among patients with an infarction, as were mean hospital costs ($17,340.65 vs. $11,308.47, p = 0.0003). Postprocedural myocardial infarction was highly predictive of mortality, bypass surgery or repeat intervention within 30 days (p < 0.0001). CONCLUSIONS: Myocardial infarction occurred commonly after coronary intervention in CAVEAT and was associated with a worse clinical outcome. Although the incidence of myocardial infarction was higher with atherectomy than with angioplasty, the baseline characteristics and consequences of the infarctions were similar between the treatments with regard to 30-day outcome. Myocardial enzyme elevations after an otherwise successful interventional procedure may identify a population at risk for a future cardiac event.
Angioplasty, Balloon, Coronary↗
Early clinical experience with integrelin, an inhibitor of the platelet glycoprotein IIb/IIIa integrin receptor.
Aggregation of platelets leading to thrombosis is one of the hallmarks of unstable angina, acute myocardial infarction, and ischaemic complications following coronary angioplasty. Activated platelets bind to fibrinogen through the glycoprotein IIb/IIIa integrin receptor. New agents have been developed to bind this receptor and thus prevent aggregation of platelets. One such compound (integrelin) is a cyclical peptide that has been shown to be a potent inhibitor of the glycoprotein IIb/IIIa receptor in man. A number of phase I and phase II clinical trials have been completed to evaluate this agent for the indications of unstable angina, acute myocardial infarction, as well as an adjunct to coronary angioplasty. This article will focus on the clinical investigation of integrelin with particular emphasis on its use during angioplasty. It has been consistently shown across different trials that integrelin can inhibit between 70% and 95% of platelet aggregation responses to 20 mumols of ADP at a variety of dosages used in the phase II trials. Preliminaray data also suggest that a more clinically unstable patient may require a higher dose of integrelin to cause a near complete inhibition of the platelet aggregation response to ADP. Future studies will need to explore more definitely the relationship between dose of glycoprotein IIb/IIIa receptor blockers and clinical instability.
Angioplasty, Balloon, Coronary↗
The use of intraaortic balloon counterpulsation in acute myocardial infarction and high risk coronary angioplasty.
Patients with complex coronary arterial stenoses, decreased ejection fraction, or acute myocardial infarction are at increased risk during percutaneous coronary interventions. Intraaortic balloon counterpulsation (IABP) can provide benefit in such cases by several mechanisms. Myocardial perfusion is improved and left ventricular afterload is reduced by balloon counterpulsation. Patients with cardiogenic shock clearly benefit from balloon counterpulsation until revascularization can be performed. Recent studies have documented the utility of balloon counterpulsation in patients undergoing angioplasty as treatment for an acute myocardial infarction. Balloon counterpulsation is also an effective means to reduce ischemia and provide hemodynamic support during complex percutaneous coronary interventions. This review will summarize the benefits, indications, and complications of balloon counterpulsation during acute myocardial infarction and high-risk coronary angioplasty.
Angioplasty, Balloon, Coronary↗
Antithrombotic therapy in patients undergoing coronary angioplasty.
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Angioplasty, Balloon, Coronary↗
Use of the perfusion balloon as a primary dilation device.
The development of more user-friendly and versatile perfusion balloon catheters has increased the use of prolonged dilations as a primary catheter treatment for coronary artery disease. In a multicenter randomized trial, the use of these devices to prolong initial inflation durations resulted in improved angiographic outcomes when compared with conventional short dilations. This benefit was most apparent in stenoses with complex morphology. Use of the perfusion balloon as a primary device is also appealing because of its ability to reduce anginal pain and hemodynamic changes during balloon inflation. Clinical experience suggests that primary use of the perfusion balloon may improve patient stability during procedures in which the treated segment jeopardizes a large percentage of the functional myocardium. An observational series has demonstrated the excellent outcomes which can be achieved in selected patients using a strategy of primary perfusion angioplasty with stent bailout when needed. Selection of a perfusion balloon rather than a conventional balloon as a primary device has the potential to decrease overall balloon usage approximately 25%, but the economic benefit of this strategy will depend on the cost of the perfusion balloon relative to a conventional balloon. Retrospective analyses suggest that perfusion angioplasty as a primary treatment strategy compares favorably with directional atherectomy for left anterior descending lesions. The use of coronary stents has not been directly compared to perfusion angioplasty as a primary treatment for coronary lesions, but use of a perfusion balloon as an initial device may have broader applicability, lower cost and less technical demands on the operator compared to stent deployment. In conclusion, when overall applicability, clinical outcome and cost are considered, the primary strategy of prolonged dilation with a perfusion balloon should have an important role in coronary intervention.
Angioplasty, Balloon, Coronary↗
Perfusion balloon angioplasty in patients with complex coronary lesion morphology.
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Angioplasty, Balloon, Coronary↗
Biochemical markers in suspected acute myocardial infarction: the need for early assessment.
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Biomarkers↗
Creatine kinase MM and MB isoforms in patients receiving thrombolytic therapy and acute angiography. TAMI Study Group.
Creatine kinase isoforms markers, including MB2 concentration, MB2/MB1 and MM3/MM1 ratios, and MT index (based on the "tissue" M subunits), were measured in serial specimens from 207 patients receiving thrombolytic therapy followed by acute angiography. The slope of release showed a significant relation (P < 0.05) between MB2 concentrations and patency, graded as TIMI 0 through TIMI 3; with regard to the precatheterization/baseline ratio, the MB2 concentrations, the MM3/MM1 ratio, and the MT index were all significantly related to graded patency (P < 0.004). Patients having patency graded as either TIMI 2/3 (Open) or TIMI 0/1 (Closed) showed highly significant differences (P < 0.03) in the slope of release and precatheterization/baseline ratio for all markers except the MB2/MB1 ratio. Defining Open as TIMI 3 and Closed as TIMI 0/1/2 showed very similar results. Despite these significant differences between the Open and Closed groups after thrombolytic therapy, none of the C index calculations (areas under ROC curves) for any of the isoform markers--either alone or combined--exceeded 0.70, suggesting that these markers have limited diagnostic utility for assessing patency.
Aged↗
A pooled analysis of coronary arterial patency and left ventricular function after intravenous thrombolysis for acute myocardial infarction.
Individual studies of patency rates and left ventricular (LV) function after thrombolysis have generally been limited by small numbers of observations, wide confidence intervals, and limited numbers of time points. To obtain a more reliable estimate of patterns of patency and LV ejection fraction, a systemic overview of angiographic studies was performed after intravenous thrombolytic therapy. A total of 14,124 angiographic observations from 58 studies evaluating patency after no thrombolytic agent, streptokinase, standard dose tissue-type plasminogen activator (t-PA), accelerated dose t-PA, or anistreplase (anisoylated plasminogen streptokinase activator complex [APSAC]) were included. At 60 and 90 minutes, streptokinase had the lowest patency rates of 48% and 51%, respectively, standard dose t-PA and APSAC had similar intermediate rates of approximately 60% and 70%, and accelerated t-PA had the highest patency rates of 74% and 84%. By 2 to 3 hours and longer, the patency rates were similar for the various regimens. Reocclusion rates in studies including 1,172 patients randomized to t-PA versus a nonfibrin-specific agent were higher after t-PA (13.4% vs 8.0%, p = 0.002). Ten studies enrolling 4,088 patients treated with thrombolytic therapy versus control demonstrated a modest improvement in mean LV ejection fraction in the thrombolytic group at each of the times after thrombolytic therapy: hour 4, day 1, day 4, day 7 to 10, and day 10 to 28 after thrombolysis. By 4 days, mean ejection fraction was 53% versus 47% (thrombolytic vs control therapy, p < 0.01); by 10 to 28 days it was 54.1% and 51.5%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Coronary Disease↗
A meta-analysis of randomized trials of calcium antagonists to reduce restenosis after coronary angioplasty.
The usefulness of calcium antagonists to reduce restenosis after coronary angioplasty remains uncertain despite 5 randomized trials involving 919 patients. Review and meta-analysis of these trials are performed to provide insight into whether calcium antagonists reduce angiographic restenosis. In aggregate, these trials suggest that patients treated with calcium antagonists had approximately a 30% reduction in the odds of angiographic restenosis (odds ratio = 0.68; 95% confidence interval of 0.49 to 0.94, p = 0.03) compared with control patients. Given the relatively low toxicity and cost of these agents, this reduction in angiographic restenosis may translate into a meaningful clinical benefit. A large, randomized clinical trial should be performed to confirm these findings before widespread adoption of this treatment strategy.
Adult↗
Intracranial hemorrhage risk and new thrombolytic therapies in acute myocardial infarction.
Thrombolytic therapy for acute myocardial infarction (AMI) has reduced mortality at the expense of additional intracranial hemorrhages. To determine whether this trade-off has been optimized, a decision analysis was performed using pooled data to determine the further reductions in mortality required to justify increased intracranial hemorrhage rates from more potent thrombolytic and adjunctive antithrombotic regimens that intravenous streptokinase. Pooled data from large clinical trials suggest that streptokinase has a 0.07% nonfatal intracranial hemorrhage rate. Approximately 54% of these result in major/moderate disability and 46% in recovery or minor residual. The early mortality rate in all AMI patients treated with thrombolytic therapy is 9.8%; it is 6.8% in patients with inferior wall AMI and 17.9% in elderly patients. If a new thrombolytic regimen provides a 1% absolute reduction in early mortality compared with streptokinase therapy, approximately a > or = 3.2% nonfatal intracranial hemorrhage rate is justified to obtain this survival benefit. For a 10% relative reduction in mortality risk, the maximal acceptable nonfatal intracranial hemorrhage rates are 2.2% for inferior wall AMI, 3.2% for all patients and 5.9% for elderly patients. Whereas intracranial hemorrhage is a catastrophic complication of thrombolytic therapy in the treatment of patients with AMI, thrombolytic regimens that result in significantly higher rates of intracranial hemorrhage than those observed with streptokinase may be preferable at surprisingly smaller additional reductions in mortality. In addition to evaluating new thrombolytic and antithrombotic regimens, this analysis, in conjunction with models that predict patient-specific intracranial hemorrhage risks and mortality benefits from thrombolytic therapy, can provide a framework for matching AMI patients with optimal thrombolytic regimens.
Aged↗
Impact of infarct artery patency on the relationship between electrocardiographic and ventriculographic evidence of acute myocardial ischaemia.
Routine invasive evaluations are being abandoned, and thus simple non-invasive methods for estimating the extent of jeopardized myocardium during evolving myocardial infarction are needed for risk stratification to guide the appropriate therapeutic intervention. With this in mind the aim of the paper was to evaluate the association between ischaemic changes in the standard electrocardiogram and the function of acutely infarcted myocardium in relation to infarct artery patency status. Forty consecutive patients with a first acute myocardial infarction, admitted within 6 h of symptom onset and without bundle branch or fascicular block were included. Summated ST segment elevation in 11 electrocardiographic leads (aVR excluded) was measured to the nearest 0.05 mV and compared to regional wall motion, estimated by the centreline method (SD/chord) and global left ventricular ejection fraction (% LVEF) after thrombolytic therapy. Acute angiographic and ST segment measurements were performed at a median 254 min (range 70-485) after the onset of symptoms. Patients were grouped according to infarct artery patency status after intravenous thrombolysis. Of the 40 patients, 27 had a patent (Thrombolysis In Acute Myocardial Infarction trial (TIMI) grade 2-3 flow) and 13 had persistently occluded (TIMI 0-1 flow) infarct arteries. Anterior myocardial infarction was present in 13 and seven patients in the two groups. In the TIMI 2-3 group, the summated ST elevation did not correlate with % LVEF or SD/chord (rs = -0.08; and rs = -0.17, respectively). In the TIMI0-1 group the summated ST elevation correlated inversely with both % LVEF and SD/chord (rs = -0.70; and rs = -0.56, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
Angiocardiography↗
The role of angioplasty after successful thrombolysis for acute myocardial infarction.
Soon after the efficacy of thrombolytic agents in recanalizing totally occluded arteries in the setting of AMI was shown, angiographic studies revealed a residual high-grade stenosis in a majority of these patients. To improve clinical outcome further, the role of coronary angioplasty at varying time intervals after myocardial infarction has been examined. In all studies examining the role of immediate angioplasty, no definite advantage was observed with the invasive strategy. In one study, a higher mortality rate was observed in the invasive group, whereas all studies demonstrated a significant increase in the number of non-fatal ischemic adverse events after PTCA. Although differences in clinical outcomes were noted, no difference in left ventricular function, the primary endpoint of all three studies, was demonstrated. Similar results were obtained in the randomized trials of delayed (< 48 h) or late (> 48 h) angioplasty versus conservative management. The majority of these latter trials suffer from the lack of a true control arm, as many patients in the conservative arms undergo PTCA. Observational series in conservatively treated patients after thrombolysis suggest that the coronary plaque remains unstable for several weeks after myocardial infarction. Pacifying the unstable plaque either by medical therapies or by PTCA with adjunctive therapies may in the future be the way to improve outcome in the post-infarction period. In the acute phase, aortic counterpulsation has been found to reduce ischemic events after PTCA in a randomized trial [36].(ABSTRACT TRUNCATED AT 250 WORDS)
Angioplasty, Balloon, Coronary↗
Randomized evaluation of coronary angioplasty for early TIMI 2 flow after thrombolytic therapy for the treatment of acute myocardial infarction: a new look at an old study. The Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) Study Group.
BACKGROUND: Patients who have suffered acute myocardial infarction (AMI) and have been treated with intravenous thrombolytic agents resulting in early 'patent' [Thrombolysis in Myocardial Infarction (TIMI) 2-3 flow grade] arteries have been shown not to benefit from early percutaneous transluminal coronary angioplasty (PTCA). Recent data, however, suggest that the clinical outcome of patients with early TIMI 2 flow is decidedly inferior to that of patients with TIMI 3 flow, raising the question whether early PTCA might be beneficial for patients with TIMI 2 flow. The clinical utility of PTCA for this particular subset of patients has never been assessed. METHODS: We analyzed left ventricular ejection fraction (LVEF) recovery by contrast ventriculography and clinical outcome in Thrombolysis and Angioplasty in Myocardial Infarction Phase I (TAMI-I) study patients with initial TIMI 2 flow grade, determined by blinded core laboratory analysis. RESULTS: No differences were observed between baseline demographic data for the 49 patients randomly assigned to undergo early PTCA compared with that from the 59 patients randomly assigned to receive early medical therapy. Patients were 56 +/- 11 years of age (mean +/- SD), 80% were men, the time from onset of chest pain to catheterization was 268 +/- 71 min, 42% had anterior AMI, and 42% had multivessel disease. Ninety minute baseline LVEF to prehospital discharge LVEF was minimally better in the group randomly assigned to undergo PTCA (51 +/- 12 to 52 +/- 11% versus 55 +/- 10 to 53 +/- 12%, P = 0.06). This contrasted with findings in patients with TIMI 3 flow grade at baseline, which showed a relative benefit for patients randomly assigned to receive early medical therapy (54 +/- 10 to 54 +/- 8% for PTCA, versus 55 +/- 10 to 58 +/- 8% for medical therapy, P = 0.01). Among patients with TIMI 2 flow grade there were no differences in in-hospital death or congestive heart failure (6.1 versus 1.7%, P = 0.25 and 18.4 versus 23.7%, P = 0.50, PTCA versus medical therapy, respectively). CONCLUSION: We conclude that (1) PTCA of infarct-related arteries with TIMI 2 flow grade may modestly improve recovery of left ventricular function, and (2) widespread application of PTCA in this setting should be deferred, pending demonstration that this benefit outweighs the risks of PTCA.
Aged↗