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Background Among patients with ST-segment elevation myocardial infarction (STEMI), rapid reperfusion is associated with improved mortality. As such, door-to-needle (D2N) and door-to-balloon (D2B) times have become metrics of quality of care and targets for intense quality improvement. Methods The National Registry of Myocardial Infarction (NRMI) collected data regarding reperfusion therapy, its timing and in-hospital mortality among STEMI patients from 1990 through 2006. Results Since 1990, NRMI has enrolled 1,374,232 STEMI patients at 2,157 hospitals. Among those, 774,279 (56.3%) were eligible for reperfusion upon arrival. The proportion receiving fibrinolytic therapy fell from 52.5% in 1990 to 27.6% in 2006 ( P P P P P Conclusions Since 1990, there has been a progressive decline in D2N and D2B time among reperfusion-eligible STEMI patients. These improvements have contributed, at least in part, to a progressive decline in mortality.

To determine whether hospitals are capable of delivering myocardial reperfusion therapy in a manner consistent with the American College of Cardiology/American Heart Association guidelines. DATA SOURCE AND STUDY SETTING: Data from the National Registry of Myocardial Infarction (NRMI)-2 and NRMI-3 were used. NRMI is an observational study, sponsored by Genentech, conducted from June 1994 through June 2000 and involving 1876 hospitals and 1,310,030 patients across the United States. The protocol calls for collecting data on all patients with a diagnosis of acute myocardial infarction. The setting was community and tertiary hospitals in the United States.This observational study used process capability analysis.Overall, no hospital was deemed capable of delivering myocardial reperfusion therapy consistent with the American College of Cardiology/American Heart Association guidelines. The highest thrombolytic and angioplasty CPUs were 0.44 and 0.52, respectively-well below the traditional value of 1.0 signifying minimum capability. In addition, among the hospitals examined, there remained a wide degree of variability in process capability, ranging from -0.69 to 0.52.Myocardial reperfusion therapy performance measurement systems relying solely on mean time-to-reperfusion conceal true process performance, thereby obscuring quality improvement opportunities and strategies for improvement. Health care providers, purchasers, regulators, and other organizations interested in measuring and improving health care quality are encouraged to incorporate process capability analysis into their myocardial reperfusion therapy performance measurement and quality management systems.

Objectives Our goals were to compare the characteristics of patients with and without prior coronary artery bypass graft (CABG) presenting with acute myocardial infarction (MI) with or without ST elevation/left bundle branch block (LBBB), and to evaluate the effect of ST shift on inhospital mortality. Methods and Results Using the National Registry of Myocardial Infarction-3 Registry, we identified 112,697 patients with acute MI without exclusion criteria. Of these, 15,936 (14.1%) had prior CABG. Patients with prior CABG had more adverse characteristics and were less likely to have ST elevation/LBBB than patients without prior CABG. The unadjusted mortality for ST elevation/LBBB patients was higher in patients with prior CABG versus without (16.2% vs 14.1%, P =.0001), whereas in patients without ST elevation/LBBB, prior CABG conferred a lower unadjusted mortality versus without (10.1% vs 12.4%, P =.0001). Adjusting for baseline differences, prior CABG was weakly associated with inhospital mortality in ST elevation/LBBB patients (odds ratio [OR], 1.11, 95% CI 1.00-1.23), but not in patients without ST elevation/LBBB (OR 0.99, 95% CI 0.92-1.07). Conclusion Acute MI patients with prior CABG are more likely to present without ST elevation/LBBB than patients without prior CABG. Prior CABG was weakly associated with inhospital mortality in patients with ST elevation/LBBB, but not in patients without these electrocardiographic findings. This suggests the differences in absolute mortality rates between patients presenting with MI with and without a history of prior CABG are largely caused by differences in baseline characteristics and presentation. (Am Heart J 2002;144:463-9.)

OBJECTIVES We sought to determine trends in the treatment of myocardial infarction from 1990 through 1999 in the U.S. and to relate these trends to current guidelines. BACKGROUND Limited data are available to show how recent clinical trials and clinical guidelines have impacted treatment of myocardial infarction. METHODS Temporal trends in myocardial infarction treatment and outcome were assessed by using data from 1,514,292 patients in the National Registry of Myocardial Infarction (NRMI) 1, 2 and 3 from 1990 through 1999. Results During this interval, the use of intravenous thrombolytic therapy declined from 34.3% to 20.8%, but the use of primary angioplasty increased from 2.4% to 7.3% (both p = 0.0001). The median “door-to-drug” time among thrombolytic therapy recipients fell from 61.8 to 37.8 min (p = 0.0001), primarily owing to shorter “door-to-data” and “data-to-decision” times. The prevalence of non–Q wave infarctions increased from 45% in 1994 to 63% in 1999 (p = 0.0001). From 1994 through 1999, there was increased usage of beta-blockers, aspirin and angiotensin-converting inhibitors, both during the first 24 h after admission and on hospital discharge (all p = 0.0001). Between 1990 and 1999, the median duration of hospital stay fell from 8.3 to 4.3 days, and hospital mortality declined from 11.2% to 9.4% (both p = 0.0001). CONCLUSIONS The NRMI data from 1990 through 1999 demonstrate that the recommendations of recent clinical trials and published guidelines are being implemented, resulting in more rapid administration of intravenous thrombolytic therapy, increasing use of primary angioplasty and more frequent use of adjunctive therapies known to reduce mortality, and may be contributing to the higher prevalence of non–Q wave infarctions, shorter hospital stays and lower hospital mortality.

Background There is an inverse relation between mortality from cardiovascular causes and the number of elective cardiac procedures (coronary angioplasty, stenting, or coronary bypass surgery) performed by individual practitioners or hospitals. However, it is not known whether patients with acute myocardial infarction fare better at centers where more patients undergo primary angioplasty or thrombolytic therapy than at centers with lower volumes. Methods We analyzed data from the National Registry of Myocardial Infarction to determine the relation between the number of patients receiving reperfusion therapy (primary angioplasty or thrombolytic therapy) and subsequent in-hospital mortality. A total of 450 hospitals were divided into quartiles according to the volume of primary angioplasty. Multiple logistic-regression models were used to determine whether the volume of primary angioplasty procedures was an independent predictor of in-hospital mortality among patients undergoing this procedure. Similar analy...

The National Registry of Myocardial Infarction 2 (NRMI-2) provides a unique opportunity to evaluate the practice patterns among participating cardiology and emergency medicine departments involved in the care of patients with acute myocardial infarction. The data from NRMI-2 suggest that almost 1/3 of all non-transfer-in and non-transfer-out patients are eligible for reperfusion therapy. Furthermore, of those patients who are clearly eligible for reperfusion therapy, 24% are not given this proven therapy. Specifically, women, the elderly, patients without chest pain on presentation, and those patients at highest risk for in-hospital mortality were least likely to be treated with reperfusion therapy. The reason for underuse of reperfusion therapy may in part reflect a concern for adverse bleeding events associated with the use of thrombolytic therapy. The data from NRMI-2 also suggest that patients with contraindications to thrombolysis may be very appropriate for primary angioplasty. Realizing the full potential benefits of reperfusion therapy in terms of reduced cardiovascular morbidity and mortality will require that clinical practice patterns be aligned more closely with the recommended national guidelines, which are based on extensive clinical trial data that show the benefit of reperfusion therapy in a wide range of patients with acute myocardial infarction. By using observational databases, such as the NRMI-2, which describe how clinical care is administered in nonclinical trial settings, we can continually monitor our progress and initiate changes to ensure that patients are given access to the many therapies that have been shown to improve their quality of life and survival.

Objectives. We sought to compare outcomes after primary percutaneous transluminal coronary angioplasty (PTCA) or thrombolytic therapy for acute myocardial infarction (MI). Background. Primary PTCA and thrombolytic therapy are alternative means of achieving reperfusion in patients with acute MI. The Second National Registry of Myocardial Infarction (NRMI-2) offers an opportunity to study the clinical experience with these modalities in a large patient group. Methods. Data from NRMI-2 were reviewed. Results. From June 1, 1994 through October 31, 1995, 4,939 nontransfer patients underwent primary PTCA within 12 h of symptom onset, and 24,705 patients received alteplase (recombinant tissue-type plasminogen activator [rt-PA]). When lytic-ineligible patients and patients presenting in cardiogenic shock were excluded, baseline characteristics were similar. The median time from presentation to initiation of rt-PA in the thrombolytic group was 42 min; the median time to first balloon inflation in the primary PTCA group was 111 min (p Conclusions. These findings suggest that in lytic-eligible patients not in shock, PTCA and rt-PA are comparable alternative methods of reperfusion when analyzed in terms of in-hospital mortality, mortality plus nonfatal stroke and reinfarction.

Intracoronary rt-PA has been used to treat patients with acute myocardial infarction primarily, after failure of intravenous thrombolytic therapy, and when angioplasty has not been technically possible. It has also been used to treat thrombotic closure complicating angioplasty, to treat nonocclusive thrombosis observed during angioplasty, and to pretreat patients with nonacute total occlusions before angioplasty. Intracoronary administration has the potential of providing high local concentrations for a given dose level and may allow lower total doses for the same degree of efficacy. More controlled data are needed on appropriate patient selection, angiographic and clinical endpoints, dose level and regimen, and comparable efficacy of rt-PA and other thrombolytic agents. However, the use of intracoronary rt-PA should be considered when intracoronary thrombus is evident and this route of administration is available.

Background Many reference levels have been proposed for the measurement of intracardiac pressures, but none have met with universal acceptance. In the first part of our study, we evaluated 10 cardiologists’ understanding of how hydrostatic pressure influences intracardiac pressures as measured with fluid-filled catheters. In the second part, we proposed and validated a new zero level (H): the uppermost blood level in the left ventricular (LV) chamber relative to the anterior chest wall for a patient in the supine position. A comparison was made of LV minimum diastolic pressure measured by reference to H versus measurements made with the zero level at midchest. Methods and Results Using two-dimensional echocardiography, we determined H in the LVs of seven normal patients (five male, two female; age, 49±9 years) undergoing routine cardiac catheterization. H was determined from a left parasternal short-axis view and calculated as the average distance between end diastole and end systole of the endocardium of the uppermost segment of the LV anterior wall below the fourth or fifth intercostal space of the left sternal border on the anterior surface of the chest wall, with the patient in the supine position. A micromanometer/fluid-filled lumen catheter was then positioned in the LV, and we compared the micromanometer LV minimum pressure (LVP min ) obtained when the reference fluid-filled transducer was aligned at midchest with the LVP min obtained when the reference fluid-filled transducer was aligned at H. LVP min referenced to a midchest fluid-filled external transducer was measured as 5.1±1.6 mm Hg (range, 2.4 to 7.2 mm Hg) versus −0.6±0.6 mm Hg (range, −1.6 to 0.4 mm Hg) when referenced to H ( P r =.88; P Conclusions External fluid-filled transducers should be used with the goal of removing hydrostatic pressure and other influences so that the presence of subatmospheric pressure during diastole in any of the cardiac chambers is accurately measured. To achieve this goal, intracardiac pressure should be referenced to an external fluid-filled transducer aligned with the uppermost blood level in the chamber in which pressure is to be measured. The current practice of referencing the zero level of LV diastolic pressure to an external fluid-filled transducer positioned at the midchest level results in systematic overestimation due to hydrostatic effects and produces physiologically significant error in the measurement of diastolic intracardiac pressure.

Background: In epidemiologic studies, excessive body weight, independent of other risk factors, portends a poor prognosis among patients with coronary artery disease experiencing acute myocardial infarction (MI). At least one recent study has suggested that patients of excessive body weight when receiving thrombolytic therapy are often underdosed, potentially reducing early coronary arterial patency and adversely affecting in-hospital clinical outcome. Concern has also been raised that body weight may influence treatment utilization, delays, and complication rates. Despite these concerns, the association between body weight and patient outcome following coronary thrombolysis has received limited attention.Methods/Results: Demographic, procedural, and outcome data from patients with MI were collected at 1073 United States hospitals participating in The National Registry of Myocardial Infarction from 1990 through 1994. Among 350,755 patients with MI enrolled, 87,688 (25.1%) were treated with tissue plasminogen activator (t-PA). Divided into body weight tertiles, 23.5% of patients were less than 70 kg (low weight), 36.8% were 70–85 kg (modrate weight), and 37.5% were greater than 85 kg (high weight). Patients of low weight were older (p < 0.001), received treatment later (p < 0.001), and were less likely to undergo cardiac catheterization, coronary angioplasty, or bypass surgery (p < 0.001) than moderate- or high-weight patients. Low-weight patients also experienced minor bleeding, major bleeding, recurrent MI, and death more often (p < 0.001). Adjusted for age, low body weight was independently associated with in-hospital mortality. Despite receiving a lower dose of t-PA per kg body weight, high-weight patients had a low incidence of cardiogenic shock, recurrent MI, death, and hemorrhagic complications. When high-weight women and men were compared, several interesting observations emerged. Mortality was increased twofold in women (6.8% vs. 3.0; p < 0.001), even adjusting for their older age. Despite being at increased risk, women were less likely than their male counterparts to undergo cardiac catheterization (p=0.001) or bypass surgery (p=0.008).Conclusions: The National Registry of Myocardial Infarction provides a unique resource for assessing health care trends in the United States. Our findings suggest that low body weight is associated with increased in-hospital morbidity and mortality. They also suggest that current dosing strategies for t-PA administration are probably adequate for high-weight patients. The excessive mortality and limited use of in-hospital interventions among high-weight women deserve further study to address gender-related differences in disease processes, as well as potential bias or discrimination.

BACKGROUND Multiple clinical trials have provided guidelines for the treatment of myocardial infarction, but there is little documentation as to how consistently their recommendations are being implemented in clinical practice. METHODS AND RESULTS Demographic, procedural, and outcome data from patients with acute myocardial infarction were collected at 1073 US hospitals collaborating in the National Registry of Myocardial Infarction during 1990 through 1993. Registry hospitals composed 14.4% of all US hospitals and were more likely to have a coronary care unit and invasive cardiac facilities than nonregistry US hospitals. Among 240,989 patients with myocardial infarction enrolled, 84,477 (35.1%) received thrombolytic therapy. Thrombolytic recipients were younger, more likely to be male, presented sooner after onset of symptoms, and were more likely to have localizing ECG changes. Among the 60,430 patients treated with recombinant tissue-type plasminogen activator (rTPA), 23.2% received it in the coronary care unit rather than in the emergency department. Elapsed time from hospital presentation to starting rTPA averaged 99 minutes (median, 57 minutes). Among patients receiving thrombolytic therapy, concomitant pharmacotherapy included intravenous heparin (96.9%), aspirin (84.0%), intravenous nitroglycerin (76.0%), oral beta-blockers (36.3%), calcium channel blockers (29.5%), and intravenous beta-blockers (17.4%). Invasive procedures in thrombolytic recipients included coronary arteriography (70.7%), angioplasty (30.3%), and bypass surgery (13.3%). Trend analyses from 1990 to 1993 suggest that the time from hospital evaluation to initiating thrombolytic therapy is shortening, usage of aspirin and beta-blockers is increasing, and usage of calcium channel blockers is decreasing. CONCLUSIONS This large registry experience suggests that management of myocardial infarction in the United States does not yet conform to many of the recent clinical trial recommendations. Thrombolytic therapy is underused, particularly in the elderly and late presenters. Although emerging trends toward more appropriate treatment are evident, hospital delay time in initiating thrombolytic therapy remains long, aspirin and beta-blockers appear to be underused, and calcium channel blockers and invasive procedures appear to be overused.

Few studies have examined the association between the number of coronary heart disease risk factors and outcomes of acute myocardial infarction in community practice.To determine the association between the number of coronary heart disease risk factors in patients with first myocardial infarction and hospital mortality.Observational study from the National Registry of Myocardial Infarction, 1994-2006.We examined the presence and absence of 5 major traditional coronary heart disease risk factors (hypertension, smoking, dyslipidemia, diabetes, and family history of coronary heart disease) and hospital mortality among 542,008 patients with first myocardial infarction and without prior cardiovascular disease.All-cause in-hospital mortality.A majority (85.6%) of patients who presented with initial myocardial infarction had at least 1 of the 5 coronary heart disease risk factors, and 14.4% had none of the 5 risk factors. Age varied inversely with the number of coronary heart disease risk factors, from a mean age of 71.5 years with 0 risk factors to 56.7 years with 5 risk factors (P for trend.001). The total number of in-hospital deaths for all causes was 50,788. Unadjusted in-hospital mortality rates were 14.9%, 10.9%, 7.9%, 5.3%, 4.2%, and 3.6% for patients with 0, 1, 2, 3, 4, and 5 risk factors, respectively. After adjusting for age and other clinical factors, there was an inverse association between the number of coronary heart disease risk factors and hospital mortality adjusted odds ratio (1.54; 95% CI, 1.23-1.94) among individuals with 0 vs 5 risk factors. This association was consistent among several age strata and important patient subgroups.Among patients with incident acute myocardial infarction without prior cardiovascular disease, in-hospital mortality was inversely related to the number of coronary heart disease risk factors.

The value of coronary artery reperfusion resulting from pharmacologically induced fibrinolysis in patients with evolving myocardial infarction has been rigorously evaluated. Improved left ventricular function and even more impressive improvements in survival rates have been demonstrated consistently in controlled studies. Benefit is related to the restoration of myocardial blood flow. Maximal benefit is achieved with early and sustained restoration of coronary artery patency. Benefits observed during initial hospitalization are sustained for at least 1 year in the majority of patients, even without subsequent mechanical revascularization. To date, analysis of subgroups has not identified a population of patients with evolving infarction that should routinely be excluded from consideration for thrombolysis. As with many potent pharmacologic agents, activators of the fibrinolytic system are associated with a degree of risk whenever they are administered to a patient. Therefore, patients must be assessed carefully prior to initiating treatment, especially for potential bleeding hazards, and appropriate follow-up evaluation and concomitant therapy needs to be planned. However, given the overwhelming body of data now available regarding its benefits and relative safety, thrombolysis should be considered as conventional therapy for patients with acute evolving myocardial infarction (AMI).

Intracoronary tissue-type plasminogen activator (t-PA) was employed successfully before, after, or in place of coronary artery angioplasty in four patients referred for emergency cardiac catheterization during evolving myocardial infarction. The potential roles of intracoronary thrombolysis, dose considerations for intracoronary t-PA, factors influencing the choice of plasminogen activator, and safety issues are discussed.

Many factors precipitate the transfer of patients hospitalized for acute myocardial infarction, including clinical status and the need for diagnostic testing and therapeutic interventions not available at the admitting hospital. The objectives of this study were to assess the frequency of transfer to another hospital and to determine whether nonmedical factors, such as age, sex, race, and insurance status, are associated with transfer.We conducted a prospective study of patients with acute myocardial infarction who were enrolled in the National Registry of Myocardial Infarction 2 from June 1994 through March 1998. The Registry involves 1674 hospitals in the United States. All patients survived to the time of hospital discharge or until transfer. Multivariable logistic regression models, with transfer as the outcome variable, were developed for the entire sample, as well as for subgroups determined by the interventional capabilities of the admitting hospital.Of 537,283 patients with acute myocardial infarction, 152,310 (28%) were transferred to another hospital after admission. After adjustment for differences in clinical and hospital characteristics, factors that were most associated with a reduced odds of transfer included older age (odds ratio [OR] = 0.43; 95% confidence interval [CI]: 0.42 to 0.44 for those aged75 vs.65 years), African-American race (OR = 0.69; 95% CI: 0.67 to 0.71 for African Americans vs. whites), and Medicaid/self-pay insurance status (OR = 0.68; 95% CI: 0.66 to 0.70 for Medicaid/self-pay vs. commercial insurance). These effects were most apparent for patients admitted to hospitals without full invasive diagnostic and therapeutic capabilities, but persisted to some extent among those admitted to hospitals with full invasive services.Our findings suggest that nonmedical factors, including age, race, and insurance type, affect decisions regarding the transfer of patients hospitalized with acute myocardial infarction. As only a minority of the nation's hospitals offers a full range of cardiovascular diagnostic and therapeutic procedures, these findings reinforce ongoing concerns about disparities in access to health care services for some patients.

We sought to determine trends in the treatment of myocardial infarction from 1990 through 1999 in the U.S. and to relate these trends to current guidelines.Limited data are available to show how recent clinical trials and clinical guidelines have impacted treatment of myocardial infarction.Temporal trends in myocardial infarction treatment and outcome were assessed by using data from 1,514,292 patients in the National Registry of Myocardial Infarction (NRMI) 1, 2 and 3 from 1990 through 1999.During this interval, the use of intravenous thrombolytic therapy declined from 34.3% to 20.8%, but the use of primary angioplasty increased from 2.4% to 7.3% (both p = 0.0001). The median "door-to-drug" time among thrombolytic therapy recipients fell from 61.8 to 37.8 min (p = 0.0001), primarily owing to shorter "door-to-data" and "data-to-decision" times. The prevalence of non-Q wave infarctions increased from 45% in 1994 to 63% in 1999 (p = 0.0001). From 1994 through 1999, there was increased usage of beta-blockers, aspirin and angiotensin-converting inhibitors, both during the first 24 h after admission and on hospital discharge (all p = 0.0001). Between 1990 and 1999, the median duration of hospital stay fell from 8.3 to 4.3 days, and hospital mortality declined from 11.2% to 9.4% (both p = 0.0001).The NRMI data from 1990 through 1999 demonstrate that the recommendations of recent clinical trials and published guidelines are being implemented, resulting in more rapid administration of intravenous thrombolytic therapy, increasing use of primary angioplasty and more frequent use of adjunctive therapies known to reduce mortality, and may be contributing to the higher prevalence of non-Q wave infarctions, shorter hospital stays and lower hospital mortality.

There is an inverse relation between mortality from cardiovascular causes and the number of elective cardiac procedures (coronary angioplasty, stenting, or coronary bypass surgery) performed by individual practitioners or hospitals. However, it is not known whether patients with acute myocardial infarction fare better at centers where more patients undergo primary angioplasty or thrombolytic therapy than at centers with lower volumes.We analyzed data from the National Registry of Myocardial Infarction to determine the relation between the number of patients receiving reperfusion therapy (primary angioplasty or thrombolytic therapy) and subsequent in-hospital mortality. A total of 450 hospitals were divided into quartiles according to the volume of primary angioplasty. Multiple logistic-regression models were used to determine whether the volume of primary angioplasty procedures was an independent predictor of in-hospital mortality among patients undergoing this procedure. Similar analyses were performed for patients receiving thrombolytic therapy at 516 hospitals.In-hospital mortality was 28 percent lower among patients who underwent primary angioplasty at hospitals with the highest volume than among those who underwent angioplasty at hospitals with the lowest volume (adjusted relative risk, 0.72; 95 percent confidence interval, 0.60 to 0.87; P0.001). This lower rate, which represented 2.0 fewer deaths per 100 patients treated, was independent of the total volume of patients with myocardial infarction at each hospital, year of admission, and use or nonuse of adjunctive pharmacologic therapies. There was no significant relation between the volume of thrombolytic interventions and in-hospital mortality among patients who received thrombolytic therapy (7.0 percent for patients in the highest-volume hospitals vs. 6.9 percent for those in the lowest-volume hospitals, P=0.36).Among hospitals in the United States that have full interventional capabilities, a higher volume of angioplasty procedures is associated with a lower mortality rate among patients undergoing primary angioplasty, but there is no association between volume and mortality for thrombolytic therapy.

Although saphenous vein graft (SVG) markers have been available for many years, they have not been widely used in coronary artery bypass graft (CABG) surgery. This is likely due to the paucity of data regarding the utility of these markers in postsurgery cardiac catheterization.We performed a prospective study of all post-CABG patients undergoing cardiac catheterization at Barnes-Jewish Hospital over a 6-month period to test our hypothesis that SVG markers would have a beneficial effect on these procedures. Differences in total procedure (arterial) time, time to image only the SVGs, fluoroscopy time, amount of contrast used, number of aortotomies, and number of views required were compared in patients with and without markers.Post-CABG patients undergoing catheterization who had markers (n = 76) required significantly less total procedure time (p = 0.007), fluoroscopy time (p = 0.02), and contrast use (p = 0.008). Even after adjusting for the numbers of SVG ostia and numbers of cine views, patients with markers still required less catheterization and fluoroscopy time (p0.01, p0.02) and time to image only the SVGs (p0.05) than those without markers (n = 106).SVG markers improve the efficiency of post-CABG catheterizations; they decrease the exposure of patients and cardiologists to ionizing radiation, and they decrease the exposure of patients to potentially toxic contrast agents. SVG markers are beneficial to the vast majority of post-CABG patients.

We reviewed data from the National Registry of Myocardial Infarction-2 to determine the differences in characteristics and outcomes in patients with acute myocardial infarction (AMI) who have undergone previous coronary artery bypass grafting (CABG), and those who have not, and between post-CABG patients who were treated with alteplase (recombinant tissue-type plasminogen activator [rt-PA]) and those who were treated with primary percutaneous transluminal coronary angioplasty (PTCA).Demographic, therapeutic, and outcome data from patients with AMI were collected at >1,000 hospitals in the United States in collaboration with National Registry of Myocardial Infarction-2. Of the 45,925 patients receiving reperfusion therapy, 2,544 of the 39,574 treated with rt-PA (6.4%) had a history of CABG, and 375 of the 6,351 treated with primary PTCA (5.9%) had a history of CABG. Patients with a history of CABG were older, more likely to be men, and had more comorbidities, but prior CABG was still an independent predictor of mortality after multivariate regression analysis (odds ratio 1.23; 95% confidence interval 1.05 to 1.44). Among the post-CABG patients who received rT-PA or underwent PTCA, there was no significant difference in in-hospital mortality rate or the combined end point of death and nonfatal stroke. Thus, (1) prior CABG is an independent predictor of mortality, and (2) for post-CABG patients with AMI who are not in shock and who are lytic-eligible, reperfusion therapy with rt-PA and PTCA result in similar outcomes with regard to in-hospital mortality and the combined end point of death and nonfatal stroke.

To determine whether there are sex differences in the demographics, treatment, and outcome of patients with acute myocardial infarction in the United States, data from the National Registry of Myocardial Infarction-I from September 1990 to September 1994 were examined.The National Registry of Myocardial Infarction-I is a national observational database consisting of 1234 US hospitals in which each hospital submits data from each patient with acute myocardial infarction to a central data collection center. For these analyses, the following variables were examined in 354 435 patients with acute myocardial infarction: demographics; use of medical therapy including thrombolytic agents; use of procedures including cardiac catheterization, percutaneous transluminal coronary angioplasty, and coronary artery bypass surgery; length of hospital stay; adverse events (stroke, major bleeding, or recurrent myocardial infarction); and causes of death.In comparison with men, women experiencing acute myocardial infarction in the United States are older, with 55.7% older than 70 years. Women have a higher mortality rate than men even when controlled for age and die less often from arrhythmia but more often from cardiac rupture whether or not thrombolytic therapy is used. Treatment with aspirin, heparin, or beta-blockers is less frequent in women. When thrombolytic therapy is used, women are treated an average of almost 14 minutes later than men and experience a greater incidence of major bleeding. Cardiac catheterization, percutaneous transluminal coronary angioplasty, and coronary artery bypass surgery are used less often in women.Observations from the National Registry of Myocardial Infarction-I document important sex differences in demographics, treatment, and outcome of patients with acute myocardial infarction in the United States.

Background —There is clear evidence that reperfusion therapy improves survival in selected patients with an acute myocardial infarction. However, several studies have suggested that many patients with an acute myocardial infarction do not receive this therapy. Whether this underutilization occurs in patients appropriate for such therapy remains unclear. Methods and Results —We examined the use of reperfusion therapy in patients with an acute myocardial infarction hospitalized at 1470 hospitals participating in the National Registry of Myocardial Infarction 2. We identified 84 663 patients who were eligible for reperfusion therapy as defined by diagnostic changes on the initial 12-lead ECG, presentation to the hospital within 6 hours from symptom onset, and no contraindications to thrombolytic therapy. Twenty-four percent of these eligible patients did not receive any form of reperfusion therapy (7.5% of all patients). When multivariate analyses were used, left bundle-branch block (odds ratio [OR]=0.22; 95% CI=0.20 to 0.24), lack of chest pain at presentation (OR=0.22; 95% CI=0.21 to 0.24), age >75 years (OR=0.40, 95% CI=0.36 to 0.43), female sex (OR=0.88, 95% CI=0.83 to 0.92), and various preexisting cardiovascular conditions were independent predictors that the patient would not receive reperfusion therapy. Conclusions —Reperfusion therapy may be underutilized in the United States. Increased use of reperfusion therapy could potentially reduce the unnecessarily high mortality rates observed in women, the elderly, and other patient groups with the highest risk of death from an acute myocardial infarction.

In hearts of experimental animals, irreversible myocardial injury occurs when perfusion is interrupted completely for intervals as brief as 20-60 minutes.45 The failure of reperfusion to salvage irreversibly injured tissue has been documented rigorously. For example, Reimer et a14 ligated coronary arteries in dogs for selected intervals and assessed necrosis morphologically. In contrast to the 55% of ischemic myocardium that remained viable when reperfusion was implemented after 40 minutes, less than 17% remained viable when reperfusion was implemented only after 6 hours (Figure 1). Similarly, in dogs with experimentally induced thrombotic coronary artery occlusion and subsequent thrombolysis induced with streptokinase, reperfusion within 2 hours salvaged approximately 50% of jeopardized myocardium as judged from positron emission tomograms.5 In contrast, late reperfusion (implemented after 6 hours) resulted in no significant salvage (Figure 2). Despite the consistency of these results, extrapolation to human hearts is neither straightforward nor necessarily justified. In patients, the impact of thrombotic occlusion will be conditioned by the severity and extent of underlying atherosclerotic coronary artery disease and variable contributions of collateral flow to protection of myocardium.6 In addition, some favorable consequences of reperfusion may depend on mechanisms independent of salvage of jeopardized myocardium, as discussed below. Nevertheless, results of several con

ContextRapid time to treatment with thrombolytic therapy is associated with lower mortality in patients with acute myocardial infarction (MI). However, data on time to primary angioplasty and its relationship to mortality are inconclusive.ObjectiveTo test the hypothesis that more rapid time to reperfusion results in lower mortality in the strategy of primary angioplasty.DesignProspective observational study of data collected from the Second National Registry of Myocardial Infarction between June 1994 and March 1998.SettingA total of 661 community and tertiary care hospitals in the United States.SubjectsA cohort of 27,080 consecutive patients with acute MI associated with ST-segment elevation or left bundle-branch block who were treated with primary angioplasty.Main Outcome MeasureIn-hospital mortality, compared by time from acute MI symptom onset to first balloon inflation and by time from hospital arrival to first balloon inflation (door-to-balloon time).ResultsUsing a multivariate logistic regression model, the adjusted odds of in-hospital mortality did not increase significantly with increasing delay from MI symptom onset to first balloon inflation. However, for door-to-balloon time (median time 1 hour 56 minutes), the adjusted odds of mortality were significantly increased by 41% to 62% for patients with door-to-balloon times longer than 2 hours (for 121-150 minutes: odds ratio [OR], 1.41; 95% confidence interval [CI], 1.08-1.84; P=.01; for 151-180 minutes: OR, 1.62; 95% CI, 1.23-2.14; P 180 minutes: OR, 1.61; 95% CI, 1.25-2.08; P

Background To determine whether there are sex differences in the demographics, treatment, and outcome of patients with acute myocardial infarction in the United States, data from the National Registry of Myocardial Infarction-I from September 1990 to September 1994 were examined. Methods The National Registry of Myocardial Infarction-I is a national observational database consisting of 1234 US hospitals in which each hospital submits data from each patient with acute myocardial infarction to a central data collection center. For these analyses, the following variables were examined in 354435 patients with acute myocardial infarction: demographics; use of medical therapy including thrombolytic agents; use of procedures including cardiac catheterization, percutaneous transluminal coronary angioplasty, and coronary artery bypass surgery; length of hospital stay; adverse events (stroke, major bleeding, or recurrent myocardial infarction); and causes of death. Results In comparison with men, women experiencing acute myocardial infarction in the United States are older, with 55.7% older than 70 years. Women have a higher mortality rate than men even when controlled for age and die less often from arrhythmia but more often from cardiac rupture whether or not thrombolytic therapy is used. Treatment with aspirin, heparin, or β-blockers is less frequent in women. When thrombolytic therapy is used, women are treated an average of almost 14 minutes later than men and experience a greater incidence of major bleeding. Cardiac catheterization, percutaneous transluminal coronary angioplasty, and coronary artery bypass surgery are used less often in women. Conclusions Observations from the National Registry of Myocardial Infarction-I document important sex differences in demographics, treatment, and outcome of patients with acute myocardial infarction in the United States.

This study was performed to determine whether patients with myocardial infarction with apparently reciprocal ST segment depression exhibit abnormal metabolism in zones distant from the primary zone of infarction. Positron emission tomography was performed after the intravenous injection of carbon-11 palmitate in 20 patients with acute myocardial infarction. Infarction was anterior in 7 patients and inferior in 13. Patients with anterior infarction did not show ST segment depression in the inferior leads and all of the patients exhibited normal homogeneous accumulation of palmitate in the inferior and posterior walls. Nine patients with inferior infarction (69%) exhibited ST segment depression (apparently reciprocal or due to anterior wall ischemia) in the anterior precordial leads. Myocardial injury tended to be greater in the primary zone of necrosis among patients with inferior infarction and "reciprocal" ST segment depression compared with those without anterior ST segment depression. This was reflected by the greater total inferior ST segment elevation (0.48 ± 0.35 versus 0.07 ± 0.19 mV [± standard deviation], p < 0.05), peak plasma MB creatine kinase activity (354 ± 134 versus 80 ± 34 IU/liter, p < 0.05) and tomographically estimated infarct size (58 ± 13 versus 33 ± 10 PET-g-eq).Three of the nine patients with inferior infarction and precordial ST depression exhibited anterior tomographic defects underlying the ST segment depression. Thus, although most of the patients with inferior infarction and precordial lead ST segment depression had no anterior wall metabolic compromise (67%) indicating that the anterior ST segment changes were truly reciprocal phenomena, in some the precordial electrocardiographic abnormalities reflected impaired metabolism in the anterior wall indicative of ischemia.

In addition to the favorable effects of calcium antagonists on symptoms related to coronary spasm, we recently documented preclusion of ergonovine-induced coronary spasm angiographically in four patients with proved Prinzmetal's angina. To determine whether nifedipine has similar "relaxing" or negative inotropic actions on left ventricular myocardial function, we studied 19 patients with various degrees of left ventricular dysfunction before and after nifedipine (20 mg sublingually) during cardiac catheterization. Left ventricular afterload was reduced, with a significant (13 percent) decline in arterial pressure; left ventricular diastolic pressures were unchanged. Left ventricular ejection function was augmented, with significant increases in ejection fraction (14 percent), mean velocity of circumferential fiber shortening (41 percent), systolic ejection rate (25 percent), and end-systolic pressurevolume ratio (19 percent). Cardiac index increased significantly by 16 percent. Early diastolic relaxation, diastolic pressure-volume relations and end diastolic stiffness remained unchanged after nifedipine. When patients were categorized (Group I: left ventricular end-diastolic volume ≤ 90 ml/m 2 , end-diastolic pressure ≤ 20 mm Hg; Group II: end-diastolic volume > 90 ml/m 2 , end-diastolic pressure > 20 mm Hg), highly pertinent differences were apparent. Nifedipine significantly reduced left ventricular preload and end-diastolic pressures in Group II but not in Group I patients. Enhancement of left ventricular ejection function in Group II patients was significantly more prominent than that in patients with normal baseline function. Although diastolic properties were insignificantly changed overall, the left ventricular diastolic pressure-volume relation was displaced downward by nifedipine in Group II, but not in Group I patients. Both systemic and pulmonary vascular resistance declined significantly more in Group II patients, whereas cardiac index was increased 25 percent compared with a negligible change in group I patients. These results indicate beneficial effects of nifedipine on myocardial oxygen requirements, particularly in patients with impaired left ventricular function in whom left ventricular preload and afterload were both significantly reduced, cardiac index augmented and the pressure-volume relation shifted downward. To confirm predicted symptomatic benefits in 13 other patients with fixed coronary, disease, incremental atrial pacing to anginal threshold was performed before and 30 minutes after nifedipine (20 mg sublingually). Mean paced heart rate at onset of angina increased 19.3 percent after nifedipine. Concomitantly, aortic pressure decreased significantly by 22.1 percent at the onset of angina; double product was unchanged at the anginal threshold. Thus, although left ventricular afterload was reduced by nifedipine, the anginal threshold was unchanged in terms of myocardial oxygen requirements. In concert, these results indicate that therapeutically effective influences of nifedipine in patients with fixed coronary disease are attributable basically to hemodynamic alterations consequent upon left ventricular afterload reduction. Nevertheless, such effects imply therapeutic benefit, the reduced afterload concomitantly permitting greater exercise-induced tachycardia before the anginal threshold is reached.

To elucidate the mechanisms of reduction of left ventricular end-diastolic pressure by nifedipine in certain individuals, we evaluated cardiac and peripheral hemodynamic responses in 32 patients after they were randomly assigned to nifedipine (20 mg sublingually) or to placebo treatment. Forearm plethysmography was performed during cardiac catheterization with micromanometers. No hemodynamic parameters were changed after placebo. Left ventricular end-diastolic pressure declined by 14% (p less than .02) after nifedipine in patients with impaired left ventricular function, but was unchanged in those with normal function; indexes of peripheral venous hemodynamics (forearm venous tone, forearm volume change) were not affected. In those patients with abnormal left ventricular function, forearm vascular resistance decreased 36% and forearm blood flow increased 31% (p less than .0005 for both), while neither changed in those with normal function. Cardiac output increased by 10% in patients with impaired left ventricular function but was unchanged in the remainder, while calculated total systemic resistance fell by 24% in those with abnormal left ventricular function (p less than .002 for both). Thus, reduction of left ventricular preload by nifedipine is not attributable to venous pooling, but rather this beneficial effect appears to be attributable to improved left ventricular systolic function in response to afterload reduction, particularly in patients with impaired left ventricular function.

Coronary thrombosis is now recognized as the most common proximate cause of acute myocardial infarction, and thrombolysis is evolving as an accepted therapeutic approach to patients presenting in the early stages of myocardial infarction. The ascent of thrombolysis in treatment hierarchies reflects multiple factors, including improved understanding of the pathophysiology of myocardial infarction, advances in the characterization of thrombosis and thrombolysis, the availability of clot-selective thrombolytic agents, the widespread availability of safe arteriographic procedures, and the contemporaneous development of effective percutaneous balloon angioplasty. Selection of patients most likely to benefit from thrombolysis with the lowest risk for complications remains difficult. Undoubtedly, some patients will benefit greatly from an aggressive approach to evolving myocardial infarction

The primary goal of this study was to assess the frequency of persistent regional wall motion abnormalities and myocardial perfusion defects detectable late after myocardial infarction with radionuclide ventriculography and thallium-201 imaging, respectively. The study was performed prospectively in 32 patients in whom infarct size was estimated enzymatically at the time of the acute episode and in 10 patients without infarction. Thallium-201 imaging and radionuclide ventriculography were performed with the patient at rest an average of 11 months after infarction (range 6 to 20 months) and analyzed independently by two observers who were unaware of results of other clinical and laboratory data. Perfusion defects were detected in 94 percent (30 of 32) by observer I and in 91 percent (29 of 32) by observer II. Wall motion abnormalities were detected in 78 percent (25 of 32) and 75 percent (24 of 32) by observers I and II, respectively, but in 10 of the patients with an infarct size less than 20 creatine kinase-gram-equivalents (CK-g-eq), wall motion abnormalities were found in only 50 and 40 percent, respectively, by these observers (p

SummaryTo characterize the duration of the fibrinolytic response to tissue-type plasminogen activator (t-PA) and streptokinase (SK) in patients with acute myocardial infarction we serially assayed crosslinked fibrin degradation products (XL-FDP) and Bβ15-42 fibrinopeptide. Use of specific monoclonal antibodies permitted quantification and differentiation of fibrin from fibrinogen degradation products. Marked elevations of XL-FDP occurred within 1 hour after administration of t-PA (n = 13) or SK (n = 35) to >1000 ng/ml in 79% of the patients. All patients given t-PA exhibited elevations of XL-FDP >1000 ng/ml, most exhibited values >5000 ng/ml (79% of patients). In contrast 6 of the patients given SK failed to exhibit XL-FDP >1000 ng/ml. XL-FDP >5000 ng/ml occurred in only 14%. The difference in the response to t-PA compared to SK was particularly striking 7 hours or more after administration of activator at which time XL-FDP were markedly elevated in patients given t-PA (5821 ± 1683 ng/ ml) compared with decreasing values in patients given SK (2924 ± 1186 ng/ml) (p

Prospective characterization of pharmacodynamics of tissue-type plasminogen activator (t-PA) is needed for diverse clinical applications. Accordingly, we used physiologically based, computer simulation of participating biochemical reactions in response to concentrations of circulating t-PA seen with infusions of 1 to 7 hr duration in 45 patients. Predicted values were compared with those from a "training set" obtained in six patients given t-PA for coronary thrombosis and six receiving therapy for peripheral arterial occlusion. Subsequently, results of simulation were compared prospectively with observations from a "test set" of 33 consecutive patients given low doses of t-PA for as long as 7 hr or higher doses for 1 to 2 hr and with data from 101 patients given t-PA in the European Cooperative Trial. Fits between observed and predicted values were close. Based on observations in the training set, the alpha 2-macroglobulin reaction with circulating plasmin and ongoing synthesis of plasminogen were incorporated in the simulations. Fibrinogenolysis in vitro was documented despite supplementation of samples with aprotinin, particularly when concentrations of t-PA were high. This phenomenon can lead to overestimation of fibrinogen depletion and was found to be obviated by the use of PPACK, a novel serine protease inhibitor. Results indicate that the simulation approach developed permits economic, prospective evaluation of regimens of t-PA suitable for diverse conditions and delineation of the impact of individual constituents and reactions on pharmacodynamics of t-PA and on the risk of induction of a systemic lytic state.

The effects of intraventricular and intracoronary contrast media on the peripheral arterial and venous beds were directly measured with forearm plethysmography. Standard dose intraventricular radiographic contrast produces a potent peripheral arterial vasodilator effect accompanied by a hypotensive and tachycardic response, followed by peripheral venoconstriction, suggesting that the net hemodynamic response is mediated peripherally. Coronary arteriography is associated with a differing pattern of response, suggesting that the most important hemodynamic effects are mediated via myocardial depression with secondary peripheral vascular responses. Hemodynamic changes occur earlier than those following ventriculography and reflect peripheral arterial and venous constriction. Dose and osmolarity of the contrast are important determinants as well as the site of administration.

Either augmentation or impairment of left ventricular function has previously been reported in different patients, in response to isometric exercise. To identify the mechanisms associated with these disparate responses, the effects of submaximal sustained handgrip upon left ventricular systolic and diastolic properties were studied in 29 patients during diagnostic catheterization. In 16 patients (group I), ejection fraction, mean Vcf, and the mean systolic ejection rate remained constant, while the ratio of peak systolic pressure to end systolic volume increased significantly from 2.81 +/- 0.6 to 3.17 +/- 0.6 ml/mm Hg. In 13 patients (group II) ejection fraction declined from 0.6 +/- 0.03 to 0.51 +/- 0.03, Vcf from 0.96 +/- 0.09 to 0.85 +/- 0.09 circ/sec, mean normalized systolic ejection rate from 1.79 +/- 0.1 to 1.50 +/- 0.09 sec-1, and the peak systolic pressure to end systolic volume ratio from 2.23 +/- 0.3 to 1.99 +/- 0.3 (p less than 0.05 for each). Systemic arterial mean pressure increased similarly by 19% and 21% in groups I and II, respectively (p less than 0.05 for each). Systemic vascular resistance increased significantly by 23% in group I and by 5% in group II (p less than 0.05). Left ventricular end diastolic volume declined from 85.4 +/- 7 to 77.3 +/- 11 ml/m2 in group I, while end diastolic and end systolic volumes increased by 13% and 35%, respectively in group II (p less than 0.05 for each). In both groups, baseline exponential pressure-volume relations were similar, though higher intercepts on the pressure-volume relations upon the Y-axis suggested greater "diastolic tone," and steeper volume-normalized pressure-volume elasticity relations indicated "stiffer" left ventricular chambers in group II patients. While the incidence of coronary artery disease was similar, both the severity and extent of left ventricular asynergy were greater in group II patients. We conclude that dilatation and deterioration of left ventricular ejection function in response to isometric exercise are causally related to, and comprise a useful predictor of, severe underlying left ventricular asynergy and impaired chamber distensibility.

To determine the mechanisms responsible for beneficial effects of nifedipine in pacing-induced angina pectoris, 20 patients undergoing diagnostic cardiac catheterization were studied. Following left ventriculography and coronary arteriography, right atrial pacing was performed before and 30 min after administration of 20 mg of nifedipine sublingually. Heart rate was increased by 10-beat-per-minute (bpm) increments every 90 sec until angina occurred. Electrocardiogram, central aortic pressure, and pulmonary arterial occlusive pressure were monitored continuously. Mean paced heart rate at the onset of angina was increased from 107 +/- 12.6 bpm to 140.6 +/- 19.9 (P less than .001) after nifedipine. Systolic arterial pressure at the time of angina declined from 143 +/- 20 mm Hg to 112 +/- 23 mm Hg (P less than .001). Consequently, the double product heart rate X systolic blood pressure was not changed significantly at the onset of chest pain (149 +/- 28 mm Hg X 10(-2) vs. 142 +/- 28 mm Hg X 10(-2) ). Pulmonary arterial occlusive pressure also did not change significantly (10.4 +/- 4.4 vs. 10.5 +/- 5.9 mm Hg). Thus, nifedipine decreased myocardial oxygen demand at a given heart rate by reducing left ventricular afterload, but did not increase the rate pressure product threshold for ischemic pain. These results indicate that peripheral arterial vasodilator effects of nifedipine, with a resultant decrease in myocardial oxygen requirements, account for its antianginal effect in this setting in patients with fixed obstructive coronary artery disease.

Pharmacologic thrombolysis is dependent on activation of endogenousplasminogen to the active proteolytic enzyme, plasmin. Agents such as tissue-plasminogen activator with a high affinity for fibrin bound plasminogen result in high local concentration of plasmin. Thus, they achieve clot lysis with less tendency to induce a systemic lytic state reflecting extensive fibrinogenolytic activity in the circulation. Appropriate dose regimens for thrombolytic agents in specific clinical situations is critical to maximize therapeutic efficacy while minimizing the risk of significant bleeding.

Objectives.This study was done to determine the incidence, timing and prevalence as a cause of death from cardiac rupture in patients with acute myocardial infarction. Background.Several clinical trials and overview analyses have suggested that the survival benefit conferred by thrombolytic therapy may be offset by a paradoxic increase in early deaths from cardiac rupture. Methods.Demographic, procedural and outcome data from patients with acute myocardial infarction were collected at 1,073 United States hospitals collaborating in the United States National Registry of Myocardial Infarction. Results.Among the 350,755 patients enrolled, 122,243 received thrombolytic therapy. In-hospital mortality for the overall patient population, those not treated with thrombolytics (m = 228,512) and those given thrombolytics were 10.4%, 12.9% and 5.9%, respectively (p < 0.001). Cardiogenic shock was the most common cause of death in each patient group. Although the incidence of cardiac rupture was low (

A 64-year-old woman with an acute exacerbation of chronic relapsing pericarditis had initial clinical and ECG features that were consistent with an acute anterior myocardial infarction. Transient Q waves were observed in the precordial leads, and she also exhibited elevated plasma MB creatine kinase (MB CK) activity. However, the overall clinical and laboratory data, including angiographic and radionuclide studies, suggest that the myocardial damage was secondary to pericarditis per se, rather than ischemic myocardial infarction. This case emphasizes that Q waves and elevated MB CK activity can be seen in association with pericarditis, and this must be differentiated from myocardial infarction secondary to coronary artery disease.

The duration of the coronary artery vasoconstrictor effect of ergonovine maleate is an important clinical parameter that has not been clearly defined. Since ergonovine is generally administered in incremental, cumulative doses and since this agent may have potentially serious toxic effects related to its vasoconstrictor properties, knowledge of duration of this effect is crucial to its safe and efficacious use. We present clinical evidence of ergonovine-induced coronary artery spasm recurring after pharmacologic relief of a first episode of ergonovine-induced spasm. Recurrent spasm occurred 18 minutes after a cumulative dose of 0.15 mg ergonovine and 14 minutes after intravenous nitroglycerin was given to ameliorate the initial spasm. Therefore, clinical monitoring of patients after ergonovine administration should be designed to identify a possibly prolonged duration of vasoconstrictor effect of the drug. Sequential doses of ergonovine at intervals of ten minutes or less should be recognized as having cumulative effect. The duration of action of pharmacologic agents utilized to alleviate ergonovine-induced coronary artery spasm should exceed the potential duration of action of ergonovine in order to minimize the possibility of late spasm.

Coronary thrombosis is now recognized as the most common proximate cause of acute myocardial infarction, and thrombolysis is evolving as an accepted therapeutic approach to patients presenting in the early stages of myocardial infarction. The ascent of thrombolysis in treatment hierarchies reflects multiple factors, including improved understanding of the pathophysiology of myocardial infarction, advances in the characterization of thrombosis and thrombolysis, the availability of clot-selective thrombolytic agents, the widespread availability of safe arteriographic procedures, and the contemporaneous development of effective percutaneous balloon angioplasty. Selection of patients most likely to benefit from thrombolysis with the lowest risk for complications remains difficult. Undoubtedly, some patients will benefit greatly from an aggressive approach to evolving myocardial infarction.