American Heart Journal

Am Heart J 2002;143:745-7.

Intravascular ultrasound imaging (IVUS) is limited by the size of the imaging catheter. To facilitate imaging before and during interventions, a 30-MHz ultrasonic imaging device was developed that is the same dimension as a 0.018-inch guide wire. The purpose of this study was to evaluate the clinical feasibility of this device. The imaging core was tested in 8 patients with the use of a monorail guiding sheath that was advanced through a 7F catheter. In addition, after coronary interventions, the standard guide wire was removed, the imaging core was placed inside a compatible balloon, and imaging was performed. In 4 patients, imaging was also performed with a standard 3.2F IVUS catheter. The lumen-plaque interface and the media-plaque interface were clearly visualized in all patients. There was no detectable loss in image quality between the new imaging device and the larger IVUS catheter, and measurements of lumen cross-sectional area were not statistically different. Improvements in manufacturing technology have permitted the development of a mechanically rotating ultrasound imaging core 0.018 inches in diameter. It is compatible with current balloon catheters without degradation of image quality.

We sought to determine whether a 600-mg loading dose of clopidogrel reduces myocardial infarct size compared with a 300-mg dose using contrast-enhanced magnetic resonance imaging in patients undergoing primary percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI). In 198 patients undergoing primary PCI for STEMI, contrast-enhanced magnetic resonance imaging was performed a median of 7 days after the index event. Infarct size was measured on delayed-enhancement imaging, and area at risk (AAR) was quantified on T2-weighted images. Baseline characteristics were not significantly different between the 600-mg clopidogrel loading group (n = 117) and the 300-mg group (n = 81). The median infarct size was significantly smaller in the 600-mg group than in the 300-mg group (17.3% [8.9%-26.2%] vs 21.7% [12.9%-30.0%], P = .03). Myocardial salvage index ([AAR - infarct size] × 100/AAR) was greater in the 600-mg group than in the 300-mg group (47.7 [33.7-60.9] vs 32.0 [23.6-51.5], P < .01). Patients in the 600-mg group also had a significantly lower extent of microvascular obstruction and smaller number of segments with >75% of infarct transmurality than did those in the 300-mg group. After propensity score matching, the 600-mg group had smaller infarct size and greater myocardial salvage index compared with the 300-mg group. In multivariate analysis, the use of a 600-mg clopidogrel loading dose significantly reduced the risk of a large infarct (odds ratio 0.53, 95% CI 0.29-0.98, P = .04). In patients undergoing primary PCI for STEMI, a 600-mg loading dose of clopidogrel reduced myocardial infarct size and improved myocardial salvage compared with a 300-mg loading dose.

An experimental model of acute myocardial infarction is presented. Intracoronary thrombus was precipitated by a mock ruptured atheromatous plaque, which is a cholesterol-collagen mixture, protruding into the stenosed left anterior descending coronary artery. Twenty-five dogs, divided into two groups, were studied: a control group of 15 dogs and a treated group of 10 dogs. Intracoronary thrombus was precipitated by the mock atheromatous plaque in 13 of 15 control animals. Myocardial infarction was induced in 10 and sudden death in two. Coronary blood flow decreased gradually or cyclically to end in myocardial infarction. The model was utilized to investigate the effects of a thromboxane synthetase inhibitor, OKY-046, on 10 additional animals. OKY-046 could significantly decrease the incidence of occlusive thrombus formation and myocardial infarction when administered intravenously during coronary blood flow reduction (3 of 10 in the treated group vs 12 of 15 in the control group, p less than 0.02). Thromboxane B2 was significantly elevated in the coronary venous blood during reduction of the coronary blood flow, while thromboxane B2 was reduced and 6-ketoprostaglandin F1 alpha increased during OKY-046 administration. The reduction in thromboxane A2 production associated with increased prostacyclin appeared to be the major mechanism of the interruption of the thrombus formation by OKY-046.

Cholesterol lowering with statins reduces the risk of vascular disease, but uncertainty remains as to whether more intensive statin therapy produces worthwhile benefits safely. Blood homocysteine level is an independent marker of vascular risk, but it is unknown whether this association is causal. 12,064 myocardial infarction survivors have been randomized to more versus less intensive cholesterol-lowering treatment using simvastatin 80 mg versus 20 mg daily. Allocation to more intensive treatment has yielded average further low-density lipoprotein cholesterol reductions of 0.5 mmol/L at 2 months and 0.4 mmol/L at 5 years. In addition, using a factorial design, these patients have been randomized to homocysteine lowering with folic acid 2 mg plus vitamin B12 1 mg daily versus matching placebo, yielding an average 3 to 4 mumol/L reduction in homocysteine. After 6 years of median follow-up, the annual overall rate of major vascular events is approximately 3%. Follow-up is scheduled to continue for a median of 7 years. SEARCH should provide reliable evidence about the efficacy and safety of prolonged use of more intensive cholesterol-lowering therapy and, separately, of folate-based homocysteine-lowering therapy in a high-risk population.

TA-064 is a new cardiotonic agent which is also effective orally, according to investigations conducted in Japan. We analyzed computer-assisted alterations of pressure-volume relationships serially and of indirect myocardial oxygen consumption (MVO2) estimations on line during TA-064 influence in 16 patients with congestive cardiomyopathy: left ventricular function was moderately decreased in seven patients (group A) and drastically decreased in nine (group B). Results showed that TA-064, 8 micrograms/kg/min intravenously, exerted positive inotropic effects in both groups and induced mean maximal delta percentage changes at about 5 minutes of infusion as follows: left ventricular stroke work index +65% and +47%; dP/dtmax +61% and 59%; left ventricular efficiency +62% and 53%; MVO2 +31% and +11% (p less than 0.05). TA-064, 20 mg by mouth induced serum levels (group A = 23.8 +/- 12ng/ml and group B = 26.4 +/- 20 ng/ml) corresponding to the effects with dosages of 1 to 2 ng/kg/min intravenously (p greater than 0.05), thus implying that significant changes in left ventricular function require higher oral dosages. We conclude that TA-064 improves left ventricular function, primarily via a contractility increase, also in group B patients without toxic side effects. On-line indirect MVO2 assessment and analysis of serial pressure-volume relationships helped to provide a more complex definition of the mechanism and efficiency of the cardiotonic agent under study.

This report describes the lipid and safety data collected during an off-drug period that followed 8 weeks of treatment with the cholesteryl ester transfer protein inhibitor, anacetrapib (ANA). A total of 589 patients with primary hypercholesterolemia or mixed hyperlipidemia were randomized to placebo, atorvastatin (ATV) 20 mg, and varying doses of ANA, provided as monotherapy or coadministered with ATV 20 mg daily. Patients were treated for 8 weeks, followed by an 8-week follow-up period, during which ANA was switched to placebo. At week 16 (8 weeks after ANA was stopped), persistent reductions in low-density lipoprotein cholesterol (LDL-C) were evident for the monotherapy groups receiving ANA 150 and 300 mg (-9.3% and -15.3%, respectively), and residual increases in high-density lipoprotein cholesterol (HDL-C) were observed for the monotherapy groups receiving ANA 40 mg (18.6%), 150 mg (40.5%), and 300 mg (43.4%). The effects on apolipoprotein B and apolipoprotein A-I were consistent with the changes observed for LDL-C and HDL-C, respectively. Corresponding residual changes in LDL-C and HDL-C were also noted in the ATV coadministration groups at the similar doses of ANA compared with ATV 20 mg alone. Residual plasma drug levels accompanied by reductions in cholesteryl ester transfer protein activity were observed at week 16 and may account for the alterations in plasma lipids 8 weeks after cessation of ANA.

Percutaneous closure of atrial septal defect (ASD) is a valid alternative to surgical approach. Current device has significantly improved the success rate also in complex cases. The aim of this study is to assess the impact of age, defect size, and morphologic features on successfully percutaneous ASD closure. Between January 2000 and September 2004, 1,013 consecutive patients underwent closure of an isolated type II ASD at our institution. The following outcomes have been evaluated: (1) role of percutaneous ASD closure as alternative to surgical repair, in current daily practice; (2) impact of age on the selected closure approach; (3) analysis of morphologic variety of ASD and its effect on the closure technique; (4) possible role of specific device selection according to ASD morphology to improve procedural success. During the study period, up to 80% of secundum ASDs were suitable for percutaneous closure with the currently available devices. Need for surgical ASD closure was more common in pediatric patients, likely reflecting the more frequent diagnosis of larger and complex defects at a young age. Accurate ADS morphology assessment and appropriate device selection are key elements to obtain procedural success. In particular, among all the ASD characteristics, the rim absence is the main limiting factor to a successful percutaneous ASD closure. A trend of reduction in peri-procedural adverse events was observed during the study period, with complications needing immediate cardiac surgery occurred only in 1% of cases. Percutaneous ASD closure is feasible and associated with low complication rate. A thorough analysis of morphologic aspects is mandatory in order to select the appropriate device and the optimal approach. Surgical closure remains the treatment of choice in selected patients.

The frequency and type of complications in a material consisting of 832 suprasternal and/or percutaneous left ventricular punctures, 72 retrograde left ventricular catheterizations, and 152 transseptal left heart catheterizations performed in this laboratory are reported.The patient material consisted of 726 persons, mainly adults and older children.Two deaths occurred during the 1,056 investigations (0.19 per cent), one after a combined suprasternal and left ventricular puncture, and the other after a transseptal left heart catheterization.Serious complications were seen a total of 19 times (1.7 per cent), as shown in Table VIII.

1.1. The clinical effect of a new coronary vasodilator, 3-dimethylamino-1,1,2-tris (4-methoxyphenyl)-1-propene hydrochloride (WIN 5494) has been studied in 13 patients with angina pectoris, using a “double-blind” technique.2.2. No significant change in either the consumption of trinitrin or in exercise tolerance tests followed administration of the drug in a dose 25 mg. four times daily.3.3. The importance of a controlled study and objective criteria of improvement in the assessment of an antianginal drug is pointed out.

The seasonal and monthly frequency of occurrence in a series of 1,386 cases of proved myocardial infarction is reported from Dallas, Texas. The greatest number of cases occurred in the summer months, and the lowest number of cases in the winter months. No previous data from the United States have been reported concerning the seasonal variation in occurrence of this disease in a hot climate. The increased summer frequency of this illness is entirely different from previous reports from northern United States cities where the greatest number of cases have been found to occur during the winter months. The importance of very hot weather as a precipitating or predisposing factor in acute myocardial infarction is discussed.

We compared the short-term hemodynamic effects of intravenous fructose 1,6-diphosphate (FDP) administration in patients with coronary artery disease. Hemodynamic measurements were performed before and after administration of FDP in two groups of patients: those with impaired left ventricular (LV) function, elevated LV end-diastolic pressures (LVEDP > or =12 mm Hg, n = 30), and those with normal LV function (LVEDP <12 mm Hg, n = 17). In those with impaired LV function, FDP induced a decrease in LVEDP from 22 +/- 1.31 to 16.73 +/- 1.46 mm Hg (p< 0.0001). The cardiac index increased (2.50 +/- 0.11 to 2.81 +/- 0.13 L/m2 [p < 0.0001]), as did the LV stroke work index (31.7 +/- 2.04 to 40.3 +/- 2.67 gm x m x m2 [p < 0.0001]). FDP induced no significant change in heart rate and mean aortic pressure. Pulmonary pressure and resistance declined (p<0.002 and p< 0.0001, respectively). Systemic vascular resistance decreased because of increased cardiac output and unchanged arterial pressure (p < 0.001). In those patients with normal baseline LVEDP (5.06 +/- 0.27 mm Hg), FDP decreased heart rate (p< 0.0001) and systemic and pulmonary resistance (p < 0.03 and p < 0.004, respectively), whereas LVEDP and mean aortic and pulmonary pressures remained unchanged. FDP moderately increased cardiac output (p < 0.05), stroke volume index, and LV stroke work index (p< 0.002 and p< 0.003, respectively). The observed improvement in LV function in those patients with elevated LV filling pressures is thought to be a result of an increased energy production by the Embden-Meyerhoff pathway and to act as a positive inotrope.

To test the mechanism of action of fructose-1,6-bisphosphate (F-1,6-P2), experiments were conducted on isolated perfused rat hearts to measure the glycolytic rate supported by exogenous glucose with simultaneous measurement of oxygen consumption and the release of lactate and pyruvate. Glycolysis was assayed in terms of the release of tritiated water from [5-3H] glucose, a measure of the rate through the aldolase step. It was found that 5 mmol/L F-1,6-P2 reduced the glycolytic rate parallel to the decrease in oxygen consumption. The results suggest that the cardioprotective action of F-1,6-P2 is related to a substrate effect and a decrease in adenosine triphosphate consumption as indicated by a decrease in oxygen consumption in accordance with the recent demonstration of Ca2+ binding by F-1,6-P2.

1. 1. Records of 1,909 patients of the Outpatient Clinic of the National Children's Cardiac Hospital, Miami, Florida, were studied to determine the relative incidence of rheumatic heart disease in those born in Florida, as against those born outside of Florida. 2. 2. The northern boundary of the state of Florida at 31° N. latitude was taken as an arbitrary dividing line. 3. 3. Control analysis of records of children 5 through 17 years of age enrolled in the Dade County school system indicated that the outpatient records were comparable to the control records as to sex, color, and birthplace. More than one-half in each group were born outside of Florida. 4. 4. Rheumatic heart disease was 5.3 times more prevalent in white non-Floridians. 5. 5. The "rheumatic state" was diagnosed 2.6 times more frequently in non-Floridians than in Florida natives. This may signify less severe illness and fewer cardiac complications because of the favorable subtropical Florida climate. 6. 6. In Negroes, the difference between Floridians and non-Floridians as regards rheumatic heart disease and the rheumatic state was not apparent. The factors contributing to this are discussed. 7. 7. The present study of records weighted heavily with children suspected of having heart disease confirms previously reported4,5 low rheumatic heart disease rates in random samples of Florida-born school children. 8. 8. Possible explanations are offered for the lower rheumatic infection rate in Floridians. 9. 9. The findings provide additional indirect evidence of the favorable effect of Florida's subtropical climate on rheumatic fever and its cardiac complications. 10. 10. Variations in the congenital heart disease rates in Floridians and non-Floridians in this study are discussed.

Until recently, the presence of a permanent pacemaker or an implantable cardioverter-defibrillator has been a relative contraindication for the performance of magnetic resonance imaging (MRI). A number of small studies have shown that MRI can be performed with minimal risk when patients are properly monitored and device programming is modified appropriately for the procedure. However, the risk of performing MRI for patients with implanted cardiac devices has not been sufficiently evaluated to advocate routine clinical use. The aim of the present protocol is to prospectively determine the rate of adverse clinical events and device parameter changes in patients with implanted non-MRI-conditional cardiac devices undergoing clinically indicated nonthoracic MRI at 1.5 T. The MagnaSafe Registry is a multicenter, prospective cohort study of up to 1500 MRI examinations in patients with pacemakers or implantable cardioverter-defibrillators implanted after 2001 who undergo clinically indicated nonthoracic MRI following a specific protocol to ensure that preventable potential adverse events are mitigated. Adverse events and changes in device parameter measurements that may be associated with the imaging procedure will be documented. Through August 2012, 701 MRI studies have been performed, representing 47% of the total target enrollment. The results of this registry will provide additional documentation of the risk of MRI and will further validate a clinical protocol for screening and the performance of clinically indicated MRI for patients with implanted cardiac devices.

The hearts of eight dogs were cooled to asystole for as long as 35 minutes by refrigeration of blood circulated by a pump-oxygenator. The hearts started to beat again upon rewarming of the blood in the extracorporeal circulation and the animals survived the experiment without any clinically detectable sequelae during a one-month observation period.Electrocardiographic recordings throughout the entire procedure and in the postoperative period showed a remarkable absence of serious arrhythmias.ResumenEsseva effectuate asystolismo del corde de 8 canes durante periodos de usque 35 minutas per medio de refrigeration extracorporee del sanguine circulante via un pumpa oxygenator. Le cordes recomenciava batter post le recalefaction del sanguine in le circulation extracorporee, e le animales superviveva sin sequelas clinicamente detegibile durante un periodo de observationes postexperimental de 4 septimanas.Le registrationes electrocardiographic durante e post le experimento se distingueva per un remarcabile absentia de arrhythmias seriose.

In vitro testing is used to determine safe parameters before performing magnetic resonance imaging (MRI) on a patient with an implant. Therefore, the objective of this study was to evaluate a cardiac pacemaker using a 1.5-T magnetic resonance (MR) system. A modern cardiac pacemaker (INSIGNIA I PLUS, Model 1298, and FINELINE II, Model 4471, pacing leads; Guidant Corporation, St Paul, MN) was evaluated for magnetic field interactions at 1.5 T. Magnetic resonance imaging-related heating was assessed using 3 different 1.5-T scanners operating at various levels of radio-frequency power and imaging conditions. Functional aspects of the pacemaker were evaluated immediately before and after MRI (9 different pulse sequences). Artifacts were also characterized. Magnetic field interactions for the pacemaker were minor. Temperature changes measured in vitro were at levels that are not expected to pose a risk for specific MR conditions (< 4.0 degrees C). The function of the pacemaker was unaffected by MRI. Artifacts were minor for the leads and relatively large for the implantable pulse generator. The findings indicated that this pacemaker exhibited acceptable safety features relative to the use of a 1.5-T MR system. If induced currents do not occur for this device, it may be safe for a patient to undergo MRI by following specific conditions. The results are specific to the pacemaker tested, the MR systems, and conditions used in this evaluation.

Recent studies suggest that magnetic resonance (MR) imaging of the brain and spine may safely be performed in patients with pacemakers (PMs) and implantable cardioverter/defibrillators (ICDs), when taking adequate precautions. The aim of this study was to investigate safety, feasibility, and diagnostic value (DV) of MR imaging in cardiac applications (cardiac MR [CMR]) in patients with PMs and ICDs for the first time. Thirty-two PM/ICD patients with a clinical need for CMR were examined. The specific absorption rate was limited to 1.5 W/kg. Devices were reprogrammed pre-CMR to minimize interference with the electromagnetic fields. Devices were interrogated pre-CMR and post-CMR and after 3 months. Troponin I levels were measured pre-CMR and post-CMR; image quality (IQ) and DV of CMR were assessed. All devices could be reprogrammed normally post-CMR. No significant changes of pacing capture threshold, lead impedance, and troponin I were observed. Image quality in patients with right-sided devices (RSD) was better compared with that in patients with left-sided devices (LSD) (P < .05), and less myocardial segments were affected by device-related artefacts (P < .05). Diagnostic value was rated as sufficiently high, allowing for diagnosis, or better in 12 (100%) of 12 patients with RSD, and only in 7 (35%) of 20 patients with LSD. Cardiac MR may be performed safely when limiting specific absorption rate, appropriately monitoring patients, and following device reprogramming. Cardiac MR delivers good IQ and DV in patients with RSD. Cardiac MR in patients with RSD may therefore be performed with an acceptable risk/benefit ratio, whereas the risk/benefit ratio is rather unfavorable in patients with LSD.

Traditional methods of using creatinine kinase (CK)-MB to diagnose acute myocardial necrosis rely on the total CK-MB exceeding a threshold of normalcy before being considered diagnostic. Because the CK-MB rapid immunoassay is both sensitive and precise, a small difference between two serial samples over an appropriate time interval may result in an increased sensitivity for acute myocardial infarction (AMI) compared with traditional methods if an appropriate cutoff value is chosen. Baseline and 2-hour CK-MB immunoassay measurements were performed in 710 patients with chest pain whose baseline CK-MB was less than two times upper limits of normal (<12 ng/ml) to determine whether a rise in CK-MB > or =+1.6 ng/ml is more sensitive and specific than an abnormal 2-hour CK-MB in the detection of patients with AMI during the initial emergency department evaluation of chest pain. The baseline (MBO) or 2-hour (MB2) CK-MB was considered positive if the CK-MB level was > or =6 ng/ml. MBdelta was defined as the difference of MB2 and MBO and was considered positive if the value was > or =+1.6 ng/ml. A positive MB2 was more sensitive for the detection of AMI (75.2% vs 17.7%; p < 0.0001) than a positive MBO. A positive MBdelta was more sensitive for the detection of AMI (93.8% vs 75.2%; p < 0.0001 ) than a positive MB2. There were no statistically significant differences in specificities for AMI for any test modality. A rise in CK-MB of > or =+ 1.6 ng/ml in 2 hours is a useful marker of AMI during the initial emergency department evaluation of patients with chest pain.

Despite advances in antithrombotic therapies and invasive technology, the risk of recurrent ischemic complications in patients with non-ST-elevation acute coronary syndromes (NSTE-ACSs) remains substantial. Ranolazine is a novel agent that inhibits the late sodium current thereby reducing cellular sodium and calcium overload and has been shown to reduce ischemia in patients with chronic stable angina. MERLIN-TIMI 36 is a phase III, randomized, double-blind, parallel-group, placebo-controlled, multinational clinical trial to evaluate the efficacy and safety of ranolazine during long-term treatment of patients with NSTE-ACS receiving standard therapy (N = 6500). Eligible patients are randomized 1:1 to ranolazine or matched placebo, initiated as 200 mg intravenously over 1 hour, followed by an 80-mg/h infusion (40 mg/h for patients with severe renal insufficiency) for up to 96 hours and oral ranolazine ER 1000 mg BID or matched placebo until the end of study. The primary end point is the time to first occurrence of any element of the composite of cardiovascular death, myocardial infarction, or recurrent ischemia. Secondary end points include ischemia on Holter monitoring, hospitalization for new or worsening heart failure, quality of life measures, and exercise performance. The evaluation of long-term safety will include death from any cause and symptomatic documented arrhythmia. Recruitment began in October 2004. The trial will continue until 730 major cardiovascular events and 310 deaths are recorded with expected completion in 24 to 28 months. MERLIN-TIMI 36 will evaluate the role of ranolazine in the acute and chronic management of patients presenting with NSTE-ACS.

The ADHERE is designed to study characteristics, management, and outcomes in a broad sample of patients hospitalized with acute decompensated heart failure. Heart failure is a leading cause of hospitalization for adults older than 65 years in the United States. Most available data on these patients are limited by patient selection criteria and study design of clinical trials and single-center studies. Participating hospitals identify patients with a primary or secondary discharge diagnosis of heart failure. Medical history, management, treatments, and health outcomes data are collected through review of medical records and entered into a database via secure web browser technology. As of January 2004, data on 107 362 patients have been received from 282 participating hospitals. Of enrollees with available analyzable data (N = 105 388 from 274 hospitals), the mean age was 72.4 (+/-14.0), and 52% were women. The most common comorbid conditions were hypertension (73%), coronary artery disease (57%), and diabetes (44%). Evidence of mild or no impairment of systolic function was found in 46% of patients. Inhospital mortality was 4.0% and the median hospital length of stay was 4.3 days. The ADHERE demonstrates both the feasibility and significant implications of gathering representative data on large numbers of patients hospitalized with heart failure. Initial data provided important insights into the clinical characteristics and patterns of care of these patients. Ongoing registry work will provide the framework for improved treatment strategies for patients hospitalized with decompensated heart failure.

More than 200,000 permanent pacemakers will be implanted in the United States in 2000 at a cost of more than $2 billion. Sick sinus syndrome (SSS) will likely account for approximately half of all cases necessitating implantation. Pacemaker technology permits the selection of ventricular (single-chamber) or dual-chamber devices. However, clinical and outcomes data are inadequate to support a clear recommendation that one or the other type of device be used. The Mode Selection Trial (MOST) is a single-blind study supported by the National Heart, Lung, and Blood Institute designed to enroll 2000 patients with SSS. All patients will receive a DDDR pacemaker programmed to VVIR or DDDR before implantation. The average time of follow-up will be 3 years. MOST has a >90% power to detect a 25% reduction in the primary end point-nonfatal stroke or total (all cause) mortality-in the DDDR-treated group. Secondary end points will include health-related quality of life and cost effectiveness, atrial fibrillation, and development of pacemaker syndrome. Prespecified subgroups for analysis will include women and the elderly. Enrollment was completed in October 1999, with a total of 2010 patients. The median age of the first 1000 enrolled patients is 74 years, with 25% of patients 80 years or older. Women comprise 49%, and 17% are nonwhite, predominantly black (13%). Before pacemaker implantation, 22% of patients reported a history of congestive heart failure, 11% coronary angioplasty, and 25% coronary bypass surgery. Supraventricular tachycardia including atrial fibrillation was present in 53% of patients. A prior stroke was reported by 12%. Antiarrhythmic therapy was in use in 18% of patients. MOST will fill the clinical need for carefully designed prospective studies to define the benefits of dual-chamber versus single-chamber ventricular pacing in patients with SSS. The MOST population is typical of the overall pacemaker population in the United States. Thus the final results of MOST should be clinically generalizable.

Cardiac tamponade is a life-threatening complication of acute myocardial infarction (MI). Data on the incidence, risk factors, and outcome of tamponade in patients with acute MI in the fibrinolytic era are limited. Data from a combined clinical trials database of ST-segment elevation MI were used to evaluate the incidence of cardiac tamponade, baseline characteristics, and outcomes in patients with and without tamponade. Univariable and multivariable analyses assessed the relationship between patient characteristics and tamponade development, and the influence of tamponade on mortality. Of 102,060 patients, 865 (0.85%) developed isolated cardiac tamponade during initial hospitalization. Patients with tamponade were older (median 71.9 vs 61.6 years, P < .001), were more likely to be female (54.0% vs 25.1%, P < .001), were more likely to have an anterior MI (61.9% vs 41.5%, P < .001), and had a longer time from symptom onset to reperfusion (median 3.5 vs 2.8 hours, P < .001) than those without tamponade. Multivariable analyses identified increasing age, anterior MI location, female sex, and increased time from symptom onset to treatment as significant independent predictors of tamponade. Patients with tamponade had an increased death rate at 30 days (hazard ratio 7.9, 95% CI 4.7-13.5). Cardiac tamponade occurs in < 1% of patients with fibrinolytic-treated acute MI and is associated with increased 30-day mortality. Time from symptom onset to treatment strongly predicted the development of tamponade, underscoring the need for continued efforts to increase speed to treatment in acute MI.

Orthogonal ECG's (Frank system) were recorded from 1,002 patients with documented nyocardial infarction. In 39 per cent of this series, tracings were obtained during the acute phase of the disease and in 61 per cent at a later date. Records from 229 normal subjects above the age of 40 years served as control. A total of 333 different ECG measurements were computed from each record in order to search for optimal discriminators between the group of normal subjects and the patients with myocardial infarct.

The present study was undertaken to investigate whether chronic smoking alters the vasodilatory capacity in the microcirculation. We assessed, in habitual cigarette smokers, the forearm skin blood flow response to iontophoretically applied acetylcholine (endothelium-dependent vasodilator) and sodium nitroprusside. Postocclusive forearm reactive hyperemia was also explored. The skin blood flow responses were determined with a laser-Doppler flowmeter that allowed us to scan the surface after acetylcholine and sodium nitroprusside application. Forty healthy male volunteers were included. Twenty subjects were aged 20 to 35 years and 20 subjects were aged 40 to 60 years. We studied the following 4 groups of 10 subjects each: group 1, younger smokers (mean of 7.2 pack-years); group 2, older smokers (mean of 30 pack-years); group 3, younger nonsmokers; and group 4, older nonsmokers. On the day of the experiment, the subjects of groups 1 and 2 were asked to smoke at least 15 cigarettes from the morning until the afternoon, when the experiments were performed. No significant difference in the studied parameters was observed between younger smokers and younger nonsmokers. In older smokers, however, both acetylcholine- and sodium nitroprusside-induced skin blood flow increases were significantly attenuated in comparison with nonsmokers. Heart rate also was significantly blunted by long-term cigarette smoking in older subjects. These data show that the vasodilatory response of the skin microvasculature is impaired in subjects who have smoked cigarettes for many years. This abnormality involves both endothelium-dependent and endothelium-independent responses.

To avoid ischemic hand complications, the percutaneous transradial approach is only performed in patients with patent hand collateral arteries, which is usually evaluated with the modified Allen's test (MAT). This qualitative test measures the time needed for maximal palmar blush after release of the ulnar artery compression with occlusive pressure of the radial artery. The objectives were to evaluate the patency of the hand collateral arteries and to compare MAT with combined plethysmography (PL) and pulse oximetry (OX) tests before the percutaneous transradial approach. Patients referred to the catheterization laboratory were prospectively examined with MAT, PL, and OX tests. PL readings during radial artery compression were divided into 4 types: A, no damping; B, slight damping of pulse tracing; C, loss followed by recovery; or D, no recovery of pulse tracing within 2 minutes. OX results were either positive or negative. Results of both tests were compared in 1010 consecutive patients. MAT results < or =9 seconds on either hand were seen in 93.7% of patients. PL and OX types A, B, or C on either hand were seen in 98.5% of patients. On the basis of the MAT < or =9 seconds criteria, 6.3% of patients were excluded from the transradial approach, whereas with PL and OX types A, B, and C, only 1.5% of patients were excluded. There was more exclusion in men and with increasing age by using both methods. In the evaluation of hand collaterals, PL and OX were found to be more sensitive than MAT. When applied to transradial approach screening, only 1.5% of patients were not suitable candidates for the transradial approach.

An electrocardiographic instrument, known as the axostat, is described which provides a simple method for rapid and accurate determination of the directions of mean QRS and T vectors in their frontal and sagittal projections without the need for planimetric evaluation of areas under electrocardiographic deflections. Such determinations were made in a group of 102 normal, youthful adults, and the orientation of the mean spatial QRS and T vectors was calculated from these data. The validity of several types of spatial electrocardiographic connections is discussed. Probably none of the associated frames of reference are accurate from the standpoint of strict geometric interpretation, but undoubtedly some of them will prove useful for the interpretation of electrocardiographic data. Other frames of reference should be discarded because they introduce certain incompatibilities. The Wilson tetrahedron is employed in this study because it introduces no such incompatibilities, the associated lead connections are simple and easily reproduced, and the frontal plane components of our spatial data are directly applicable to conventional extremity lead electrocardiography. The directions of mean QRS and T vectors in our group of normals display as much variability in the sagittal plane as they do in the frontal plane. However, the two sets of data are interrelated in a highly significant manner. Analysis of these relationships strongly suggests that three spatial electrocardiographic indices be firmly established and further investigated: (a) the locus of the mean spatial QRS vector, (b) the locus of the mean spatial T vector, and (c) the angle between the mean spatial QRS and T vectors. The primary virtue of these spatial indices appears to be reduced variability in the range of normal values. According to the standard deviations in our group of normals the scatter of the spatial electrocardiographic indices about their average values is reduced to almost one-half the scatter in the case of the corresponding planar indices. It is anticipated that this reduction in scatter will result in more precise criteria of normality and abnormality.

It has been shown that patients with an acute myocardial infarction and persistent electrocardiographic ST-segment depression are at high risk for subsequent cardiac events. The purpose of this retrospective analysis was to examine the long-term effects of propranolol therapy in patients with their first acute myocardial infarction and persistent electrocardiographic ST-segment depression. The outcomes of 2877 patients enrolled in the Beta-Blocker Heart Attack Trial (BHAT) with their first myocardial infarction (75% of patients in BHAT) were reviewed. Patients were divided into three groups on the basis of presence or absence of > or =1 mm ST-segment depression in two contiguous leads of the 12-lead electrocardiogram obtained soon after admission or at the time of randomization, which occurred 10.1+/-3.5 days after the index myocardial infarction. Group 1 included 774 patients (392 randomly assigned to placebo and 382 to propranolol) with no ST-segment depression; group 2 included 1447 patients (713 placebo, 734 propranolol) with ST-segment depression at admission or at the time of randomization (labeled as transient); and group 3 included 656 patients (339 placebo and 317 propranolol) who had electrocardiographic ST-segment depression from the time of admission to the time of randomization (labeled as persistent). In group 3, patients with persistent electrocardiographic ST depression, the mortality rate in patients randomly assigned to placebo was 13.6% compared with 7.6% in patients with propranolol (p = 0.012; log rank test). Sudden death in the placebo arm was 9.7% compared with 4.7% in the propranolol group (p = 0.012, log rank test). The results of the Cox regression analysis, adjusting for all baseline variables with p values <0.25, showed the relative risk of overall mortality rate and the relative risk of sudden death were 2.13 ( 1.22, 3.70) and 2.56 (1.27, 5.26), respectively, for the placebo group compared with the propranolol group. Patients with persistent ST-segment depression had the greatest benefit from propranolol (47.2 fewer events [deaths/reinfarctions] per 1000 person-years compared with 78 and 2.1 fewer events in patients with transient and no ST-segment depression, respectively). It appears that the greatest benefit for beta-blocker therapy in patients after myocardial infarction is observed in patients with persistent ST-segment depression who are at greatest risk for death and reinfarction. Definitive conclusions regarding therapy with beta-adrenergic blocking agents in patients with persistent ST-segment depression cannot be made because our analysis, given its retrospective nature, is only hypothesis generating.

Echocardiography was used to indirectly assess the effects of marathon running on myocardial performance. Thirteen marathon runners (mean +/- SEM:30 +/- 1.6 years) were submitted to a resting echocardiographic examination before racing and during early recovery from marathon racing. Indices of left ventricular performance were computed from M-mode recordings of left ventricular dimensions and aortic valve motions. Comparison of basal and post-marathon indices of left ventricular performance showed no significant differences in either pre-ejection period (PEP), left ventricular ejection index (LVEI), fractional shortening (% delta D), ejection fraction (EF), or mean rate of circumferential fiber shortening (mVcf). Cardiac output (Qc) computed from left ventricular end-diastolic (LVEDV) and end-systolic volumes (LVESV) were significantly higher following marathon running (4.9 +/- 0.4 to 6.7 +/- 0.7 L/min) because of a marked increase in resting heart rate (HR) (58 +/- 3 to 76 +/- 3 bpm). A significant decrease in systolic blood pressure (118 +/- 4 to 108 +/- 3 mm Hg), associated with a slight reduction in calculated total peripheral resistance was also observed after the race. These circulatory adjustments probably reflect thermoregulatory activity that allows a greater blood flow to the skin for heat dissipation, as well as persistence of reactive muscle hyperemia. Echocardiographic evidence suggests that marathon running does not lead to marked impairments in left ventricular performance. However, the absence of change in the end-systolic volume, despite a marked reduction in cardiac afterload, may suggest a slight alteration in contractility that could not be detected with the use of echocardiography.

The authors have analyzed the rhythm of 124 electrocardiograms from 103 autopsied patients with chronic chagasic myocarditis. The most frequent types of arrhythmias were ventricular extrasystoles, atrioventricular block, and bundle branch block. A higher incidence of right bundle branch block was found, but left bundle branch block was more frequently encountered than usually reported. Complete right bundle branch block showed a peculiar distribution of ÂQRS between -60° and -90°, and terminal QRS vectors between -100° and -150°. These orientations seem to be related to the anatomic findings of hypertrophy, dilatation, and apical fibrosis of the ventricles. The presence of right bundle branch block with an upward and left deviation of the ÂQRS, frequently associated with another kind of arrhythmia, is so characteristic in Chagas' disease that if these electrocardiographic signs are found in a young patient with an acquired cardiopathy, they will strongly suggest that we are dealing with chagasic myocarditis, at least in countries where Chagas' disease is endemic. The vectorial analysis of left bundle branch block was without peculiarities, but Q waves in Leads I, aVL, and V5 even in the presence of complete left bundle branch block was frequently found (45.5 per cent). In 5 of 11 patients showing complete left bundle branch block the ages were 18, 20, 20, 22, and 23 years, respectively. An electrocardiographic diagnosis of bilateral "focal" block was made in 8 cases showing disturbances of the intraventricular conduction and QRS complexes predominantly positive in all precordial leads.

1.1. The long-term effects of a typical monoamine oxidase inhibitor, DL-serine-N2-isopropylhydrazide monohydrochloride (RO 4-1038), alone or in combination with chlorothiazide were studied in 53 patients with moderate arterial hypertension.2.2. There was a highly significant decrease in mean arterial pressure in both the supine and standing positions after 6 weeks of therapy, with a more marked response in the standing position. After prolonged administration, the hypotension was still significant. The addition of chlorothiazide did not appear to cause a significant further reduction in blood pressure.3.3. Side effects of RO 4-1038 were mild and seldom necessitated discontinuation of therapy. No major toxicity was found.4.4. No correlation was found between the increase in urinary tryptamine excretion and the hypotensive response in individual patients, which suggests that the antihypertensive effects of RO 4-1038 and similar compounds may be unrelated to their MAO inhibiting properties.5.5. It is thought that RO 4-1038 is a valuable adjunct in the treatment of hypertension.

To assess the effect of long-term athletic training on the heart, 104 professional cyclists and 40 sedentary controls (69 younger cyclists and 26 controls aged 20 to 39 and 35 older cyclists and 14 controls aged 40 to 60) were examined by using M-mode and pulsed Doppler echocardiography. Cyclists had larger and more hypertrophied left ventricle than did controls (p < 0.001) and had normal percentages of fractional shortening (%FS). The ratio of left ventricular late-to-early diastolic peak filling velocity (A/R) of younger cyclists was normal, but the A/R of older cyclists was larger than that of controls (p < 0.001). Of the 104 cyclists, 95 continued cycling and were reexamined 2 years later; 9 of 40 older cyclists retired and were reexamined 20 +/- 8 months after retirement. During the follow-up period for the active cyclists, left ventricular dilatation, hypertrophy, and %FS of both younger and older cyclists and the A/R of younger cyclists did not change. However, the A/R of older cyclists increased (p < 0.01). For the nine retired cyclists, left ventricular dimension decreased (p < 0.001), left ventricular wall thickness and %FS did not change, and A/R increased (p < 0.05) after retirement. We concluded that (1) cyclists had large and hypertrophied left ventricles with normal systolic function, and (2) some cyclists with long-term athletic training may have partly irreversible left ventricular hypertrophy with impaired left ventricular diastolic filling.

Of 105 cases of lesions of the sinus of Valsalva found over a 25-year period at the Shanghai Chest Hospital, 90 were ruptured sinuses or sinus aneurysms and 15 were unruptured aneurysms. The cases were classified roentgenologically according to the method of Sakakibara and Konno: 64.5% were type I, 23.7% type II, 1.1% type IIIv, 6.4% type IIIa, 1.1% type IIIa + v, and 3.2% type IV. A new and simplified method of classification has been devised in the Shanghai Chest Hospital and shows the highest incidence to be the type of aneurysm of the sinus of Valsalva associated with ventricular septal defect. On aortography three types of morphologic changes--aneurysmal formation, enlargement of the sinus with no definite aneurysm, and sinus rupture with no enlargement or aneurysmal formation--are observed. Angiographically, shunting from ruptured sinus or sinus aneurysm begins in middiastole and gradually increases to end diastole. Aortic insufficiency, if present, usually begins in early diastole and extends over the whole diastolic phase in a decrescendo fashion. Special attention should be paid to the differentiation between ruptured sinus of Valsalva with or without aneurysmal formation and ventricular septal defect with aortic insufficiency.

Thiazides produce an average loss of 2 L of extracellular fluid volume, of which about 300 ml is plasma volume, during the first 48 hours of administration, and this reduction is maintained without further loss for as long as the drug is given. Do thiazides lower blood pressure by volume depletion or by direct vasodilator action? As evidence against the vasodilator theory, these facts may be adduced: (1) thiazides do not lower blood pressure in patients (with renal disease) who cannot obtain a diuresis, and (2) other diuretics and diets very low in sodium also reduce blood pressure and volume to a similar degree. A related hypothesis is that thiazides reduce total peripheral vascular resistance (TPR) by "dehydrating" vascular walls. However, direct measurements in small arteries failed to confirm such changes. There is, however, a fall in TPR after long-term treatment, although initially cardiac output falls and TPR remains unchanged. How these long-term readjustments occur remains unknown, although several hypotheses have been advanced.

To test the applicability of Doppler ultrasound in the evaluation of prosthetic valve function, 107 patients with normal ejection fractions in whom Starr-Edwards, Björk-Shiley, Carpentier-Edwards, and Hancock models had been implanted in the aortic position were examined. Maximal transvalvular velocity was recorded by non-imaging continuous wave Doppler ultrasound. Means of maximal velocities by model and size ranged from less than 2 to 4 m/sec. The Starr-Edwards valve showed the highest velocities, the Björk-Shiley the lowest, and the bioprosthetic models showed velocities in between. A significant inverse relation between velocity and size, and standard deviations averaging +/- 14% enabled the technique to measure differences between sizes of the same model. Aortic regurgitation was detected in 24% of the patients. This study, conducted in well and stable patients, established values for maximal velocity across normally functioning aortic mechanical and tissue prostheses of different models and sizes. The intersubject variability was relatively small which, together with a previously shown minimal intrasubject variability, was testimony to a methodology that should prove useful in longitudinal postoperative evaluations.

The clinical experience derived from the retrospective study of 107 cases of TA over a 19 year period is presented. The disease predominated in females (8.5:1), with age of onset usually less than 20 years. In half of the cases an acute inflammatory phase was observed, characterized mainly by systemic and cardiovascular symptoms. Subsequently the natural course of TA was toward chronicity with gradual deterioration. The most frequent variety of TA (65 per cent of the patients) was Type III, in which the supra-aortic trunks and the abdominal aorta were involved. The predominant clinical features were reduction of amplitude of peripheral arterial pulses (96 per cent), vascular bruits (94 per cent), and raised blood pressure (72 per cent), mainly resulting from renal arterial involvement (62 per cent). Heart failure (28 per cent) is rarely the result of direct coronary arteritis. TA is most often confused with aortic coarctation, but usually the aortogram distinguishes these. The etiology of TA is discussed. The high incidence of previous and present active tuberculous (48 per cent) in the present series and previous experimental work suggest that tuberculosis may play an important role in the etiology of TA. Treatment for antihypertension and heart failure should be employed when indicated. Treatment with corticosteroids requires further evaluation. Treatment for tuberculosis is not justified in all cases until the exact role of tuberculosis is well established.

Prior studies on chronic systolic heart failure (HF) have demonstrated that body mass index (BMI) is inversely associated with mortality, the so-called obesity paradox. The aim of this study was to determine whether BMI influences the mortality risk in acute decompensated HF, a subject not previously studied. The Acute Decompensated Heart Failure National Registry was analyzed for acute HF hospitalizations in 263 hospitals in the United States from October 2001 through December 2004. Patients with documented height and weight were divided into BMI (measured in kilograms per square meter) quartiles. Inhospital mortality by BMI quartile for all the patients and for those with reduced (n = 43,255) and preserved (n = 37,901) systolic function was assessed. Body mass index quartiles in the 108,927 hospitalizations were QI (16.0-23.6 kg/m2), QII (23.7-27.7 kg/m2), QIII (27.8-33.3 kg/m2), and QIV (33.4-60.0 kg/m2). Patients in the higher BMI quartiles were younger, had more diabetes, and had a higher left ventricular ejection fraction. Inhospital mortality rates decreased in a near-linear fashion across successively higher BMI quartiles. After adjustments for age, sex, blood urea nitrogen, blood pressure, creatinine, sodium, heart rate, and dyspnea at rest, BMI quartile still predicted mortality risk. For every 5-U increase in BMI, the odds of risk-adjusted mortality was 10% lower (95% CI 0.88-0.93, P < .0001). In this cohort of hospitalized patients with HF, higher BMI was associated with lower inhospital mortality risk. The relationship between BMI and adverse outcomes in HF appears to be complex and deserving of further study.

Serial intravascular ultrasonographic (IVUS) studies have shown that in-stent restenosis is the result of intimal hyperplasia (IH). However, routine preintervention IVUS imaging has suggested that many restenotic stents were inadequately deployed. The purpose of this IVUS study was to determine the incidence of mechanical problems contributing to in-stent restenosis (ISR). Between April 1994 and June 2000, 1090 patients with ISR were treated at the Washington Hospital Center. All underwent preintervention IVUS imaging. IVUS measurements included proximal and distal reference lumen areas and diameters; stent, minimum lumen, and IH (stent minus lumen) areas; and IH burden (IH/stent area). In 49 ISR lesions (4.5%), there were morphologic findings that contributed to the restenosis. These were termed mechanical complications. Examples include (1) missing the lesion (eg, an aorto-ostial stenosis), (2) stent "crush," and (3) having the stent stripped off the balloon during the implantation procedure. Excluding mechanical complications, stent underexpansion was common. In 20% of the ISR cases the stents had a cross-sectional area (CSA) at the site of the lesion <80% of the average reference lumen area. Twenty percent of lesions had a minimum stent area <5.0 mm(2) and an additional 18% had a minimum stent area of 5.0 to 6.0 mm(2). Twenty-four percent of lesions had an IH burden <60%. Mechanical problems related to stent deployment procedures contribute to a significant minority of ISR lesions (approximately 25%).

RPR 109891 is a modified tetrapeptide glycoprotein IIb/IIIa inhibitor available in intravenous and oral formulations. Two phase II dose-ranging studies were performed to investigate pharmacodynamics and safety in acute coronary syndromes. The Thrombolysis In Myocardial Infarction (TIMI) 15A trial was a randomized, open-label, study of RPR 109891 administered intravenously for 24 to 96 hours in 91 patients. TIMI 15B was a randomized, double-blind comparison of intravenous RPR 109891 plus 4 weeks of oral RPR 109891 (n = 142) compared with placebo (n = 50). Intravenous RPR 109891 exhibited a dose-response inhibition of platelet aggregation; mean inhibition after a bolus ranged from 53% to 92%, and at steady state 49% to 98%. Oral RPR 109891 demonstrated less platelet inhibition (peaks, range 48% to 59%; troughs, range 18% to 39%). Mean glycoprotein IIb/IIIa receptor occupancy and platelet inhibition were highly correlated (r = 0.82, 95% confidence interval 0.74-0.88). There were trends for increased major hemorrhage (10% vs 6%, P =.57), thrombocytopenia <90,000 cells/mm(3) (13% vs 4%, P =.11), and profound thrombocytopenia <20, 000 (3.5% vs 0%, P =.33) with intravenous plus oral RPR 109891 compared with placebo. In 3 of 5 cases of profound thrombocytopenia, RPR 109891 had been interrupted because of bypass surgery, and a precipitous fall in platelet count occurred after the first postoperative oral dose. Intravenous RPR 109891 is a potent, predictable, dose-related platelet inhibitor. Oral RPR 109891 (</=600 mg/d) achieves moderate platelet inhibition. Interrupted glycoprotein IIb/IIIa blockade may be associated with a higher risk of profound thrombocytopenia and deserves closer examination in future studies.

The availability of a reliable, noninvasive serum marker of reperfusion may permit early identification of patients with occlusion after thrombolysis who might benefit from further interventions. We measured myoglobin, creatine kinase MB (CK-MB), and cardiac troponin-I (cTnI) concentrations in sera obtained just before thrombolysis (T0) and 60 minutes later (T60) in 30 patients given TNK-tPA for acute myocardial infarction as part of the Thrombolysis in Myocardial Infarction (TIMI) 10A trial. Angiography at T60 showed reperfusion (TIMI flow grade 2 to 3; n = 19) or occlusion (TIMI flow grade 0 to 1; n = 8). The median serum T60 concentration, the ratio of the T60 and T0 serum concentration, and the slope of increase over a 60-minute period for each serum marker were significantly higher in patients with patent arteries compared with patients with occluded arteries. The areas under the receiver operator characteristics curve for diagnosis of occlusion were 0.96, 0.91, and 0.87 for the T60 concentration of myoglobin, CK-MB and cTnI, respectively. Although the T60 levels of <469 ng/ml for myoglobin, <11.5 ng/ml for CK-MB, and < 1.1 ng/ml for cTnI identified all patients with occlusion, the specificity of myoglobin (94%) was higher than that of CK-MB (61%) and cTnI (67%). Similar results were obtained for the 60-minute ratios and 60-minute slopes for each marker, with indexes for myoglobin having the highest specificity. In this pilot study, noninvasive diagnosis of occlusion 60 minutes after thrombolysis was achieved with a high degree of sensitivity and specificity with the myoglobin, CK-MB, and cTnI concentrations measured at that time point. These preliminary findings may permit a new strategy for assessment of the success of reperfusion, with triage to rescue angioplasty for patients in whom the 60-minute cardiac marker values or indexes are consistent with occlusion of the infarct-related artery.

We sought to identify, by use of serum cardiac markers, patients at low risk for 30-day mortality after ST-segment elevation myocardial infarction. Baseline cardiac markers are currently used to identify patients at increased risk for short-term events. We hypothesized that serum markers measured after treatment could identify patients at low risk for 30-day mortality. A total of 839 patients from the Thrombolysis in Myocardial Infarction (TIMI) 10B study had myoglobin, cardiac-specific troponin-I, creatine kinase (CK)-MB measurements at the following time points; baseline, 90 minutes, and 3 and 12 hours after thrombolysis. By use of receiver operating characteristic analysis, thresholds were derived to predict 30-day mortality with at least 95% negative predictive value. Ninety minutes after thrombolysis myoglobin was superior to troponin-I or CK-MB in identifying patients at low risk for mortality. The 30-day mortality for 12-hour myoglobin < or = 239 ng/mL was 1.4% compared with 9.1% for levels > 239 ng/mL (P < .001). For 12-hour troponin-I (threshold 81.5 ng/mL), mortality was 1.9% versus 6.6% (P = .001) if above threshold; similarly for CK-MB at 12 hours (threshold 191 ng/mL) it was 3.3% versus 7.9% (P = .02). Multivariate analysis of baseline and posttreatment cardiac markers, age, sex, infarct artery location, and 90-minute TIMI flow grade identified only 12-hour myoglobin among the cardiac markers as independently predicting a low 30-day mortality (odds ratio 0.11, 95% confidence interval 0.02-0.50, P < .004). Serum cardiac markers can identify greater than two thirds of patients at low risk for 30-day mortality. A low 12-hour myoglobin level (< or = 239 ng/mL in this substudy) identifies such patients at low risk and could potentially assist in early risk stratification and triage after ST-segment elevation myocardial infarction.