J. Am. Coll. Cardiol. 1998;31;783-789 PW Armstrong A Langer, MW Krucoff, P Klootwijk, ML Simoons, CB Granger, A Barr, RM Califf, andST Segment Monitoring Substudy patients with myocardial infarction treated with thrombolytic therapy: the GUSTO-I Prognostic significance of ST segment shift early after resolution of ST elevation inThis information is current as of July 24, 2011 http://content.onlinejacc.org the World Wide Web at: The online version of this article, along with updated information and services, is located onDownloaded from content.onlinejacc.org

BACKGROUND:A number of case reports link the use of 5-aminosalicylic acid (5-ASA) to interstitial nephritis in patients with inflammatory bowel disease (IBD).OBJECTIVE:To investigate whether the long-term use of 5-ASA has harmful effects on renal function in patients with IBD.METHODS:A retrospective analysis of 171 consecutive outpatients with Crohn's disease or ulcerative colitis was conducted. Serum creatinine levels and body weight were measured before and after treatment to calculate the creatinine clearance (CrCl) rate.RESULTS:In 171 patients (93 women, 78 men), the mean (+/- SD) dose of 5-ASA was 3.65+/-0.85 g/day with a cumulative dose of 11+/-7.7 kg over an interval of 8.4+/-5.9 years. Serum creatinine concentrations increased from 76.8 micromol/L to 88.7 micromol/L (n=171; P<0.0001) and the CrCl rate fell significantly from 104.6 mL/min to 93.1 mL/min (n=81; P<0.0001). There was one case of interstitial nephritis reported. Treatment groups included mesalamine (74.3%), sulfasalazine (15.2%) and combination (sulfalsalazine/mesalamine [10.5%]) with treatment durations of 7.2+/-4.5, 12.3+/-8.7 and 11.2+/-6.7 years, respectively. The duration of treatment was the most important covariate for change in CrCl and when analyzed by treatment group, those treated with sulfasazine had a strong correlation (r=-0.54, P=0.0145), while nonsignificant in the mesalamine group (r=0.06, P=0.7017). The decline in CrCl was negatively correlated with the pretreatment CrCl rate (r=-0.34; P=0.0024) and positively correlated with the mean daily dose of 5-ASA (r=0.32; P=0.0034).CONCLUSION:The present study is the first to demonstrate a significant dose- and treatment duration-dependant decline in CrCl. The risks need to be further evaluated because 5-ASA is widely used for long-term maintenance therapy in patients with IBD.

The impact of heart failure and its treatment on specific nutrient requirements is unknown. Furthermore, depletion of water-soluble B vitamins that play key roles in the production of cellular energy in patients with heart failure can contribute to depletion of energy reserves observed in the failing heart. A cross-sectional study recently reported that approximately one third of hospitalized patients with heart failure had tissue levels suggestive of thiamin deficiency (vitamin B-1). Riboflavin (vitamin B-2) and pyridoxine (vitamin B-6) are similar to thiamin in that they are water-soluble, subject to renal excretion, have limited tissue storage, and are dependent on intake. Therefore, it was hypothesized that the status of these B vitamins may also be adversely affected by heart failure. As a result, the prevalence of patients at risk of vitamin B-2 (erythrocyte glutathione reductase activity coefficient > or = 1.2) and B-6 deficiency (plasma B-6 < or = 20 nmol/L) was determined in a cross-section of 100 patients hospitalized with heart failure between April 2001 and June 2002 as well as in a group of volunteers without heart failure. Twenty-seven percent of patients with heart failure had biochemical evidence of vitamin B-2 deficiency, while 38% had evidence of B-6 deficiency. These prevalence rates were significantly higher than those observed in the volunteers without heart failure (2% and 19%, respectively; P < or = 0.02). Use of common B-vitamin-containing supplements by patients with heart failure did not significantly reduce deficiency rates in comparison with those who did not use supplements (B-2 P=0.38 or B-6 P=0.18)). Finally, while 80% of patients with heart failure took diuretics, neither the dose nor the duration of furosemide use was related to the presence of either B-2 or B-6 deficiency. Given the physiologic importance of these vitamins, further investigations aimed at determining the effect of heart failure on specific nutrient requirements as well as the safety and efficacy of B-vitamin supplementation are warranted.

BACKGROUND Survivors of ARDS report depressive symptoms and memory complaints, the prevalence of which after 5 years is unknown. METHODS We administered instruments assessing symptoms of depression (Beck Depression Inventory II [BDI-II]) and memory complaints (Memory Assessment Clinics Self-Rating Scale [MAC-S]) to 64 survivors of ARDS from four university-affiliated ICUs 5 years after ICU discharge. We compared BDI-II scores to quality of life (Medical Outcomes Study 36-Item Short Form [SF-36]) mental health domains (role emotional, mental health, mental component summary), compared BDI-II and MAC-S scores to earlier scores (median, 22 months postdischarge), and examined return to work. RESULTS Forty-three (67.2%), 46 (71.9%), and 38 (59.4%) patients fully completed the BDI-II, MAC-S ability subscale, and MAC-S frequency of occurrence subscale, respectively. Responders were young (median, 48 years; first-third quartile [Q1-Q3], 39-61 years) with high illness severity. The median BDI-II score was 10 (Q1-Q3, 3-18); eight of 43 (18.6%) had moderate to severe depressive symptoms compared with 14 of 43 (32.6%) earlier (P = .15, n = 38 with paired data). Median MAC-S ability and MAC-S frequency scores were 81 (Q1-Q3, 57-92) and 91.5 (Q1-Q3, 76-105), respectively, similar to earlier scores (P = .67 and P = .64, respectively); 0% to 4.3% scored > 2 SDs below population norms. Higher BDI-II score was predicted by higher earlier BDI-II score, slower recovery of organ function, and longer duration of mechanical ventilation and ICU stay. Higher MAC-S score was predicted by higher earlier MAC-S score. SF-36 mental health domain scores were very stable (P = .57-.83). BDI-II and SF-36 mental health domains were negatively correlated (Spearman coefficient, -0.50 to -0.82). Most patients returned to work regardless of depressive symptoms (minimal to mild, 31 of 35 [88.6%]; moderate to severe, five of eight [62.5%]; P = .12). CONCLUSIONS Compared with ∼ 2 years postdischarge from the ICU, depressive symptoms and memory complaints were similar at 5 years. Mental health domains of the SF-36 may not be sensitive to small changes in mood symptoms.

This study employed an Experience Sampling Methodology (ESM) to test whether various elements of affective instability can predict future suicide ideation in patients with borderline personality disorder (BPD) and a history of recurrent suicidal behavior. Eighty-two individuals with BPD and a history of recurrent suicidal behavior were followed prospectively for one month during which time they recorded their current mood states, 6 times daily over three weeks. Accounting for a set of robust suicide risk factors in multiple regression analyses, only negative mood intensity was significantly related to intensity of self-reported suicide ideation and to number of suicidal behaviors over the past year. Other elements of affective instability examined (e.g., mood amplitude, dyscontrol, and reactivity) were not associated with future suicide ideation or with recent suicidal behavior. Affective instability in patients with BPD is highly variable from one individual to another and is characterized by high levels of intense negative mood. These negative mood states, versus other aspects of mood variability, seem to be more closely tied to the occurrence of suicidal ideation and behavior.

OBJECTIVES:The purpose of this study was to determine the prevalence of thiamin deficiency (TD) in a cross section of hospitalized congestive heart failure (CHF) patients and to investigate factors that contribute to its development.BACKGROUND:Thiamin deficiency manifests as symptoms of CHF and, therefore, may worsen existing heart failure. Congestive heart failure patients may be at increased risk for TD as a result of diuretic-induced urine thiamin excretion, disease severity, malnutrition, and advanced age.METHODS:Erythrocyte thiamin pyrophosphate concentrations, using high-performance liquid chromatography, were measured in 100 CHF patients and compared to 50 control subjects. Variables including diuretics (type and dose), left ventricle dysfunction, New York Heart Association functional classification, creatinine clearance, thiamin intake (diet and supplements), malnutrition, appetite ratings, and age were related to TD using univariate statistics and multiple logistic regression analysis.RESULTS:Thiamin deficiency was more prevalent in CHF patients (33%) compared to control subjects (12%) (p = 0.007). Thiamin deficiency was related to urine thiamin loss (p = 0.03), non-use of thiamin-containing supplements (p = 0.06), and preserved renal function (p = 0.05). Increased urinary thiamin loss (mug/g creatinine) was found to be the only significant positive predictor of thiamin status on multiple logistic regression analysis (p = 0.03).CONCLUSIONS:One-third of hospitalized CHF patients were TD. In contrast to previous studies, increased urinary losses of thiamin were predictive of improved thiamin status. Thiamin supplementation may be protective against TD in the clinical setting. Future studies are warranted to determine if thiamin supplementation improves thiamin status and disease severity in CHF patients.

Rationale: Little is known about the long-term outcomes and costs of survivors of acute respiratory distress syndrome (ARDS).Objectives: To describe functional and quality of life outcomes, health care use, and costs of survivors of ARDS 2 yr after intensive care unit (ICU) discharge.Methods: We recruited a cohort of ARDS survivors from four academic tertiary care ICUs in Toronto, Canada, and prospectively monitored them from ICU admission to 2 yr after ICU discharge.Measurements: Clinical and functional outcomes, health care use, and direct medical costs.Results: Eighty-five percent of patients with ARDS discharged from the ICU survived to 2 yr; overall 2-yr mortality was 49%. At 2 yr, survivors continued to have exercise limitation although 65% had returned to work. There was no statistically significant improvement in health-related quality of life as measured by Short-Form General Health Survey between 1 and 2 yr, although there was a trend toward better physical role at 2 yr (p = 0.0586). Apart from emotional role and mental health, all other domains remained below that of the normal population. From ICU admission to 2 yr after ICU discharge, the largest portion of health care costs for a survivor of ARDS was the initial hospital stay, with ICU costs accounting for 76% of these costs. After the initial hospital stay, health care costs were related to hospital readmissions and inpatient rehabilitation.Conclusions: Survivors of ARDS continued to have functional impairment and compromised health-related quality of life 2 yr after discharge from the ICU. Health care use and costs after the initial hospitalization were driven by hospital readmissions and inpatient rehabilitation.

Background Prior research suggests that patients may be entered into clinical trials with different electrocardiographic (ECG) findings than specified by study protocol criteria; the extent and impact of this variability in a large-scale trial have not been previously described.Methods We evaluated the relationship between case report form (CRF) categorization of the admission ECG and a Core Laboratory,and subsequent outcome in a retrospective analysis of a trial of patients with acute ischemia and a broad spectrum of ECG changes (the GUSTO-IIb trial).Results In 11037 patients with CRF information and an interpretable ECG, there was agreement in 89.1 % of ST-elevation and 81.9% of non-ST-elevation cases. Among patients designated as having no ST elevation on the CRF, 1-year mortality rates were significantly higher in the subgroup of patients with Core Laboratory-determined ST elevation as compared with those where both the CRF and Core Laboratory classification were in agreement (8.8% vs 6.8%, P =.0093). Among patients designated as having ST elevation by the CRF, 1-year mortality rates were similar in both the subgroup of patients with and without Core Laboratory agreement (7.7% vs 8.2%, P =.72).Conclusions These findings have important implications for clinicians in routine practice because even a simple evaluation (presence or absence of ST elevation) on the admission ECG was often discordant and was associated with adverse clinical outcome.

Assertive community treatment appears to have limited impact on the risk of suicide in persons with severe and persistent mental illness (SPMI). This exploratory prospective study attempts to understand this observation by studying the contribution of suicidality to the occurrence of crisis events in patients with SPMI. Specifically, an observer-rated measure of the need for hospitalization, the Crisis Triage Rating Scale, was completed at baseline, crisis occurrence, and resolution to determine how much the level of suicidality contributed to the deemed level of crisis. Second, observer-ratings of suicidal ideation, the Modified Scale for Suicide Ideation, and psychopathology and suicidality, Brief Psychiatric Rating Scale, were measured at baseline, crisis occurrence, and resolution. A self-report measure of distress, the Symptom Distress Scale, was completed at baseline, crisis occurrence, and resolution. Finally, the patients' crisis experiences were recorded qualitatively to compare with quantitative measures of suicidality. Almost 40% of the subjects experienced crisis events and more than a quarter of these events were judged to be severe enough to warrant the need for hospitalization. Our findings suggest that elevation of psychiatric symptoms is a major contributor to the crisis occurrences of individuals with SPMI; although the risk of suicide may have to be conceived as somewhat separate from crisis occurrence.

BACKGROUND:Percutaneous coronary interventions (PCIs) are often complicated by postprocedural myocardial necrosis as manifested by elevated cardiac markers. PURPOSE:To assess the incidence and risk factors of elevated troponin-I (TnI) after PCI. METHODS AND RESULTS:We performed a retrospective analysis on 522 PCI cases over a 1-year period at a single center. An elevated postprocedural TnI (>1.0 ng/ml) occurred in 213 patients (40.8%). Overall, glycoprotein (GP) IIb/IIIa inhibitors were used in 52% of cases. Baseline clinical characteristics were similar between the positive and the negative TnI groups. A univariate analysis revealed that patients with elevated TnI post-PCI had significantly more multivessel (28% vs. 15%, P = .001) and multilesion interventions (44% vs. 27%, P<.0001). The lesions were longer, more often angulated and involving bifurcations, and more complex in the TnI-positive group. Stent use and number of stents was higher in the TnI-positive group, and longer inflation times (>30 s) or higher inflation pressures (>14 atm) were used more often in the TnI-positive group. GP IIb/IIIa inhibitor use was higher in the TnI-positive group (61% vs. 45%, P = .0007). After multivariable analysis, independent predictors of elevated TnI after PCI included multilesion intervention, lesion length, lesion angulation, and GP IIb/IIIa inhibitor use. CONCLUSION:TnI is elevated in approximately 40% of cases after PCI. TnI is more likely to be elevated after intervention on multiple lesions, angulated or long lesions.

OBJECTIVES The purpose of this study was to compare rate-only detection to enhanced detection in a dual-chamber implantable cardioverter-defibrillator (ICD), to discriminate ventricular tachycardia from supraventricular tachycardia.BACKGROUND ICDs are highly effective in treating ventricular tachycardia (VT) or ventricular fibrillation (VF). However, they frequently deliver inappropriate therapy during supraventricular tachycardia (SVT).METHODS We conducted a randomized clinical trial of detection enhancements in a dual-chamber ICD compared to control (rate-only) detection to discriminate VT from SVT. Detection enhancements included a specific standardized protocol identical for all patients for programming rate stability, sudden onset, atrial-to-ventricular relationship (sudden onset = 9% and rate stability = 10 ms; V > A "on"), and "sustained rate duration" (3 minutes). The primary endpoint was the time to first inappropriate therapy classified by a blinded events committee.RESULTS One hundred forty-nine patients had a history of sustained VT or VF. Mean age ( +/- SD) was 60 +/- 13 years; 83% were male, and mean ejection fraction was 35 +/- 15%. Control (n = 70) and "enhanced" (n = 79) groups did not differ with regard to age, sex, ejection fraction, or primary arrhythmia. The proportion of patients free of inappropriate therapy over time was significantly higher in the enhanced versus the control group (hazard ratio = 0.47, P =.011). High-energy shocks were reduced from 0.58 +/- 4.23 shocks/patient/month in the control group to 0.04 +/- 0.15 shocks/patient/ month in the enhanced group (P = .0425). No patient programmed per protocol failed to receive therapy for VT detected by the ICD (422 VT episodes).CONCLUSIONS Standardized programming in a dual-chamber ICD leads to a significant and clinically important reduction in inappropriate therapies compared to rate-only detection and does not compromise safety with respect to appropriate treatment of VT. (C) 2004 Heart Rhythm Society. All rights reserved.

Transfusion of anemic patients with hemoglobin-based oxygen carriers (HBOCs) may improve cerebral oxygen delivery. Conversely, cerebral vasoconstriction, associated with HBOC transfusion, could limit optimal cerebral tissue oxygenation. We hypothesized that hemodilution with a HBOC would maintain cerebral tissue oxygenation, despite the occurrence of cerebral vasoconstriction. Isoflurane-anesthetized rats (100% oxygen) underwent direct measurement of mean arterial blood pressure (MAP), caudate tissue oxygen tension (PBrO2), and regional cortical cerebral blood flow (rCBF) before and after 50% of the estimated blood volume (30 mL/kg) was exchanged with either an HBOC (hemoglobin raffimer; Hemolink™) or pentastarch (n = 6). Hemodilution with hemoglobin raffimer caused a transient increase in PBrO2 from 24.9 ± 13.3 mm Hg to 32.2 ± 19.1 mm Hg (P < 0.05), a sustained increase in MAP, and no change in rCBF. Arterial blood oxygen content was maintained despite an increase in methemoglobin and reduced oxygen saturation. Hemodilution with pentastarch caused a transient increase in MAP, no change in PBrO2, and a sustained increase in rCBF (P < 0.05), whereas the hemoglobin concentration and oxygen content were significantly reduced. Hemodilution with hemoglobin raffimer augmented PBrO2 and prevented the increase in rCBF observed after similar hemodilution with pentastarch. These data suggest that transfusion with hemoglobin raffimer may help to maintain cerebral oxygenation during severe anemia.

Severe hemodilutional anemia may reduce cerebral oxygen delivery, resulting in cerebral tissue hypoxia. Increased nitric oxide synthase (NOS) expression has been identified following cerebral hypoxia and may contribute to the compensatory increase in cerebral blood flow (CBF) observed after hypoxia and anemia. However, changes in cerebral NOS gene expression have not been reported after acute anemia. This study tests the hypothesis that acute hemodilutional anemia causes cerebral tissue hypoxia, triggering changes in cerebral NOS gene expression. Anesthetized rats underwent hemodilution when 30 ml/kg of blood were exchanged with pentastarch, resulting in a final hemoglobin concentration of 51.0 +/- 1.2 g/l (n = 7 rats). Caudate tissue oxygen tension (Pbr(O(2))) decreased transiently from 17.3 +/- 4.1 to 14.4 +/- 4.1 Torr (P < 0.05), before returning to baseline after approximately 20 min. An increase in CBF may have contributed to restoring Pbr(O(2)) by improving cerebral tissue oxygen delivery. An increase in neuronal NOS (nNOS) mRNA was detected by RT-PCR in the cerebral cortex of anemic rats after 3 h (P < 0.05, n = 5). A similar response was observed after exposure to hypoxia. By contrast, no increases in mRNA for endothelial NOS or interleukin-1beta were observed after anemia or hypoxia. Hemodilutional anemia caused an acute reduction in Pbr(O(2)) and an increase in cerebral cortical nNOS mRNA, supporting a role for nNOS in the physiological response to acute anemia.

PURPOSE:To test the hypotheses that deliberate elevation of PaCO(2) increases cerebral tissue oxygen tension (PBrO(2)) by augmenting PaO(2) and regional cerebral blood flow (rCBF).METHODS:Anesthetized rats were exposed to increasing levels of inspired oxygen (O(2)) or carbon dioxide (CO(2); 5%, 10% and 15%, n = 6). Mean arterial blood pressure (MAP), PBrO(2) and rCBF were measured continuously. Blood gas analysis and hemoglobin concentrations were determined for each change in inspired gas concentration. Data are presented as mean +/- standard deviation with P < 0.05 taken to be significant.RESULTS:The PBrO(2) increased in proportion to arterial oxygenation (PaO(2)) when the percentage of inspired O(2) was increased. Proportional increases in PaCO(2) (48.7 +/- 4.9, 72.3 +/- 6.0 and 95.3 +/- 15.4 mmHg), PaO(2) (172.2 +/- 33.1, 191.7 +/- 42.5 and 216.0 +/- 41.8 mmHg), and PBrO(2) (29.1 +/- 9.2, 49.4 +/- 19.5 and 60.5 +/- 23.0 mmHg) were observed when inspired CO(2) concentrations were increased from 0% to 5%, 10% and 15%, respectively, while arterial pH decreased (P < 0.05 for each). Exposure to CO(2) increased rCBF from 1.04 +/- 0.67 to a peak value of 1.49 +/- 0.45 (P < 0.05). Following removal of exogenous CO(2), arterial blood gas values returned to baseline while rCBF and PBrO(2) remained elevated for over 30 min. The hypercapnia induced increase in PBrO(2) was threefold higher than that resulting from a comparable increase in PaO(2) achieved by increasing the inspired O(2) concentration (34.9 +/- 14.5 vs 11.4 +/- 5.0 mmHg, P < 0.05).CONCLUSION:These data support the hypothesis that the combined effect of increased CBF, PaO(2) and reduced pH collectively contribute to augmenting cerebral PBrO(2) during hypercapnia.

Background Congestive heart failure depletes the myocardium of carnitine, coenzyme Q10 (CoQ10), and taurine—substances known to influence mitochondrial function and cell calcium. We hypothesized that feeding patients a nutritional supplement that contained carnitine, CoQ10, and taurine would result in higher myocardial levels of these nutrients and improve left ventricular function. Methods Forty-one patients who underwent aortocoronary artery bypass with an ejection fraction ≤40% at referral were randomly assigned to a double-blind trial of supplement or placebo. Radionuclide ventriculography was performed at randomization and before surgery. Surgical myocardial biopsies, adjusted for protein content, were analyzed for carnitine, CoQ10, and taurine levels. Results The groups were well matched. Minor exceptions were supplement group versus placebo group for digoxin use (7 vs 0, respectively; P =.009) and age (62 ± 11 years vs 69 ± 5 years, respectively; P =.04). There were significantly higher levels in the treated group compared with the placebo group for myocardial levels of CoQ10 (138.17 ± 39.87 nmol/g wet weight and 56.67 ± 23.08 nmol/g wet weight; P =.0006), taurine (13.12 ± 4.00 μmol/g wet weight and 7.91 ± 2.81 μmol/g wet weight; P =.003), and carnitine (1735.4 ± 798.5 nmol/g wet weight and 1237.6 ± 343.1 nmol/g wet weight; P =.06). The left ventricular end-diastolic volume fell by −7.5 ± 21.7 mL in the supplement group and increased by 10.0 ± 19.8 mL in the placebo group (P =.037). Conclusions Supplementation results in higher myocardial CoQ10, taurine, and carnitine levels and is associated with a reduction in left ventricular end-diastolic volume in patients with left ventricular dysfunction before revascularization. Because the risk of death for surgical revascularization is related to preoperative left ventricular end-diastolic volume, supplementation could improve outcomes. (Am Heart J 2002;143:1092-100.)

BACKGROUND:Data on non-Q myocardial infarctions (MI) are derived primarily from prethrombolytic era studies. Previous trials demonstrated different development rates and none reported on clinical outcomes.METHODS:Our goal was to determine the incidence and prognosis of non-Q-wave MI among patients with ST-segment elevation receiving thrombolysis. A retrospective analysis of 5 randomized controlled trials was made. The main outcome measures included rates of (1) transformation of ST-segment elevation to Q- and non-Q-wave MI and (2) inhospital and 1-year mortality and reinfarction among patients who subsequently develop a Q or non-Q MI postthrombolysis as compared to controls.RESULTS:Non-Q wave development was greater among patients receiving thrombolysis versus placebo/control (3.1% absolute difference, 95% CI 1.2%-5.0%). Among patients receiving thrombolysis, those who developed a non-Q MI experienced significantly lower inhospital and 1-year mortality (absolute differences -3.8% [95% CI -5.2% to -2.4%] and -6.4% [95% CI -9.9% to -3.0%], respectively) and reinfarction (absolute differences -2.9% [95% CI -4.3% to -1.6%] and -3.5% [95% CI -6.1% to -0.9%], respectively) rates, compared with those who evolved a Q MI. Inhospital and 1-year mortality was also significantly lower when compared to placebo/control patients who developed a non-Q MI (absolute differences 4.6% [95% CI -8.2% to -1.1%] and -7.5% [95% CI -12.5% to -2.5%], respectively).CONCLUSIONS:Patients receiving thrombolysis more often develop a non-Q-wave MI and have a better prognosis than either those who develop a Q MI postthrombolysis or a non-Q MI after standard medical therapy.

We investigated the impact of primary angioplasty compared with thrombolysis in 894 patients with ST elevation acute myocardial infarction and electrocardiographic grades II and III ischemia on enrollment. Patients were divided into 2 groups based on the enrollment electrocardiogram-grade III: (1) absence of an S wave below the isoelectric baseline in leads that usually have a terminal S configuration (leads V(1) to V(3)), or (2) ST J-point amplitude > or =50% of the R-wave amplitude in all other leads. To be included in the grade III group, grade III criteria in > or =2 adjacent leads were required. Patients with ST elevation but without grade III criteria were classified as having grade II. In-hospital mortality was 3.2% and 6.8% in the grade II (n = 616) and grade III (n = 278) groups, respectively (p = 0.016). In the grade II group, in-hospital mortality was similar in the thrombolysis and angioplasty subgroups (3.2% and 3.3%, p = 0.941). In patients with grade III, in-hospital mortality was 6.4% and 7.3%, respectively (p = 0.762). The odds ratio for the grade III group for death with thrombolysis was 2.06 (95% confidence intervals [CI] 0.82 to 5.19; p = 0.125); the odds ratio for primary angioplasty was 2.30 (95% CI 0.93 to 5.66; p = 0.07). In the thrombolysis group, reinfarction occurred in 3.3% and 6.5% of the grade II and grade III subgroups (p = 0.137). In the angioplasty group, reinfarction occurred in 1.3% and 4.4%, respectively (p = 0.239). Grade III ischemia on admission was associated with higher in-hospital and 30-day mortality and a higher rate of reinfarction. There was no difference in mortality between primary angioplasty and thrombolysis in the grade II and grade III ischemia patients.