Prognostic value of NH2-terminal pro B-type natriuretic peptide in patients with diabetes and stable coronary heart disease.
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Publications and source records attributed to Lars Køber.
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BACKGROUND: The results of randomised control trials (RCTs) evaluating the effect of beta-blockers on functional status in patients with chronic heart failure are conflicting. AIM: To perform a systematic review and meta-analysis of RCTs evaluating the effect of beta-blockers on New York Heart Association (NYHA) classification and exercise tolerance in chronic heart failure. METHODS AND RESULTS: We selected 28 RCTs evaluating beta-blocker versus placebo in addition to ACE inhibitor therapy. Combined results of 23 RCTs showed that beta-blockers improved NYHA class by at least one class with odds ratio (OR) 1.80 (1.33-2.43) p<0.0001. Meta-analysis of 10 RCTs showed a significant prolongation of exercise time by 44.19 (6.62-81.75) s p=0.021. Combining 8 RCTs evaluating the maximal peak oxygen uptake and 9 RCTs evaluating 6-min walk distance showed that beta-blockers had no significant effect compared with placebo, p=0.484, and p=0.730, respectively. Combined results of the 23 RCTs showed significant reducing effect on all cause mortality with OR=0.69 (0.59-0.82) p<0.0001. CONCLUSION: Chronic use of a beta-blocker in conjunction with ACE inhibitor therapy improves dyspnoea and prolongs exercise tolerance time, but has no significant effect on 6-min walk test or maximal oxygen uptake in patients with heart failure.
AIMS: Atrial fibrillation (AF) is a common complication in patients with acute myocardial infarction and is associated with an increase in the risk of death. The excess mortality associated with AF complicating acute myocardial infarction has not been studied in detail. Observations indicate that AF facilitates induction of ventricular arrhythmias, which may increase the risk of sudden cardiovascular death (SCD). A close examination of the mode of death could potentially provide useful knowledge to guide further investigations and treatments. METHODS AND RESULTS: We analysed the relation between AF/atrial flutter (AFL) and modes of death in 5983 consecutive patients discharged alive after an acute myocardial infarction screened in the TRAndolapril Cardiac Evaluation registry. This cohort of patients with an enzyme-verified acute myocardial infarction was admitted to 27 centres in 1990-92. Survival status was obtained 2 years after screening of the last patient. An independent endpoint committee assessed the modes of death. Left ventricular ejection fraction was determined in all the screened patients and information about presence or absence of AF/AFL was prospectively collected. Sustained or paroxysmal AF/AFL was observed in 1149 patients (19%) during hospitalization. During follow-up, 1659 patients (34%) died: 482 (50%) patients with AF/AFL and 1177 (30%) patients without AF/AFL, P<0.001. SCD occurred in 536, non-SCD occurred in 725, and 398 died of non-cardiovascular causes (includes 142 unclassifiable cases). The adjusted risk ratio of AF/AFL for total mortality was 1.33 (95% CI: 1.19-1.49; P<0.0001) and the risk ratio for SCD was 1.31 (95% CI: 1.07-1.60; P<0.009). The adjusted risk ratio of AF/AFL for non-SCD was 1.43 (95% CI: 1.21-1.70; P<0.0001). CONCLUSION: The excess mortality observed in patients with AF/AFL following acute myocardial infarction is due to a significant increase in both SCD and non-SCD.
BACKGROUND: To study the prognostic information of congestive heart failure (CHF) and left ventricular systolic dysfunction regarding sudden and non-sudden cardiovascular death (SCD and non-SCD) in patients with acute myocardial infarction (MI), as this may indicate the potential benefit of implantable defibrillators. METHODS: Data from consecutive patients with acute MI screened in 1990-92 for the TRAndolapril Cardiac Evaluation (TRACE) study were entered into a registry. A total of 5502 patients were alive 30 days after the MI and were followed for up to 4 years with respect to cause of death. SCD was defined as cardiovascular death within 1 h of onset of symptoms. An echocardiography was performed 1-6 days after the admission and evaluated centrally using the wall motion index (WMI). RESULTS: Half of the patients had CHF and 17% of the patients had WMI < or =1.0 (corresponding to an ejection fraction < or =0.30). During follow-up 431 patients died from SCD and 606 from non-SCD. The risk ratios for SCD and non-SCD associated with WMI < or =1.0 were 3.17 and 2.95, transient CHF 2.01 and 1.46, and permanent CHF 3.71 and 4.42, respectively. No risk factor was a specific marker of SCD or non-SCD. The 3-year probability of SCD was 7.9% for patients with transient CHF, 13.3% for permanent CHF, and 15.5% for WMI < or =1.0. CONCLUSIONS: CHF and low WMI identify a relevant proportion of patients with MI who are at high absolute risk of SCD. This study indicates the relevance of defibrillators in consecutive post-MI patients with left ventricular dysfunction or clinical signs of heart failure.
BACKGROUND: The effect of angiotensin converting enzyme (ACE) inhibitors on symptoms in patients with left ventricular systolic dysfunction (LVSD) is controversial. AIMS: To perform a meta-analysis of studies evaluating effect of ACE inhibitors on New York Heart Association (NYHA) class in patients with LVSD. METHODS: Individual data from 10389 patients in NYHA classes I-IV from four large long-term studies (2-4-year follow-up) and summary data from 2302 patients in NYHA classes II-IV from 16 short-term studies (3 months follow-up) were meta-analysed to assess changes in NYHA class. RESULTS: The large long-term studies showed a significant improvement in the worst NYHA classes (classes II-IV compared to class I) in the ACE inhibitor arm versus placebo, odds ratio (OR) = 0.875 (0.811-0.943) p = 0.0005. This effect was only present in studies which included patients with chronic heart failure and was particularly pronounced on deterioration to the worst NYHA class IV, OR = 0.66 (0.52-0.84) p = 0.001. There was no effect in the studies which included patients after myocardial infarction. The short-term chronic heart failure studies showed a significant improvement in NYHA class; OR for improvement of at least one NYHA class was 2.11 (1.48-2.98, 95% CI) p < 0.0001. CONCLUSION: ACE inhibition significantly improves symptomatic status measured as NYHA classification in patients with chronic heart failure.
AIMS: An understanding of the temporal trends on the risks of arrhythmic death (AD) vs. non-arrhythmic deaths (NAD) after myocardial infarction (MI) is crucial in deciding the optimal timing for risk stratification and treatment window for prophylactic antiarrhythmic treatment. However, contemporary data on such information is lacking. METHODS AND RESULTS: Individual patient data were pooled from the placebo arms of EMIAT, CAMIAT, SWORD, TRACE, and DIAMOND-MI who had a recent MI and left ventricular ejection fraction (LVEF) <40% or frequent ventricular premature beats (VPBs). Temporal trends were investigated for all studies from day 45 after acute myocardial infarction (AMI) to account for different recruitment periods between trials, and then from the onset of MI for TRACE and DIAMOND-MI that recruited patients within 2 weeks after MI. In total, 3104 patients (median age 65, range: 23-92; 2471 males) were pooled from all five studies, with a total of 487 deaths at 2-year follow-up; 220 deaths were ADs and 172 were NADs. The risks of both AD and NAD were highest in the first 6 months but the risk of AD was consistently higher than that of NAD throughout the 2-year period [rate of death/100 person-year at risk (AD/NAD): 8.09/6.07 (45 days to 6 months), 4.07/3.35 (>6-12 months), 4.34/3.60 (>12-18 months), 3.76/2.77 (>18-24 months)]. There were significant interactions between the temporal trends of mortalities and gender (P=0.03) and history of hypertension (P=0.04). A similar trend was observed when mortality was measured from time of onset of MI from the combined TRACE and DIAMOND-MI dataset. CONCLUSION: Our study provided the first contemporary evidence that in high-risk post-MI patients with LVEF <40% or frequent VPBs, the risk of AD was higher than that of NAD for up to 2 years although in female patients, they became increasingly more likely to die from NAD after 6 months. Therefore, risk stratification of post-MI patient at high risk of AD remains a worthwhile exercise. However, the risks of AD (and NAD) were highest in the first 6 months after AMI and level-off thereafter, suggesting that the optimal window period for risk stratification for implantable cardioverter defibrillator after AMI is in the first 6 months.
BACKGROUND: Reports on the prognostic importance of atrial fibrillation following myocardial infarction have provided considerable variation in results. Thus, this study examined the impact of left ventricular systolic function and congestive heart failure on the prognostic importance of atrial fibrillation in acute myocardial infarction patients that might explain previous discrepancies. METHODS: The study population was 6676 patients consecutively admitted to hospital with acute myocardial infarction. Information on the presence of atrial fibrillation/flutter, left ventricular systolic function and congestive heart failure were prospectively collected. Mortality was followed for 5 years. RESULTS: In patients with left ventricular ejection fraction<0.25, atrial fibrillation/atrial flutter was associated with an increased in-hospital mortality (OR=1.8 (1.1-3.2); p<0.05) but not an increased 30-day mortality. In patients with 0.25 0.35. In patients with congestive heart failure, atrial fibrillation/atrial flutter was associated with an increased in-hospital mortality (OR=1.5 (1.2-1.9); p<0.001) and increased 30-day mortality (OR=1.4 (1.1-1.7); p<0.001) but not in patients without congestive heart failure. In hospital survivors, atrial fibrillation/atrial flutter was associated with an increased long-term mortality in all subgroups except those with left ventricular ejection fraction<0.25. CONCLUSIONS: Atrial fibrillation/atrial flutter is primarily associated with increased in-hospital mortality in heart failure patients. Long-term mortality is increased in all subgroups except those with left ventricular ejection fraction<25%.
BACKGROUND: The level of the inactive N-terminal fragment of pro-brain (B-type) natriuretic peptide (BNP) is a strong predictor of mortality among patients with acute coronary syndromes and may be a strong prognostic marker in patients with chronic coronary heart disease as well. We assessed the relationship between N-terminal pro-BNP (NT-pro-BNP) levels and long-term mortality from all causes in a large cohort of patients with stable coronary heart disease. METHODS: NT-pro-BNP was measured in baseline serum samples from 1034 patients referred for angiography because of symptoms or signs of coronary heart disease. The rate of death from all causes was determined after a median follow-up of nine years. RESULTS: At follow-up, 288 patients had died. The median NT-pro-BNP level was significantly lower among patients who survived than among those who died (120 pg per milliliter [interquartile range, 50 to 318] vs. 386 pg per milliliter [interquartile range, 146 to 897], P<0.001). Patients with NT-pro-BNP levels in the highest quartile were older, had a lower left ventricular ejection fraction (LVEF) and a lower creatinine clearance rate, and were more likely to have a history of myocardial infarction, clinically significant coronary artery disease, and diabetes than patients with NT-pro-BNP levels in the lowest quartile. In a multivariable Cox regression model, the hazard ratio for death from any cause for the patients with NT-pro-BNP levels in the fourth quartile as compared with those in the first quartile was 2.4 (95 percent confidence interval, 1.5 to 4.0; P<0.001); the NT-pro-BNP level added prognostic information beyond that provided by conventional risk factors, including the patient's age; sex; family history with respect to ischemic heart disease; the presence or absence of a history of myocardial infarction, angina, hypertension, diabetes, or chronic heart failure; creatinine clearance rate; body-mass index; smoking status; plasma lipid levels; LVEF; and the presence or absence of clinically significant coronary artery disease on angiography. CONCLUSIONS: NT-pro-BNP is a marker of long-term mortality in patients with stable coronary disease and provides prognostic information above and beyond that provided by conventional cardiovascular risk factors and the degree of left ventricular systolic dysfunction.
OBJECTIVES: Whether beta-blockers reduce atrial arrhythmias and, when added to an angiotensin-converting enzyme (ACE) inhibitor, ventricular arrhythmia is unknown. BACKGROUND: Ventricular and atrial arrhythmias are common after acute myocardial infarction (AMI) and are associated with a poor prognosis. Angiotensin-converting enzyme inhibitors reduce the incidence of both types of arrhythmia. METHODS: The antiarrhythmic effect of carvedilol was examined in a placebo-controlled multicenter trial, the Carvedilol Post-Infarct Survival Control in Left Ventricular Dysfunction (CAPRICORN) study, which enrolled 1,959 patients with reduced left ventricular systolic function after AMI, 98% of whom were treated with an ACE inhibitor. RESULTS: The incidence of atrial fibrillation/flutter was 53 to 984 (5.4%) in the placebo group and 22 to 975 (2.3%) in the carvedilol group, giving a carvedilol/placebo hazard ratio (HR) of 0.41 (95% confidence interval [CI] 0.25 to 0.68; p = 0.0003). The corresponding rates of ventricular tachycardia/flutter/fibrillation were 38 to 984 (3.9%) and 9 to 975 (0.9%) (HR 0.24, 95% CI 0.11 to 0.49; p < 0.0001). CONCLUSIONS: Carvedilol has a powerful antiarrhythmic effect after AMI, even in patients already treated with an ACE inhibitor. Carvedilol suppresses atrial as well as ventricular arrhythmias in these patients.
BACKGROUND: Contemporary information is lacking on the effect of demographic features and clinical features on the specific mode of mortality after myocardial infarction (MI) in the thrombolytic era. HYPOTHESIS: The aims of this study were (1) to examine the risk and trend of a different mode of mortality (i.e., all-cause, arrhythmic, and nonarrhythmic cardiac mortality) in high-risk patients post MI with reduced left ventricular ejection fraction (LVEF) or ventricular arrhythmias; and (2) to assess the predictive value of demographic and clinical variables in the prediction of specific modes of death in high-risk patients post MI in the thrombolytic era. METHODS: In all, 3,431 patients receiving placebo (2,700 men, median age 64 +/- 11 years) from the EMIAT, CAMIAT, SWORD, TRACE, and DIAMOND-MI studies, with LVEF < 40% or ventricular arrhythmia were pooled. Risk factors for mortality among patients surviving > or = 45 days after MI up to 2 years were examined using Cox regression. Short-term survival (from onset of MI to Day 44 after MI) was also examined for TRACE and DIAMOND-MI, in which patients were recruited within 2 weeks of MI. RESULTS: After adjustment for treatment and study effects, age, previous MI/angina, increased heart rate, and higher New York Heart Association functional class increased the risk of all-cause, arrhythmic, and cardiac mortality. Male gender, history of hypertension, low baseline systolic blood pressure, and Q wave were predictive of all-cause and arrhythmic mortality, whereas diabetes was only predictive of all-cause mortality. Smoking habit and atrial fibrillation had no prognostic value. Similar parameters were also predictive of short-term mortality, but not identical. CONCLUSIONS: Our study has shown that in high-risk patients post MI, who have been preselected using LVEF or frequent ventricular premature beats, demographic and clinical features are powerful predictors of mortality in the thrombolytic era. We propose that demographic and clinical factors should be considered when designing risk stratification or survival studies, or when identifying high-risk patients for prophylactic implantable cardiodefibrillator therapy.
AIMS: To study the prognostic importance of left ventricular systolic function in patients with heart failure (HF) and acute myocardial infarction (AMI) with respect to the presence of prior heart failure and known ischemic heart disease. METHODS: In 13,084 consecutive patients diagnosed with either AMI or HF, a medical history and an echocardiographic assessment of left ventricular systolic function by wall motion index (WMI) were obtained. Patients were divided into four groups: AMI with or without a history of HF, and primary HF (no recent AMI) with or without a history of ischemic heart disease (IHD). Mortality was assessed after nine years of follow-up. RESULTS: WMI stratified patients according to all-cause mortality in all four groups of patients (p<0.0001). For a decrease in WMI of 0.3 (corresponding to a decrease in left ventricular ejection fraction of 0.1), the hazard ratio was 1.61 (95% CI: 1.48-1.76) for AMI patients without prior HF, 1.43 (1.38-1.48) for AMI patients with prior HF, 1.26 (1.22-1.30) for primary HF patients with IHD and 1.23 (1.18-1.27) for HF patients without IHD. CONCLUSION: WMI stratifies patients with IHD and/or HF according to risk of all-cause death. The presence of HF attenuates the prognostic power of WMI.
OBJECTIVE: To evaluate the impact of obesity on mortality in patients with acute myocardial infarction. METHODS: This study comprises 6676 consecutive patients with acute myocardial infarction screened for entry into the Danish Trandolapril Cardiac Evaluation (TRACE) study. At baseline, body mass index (BMI) and waist to hip ratio (WHR) were measured. Survival status was determined after 8-10 years. RESULTS: BMI was used to divide patients into 4 groups: underweight, normal weight, overweight and obese. The normal weight group was used as reference for the other groups. WHR was divided in quartiles and the lowest quartile was used as reference for the three other quartiles. The prevalence of overweight (BMI 25-29.9 kg/m(2)) and obesity (BMI>30 kg/m(2)) were 48% and 13% in males and 31% and 13% in females. Obese patients were younger, less often smokers and more frequently suffered from diabetes and hypertension. In both men and women, there was no association between obesity assessed as BMI and mortality [men: adjusted RR=0.99 (0.85-1.14, p=0.3); women: adjusted RR=0.90 (0.74-1.10, p=0.2)]. Men with WHR in the upper quartile had an increased mortality [adjusted RR=1.21 (1.07-1.37, p<0.01)]. Increasing WHR in women showed a trend of increased mortality, although this was not significant [adjusted RR=1.13 (0.95-1.34, p=0.2)]. CONCLUSION: In patients with acute myocardial infarction overall obesity as assessed by body mass index is inversely related to mortality. However, abdominal obesity appears to be an independent predictor of all-cause mortality in men and perhaps also in women.
Familial hypertrophic cardiomyopathy (FHC) is, in most cases, a disease of the sarcomere, caused by a mutation in one of 10 known sarcomere disease genes. More than 266 mutations have been identified since 1989. The FHC disease gene first characterized MYH7, encodes the cardiac beta-myosin heavy chain, and contains more than 115 of these mutations. However, in most studies, only the region encoding the globular head and the hinge region of the mature cardiac beta-myosin heavy chain have been investigated. Furthermore, most studies carries out screening for mutations in the most prevalent disease genes, and discontinues screening when an apparent disease-associated mutation has been identified. The aim of the present study was to screen for mutations in the rod region of the MYH7 gene in all probands of the cohort, regardless of the known genetic status of the proband. Three disease-causing mutations were identified in the rod region in four probands using capillary electrophoresis single-strand conformation polymorphism as a screening method. All mutations were novel: N1327K, R1712W, and E1753K. Two of the probands had already been shown to carry other FHC-associated mutations. In conclusion, we show that in the Danish cohort we find one third of all MYH7 mutations in the rod-encoding region and we find that two of the patients carrying these mutations also carry mutations in other FHC disease genes stressing the need for a complete screening of all known disease genes in FHC-patients.
OBJECTIVES: To study the use of beta-blockers and angiotensin-converting enzyme (ACE) inhibitors after acute myocardial infarction (AMI) in Denmark from 1995 to 2002. DESIGN: Information about patients with first AMI aged > or = 30 years and the dispensing of beta-blockers and ACE inhibitors from pharmacies within 30 d from discharge was obtained from the National Patient Registry and the Danish Registry of Medicinal Product Statistics. RESULTS: Beta-blocker use increased from 38.1% of patients in 1995 to 67.9% in 2002 (OR = 3.85, CI: 3.58-4.13). Women, elderly patients and patients taking loop-diuretics and antidiabetic drugs received beta-blockers less frequently, but patients taking loop-diuretics or antidiabetic drugs had the greatest increase. ACE inhibitor use increased from 24.5 to 35.5% (OR = 1.86, CI: 1.72-2.01). Women, patients aged < 60 years or > or = 80 years and patients not taking loop-diuretics received ACE inhibitors less frequently, but patients not taking loop-diuretics had the greatest increase. CONCLUSIONS: Beta-blocker use increased markedly post-AMI from 1995 to 2002, whereas ACE inhibitor use increased modestly. The results suggested undertreatment of women, elderly patients and people with diabetes.
AIMS: To study outpatient statin use after first acute myocardial infarction (AMI) in Denmark between 1995 and 2002 and to determine the predictors of statin use. METHODS: This is a nationwide population-based study using administrative registries. Patients with first AMI between 1995 and 2002 older than 30 years of age and alive 6 months after discharge (n = 45 219) were identified through the National Patient Registry. The statins purchased by these patients within 6 months after discharge were determined using the Registry of Medicinal Product Statistics, a nationwide prescription database. RESULTS: Statin use following AMI increased from 13% in 1995 to 61% in 2002. In 2002, 81% of patients aged 30-64 years used statins. Older patients used fewer statins, but use increased more among patients aged 75-84 years: from 1.3% to 43%. Use in elderly patients did not differ according to gender in 2000-02, but young men used more than younger women. In 2000-02, patients with diabetes (odds ratio (OR): 0.84; 95% confidence interval (CI): 0.74-0.95) and with heart failure (OR: 0.70; 95% CI: 0.64-0.76) were undertreated; this trend was present throughout the period. CONCLUSIONS: In this nationwide study, younger patients after AMI had high statin use in 2002, but high-risk patients such as those with diabetes and heart failure were still being undertreated.
AIMS: To investigate the long-term benefits of treatment with angiotensin-converting enzyme (ACE)-inhibitors in patients with myocardial infarction (MI) and left ventricular dysfunction (LVD). METHODS AND RESULTS: In the trandolapril cardiac evaluation (TRACE) study, 1749 patients with LVD (ejection fraction< or =35%) were randomized to trandolapril (n=876) or placebo (n=873) 3-7 days post-MI. Enrolment lasted from 1990 to 1994; on-treatment follow-up ranged from 2 to 4 years. At study closure, all patients were recommended continued ACE-inhibitor use. National registries were used to track deaths and hospitalizations until 2002. Mortality was analysed with Cox proportional hazard models and hospitalization with Poisson regression models (models adjusted for observation time). Over 10-12 years of follow-up, a total of 1283 deaths and 9220 hospitalizations were registered. Compared with the placebo group, the trandolapril group had a significantly reduced risk of all-cause mortality (relative risk 0.89, 95% CI 0.80-0.99, P=0.03), all-cause hospitalizations (rate ratio 0.92, 95% CI 0.88-0.96, P<0.001), and cardiovascular hospitalizations (rate ratio 0.95, 95% CI 0.91-1.00, P=0.047), including congestive heart failure hospitalizations (rate ratio 0.85, 95% CI 0.77-0.93, P<0.001). CONCLUSION: In patients with LVD, use of trandolapril shortly after an MI for 2-4 years has long-term benefits. The beneficial effect on mortality and hospitalization rates is maintained for at least 10-12 years.
AIMS: Previous studies have suggested that a high body mass index (BMI) is associated with an improved outcome in congestive heart failure (CHF). However, the studies addressing this problem have not included enough patients with non-systolic heart failure to evaluate how left ventricular systolic function interacts with obesity on prognosis in CHF. The aim of this study was to evaluate how BMI influences mortality in patients hospitalized with CHF, and to address in particular whether the effect of BMI is influenced by left ventricular (LV) systolic function. METHODS AND RESULTS: Retrospective analysis of baseline and survival data for 4700 hospitalized CHF patients for whom BMI was available. LV systolic function, as assessed by wall motion index was available for 95% of the patients. Follow-up time ranged from 5 to 8 years. In the total population, the risk of death decreased steadily with increasing BMI from the underweight to the obese. Compared with normal weight, and adjusted for sex and age, risk ratios (RR) and 95% confidence limits were: underweight 1.56 (1.33-1.84), overweight 0.90 (0.83-0.97), obese 0.77 (0.70-0.86). Being underweight conferred a greater risk in CHF patients with normal systolic function [RR 1.66 (1.29-2.14), compared with normal weight] than in patients with reduced systolic function [RR 1.11 (0.87-1.42), P for interaction 0.03]. In patients with systolic dysfunction, obesity was associated with increased risk compared with normal weight [RR 1.21 (1.01-1.45)]. CONCLUSION: Increasing BMI in CHF is associated with a lower mortality, but the influence is complex and depends on left ventricular systolic function. Hence, in patients with systolic dysfunction obesity may indicate an increased risk.
BACKGROUND: A prior diagnosis of diabetes mellitus is associated with adverse outcomes after acute myocardial infarction (MI), but the risk associated with a new diagnosis of diabetes in this setting has not been well defined. METHODS AND RESULTS: We assessed the risk of death and major cardiovascular events associated with previously known and newly diagnosed diabetes by studying 14,703 patients with acute MI enrolled in the VALsartan In Acute myocardial iNfarcTion (VALIANT) trial. Patients were grouped by diabetic status: previously known diabetes (insulin use or diagnosis of diabetes before MI, n=3400, 23%); newly diagnosed diabetes (use of diabetic therapy or diabetes diagnosed at randomization [median 4.9 d after infarction], but no known diabetes at presentation, n=580, 4%); or no diabetes (n=10,719). Patients with newly diagnosed diabetes were younger and had fewer comorbid conditions than did patients with previously known diabetes. At 1 year after enrollment, patients with previously known and newly diagnosed diabetes had similarly increased adjusted risks of mortality (hazard ratio [HR] 1.43; 95% confidence interval [CI], 1.29 to 1.59 and HR, 1.50; 95% CI, 1.21 to 1.85, respectively) and cardiovascular events (HR, 1.37; 95% CI, 1.27 to 1.48 and HR, 1.34; 95% CI, 1.14 to 1.56). CONCLUSIONS: Diabetes mellitus, whether newly diagnosed or previously known, is associated with poorer long-term outcomes after MI in high-risk patients. The poor prognosis of patients with newly diagnosed diabetes, despite having baseline characteristics similar to those of patients without diabetes, supports the idea that metabolic abnormalities contribute to their adverse outcomes.