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Methods We identified patients 30 years of age or older in a large, diverse, community-based population who were hospitalized for incident myocardial infarction between 1999 and 2008. Age- and sex-adjusted incidence rates were calculated for myocardial infarction overall and separately for ST-segment elevation and non–ST-segment elevation myocardial infarction. Patient characteristics, outpatient medications, and cardiac biomarker levels during hospitalization were identified from health plan databases, and 30-day mortality was ascertained from administrative databases, state death data, and Social Security Administration files. Results We identified 46,086 hospitalizations for myocardial infarctions during 18,691,131 person-years of follow-up from 1999 to 2008. The age- and sex-adjusted incidence of myocardial infarction increased from 274 cases per 100,000 person-years in 1999 to 287 cases per 100,000 person-years in 2000, and it decreased each year thereafter, to 208 cases per 100,000 person-years in 2008, representing a 24% relative decrease over the study period. The age- and sex-adjusted incidence of ST-segment elevation myocardial infarction decreased throughout the study period (from 133 cases per 100,000 person-years in 1999 to 50 cases per 100,000 person-years in 2008, P. Many primary and secondary prevention strategies for acute myocardial infarction that have been shown to be efficacious in randomized trials have been implemented by physicians and health systems, resulting in improved control of cardiovascular risk factors in several populations.
However, although better management of risk factors is an important quality benchmark, reductions in the incidence of myocardial infarction and adjusted case fatality rates are better measures of quality. Previous studies of the incidence of myocardial infarction and case fatality rates have often focused on selected subgroups (e.g., the elderly) in populations with limited diversity with respect to race and ethnic group, age, sex, and coexisting conditions, and most have not examined ST-segment elevation and non–ST-segment elevation myocardial infarction separately, although the management and outcomes of these entities differ markedly. The increased use of highly sensitive cardiac biomarkers, particularly troponin, over time might also have contributed to both an artifactually higher incidence of myocardial infarction and a lower level of severity among diagnosed cases. To disentangle these various factors, we examined trends between 1999 and 2008 in the incidence of myocardial infarction, severity as measured by cardiac biomarker levels, and short-term mortality within a large, diverse, community-based cohort. Identification and Characterization of Acute Myocardial Infarction Kaiser Permanente Northern California is a large, integrated health care delivery system caring for more than 3 million persons who are broadly representative of the local and statewide population. Among members who were 30 years of age or older, we identified hospitalizations between 1999 and 2008 with a primary discharge diagnosis of acute myocardial infarction based on the International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) codes 410. Hoover Windtunnel Turbopower 7500 Manual on this page. x0 or 410.x1 from databases of hospital-discharge information and billing claims. This health system's databases capture data on approximately 90% of myocardial infarctions among its members, through either their initial presentation to one of its facilities or their transfer from other hospitals.
And Torus Maps, Dynamics and. Stability of Systems, 11, No. Blanchard, R. Devaney) Differential Equations, Preliminary Edition, PWS. Blanchard, R. Devaney) Differential Equations, Brooks Cole, First Edition. Second Edition 2002, Third Edition 2006, Fourth Edition 2012.
Myocardial infarctions in patients hospitalized solely at other facilities were identified through billing claims. Data on patients with any hospitalization for myocardial infarction within 8 years before the year of interest were censored. The institutional review board of the Kaiser Foundation Research Institute approved the study and granted a waiver of informed consent because of its nature. We classified hospitalizations for myocardial infarction as ST-segment elevation myocardial infarction or non–ST-segment elevation myocardial infarction using primary discharge ICD-9-CM codes: 410.0 to 410.6 and 410.8 for ST-segment elevation myocardial infarction and 410.7 and 410.9 for non–ST-segment elevation myocardial infarction. In 2005, the ICD-9-CM code descriptions were revised to distinguish more explicitly between codes for ST-segment elevation myocardial infarction (410.0 to 410.6 and 410.8) and non–ST-segment elevation myocardial infarction (410.7x).
We assigned ICD-9-CM code 410.9 as non–ST-segment elevation myocardial infarction on the basis of a chart review of a random sample of 37 hospitalizations with ICD-9-CM code 410.9 showing a positive predictive value of 81.1% for this condition. To determine the accuracy and consistency of diagnostic coding over time, we performed a detailed chart review of random samples of 80 hospitalizations per year (40 presumed ST-segment elevation myocardial infarctions and 40 presumed non–ST-segment elevation myocardial infarctions, based on codes) between 1999 and 2007. We applied standardized criteria from the joint European Society of Cardiology and American College of Cardiology Global Task Force. The positive predictive value of the categorization scheme was 96.7% for any myocardial infarction, 79.2% for ST-segment elevation myocardial infarction, and 91.0% for non–ST-segment elevation myocardial infarction, with no significant differences for the latter two conditions across years (P=0.24 and P=0.71, respectively).
For each identified myocardial infarction, we obtained information from laboratory databases on testing for the MB fraction of creatine kinase (CK-MB index) and on CK-MB values for the period from 72 hours before admission until hospital discharge or death, if it occurred during the index hospitalization. For patients undergoing coronary-artery bypass surgery (CABG) during the index hospitalization, only preoperative biomarker levels were included.
We also examined the proportion of patients for whom cardiac troponin I levels were measured; however, troponin levels were not analyzed, since they were not checked systematically in patients with myocardial infarction throughout the entire study period, nor were they commonly used to quantify the severity of the infarct. Patient Characteristics Data on age, sex, and self-reported race or ethnic group were obtained from health plan databases. We recorded information on cardiovascular disease during the 8 years before cohort entry (e.g., angina, ischemic stroke or transient ischemic attack, heart failure, peripheral arterial disease, and percutaneous coronary intervention [PCI] or CABG), cardiovascular risk factors (e.g., hypertension, diabetes mellitus, and dyslipidemia), and other coexisting illnesses such as cancer or lung disease, using previously validated approaches. Preadmission Medication Use The use of medication on an outpatient basis within 30 days before the first hospitalization for myocardial infarction was ascertained from health plan pharmacy records for therapies known to lower cardiovascular risk, including beta-blockers, angiotensin-converting–enzyme (ACE) inhibitors or angiotensin II–receptor blockers (ARBs), statins, and thienopyridines. Statins and beta-blockers may also reduce the severity of the type of clinical presentation of coronary disease. More than 90% of the patients had a drug benefit that provided strong financial incentives to obtain medications from health plan pharmacies. Statistical Analysis Analyses were performed with the use of SAS software, version 9.1 (SAS Institute).
We calculated the incidence rates of myocardial infarction (per 100,000 person-years) for each year. For the denominator, total person-months in each year were calculated in 10-year age intervals (30 to 39 years, 40 to 49 years, 50 to 59 years, 60 to 69 years, 70 to 79 years, 80 to 89 years, and ≥90 years). Direct methods for adjustment were used on the basis of the distribution for age and sex in the 2008 Kaiser Permanente Northern California membership. Cochran–Armitage testing was used to assess for linear trend in incidence rates for myocardial infarction, if appropriate. Sensitivity analyses were performed to determine whether decreases in observed incidence rates for myocardial infarction were strongly influenced by misclassification because of possible miscoding of acute myocardial infarction or differential patterns of persons joining the health plan (in-migration) and existing members leaving the health plan (out-migration) during the study period. We addressed the former by expanding the definition of myocardial infarction to include ICD-9-CM codes 411.x, 413.x, and 414.x in association with elevated cardiac biomarker levels; we addressed the latter by restricting analyses to the subgroup with no in- or out-migration. Temporal trends in the incidence of myocardial infarction, ST-segment elevation myocardial infarction, and non–ST-segment elevation myocardial infarction in all sensitivity analyses were similar to results from the main analysis (see the, available with the full text of this article at NEJM.org), so only the main results are presented here.
We also observed that the proportion of 410.x hospital-discharge codes in the 410.x, 411.x, 413x, and 414.x grouping increased during the study period, suggesting that miscoding of myocardial infarction was unlikely to have contributed to the decrease in rates of myocardial infarction. To explore the potential influence of troponin I testing on the incidence of diagnosed myocardial infarction, we determined the proportion of patients with myocardial infarction who underwent this testing (AxSYM, Abbott Laboratories; AccuTnI, Beckman Coulter) in each study year. We identified the proportion of patients in whom CK-MB was measured and determined the median values for the peak CK-MB level and CK-MB fraction. Temporal trends were assessed with the use of Kendall's tau rank test.
We examined the independent association between calendar year and 30-day case fatality rates using logistic regression with generalized estimating equations that accounted for clustering of patients within each Kaiser Permanente Northern California facility. We adjusted for sociodemographic characteristics, previous cardiovascular diseases, vascular risk factors, and other coexisting illnesses. Incidence of Myocardial Infarction We identified 46,086 patients 30 years of age or older who were hospitalized for incident myocardial infarction between 1999 and 2008 (representing a period of 18,691,131 person-years). Overall, 15,271 patients (33.1%) presented with ST-segment elevation myocardial infarction and 30,815 patients (66.9%) presented with non–ST-segment elevation myocardial infarction. The proportion of myocardial infarctions that were ST-segment elevation myocardial infarctions decreased from 47.0% in 1999 to 22.9% in 2008.
The age- and sex-adjusted incidence of myocardial infarction increased from 274 cases per 100,000 person-years in 1999 to a peak of 287 cases per 100,000 person-years in 2000, and then decreased each year thereafter, to 208 cases per 100,000 person-years in 2008 (relative decrease between 1999 and 2008, 24%) ( Figure 1 Age- and Sex-Adjusted Incidence Rates of Acute Myocardial Infarction, 1999 to 2008. I bars represent 95% confidence intervals. MI denotes myocardial infarction, and STEMI ST-segment elevation myocardial infarction. The age- and sex-adjusted incidence of ST-segment elevation myocardial infarction decreased each year, from 133 cases per 100,000 persons in 1999 to 50 cases per 100,000 persons in 2008 (relative decrease between 1999 and 2008, 62%; P. Patient Characteristics and Medication Use Patients hospitalized with myocardial infarction in the latter part of the study period were older, more likely to be female, less likely to be white, more likely to have coexisting illnesses such as hypertension, dyslipidemia, and diabetes mellitus, and more likely to have undergone previous coronary revascularization ( Table 1 Characteristics of Hospitalized Patients with Incident Myocardial Infarction, 1999 to 2008. These trends were related to the decrease in ST-segment elevation myocardial infarctions as compared with non–ST-segment elevation myocardial infarctions (see Tables B and C in the for the characteristics of the patients).
The use of ACE inhibitors and ARBs, beta-blockers, and statins before myocardial infarction all increased significantly over time ( Figure 2 Previous Use of Medication on an Outpatient Basis. The use of medications in patients presenting with myocardial infarction (MI) (Panel A), ST-segment elevation myocardial infarction (STEMI) (Panel B), and non-STEMI (Panel C) is shown. Chembiodraw Ultra 11 0 Cracked there.
ACE denotes angiotensin-converting enzyme, and ARB angiotensin II–receptor blocker. Cardiac Biomarkers The proportion of patients with myocardial infarction who were known to have undergone troponin I testing increased from 53% in 1999 to 84% in 2004, with stable testing rates between 2004 and 2008. The proportion of patients who underwent CK-MB testing decreased from 75% in 1999 to 56% in 2008 (P. Revascularization and Case Fatality Rates The proportion of patients who underwent revascularization within 30 days after myocardial infarction increased from 40.7% in 1999 to 47.2% in 2008 (P. Discussion Our data from a large, diverse, community-based population show a significant decrease in the incidence of myocardial infarction after 2000 and a dramatic decrease in the incidence of ST-segment elevation myocardial infarction throughout the past decade. The overall adjusted case fatality rate has decreased over time, although it has not decreased among patients with ST-segment elevation myocardial infarctions. Increasing emphasis has been put on measures to reduce risk factors at the individual and community levels, including public bans on smoking and lower target levels of low-density lipoprotein (LDL) cholesterol and blood pressure; these changes have resulted in improved control of risk factors over time.
Substantial reductions in levels of blood pressure and LDL cholesterol occurred during this period within the Kaiser Permanente Northern California population, as compared with other providers, according to reports from the Healthcare Effectiveness Data and Information Set. For example, the proportion of patients meeting target blood-pressure levels increased from 40% in 1999 to 80% in 2008, and the proportion of patients with coronary disease in whom target LDL levels (. Source Information From the Cardiology Division, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston (R.W.Y.); the Division of Research, Kaiser Permanente Northern California (S.S., M.C., M.S., J.V.S., A.S.G.) and the Permanente Medical Group (S.S., J.V.S., A.S.G.) — both in Oakland; and the Departments of Epidemiology, Biostatistics, and Medicine, University of California, San Francisco, San Francisco (A.S.G.). Address reprint requests to Dr. Go at the Division of Research, Kaiser Permanente Northern California, 2000 Broadway St., 3rd Fl., Oakland, CA 94612,. References • 1 Dahlof B, Sever PS, Poulter NR, et al. Prevention of cardiovascular events with an antihypertensive regimen of amlodipine adding perindopril as required versus atenolol adding bendroflumethiazide as required, in the Anglo-Scandinavian Cardiac Outcomes Trial-Blood Pressure Lowering Arm (ASCOT-BPLA): a multicentre randomised controlled trial.
Lancet 2005;366:895-906 • 2 Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic: the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). JAMA 2002;288:2981-2997[Erratum, JAMA 2003;289:176, 2004;291:2196.] • 3 Shepherd J, Cobbe SM, Ford I, et al. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia.
N Engl J Med 1995;333:1301-1307 • 4 Downs JR, Clearfield M, Weis S, et al. Primary prevention of acute coronary events with lovastatin in men and women with average cholesterol levels: results of AFCAPS/TexCAPS. JAMA 1998;279:1615-1622 • 5 Yusuf S, Sleight P, Pogue J, Bosch J, Davies R, Dagenais G. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients.
N Engl J Med 2000;342:145-153[Erratum, N Engl J Med 2000;342:748, 1376.] • 6 LaRosa JC, Grundy SM, Waters DD, et al. Intensive lipid lowering with atorvastatin in patients with stable coronary disease. N Engl J Med 2005;352:1425-1435 • 7 Yusuf S, Zhao F, Mehta SR, Chrolavicius S, Tognoni G, Fox KK.
Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. N Engl J Med 2001;345:494-502[Erratum, N Engl J Med 2001;345:1506, 1716.] • 8 Cannon CP, Weintraub WS, Demopoulos LA, et al. Comparison of early invasive and conservative strategies in patients with unstable coronary syndromes treated with the glycoprotein IIb/IIIa inhibitor tirofiban.
N Engl J Med 2001;344:1879-1887 • 9 Montalescot G, Barragan P, Wittenberg O, et al. Platelet glycoprotein IIb/IIIa inhibition with coronary stenting for acute myocardial infarction. N Engl J Med 2001;344:1895-1903 • 10 Cutler JA, Sorlie PD, Wolz M, Thom T, Fields LE, Roccella EJ. Trends in hypertension prevalence, awareness, treatment, and control rates in United States adults between 1988-1994 and 1999-2004. Hypertension 2008;52:818-827 • 11 Hoerger TJ, Segel JE, Gregg EW, Saaddine JB. Is glycemic control improving in U.S. Diabetes Care 2008;31:81-86 • 12 Mann D, Reynolds K, Smith D, Muntner P.
Trends in statin use and low-density lipoprotein cholesterol levels among US adults: impact of the 2001 National Cholesterol Education Program guidelines. Ann Pharmacother 20-1215 • 13 McWilliams JM, Meara E, Zaslavsky AM, Ayanian JZ. Differences in control of cardiovascular disease and diabetes by race, ethnicity, and education: U.S. Trends from 1999 to 2006 and effects of Medicare coverage. Ann Intern Med 2009;150:505-515 • 14 Steinberg BA, Bhatt DL, Mehta S, et al. Nine-year trends in achievement of risk factor goals in the US and European outpatients with cardiovascular disease.
Am Heart J 2008;156:719-727 • 15 Fox CS, Evans JC, Larson MG, Kannel WB, Levy D. Temporal trends in coronary heart disease mortality and sudden cardiac death from 1950 to 1999: the Framingham Heart Study. Circulation 2004;110:522-527.