- J P Pell, consultant in public health medicinec,
- E Simpson, consultant clinical scientistb,
- J C Rodger, consultant cardiologista,
- A Finlayson, principal statisticiand,
- D Clark, senior statisticiand,
- J Anderson, research assistanta,
- A C H Pell (), consultant cardiologista
- a Department of Medicine, Monklands Hospital, Airdrie, Lanarkshire ML6 0JS
- b Department of Biochemistry, Monklands Hospital
- c Department of Public Health, Greater Glasgow NHS Board, Glasgow
- d Record Linkage Department, Information and Statistics Division, Common Services Agency, Edinburgh
- Correspondence to: A Pell
- Accepted 5 May 2002
Acute myocardial infarction used to be defined by criteria based on symptoms, changes in electrocardiograms and the concentrations of cardiac enzymes, as recommended by the World Health Organization.1 Specific markers of myocardial damage, including troponin T, are more sensitive indicators than total creatine kinase concentration for ischaemic myocardial necrosis and prognosis.2
In 2000, the European Society of Cardiology and the American College of Cardiology recommended changing the diagnostic criteria for acute myocardial infarction to include raised troponin T concentrations in addition to changes in electrocardiograms or coronary intervention.3 Some patients with acute coronary syndrome who had been diagnosed as having unstable angina are now classified as having myocardial infarction. We investigated the impact of using the new criteria on the incidence, management, and outcome of myocardial infarction.
Participants, methods, and results
Since 1997, all patients admitted with chest pain to Monklands Hospital, Airdrie, had their troponin T concentrations measured. We identified patients admitted between April 1997 and December 2000 with a principal diagnosis of acute myocardial infarction, according to the old criteria, from routine discharge data, the databases of the coronary care unit and laboratory, and case notes. We used the databases to identify patients admitted for chest pain who had raised troponin T concentrations (≥0.1 ng/ml) in the absence of non-myocardial causes such as renal failure, thromboembolic disease, or myocarditis. The new criteria increased admissions for myocardial infarction by 58%, from 1671 to 2637; this equated to approximately 160 000 additional myocardial infarctions per year in the United Kingdom.
Compared with patients who met the old criteria, the additional 966 patients identified were older (median age 74 v 68 years; P<0.001; Mann Whitney U test) and a higher proportion were women (47% v 38%; P<0.0001, χ2 test). Thrombolysis was given to only 13 of the additional patients compared with 672 patients who met the old criteria (1% v 40%; P<0.0001; χ2 test). As a result, thrombolysis rates fell from 40% (95% confidence interval 38% to 42%) to 26% (24% to 28%).
Linkage to national admission (Scottish morbidity record) and death data (General Registrar's Office) provided information on survival, readmission for ischaemic heart disease, coronary angiography, and coronary revascularisation. We calculated cumulative probabilities of these outcomes up to one year of follow up using Kaplan-Meier product limit estimates.
The additional patients had higher 30 day mortality (P=0.016, log rank test) (table). The difference in mortality increased over one year (P<0.0001, log rank test). In a Cox proportional hazards model, the difference in survival on univariate analysis (hazard ratio 2.69; 2.32 to 3.12) was slightly attenuated after adjustment for age, sex, and deprivation (2.07; 1.77 to 2.42) and attenuated further after we adjusted for thrombolysis administration (1.87; 1.58 to 2.20). However, the difference remained significant (P<0.001). The univariate differences in readmission (0.71; 0.60 to 0.84; P<0.001), coronary angiography (0.60; 0.47 to 0.76; P<0.001), and revascularisation (0.69; 0.52 to 0.91; P<0.001) were no longer significant after we adjusted for demography.
The new criteria identified additional patients who were significantly different from those previously classified as having myocardial infarction in terms of demography, eligiblity for thrombolysis, and outcome. Their poorer survival may be, in part, because they are older and ineligibile for thrombolysis because ST segments are not elevated in electrocardiograms. Less frequent revascularisation may be because of poorer survival but may also reflect real differences in practice. Recent evidence suggests these patients might benefit from early revascularisation.4 Thrombolysis rates, 30 day mortality, readmission, and revascularisation are commonly used to assess and compare the quality of care provided by hospitals. Because hospitals vary in both access to troponin assays and adoption of the new diagnostic criteria,5 comparisons between hospitals are misleading. Similarly, longitudinal studies will be unable to differentiate between real changes and artefacts. Our findings have serious implications for auditing, benchmarking, and epidemiology.
We thank Tom Faichen and Maria Ferguson for providing extracts of data from the laboratory and coronary care unit databases respectively.
Contributors: ACHP had the original concept. ACHP and JPP designed the study. AF and DC linked data from the four sources. AF and JPP did the statistical analyses. JA and ACHP reviewed case notes. JPP wrote the original draft and redraft. ES and JCR contributed data and helped with the methodology. All authors agreed the interpretation and approved the final version. ACHP is guarantor.
Funding Chief Scientist Office, Department of Health, Scottish Executive (CZG 4240).
Competing interests None declared.