Journal of the New Zealand Medical Association, 07-October-2005, Vol 118 No 1223
Heart attacks and unstable angina (acute coronary syndromes) have doubled in New Zealand since 1989: how do we best manage the epidemic?
John Elliott, Mark Richards
While falls in age-standardised mortality have been well publicised over the last 30 years, heart disease continues to account for 30% of all deaths in New Zealand.1 There were 5973 deaths in 2000 and 6368 deaths in 2001 due to disease of the coronary (heart) arteries. Recent surveys also suggest a large number of older New Zealanders have been diagnosed with coronary artery disease. Indeed, 40% of those aged over 75, and 30% of those aged 65 to 74, have symptoms of coronary disease.2 Therefore, it is important to treat such a prevalent disease well to optimise wellbeing of (and minimise costs to) individuals, the health system, and our society.
The treatment of acute coronary syndromes (ACS) in New Zealand was audited in 2002 in a nationwide study in which data was collected on all patients presenting with suspected or definite ACS to all 36 hospitals in the country accepting such admissions.3 Over a 14-day period in May 2002, there were 721 patients with a confirmed ACS (101 were diagnosed with ST-elevation myocardial infarction, 287 with non ST-elevation myocardial infarction, and 333 with unstable angina); this translates to nearly 19,000 New Zealanders requiring treatment over 1 calendar year.
Results suggested low levels of appropriate investigations and evidence-based treatments compared with contemporary international guidelines, including revascularisation before discharge. Furthermore, treatments received varied between one region and another, and depended on whether the hospital had on-site angiography or cardiac catheterisation facilities. If there was no angiography facility on-site, the chances of having an angiogram or in-hospital revascularisation were significantly lower. 4
In this issue of the Journal, New Zealand Guidelines formulated by New Zealanders for New Zealanders are published.5,6 These Guidelines outline appropriate standards of care for in-hospital treatment of people presenting with ST-elevation myocardial infarction (STEMI) or non ST-elevation acute coronary syndromes (nonSTEACS). There is a gap between the standards of care outlined in these guidelines and the treatments received by New Zealanders in 2002.3 Before estimating the extra resources required to close the gap, we need to know just how many New Zealanders are presenting to hospitals with STEMI or nonSTEACs each year.
Age- and gender-specific data on the incidence of ACS was extracted from an annual publication titled Selected Hospital Morbidity and Mortality Data for calendar years till 1995 inclusive then for financial years including 1995/96 through 2000/2001. Unpublished data for 2001/02 and 2002/03 was kindly supplied by the New Zealand Health Information Service.
Between 1989 and 2002/2003, hospital discharges for acute myocardial infarction have more than doubled from 5496 to 11,454 per year or 31 each day in New Zealand, increasing by an average of 4% per year from 1989 to 1999/2000 then by 17% per year till 2002/2003 (Figure 1). During the same period, hospital discharges for all acute coronary syndromes combined increased by 5% per year from 14,777 to peak at 25,692 in 2000/2001 and then fell to 23,978 or 66 each day in 2002/2003 (Figure 2).
Figure 1. Hospitalisation for treatment of acute myocardial infarction (DRG 410 up to and including 1999/2000, thereafter code I21) in all New Zealanders (closed squares), men (closed circles), and women (open circles)
Figure 2. Hospitalisation for treatment of acute coronary syndromes in all New Zealanders (closed squares), men (closed circles), and women (open circles)
The recent accelerated increase in the number of acute myocardial infarctions (AMIs) per year may be due to changes in the definition of AMI. Rises in troponin T and troponin I are specific for myocardial cell necrosis. Guidelines for the diagnosis and treatment of AMI have been changed to incorporate the use of troponins in differentiating between AMI and unstable angina. This has increased the number of AMI diagnosed by at least 20% in the GRACE registry, a contemporary international ACS registry.7
The risk of death and reinfarction in the years after these “small” infarcts, with raised troponins but normal creatine kinase levels, is the same as that after “bigger” heart attacks with raised creatine kinase levels. Therefore, international guidelines have recommended that these “small” AMIs diagnosed using troponin levels should be investigated and treated in the same way as AMI with raised creatine kinase. Thus, however they are defined, all patients currently diagnosed with AMI must be considered for in-hospital angiography and revascularisation as appropriate. The redefinition of AMI in no way confounds the observed increase in total admissions for ACS (although it clearly recategorised a significant minority from unstable angina to AMI within the overall population incurring ACS).
It is not known how many of the 11,454 AMIs in 2002/2003 presented with ST-elevation and required immediate thrombolysis or direct angioplasty. The coding system is based on primary discharge diagnosis and does not categorise AMI according to ECG changes at presentation. Also there are no discharge codes for thrombolysis, direct angioplasty, or glycoprotein IIbIIIa inhibitors. This has two important consequences: there is no data on how many New Zealanders receive these treatments, and DHBs who choose to use these interventions do not receive any extra payment for the extra costs of evidence-based treatment in these subgroups. Coding updates that have been adopted in Australia in recent years have not been adopted in New Zealand pending reassessment of the cost implications. In the NZ ACS Audit, 26% of all infarcts presented with ST elevation.3
ACS may be increasing more rapidly in women than in men. Between 1989 and 2002/2003, AMI has increased by 102% in men and 119% in women. In 1989, 35% of AMI were in women, this has increased to 38% in 1999/2000 and 37% in 2002/03. The proportion of women with acute coronary syndromes has increased from 36% to 39%.
ACS is also increasing more rapidly in Maori and Pacific Island groups than in other New Zealanders. Between 1995/96 and 2000/2001, acute coronary syndromes overall increased by 15% per year in Maori (15% in men and women), 25% per year in Pacific Islanders (26% in men and 24% in women), and 5% per year in other New Zealanders ( 4.1% in men and 6.4% in women) (Figure 3).
In 1995/96, 5.5% of all New Zealanders discharged with ACS were Maori and 1.6% were Pacific Islanders, this increased to 7.2% and 2.7% in 2000/01. Discharge after treatment for AMI increased by 14% per year in Maori (17% in men and 13% in women and 4% in other New Zealanders. In 1995/96, 5.5% of AMI were in Maori, this increased to 6.7% in 2000/01. Data on AMI in Pacific Islanders was not published.
We have calculated age-specific data for ACS hospital discharges for all New Zealand men from 1991 to 2000 by adjusting increases in hospital discharges for increases in population numbers for each age group using 1991 and 2001 census data. There were increases in all age groups with the greatest absolute increase in numbers in the 65 to 74 year age group, but the largest percentage change in the age-specific discharge rates was in the youngest age group of men aged 25 to 34 years. Age-specific discharge rates increased by 2 to 3% per year in all age groups except those aged 55-64 where the increase was just over 1% per year. Similar changes were present in women. Thus the increases in numbers of patients are not confined to elderly age groups.
In 2002/2003, more than twice as many New Zealanders had a heart attack than in 1989, and 9,000 more New Zealanders were admitted to hospital with ACS than in 1989. While these data may be influenced by changes in coding systems over the last 15 years, and do not distinguish repeat admissions from first admissions, our observations suggest an epidemic in acute coronary syndromes is in progress. The aging population contributes to this epidemic but increases have occurred in men and women of all age groups. Of further concern, increases in the incidence of ACS in Maori and Pacific Islanders appear to outstrip trends in other New Zealanders.
Figure 3 Hospitalisation with acute coronary syndromes in Maori men (closed diamonds), Maori women (open diamonds), Pacific Island men (closed squares), and Pacific Island women (open squares) from 1995/96 to 2000/01
These findings have important implications for resource allocation and planning, particularly as this increase in numbers of New Zealanders hospitalised with ACS has coincided with a wealth of evidence that supports more aggressive and invasive treatments to improve prognosis and outcomes (see Guidelines published in this issue of the Journal).
The cost of treating New Zealanders with “best practice” treatments, which have been available for more than 10 years, needs to be acknowledged by funders by urgently updating the coding system to include codes for such treatments. It is indefensible that DHBs are not compensated for the costs of treating patients with thrombolysis or IIbIIIa inhibitors because these proven agents have not made it into the coding system.
The lack of a code or payment for direct angioplasty for STEMI patients will impede appropriate development of such services. Pre-discharge angioplasty or bypass surgery attracts 1.84 fewer case weights or approximately $5000 less than discharge without appropriate investigation with later elective readmission for angiography then further admission for revascularisation in those who have survived this stepwise process. The funding system is backward and broken and will hamper efforts by providers or DHBs to follow the Guidelines.
Hospital funding will also have to keep pace with the epidemic until primary prevention efforts become more effective and adverse trends in smoking in the young, and insufficient exercise as well as obesity in all age groups, are reversed.2
Author information: John M Elliott, Associate Professor of Medicine; Mark Richards, National Heart Foundation Professor of Cardiovascular Studies, Department of Medicine; Christchurch School of Medicine and Health Sciences, University of Otago, Christchurch
Correspondence: Assoc Professor John Elliott, Department of Medicine, Christchurch School of Medicine and Health Sciences, PO Box 4345, Christchurch. Fax: (03) 364 0935; email: email@example.com
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