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Coronary Heart Disease Incidence, Prevalence and Survival Among The Maori Population, 2000–2002
S22
Abstracts
ABSTRACTS
winter hospitalisations (EWH) and whether this applied to all subcategories of CVD. Methods: We obtained CVD data (ICD.9 principal diagnosis code 390-459 and ICD.10 code I00-I99) from the New Zealand Health Information Service, including all deaths (1988–2005) and hospitalisations (1988–2007). We derived EWM and EWH for each subcategory of CVD using the ratio between episodes in the winter months (June, July and August) compared with summer (December, January, February). We excluded inter-hospital transfers, readmissions within 30 days, planned admissions and day patients. Results: Over this period there were 207,012 deaths and 757,870 hospitalisations coded as CVD (42% and 8.8% of the total deaths and admissions, respectively). Mortality and morbidity were dominated by coronary disease (56.9% and 39.7%) and stroke (23.4% and 14.6%); heart failure also contributing substantially to admissions (13.8%). All 14 subcategories of CVD with total deaths >100 showed EWM with ratios >1.0, most notable being cardiac infections (1.43), heart failure (1.42) and coronary disease (1.32). Similarly all classes showed EWH, especially heart failure (ratio 1.47) although ratios for other diagnostic categories were smaller. Conclusion: All types of CVD deaths and hospitalisations are markedly higher in winter with greater differences among the sickest patients—those dying and those with heart failure. Further research will help to correlate regional differences in such ratios with other environmental influences in an attempt to identify factors amenable to intervention. doi:10.1016/j.hlc.2009.04.050 48 CORONARY HEART DISEASE INCIDENCE, PREVALENCE AND SURVIVAL AMONG THE MAORI POPULATION, 2000–2002 S Mann 3,∗ , M Tobias 1 , L Yeh 1 , C Wright 1 , T Riddell 2 , W Chan 2 , R Jackson 2 1 Public Health Intelligence, Ministry of Health, Auckland, New
Zealand 2 School
of Population Health, University of Auckland, New Zealand 3 Department of Medicine, University of Otago, Wellington, New Zealand Background: Maori appear to have a higher incidence and mortality from coronary heart disease (CHD) than the wider population in New Zealand. We wished to examine this in detail using existing health information compiled for the years 2000–2002. Methods: We obtained data for 2000–2002 from the New Zealand Health Information Service and undertook record linkage using unique national patient identifier numbers. Incidence included all first CHD hospital admissions and all out-of-hospital deaths attributed to CHD where no previous admission had been recorded in the preceding 5 years. Prevalence, survival and other parameters were derived using multi-state lifetables.
Heart, Lung and Circulation 2009;18S:S1–S31
Results: Maori had a higher CHD incidence and higher case fatality than non-Maori. Maori developed CHD at a younger age (medians 56.5 years for males and 58.8 years for females) than non-Maori (medians 67.5 and 77.5, respectively). The lifetime risk of CHD for Maori (36% for males and 34% for females) was only slightly higher than that for the non-Maori population (35% and 28%, respectively) despite higher Maori CHD incidence. This appears to reflect increased age-specific mortality for non-CHD illnesses as well as CHD. Duration of survival with CHD in Maori (9.2 years) was similar to that of the non-Maori population for males (9.5 years) but longer for females (11.2 vs. 6.2 years), which is most likely related to the earlier age of onset in the Maori population. Conclusions: CHD has a markedly higher impact in Maori and at younger ages than in the wider population identifying areas requiring prioritisation. doi:10.1016/j.hlc.2009.04.051 49 PLASMA MYELOPEROXIDASE AT THE CULPRIT CORONARY LESION IN ACUTE MYOCARDIAL INFARCTION CJ Marshall 1,∗ , M Nallaratnam 1 , T Mocatta 2 , D Smyth 1 , AM Richards 1 , JM Elliott 1 , J Blake 1 , C Winterbourn 2 , AJ Kettle 2 , DR McClean 1 1 Cardiology Department, Christchurch Hospital, Christchurch,
New Zealand Radical Research Group, University of Otago, Christchurch, New Zealand
2 Free
Background: Acute ST elevation myocardial infarction (STEMI) is associated with the release of neutrophil enzymes such as myeloperoxidase (MPO). It is unclear whether MPO release is due to acute coronary plaque disruption, or a generalized systemic process. We investigated plasma MPO levels at the culprit coronary lesion in patients undergoing primary PCI for STEMI. Methods: 54 STEMI patients had blood sampled at the femoral artery (FA) prior to anticoagulants. Further samples were drawn across the heart including culprit coronary artery (CA) at the site of occlusive thrombus, and coronary sinus (CS), pre- and post-PCI. Twelve elective PCI patients provided a control. MPO was measured by ELISA. Results: FA MPO was elevated in STEMI vs. elective PCI (median, IQR; 45 ng/ml 34 – 83 vs. 25 ng/ml, 19 – 29, p < 0.001). Following heparin, MPO increased at all sites compared to FA (p < 0.05). Plasma MPO at CA pre was elevated in STEMI compared to elective PCI (171, 122 – 230 vs.136, 109 – 151, p < 0.05). MPO was higher in STEMI patients with culprit coronary artery TIMI 0-1 flow (192 ng/ml, 136 – 241, n = 37), compared to TIMI 2-3 flow (137 ng/ml, 98 – 158, n = 14, p = 0.015). Post PCI, MPO at CS was higher in STEMI vs. controls (154.4, 118 – 216 vs. 90, 70 – 124, p = 0.002). Conclusion: Elevated plasma MPO locally at culprit coronary lesion in STEMI suggests a possible role of MPO
Abstracts
ABSTRACTS
winter hospitalisations (EWH) and whether this applied to all subcategories of CVD. Methods: We obtained CVD data (ICD.9 principal diagnosis code 390-459 and ICD.10 code I00-I99) from the New Zealand Health Information Service, including all deaths (1988–2005) and hospitalisations (1988–2007). We derived EWM and EWH for each subcategory of CVD using the ratio between episodes in the winter months (June, July and August) compared with summer (December, January, February). We excluded inter-hospital transfers, readmissions within 30 days, planned admissions and day patients. Results: Over this period there were 207,012 deaths and 757,870 hospitalisations coded as CVD (42% and 8.8% of the total deaths and admissions, respectively). Mortality and morbidity were dominated by coronary disease (56.9% and 39.7%) and stroke (23.4% and 14.6%); heart failure also contributing substantially to admissions (13.8%). All 14 subcategories of CVD with total deaths >100 showed EWM with ratios >1.0, most notable being cardiac infections (1.43), heart failure (1.42) and coronary disease (1.32). Similarly all classes showed EWH, especially heart failure (ratio 1.47) although ratios for other diagnostic categories were smaller. Conclusion: All types of CVD deaths and hospitalisations are markedly higher in winter with greater differences among the sickest patients—those dying and those with heart failure. Further research will help to correlate regional differences in such ratios with other environmental influences in an attempt to identify factors amenable to intervention. doi:10.1016/j.hlc.2009.04.050 48 CORONARY HEART DISEASE INCIDENCE, PREVALENCE AND SURVIVAL AMONG THE MAORI POPULATION, 2000–2002 S Mann 3,∗ , M Tobias 1 , L Yeh 1 , C Wright 1 , T Riddell 2 , W Chan 2 , R Jackson 2 1 Public Health Intelligence, Ministry of Health, Auckland, New
Zealand 2 School
of Population Health, University of Auckland, New Zealand 3 Department of Medicine, University of Otago, Wellington, New Zealand Background: Maori appear to have a higher incidence and mortality from coronary heart disease (CHD) than the wider population in New Zealand. We wished to examine this in detail using existing health information compiled for the years 2000–2002. Methods: We obtained data for 2000–2002 from the New Zealand Health Information Service and undertook record linkage using unique national patient identifier numbers. Incidence included all first CHD hospital admissions and all out-of-hospital deaths attributed to CHD where no previous admission had been recorded in the preceding 5 years. Prevalence, survival and other parameters were derived using multi-state lifetables.
Heart, Lung and Circulation 2009;18S:S1–S31
Results: Maori had a higher CHD incidence and higher case fatality than non-Maori. Maori developed CHD at a younger age (medians 56.5 years for males and 58.8 years for females) than non-Maori (medians 67.5 and 77.5, respectively). The lifetime risk of CHD for Maori (36% for males and 34% for females) was only slightly higher than that for the non-Maori population (35% and 28%, respectively) despite higher Maori CHD incidence. This appears to reflect increased age-specific mortality for non-CHD illnesses as well as CHD. Duration of survival with CHD in Maori (9.2 years) was similar to that of the non-Maori population for males (9.5 years) but longer for females (11.2 vs. 6.2 years), which is most likely related to the earlier age of onset in the Maori population. Conclusions: CHD has a markedly higher impact in Maori and at younger ages than in the wider population identifying areas requiring prioritisation. doi:10.1016/j.hlc.2009.04.051 49 PLASMA MYELOPEROXIDASE AT THE CULPRIT CORONARY LESION IN ACUTE MYOCARDIAL INFARCTION CJ Marshall 1,∗ , M Nallaratnam 1 , T Mocatta 2 , D Smyth 1 , AM Richards 1 , JM Elliott 1 , J Blake 1 , C Winterbourn 2 , AJ Kettle 2 , DR McClean 1 1 Cardiology Department, Christchurch Hospital, Christchurch,
New Zealand Radical Research Group, University of Otago, Christchurch, New Zealand
2 Free
Background: Acute ST elevation myocardial infarction (STEMI) is associated with the release of neutrophil enzymes such as myeloperoxidase (MPO). It is unclear whether MPO release is due to acute coronary plaque disruption, or a generalized systemic process. We investigated plasma MPO levels at the culprit coronary lesion in patients undergoing primary PCI for STEMI. Methods: 54 STEMI patients had blood sampled at the femoral artery (FA) prior to anticoagulants. Further samples were drawn across the heart including culprit coronary artery (CA) at the site of occlusive thrombus, and coronary sinus (CS), pre- and post-PCI. Twelve elective PCI patients provided a control. MPO was measured by ELISA. Results: FA MPO was elevated in STEMI vs. elective PCI (median, IQR; 45 ng/ml 34 – 83 vs. 25 ng/ml, 19 – 29, p < 0.001). Following heparin, MPO increased at all sites compared to FA (p < 0.05). Plasma MPO at CA pre was elevated in STEMI compared to elective PCI (171, 122 – 230 vs.136, 109 – 151, p < 0.05). MPO was higher in STEMI patients with culprit coronary artery TIMI 0-1 flow (192 ng/ml, 136 – 241, n = 37), compared to TIMI 2-3 flow (137 ng/ml, 98 – 158, n = 14, p = 0.015). Post PCI, MPO at CS was higher in STEMI vs. controls (154.4, 118 – 216 vs. 90, 70 – 124, p = 0.002). Conclusion: Elevated plasma MPO locally at culprit coronary lesion in STEMI suggests a possible role of MPO