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Chest pain triage-outcome after inappropriate discharge
Heart,
Lung
and Circulation
2000; 9
48th Annual
Scientific
Meeting
of CSANZ
A10’
A PLAQUE RUPTURE MODEL FOR ISCHAEMIA IN THE RABBIT HINDLIMB AJ. Tavla*. A Boblk. M Bcrudt G Jctmluas. Baker Medical Research Institute, Melbourne, Australii. Background: Rupture of atherosclerotic pIaque is the pivotal event iu uustable coronary syndromes, including uustable angina and acute myocardlal iotbrctlou (AMI). To tmdersumd tbe patltogeuesis of AMI, functlaral aud histological loformaticu regardbtg both the adtcmsclerotic plaque ruptureAbrombosis itself and also the effects on the distal vascttlature needs to be obtaiued. Ao animal model of plaque rupture attd tbrombcais would be highly desirable. Methods: A total of 19 Baker rabbits tmdmveut one of two regimens. Rabbits io group I (n=8) uudmveot balloou-iuduced arteial injury followed by the placement of au iodwelliog ltttra-art&al wire to eubaoce lesion development. Rabbits lu group II (n=ll) also uoderweut balloon-induced arterial injury but did not have au indwelling imra-m wire left in-situ. AU rabbits commenced a diet of 1% cholesterol 3 days prior to the balloon injury and rmuatued 00 this until completion of tbe study. After a prcdetermlued time @out 1 to 4 weeks) the rabbits uoderweut a repeat study cousistiog of attg&mplty to document stestosis severity, aud thee smilice for histological examiuaticu. Ju those rabbits restudied at 4 weeks, au attempt at plaque rupture was made. Serial augiograpbic data was also obtaiued at 2, 3 and 4 weeks in the group II rabbits. Resulb: Of the 8 rabbits iu group I, 4 were restudied at 1 week and 4 were restudied at 2 weeks. lo all cases the leslous bad progressed so rapidly dmt the vessel was totally cccluded at the time of restudy. Of dte 11 rabbits in group II,4 were restudied at 2 weeks wltb tie remainder being restudied at 4 weeks. Serial augiogmpby in group II revealed a steady iucrease lu stenosis severity, from a mean of 10% at 2 weeks to a meatt of 68% at 4 we&s (PcO.@Xt5). Histological examluatiou showed a progressiou of me lesious over rime, wltb tbcee at 4 weeks showing heavy foam cell itt6bmtiat and rich lipid depositlou. Mechanical plaque rupture was attempted iu all r&bits re.studied at 4 weeks. Hlstopadtological examluatlou revealed local tbrmubosis in 4 of 5 rabbits, with complete vessel ix.clusiou in me case. Coucluslons: Our model demmtstrates progressiou wltb time of adtaosclerotic plaques in the rabbit hlttdllbnb botb augiograpbically and histologically. At 4 weeks, the lesicms appeared similar to unstable human plaques and were suitable for mecbauicai disruptiou to luduce local tbrcdubosis. We couflrmed histopatbologically that local drrombosls occurred following mechanical plaque rupture, and that lu one case the local tbrmubosis was so extensive that complete vessel occlusiou occurred. We believe dtis model will enable further exatuiuatioo of the effect.3 of plaque rupture and tbrombodc occlusion, both locally and iu the distal vessel.
PAIN EVALUATION AREAS IN MELBOURNE: A PILOT 1 Dart. 1 G Je 1 1. Holsworth”‘. L Dud rz P Cameron P LeBroca . A Kambourakrs . R Pevenl . S , ‘Dept of Cardiology ,‘d Emergency Meicine The Add Hospital, Prabran, Vie. *Dept of Cardiology and Emerge& Medicine, Royal Melbourne Hospital, Parkville, Vie. ‘Dept of Cardiology and Emergency Medicine, Monash Medical Center, Clayton, Vie. Background American studies support the introduction of Chest Pain Evaluation Areas (CPEA) as an adjunct to emergency department (ED) management of chest pain. Aim To assess the safety and effectiveness of an accelerated diagnostic protocol witbin a CPEA in the Australian setting. Method CFEA’s were established in three major Melbourne tertiary referral hospitals. All patients presenting to the ED with possible ischaemic chest pain and low to intermediate risk of adverse events were admitted to these areas. Management protocols included continuous ECG and ST segment monitoring, serial cardiac enzyme measurements, carcliology review and investigations to exclude myocarclial ischaemia. All patients were followed up at 30 days to confirm final diagnosis and exclude post discharge acute coronaty events. Results During the initial six month period 656 patients were admitted to the CPEA’s, representing 13% of total chest pain presentations to ED. Of these, 78%(n-513) completed the protocol and were discharged to home. Subsequent investigations within this sub group diagnosed new onset acute coronary syndrome in 3%(n=lS) patients at 30 days. Post discharge events were identified in <0.6%(n=3) of these patients, these were AMI <0.4%(n-2) and death <0.2%(n= 1). The remainin g 22%(n=143) of CPEA patients required in-patient admission and one non-cardiac death occurred whilst in CPEA. Final discharge diagnosis confirmed 17%(n=25) AM1 and 29%(n-41) Unstable Angina. Conclusion Accelerated diagnostic protocols witbin a CPEA provide effective, safe management of chest pain within the ED.
TROPONIN I IN PULMONARY EMBOLISM. A Z Rij& R.SlauehterCarAronev.iology Department, The Prince Charles Hospital, Brisbane, Qld. Aim: There have been a growing number of isolated reports of an elevation of troponin I in patients with pulmonary embolism. The aim of this study is to demonstrate whether troponin I (TnI) is elevated in acute pulmonary embolism (PE) in patients without evidence of ischaemic heart disease and to determine if an elevated TnI correlates with embohts load, as determined by CT pulmonaty angiogram (CTPA), ECG changes and echocardiographic parameters related to right ventricular overload. Methods: This was a prospective study of patients who presented to the emergency department with PE confirmed on CTPA and no evidence of active coronary disease. Tn I was measured at presentation or 8 hours after symptom onset (whichever was later), at 24 hours and at 4 days. ECGs were performed on presentation and all patients had an echocardiogram to assess right ventricular function within two days. Results: Of the 8 cases of acute PE presenting to the hospital, 6 had a “large” embolus loads as judged on CTPA, one “medium” and one “small”. Of the large PEs, 4 had echocardiographic evidence of right ventricular dilatation and reduced function and all had ECG changes consistent with a diagnosis of PE. Neither ECG nor ECHO changes were evident in the small or medium PEs. All the large PEs had an elevated TnI which persisted for 4 days, but neither of the small or medium PEs had an elevation of TnI. Conclusion: The study confirms that troponin I is elevated in some patients with pulmonary embolism, specifically those assessed with a large thrombus load and “right ventricular strain”. The persistence of troponin I elevation for 4 days suggests myocardial necrosis rather than “cytosolic 1eakage”of troponin.
CHEST PAIN TRIAGE - OUTCOME AFTER INAPPROPRIATE DISCHARGE: M. A. Fitzuatrlck*. M. Dodd E. Hutcbiues. D. Schoevers, A. Grouse. Cardiology and Emergency Depts, Nepeau Hospital, NSW. Introduction: Chest pain (CP) patients (pts) wltb an intermediate risk (IntRisk) of short-term adverse events are frequently discharged inappropriately (IuDis) without exclusion of Ml at 8 brs or exercise testing (EST) contrary to National Guidelines (NGL) (MJA 1997; 166:644). Aim: To compare the outcomes (death, MI or recurrent CP admission) of IuDis pts with those managed by a chest pain unit strategy (CPU - exclude Ml t EST + discharge iu < 24 brs). Methods: Prospective cohort study of 1,013 patients presenting for the first time to the NH ED with CP between 29/6/98 and 28/2/99. Of 370 IntRisk pts, 173 were discharged <24 brs: 75 CPU; 100 IuDis (43 < 6brs; 57 No EST). Of 205 high risk or ST elevation MI pts, 20 of the high tisk pts were discharged <24 brs: 6 CPU; 14 IuDis (5 < 6brs; 9 No EST). Of the CPU pts, 27 participated in a randomlsed study comparing outcomes witlt usual care. Of tlte remaiuiug CPU pts, 36/54 would have met inclusion criteria for the study, while 51/106 IttDis pts met these criteria. Outcomes were determined by &art review and telephone at 4 months. Results: At entry, the CPU & InDis pts had a similar age and sex distribution and frequency of CAD risk factors. However, IuDis pts bad a higher prevalence of prior CAD (43% v 7%, p
CHEST STUDY
Lung
and Circulation
2000; 9
48th Annual
Scientific
Meeting
of CSANZ
A10’
A PLAQUE RUPTURE MODEL FOR ISCHAEMIA IN THE RABBIT HINDLIMB AJ. Tavla*. A Boblk. M Bcrudt G Jctmluas. Baker Medical Research Institute, Melbourne, Australii. Background: Rupture of atherosclerotic pIaque is the pivotal event iu uustable coronary syndromes, including uustable angina and acute myocardlal iotbrctlou (AMI). To tmdersumd tbe patltogeuesis of AMI, functlaral aud histological loformaticu regardbtg both the adtcmsclerotic plaque ruptureAbrombosis itself and also the effects on the distal vascttlature needs to be obtaiued. Ao animal model of plaque rupture attd tbrombcais would be highly desirable. Methods: A total of 19 Baker rabbits tmdmveut one of two regimens. Rabbits io group I (n=8) uudmveot balloou-iuduced arteial injury followed by the placement of au iodwelliog ltttra-art&al wire to eubaoce lesion development. Rabbits lu group II (n=ll) also uoderweut balloon-induced arterial injury but did not have au indwelling imra-m wire left in-situ. AU rabbits commenced a diet of 1% cholesterol 3 days prior to the balloon injury and rmuatued 00 this until completion of tbe study. After a prcdetermlued time @out 1 to 4 weeks) the rabbits uoderweut a repeat study cousistiog of attg&mplty to document stestosis severity, aud thee smilice for histological examiuaticu. Ju those rabbits restudied at 4 weeks, au attempt at plaque rupture was made. Serial augiograpbic data was also obtaiued at 2, 3 and 4 weeks in the group II rabbits. Resulb: Of the 8 rabbits iu group I, 4 were restudied at 1 week and 4 were restudied at 2 weeks. lo all cases the leslous bad progressed so rapidly dmt the vessel was totally cccluded at the time of restudy. Of dte 11 rabbits in group II,4 were restudied at 2 weeks wltb tie remainder being restudied at 4 weeks. Serial augiogmpby in group II revealed a steady iucrease lu stenosis severity, from a mean of 10% at 2 weeks to a meatt of 68% at 4 we&s (PcO.@Xt5). Histological examluatiou showed a progressiou of me lesious over rime, wltb tbcee at 4 weeks showing heavy foam cell itt6bmtiat and rich lipid depositlou. Mechanical plaque rupture was attempted iu all r&bits re.studied at 4 weeks. Hlstopadtological examluatlou revealed local tbrmubosis in 4 of 5 rabbits, with complete vessel ix.clusiou in me case. Coucluslons: Our model demmtstrates progressiou wltb time of adtaosclerotic plaques in the rabbit hlttdllbnb botb augiograpbically and histologically. At 4 weeks, the lesicms appeared similar to unstable human plaques and were suitable for mecbauicai disruptiou to luduce local tbrcdubosis. We couflrmed histopatbologically that local drrombosls occurred following mechanical plaque rupture, and that lu one case the local tbrmubosis was so extensive that complete vessel occlusiou occurred. We believe dtis model will enable further exatuiuatioo of the effect.3 of plaque rupture and tbrombodc occlusion, both locally and iu the distal vessel.
PAIN EVALUATION AREAS IN MELBOURNE: A PILOT 1 Dart. 1 G Je 1 1. Holsworth”‘. L Dud rz P Cameron P LeBroca . A Kambourakrs . R Pevenl . S , ‘Dept of Cardiology ,‘d Emergency Meicine The Add Hospital, Prabran, Vie. *Dept of Cardiology and Emerge& Medicine, Royal Melbourne Hospital, Parkville, Vie. ‘Dept of Cardiology and Emergency Medicine, Monash Medical Center, Clayton, Vie. Background American studies support the introduction of Chest Pain Evaluation Areas (CPEA) as an adjunct to emergency department (ED) management of chest pain. Aim To assess the safety and effectiveness of an accelerated diagnostic protocol witbin a CPEA in the Australian setting. Method CFEA’s were established in three major Melbourne tertiary referral hospitals. All patients presenting to the ED with possible ischaemic chest pain and low to intermediate risk of adverse events were admitted to these areas. Management protocols included continuous ECG and ST segment monitoring, serial cardiac enzyme measurements, carcliology review and investigations to exclude myocarclial ischaemia. All patients were followed up at 30 days to confirm final diagnosis and exclude post discharge acute coronaty events. Results During the initial six month period 656 patients were admitted to the CPEA’s, representing 13% of total chest pain presentations to ED. Of these, 78%(n-513) completed the protocol and were discharged to home. Subsequent investigations within this sub group diagnosed new onset acute coronary syndrome in 3%(n=lS) patients at 30 days. Post discharge events were identified in <0.6%(n=3) of these patients, these were AMI <0.4%(n-2) and death <0.2%(n= 1). The remainin g 22%(n=143) of CPEA patients required in-patient admission and one non-cardiac death occurred whilst in CPEA. Final discharge diagnosis confirmed 17%(n=25) AM1 and 29%(n-41) Unstable Angina. Conclusion Accelerated diagnostic protocols witbin a CPEA provide effective, safe management of chest pain within the ED.
TROPONIN I IN PULMONARY EMBOLISM. A Z Rij& R.SlauehterCarAronev.iology Department, The Prince Charles Hospital, Brisbane, Qld. Aim: There have been a growing number of isolated reports of an elevation of troponin I in patients with pulmonary embolism. The aim of this study is to demonstrate whether troponin I (TnI) is elevated in acute pulmonary embolism (PE) in patients without evidence of ischaemic heart disease and to determine if an elevated TnI correlates with embohts load, as determined by CT pulmonaty angiogram (CTPA), ECG changes and echocardiographic parameters related to right ventricular overload. Methods: This was a prospective study of patients who presented to the emergency department with PE confirmed on CTPA and no evidence of active coronary disease. Tn I was measured at presentation or 8 hours after symptom onset (whichever was later), at 24 hours and at 4 days. ECGs were performed on presentation and all patients had an echocardiogram to assess right ventricular function within two days. Results: Of the 8 cases of acute PE presenting to the hospital, 6 had a “large” embolus loads as judged on CTPA, one “medium” and one “small”. Of the large PEs, 4 had echocardiographic evidence of right ventricular dilatation and reduced function and all had ECG changes consistent with a diagnosis of PE. Neither ECG nor ECHO changes were evident in the small or medium PEs. All the large PEs had an elevated TnI which persisted for 4 days, but neither of the small or medium PEs had an elevation of TnI. Conclusion: The study confirms that troponin I is elevated in some patients with pulmonary embolism, specifically those assessed with a large thrombus load and “right ventricular strain”. The persistence of troponin I elevation for 4 days suggests myocardial necrosis rather than “cytosolic 1eakage”of troponin.
CHEST PAIN TRIAGE - OUTCOME AFTER INAPPROPRIATE DISCHARGE: M. A. Fitzuatrlck*. M. Dodd E. Hutcbiues. D. Schoevers, A. Grouse. Cardiology and Emergency Depts, Nepeau Hospital, NSW. Introduction: Chest pain (CP) patients (pts) wltb an intermediate risk (IntRisk) of short-term adverse events are frequently discharged inappropriately (IuDis) without exclusion of Ml at 8 brs or exercise testing (EST) contrary to National Guidelines (NGL) (MJA 1997; 166:644). Aim: To compare the outcomes (death, MI or recurrent CP admission) of IuDis pts with those managed by a chest pain unit strategy (CPU - exclude Ml t EST + discharge iu < 24 brs). Methods: Prospective cohort study of 1,013 patients presenting for the first time to the NH ED with CP between 29/6/98 and 28/2/99. Of 370 IntRisk pts, 173 were discharged <24 brs: 75 CPU; 100 IuDis (43 < 6brs; 57 No EST). Of 205 high risk or ST elevation MI pts, 20 of the high tisk pts were discharged <24 brs: 6 CPU; 14 IuDis (5 < 6brs; 9 No EST). Of the CPU pts, 27 participated in a randomlsed study comparing outcomes witlt usual care. Of tlte remaiuiug CPU pts, 36/54 would have met inclusion criteria for the study, while 51/106 IttDis pts met these criteria. Outcomes were determined by &art review and telephone at 4 months. Results: At entry, the CPU & InDis pts had a similar age and sex distribution and frequency of CAD risk factors. However, IuDis pts bad a higher prevalence of prior CAD (43% v 7%, p
CHEST STUDY