Maruti Suzuki India Ltd In line with expectations Result Update Maruti’s 4QFY08 operating performance was in line with our estimates, adjusting for 28tH April 2008 MTM loss provision on its forex derivatives and the one time expense of Rs 545 mn, representating compensation to dealer. The MTM provision is with respect to forward cover for its European exports (commenc
Bardzo tanie apteki z dostawą w całej Polsce kupic levitra i ogromny wybór pigułek.
Acutemed.co.uk2Emergency management of cardiac chest pain: a
Emerg. Med. J.
doi:10.1136/emj.18.1.6 Updated information and services can be found at: References
This article cites 30 articles, 14 of which can be accessed free at: 2 online articles that cite this article can be accessed at: Rapid responses
Receive free email alerts when new articles cite this article - sign up in the box at the To order reprints of this article go to: Emerg Med J 2001;18:6–10
Emergency management of cardiac chest pain: areview Chest pain accounts for 2%–4% of all new fer to coronary care, and also to limit the attendances at emergency departments (ED) impact on the patient and healthcare resources.
in the United Kingdom.1 2 Chest pain can be The diagnosis of chest pains less than 12 the presenting complaint in a myriad of disor- hours in duration is an important challenge.
ders ranging from life threats such as acute This is for three reasons. Firstly, individual myocardial infarction (AMI) to mild self limit- biochemical markers cannot eVectively rule ing disorders such as muscle strain. Possible out myocardial infarction in the initial 12 hour cardac chest pain can be viewed as a con- period.13 14 Secondly, aspirin and the fibrino- tinuum, ranging from total global AMI to sim- lytic agents are at their most potent during this ple short lived angina. Within this spectrum lie period,8 15 and finally the majority of AMI the acute coronary syndromes with critical car- related deaths occur in the first 12 hours.4 diac ischaemia and minimal myocardial dam- identifies all AMIs immediately and confi- Nationally over 129 000 deaths a year are dently excludes all non-AMIs. No perfect test attributable to ischaemic heart disease.3 AMI exists; instead tests are combined initially to case mortality is currently 45% with over 70% rule in myocardial infarction (RIMI), and then of these dying before they reach medical care.4 to eVectively rule out myocardial infarction One in eight patients with unstable angina will (ROMI). The clinical eYcacy of diagnostic infarct within two weeks without appropriate tests is evaluated using sensitivity and specifi- treatment. In the UK around 30% of patients city. To be certain of the diagnosis (in this case RIMI) a test must be have very few false posi- discharged from the ED1 while in the United tives (high specificity). However, to confidently States 60% are admitted and 40% discharged.4 rule out a condition (in this case ROMI) the Despite such high admission rates 3%–4% of test must have minimal false negatives (high EDs. In the UK significantly fewer patients are admitted; while the number of missed AMIs is evidence base underlying diagnostic and treat- unknown, recent evidence suggests that some ment strategies for patients with cardiac 6% of patients discharged from EDs may have prognostically significant myocardial damage.5 The initial approach to cardiac sounding
accounts for 20% of US emergency medicine Patients with cardiac sounding chest pain must related litigation dollars.7 Many interventions have rapid access to appropriate care. This including drug therapy and surgery reduce requires robust recognition of the problem, mortality in patients with AMI.8–11 However, the patient can only benefit if correctly identi- trained to assess clinical risk. This is summa- Although it is essential to identify all patients Department of
important to control costs and not subject Accident and
patients to unnecessary investigations, in- Emergency,
patient care and resultant psychological stress.
Forty per cent of patients admitted to CCU Road, Manchester
with chest pain will have all ischaemic heart M13 9WL, UK
disease ruled out.12 The emotional, physical and economic impact on the patient, their family, their friends and the limited resources of the healthcare system should not be under- estimated. The process of chest pain evaluation must therefore be both timely and accurate in order to facilitate early thrombolysis and trans- Emergency management of cardiac chest pain History suggesting unstable cardiac ischaemia The first clinical contact between the patientand the ED is usually at nurse triage. It is Cardiac sounding chest pain and any of: essential that cardiac sounding chest pain is identified at this stage, and accorded an appro- + Pain not relieved by standard treatment in standard time priately high (very urgent) clinical priority.17 + Pain occurring with increasing frequency over the previous This will ensure that an appropriate early path- way of care is followed. Once this group of + Pain within six weeks of AMI or revascularisation patients have been identified subsequent man-agement should be presentation sensitive— tion. This will allow appropriate decisions very urgent cardiac pain patients should be ischaemic changes not known to be old predictboth a high risk of myocardial infarction and also a high risk of complications. If the ECG is The initial ECG is performed to RIMI, and normal then clinical risk factors are sought.
should be recorded as soon as possible—and Firstly, any history consistent with unstable certainly within 10 minutes. The ECG is an ischaemic heart disease is elicited—a practical excellent tool for RIMI as it is highly specific (77%–100%) depending on the criteria used.
Secondly, any findings of either hypotension However, the sensitivity of ECG is poor (28%– (systolic blood pressure less than 120 mm Hg) 54%) in the first 12 hours,11 18 and the presence or significant heart failure (crepitations not just including the bases) are noted. If more than provides suYcient assurance to discharge the two clinical risk factors are present then the patient from the ED. At this stage, therefore, the ECG is a tool to identify patients for If only one risk factor is present or there are consideration of fibrinolytic drugs.18–20 none at all, then the history should bereconsidered to see whether one of two CLINICAL RISK STRATIFICATIONAcute MI patients with ECG changes should particular scenarios that go along with a mod- therefore be spotted straight away and should erate risk of myocardial infarction are present.
then be treated appropriately (see below). The patients who remain will range from those with The whole approach to clinical risk assess- unstable angina to those with musculoskeletal pain. While the particular diagnosis in indi- vidual patients may take some time to estab- multicentre chest pain study19 20 and provides lish, the risks of either myocardial infarction or an objective, evidence based tool for use in the of later complications can be rapidly assessed by considering the ECG, by taking a focused patients are identified rapidly and provides a history and by carrying out a brief examina- framework for subsequent care of all thoseremaining.
Clinical scenarios indicating a moderate risk of myocardial infarction in patients Management
Typical cardiac pain in a patient over 40 years old where the pain is not The management of the patients will depend reproduced by palpation, is not stabbing in nature and does not radiate on the outcome of the initial screen. Some A history of anginal pain lasting longer than one hour that was either worse patients will have an ECG positive diagnosis of than usual angina pain or as bad as the pain of a previous AMI.
myocardial infarction and will need immediateintervention. Others will be at high risk andwill need admission for both treatment and further diagnosis. Those at moderate and low risk will need myocardial infarction ruled out, ST elevation (>1 mm in two limb leads or >2 mm in two chest leads) or acute left bundlebranch block in a patient with chest pain arediagnostic of AMI and indicators for the use of Patients should receive aspirin unless they have a major contraindication (active pepticulceration, bleeding disorders and severe al-lergy).21 dependent platelet activity—taking one hour toinduce oxygenase.22 Therefore the earlier aspirin isgiven the greater the eVect. Aspirin given immediately and continued for one monthafter AMI prevents 25 deaths and 13 other vas- Clinical risk assessment overview. cular events per 1000 patients treated.10 Contraindications to the use of fibrinolytic drugs MODERATE RISK GROUPThe care of the moderate risk group is moot at Bleeding disorders, for example, haemophilia, severe liver History of bleeding, for example, cerebral bleed, GI bleed managed by admission as high risk patients, or by entry into a ROMI protocol (see below).
Cavitating lung diseaseAcute pancreatitis LOW RISK GROUPSome 65% of all patients presenting to an ED Indications for the use of t-PA in patients with ST segment elevation or acute LBBB with cardiac sounding chest pain fall into thelow risk group. These patients do not have a clear cut clinical diagnosis, the risk of AMI is less than 7% and the risk of a major complica- Aged under 75Anterior myocardial infarction tion is around 2%. All patients should bescreened for evidence of myocardial dam-age.19 20 admitted to hospital for a ROMI protocol— are streptokinase and recombinant tissue plas- minogen activator (rtPA). Fibrinolytic agents others are discharged without further investi- work by direct action upon the coronary artery gation. This approach results in a proportion of thrombosis leading to recanalisation and reper- patients with AMI being inadvertently dis- charged. Matching the clinical resource with artery.23 Fibrinolytics and aspirin used in the clinical need has led to the development of conjunction result in a reduction in mortality of 52 deaths per 1000 AMIs.10 The indications purpose of these is twofold—firstly, to identify and contraindications for fibrinolytic agents patients with myocardial damage rapidly and secondly, to facilitate discharge for the rest as Individual hospitals have defined guidelines quickly as safely possible.25–30 All this must be on the use of these drugs taking into account the cost diVerential and the relative clinicaleYcacy; currently rtPA costs up to eight times A variety of strategies currently exist for The benefit of thrombolysis is not age or sex ROMI. These include cardiac enzyme assays, dependent and fibrinolytics should be given to all indicated patients with no contraindica- approach of serial ECGs and enzyme testing tions. The benefits are greatest in the sickest (also known as the World Health Organisation patients, those with hypotension and tachycar- criteria) is still the most commonly used dia. However, benefit is time dependent and rapid identification and initiation of treatment once two samples have been taken, the WHO criteria are 96% sensitive.31 In low risk patientsin whom no further pain has occurred the sen-sitivity is 99.4%.30 This test is relatively cheap but not timely, requiring the patient to remain Patients at high risk of either myocardial infarction or complications will require emer-gency treatment and admission. Many of these patients have ST-T segment changes suggestive The traditional markers of creatinine kinase of myocardial ischaemia or subendocardial myocardial infarction, while others have a lactate dehydrogenase (LDH) are being super- history strongly sugggestive of unstable ischae- seded by newer tests. Entirely new markers mic heart disease. This group has around a such as the cardiac troponins have been devel- 25% chance of AMI, and a moderate to high risk of major complications developing.19 20 In common with all patients with possible cardiac chest pain they should receive aspirin The two new tests for troponins (cTnT and be started unless specifically contraindicated cTnI) are both highly specific and sensitive.
(by the presence of significant conduction dis- order, definite asthma or overt heart failure) as tropomyosin regulatory complex (TRC). The should antithrombotic therapy. Low molecular TRC regulates the actin-myosin complex in weight heparin is more eVective than unfrac- muscle. Troponin T and I in cardiac muscle tionated heparin at reducing the incidence of are unique in that they are virtually only ischaemic events and the need for revasculari- produced by cardiac myocytes.32 The test iden- sation procedures. The incidence of major tifies the amount of each protein in the blood.
bleeding complications is the same for both Testing for either TnT orTnI is both cost and forms of heparin. Thus all patients who fall clinically eVective after 12 hours, but misses into the high risk chest pain group who are not the early diagnostic window available to EDs.
eligible for fibrinolytic drugs should receive These enzymes are therefore better as late markers and not as ROMI tests in a six or nine Emergency management of cardiac chest pain combination of CK-MB assay and ST segment monitoring has been extensively used in this way; a prospective randomised controlled trialhas shown this approach to be safe, when com-pared with inpatient care.28 One approach is the six hour CPAU protocol CPAU protocols can deliver high sensitivity and specificity and provide a rapid evidence-based protocol for ROMI in the ED. A negativetest eVectively rules out significant myocardial damage and allows safe discharge from the ED.
have been proposed as possible protocol addi-tions for a chest pain service. These includetroponin echocardiography.36–38 The main problem at present in including these technologies in EDprotocols is that they are not validated for usein patients with the same spectrum of diseaseas ED patients All patients attending an ED with chest painthat could be cardiac should be given a hightriage priority to allow rapid assessment andtreatment.
All patients should receive adequate analge- sia and aspirin. Patients with AMI who require fibrinolytic agents should be identified and treatment started. Other high risk patientsneed inpatient care and may need low molecu- Low risk patients require rapid, cost eVective patients did not adequately evaluate dis- and eYcacious ROMI protocols, so they can be charged patients—the incidence of missed discharged safely. CPAUs provide the best way of achieving this. Currently the best early pro- tocol seems to be serial CK-MB measurementsand continuous ST segment monitoring CK-MB isoforms and massCK has three isoenzymes (MM, BB, MB).
1 Fothergill NJ, Hunt MT, Touquet R. Audit of patients with chest pain presenting to an accident and emergency CK-MB has a higher cardiac specificity than department over a 6-month period. Arch Emerg Med CK, and is a more sensitive and specific marker 1993;10:155–60.
2 Emerson PA, Russell NJ, Wyatt J, et al. An audit of doctors of myocardial damage. A number of isoforms management of patients with chest pain in the accident and of these enzymes exist. These isoforms are emergency department. Q J Med 1989;70:213–20.
3 Mortality statistics. Series DH2. London: HMSO, 1996:23.
4 Norris RM. On behalf of the United Kingdom heart attack technically diYculties make their assay diYcult study collaborative group. Fatality outside hospital fromacute coronary events in three British health districts to perform as an emergency service; further- 1994–5. BMJ 1998;316:1065–70.
more the interpretation of the results (which 5 Collinson PO, Premachandram S, Hashemi K. Prospective audit of incidence of prognostically important myocardial are given as ratios) can be diYcult. CK mass damage in patients discharged from emergency depart- measurement is now possible—this measures ment. BMJ 2000;320:1702–5
6 Lee TH, Rouan GW, Weisberg M, et al. Clinical character- the absolute amount of the enzyme—and is istics and natural history of patients with acute myocardial both easy to perform and interpret. Both CK infarction sent home from the emergency department. Am
J Cardiol 1987;60:219–24.
7 Karcz A, Holbrook J, Burke MC, et al. Massachusetts reasonably sensitive at six hours after onset of Emergency Medicine closed malpractice claims:1988–90.
Ann Emerg Med 1993;22:553–9.
pain (78%–100%). These tests are significantly 8 Fibrinolytic Therapy Trialists collaborative group. Indica- cheaper than the cost of inpatient care, and so tions for fibrinolytic therapy in suspected acute myocardialinfarction: collaborative overview of early mortality and can be cost eVective if they facilitate early safe major morbidity results from all major randomised trials of more than 1000 patients. Lancet 1994;343:311–22.
9 ISIS-1 (First international study of infarct survival) collabo- rative group. Randomised trial of intravenous atenolol among 16027 cases of suspected acute myocardialinfarction:ISIS-1. Lancet 1986;ii:57–66.
There are now multitudes of diagnostic tests to 10 ISIS-2 (Second international study of infarct survival) collaborative group. ISIS-3: a randomised comparison ofstreptokinase vs tissue plasminogen activator vs anis- cheaper than others are and some are more treplase and of aspirin plus heparin vs aspirin alone in specific or sensitive. However, no single test 41299 cases of suspected acute myocardial infarction. Lan-
will reliably ROMI in patients with fewer than 11 King III SB, Lembo NJ, Weintraub WS, et al. A randomised controlled trial comparing coronary angioplasty with
coronary bypass surgery. N Engl J Med 1994;331:1044–50.
One way to increase sensitivity is to do a 12 Schroeder JS, Lamb IH, Harrison DC. Patients admitted to series of tests. This is the premise behind the coronary care unit for chest pain: High risk subgroup
for subsequent cardiovascular death. Am J Cardiol 1977;39:
13 Young GP, Green TR. The role of single ECG, creatine 28 Zalenski RJ, McCarren M, Roberts R, et al. An evaluation of kinase, and CKMB in diagnosing patients with acute chest a chest pain diagnostic protocol to exclude acute cardiac pain. Am J Emerg Med 1993;11:444–9.
ischaemia in the emergency department. Arch Intern Med 14 Bakker AJ, Koelemay MJW, Gorgels PMC, et al. Failure of 1997;157:1085–91.
new biochemical markers to exclude acute myocardial inf- 29 Farkouh ME, Smars PA, Reeder GS, et al. A clinical trial of arction at admission. Lancet 1993;342:1220–2.
a chest pain observation unit for patients with unstable 15 GUSTO investigators. An international randomised trial angina. N Engl J Med 1998;339:1882–8.
comparing four thrombolytic strategies for acute myocar-dial infarction.
N Engl J Med 1993;329:673–2.
16 Sackett DL, Haynes RB, Guyatt GH, et al. Clinical infarction: A prospective multicenter validation of a 12 epidemiology: a basic science for clinical epidemiology. 2nd ed.
hour strategy for patients at low risk. N Engl J Med 1996;334:1498–504.
17 Mackway-Jones K, ed. Emergency triage. London: BMJ Pub- 31 Lee TH, Rouan GW, Weisberg M, et al. Sensitivity of routine clinical criteria for diagnosing myocardial infarc- 18 Brush JE, Brand DA, Acampora D, et al. Use of the initial tion within 24 hours of hospitalisation. Ann Intern Med electrocardiogram to predict in hospital complications of 1987;106:181–6.
acute myocardial infarction. N Engl J Med 1985;312:1137–
32 Mair J. Progress in myocardial damage detection: new biochemical markers for clinicians. Crit Rev Lab Sci 1997; 19 Goldman L, Cook EF, Brand DA, et al. A computer protocol 34:1–66.
to predict myocardial infarction in emergency department 33 Hamm CW, Goldmann BU, Heeschen C, et al. Emergency patients with chest pain. N Engl J Med 1988;318:797–803.
room triage of patients with acute chest pain by means of 20 Goldman L, Cook EF, Johnson PA, et al. Prediction of the rapid testing for cardiac troponin T or troponin I.
need for intensive care in patients who come to emergency departments with acute chest pain. N Engl J Med Med 1997;337:1648–53.
34 Young GP, Gibler WB, Hedges JR, et al. Serial creatinine 21 British National Formulary. 33rd ed. London: British Medi- kinase-MB results are a sensitive indicator of acute cal Association and Royal Pharmaceutical Society of Great myocardial infarction in chest pain patients with non diag- nostic electrocardiograms: The second emergency medi- 22 Clarke RJ, Mayo G, Price P, et al. Suppression of thrombox- cine cardiac research group study. Acad Emerg Med 1997;4:
ane A2 but not of systemic prostacyclin by controlled release aspirin. N Engl J Med 1991;325:1137–41.
35 Mair J, Morandell D, Genser N, et al. Equivalent early sen- 23 Schoder R, Biamono G, Von Leitner ER. Intravenous short sitivities of myoglobin, creatinine kinase MB mass, term infusion of streptokinase in acute myocardial creatinine kinase isoform ratios and cardiac troponins I and infarction. Circulation 1983;67:536–48.
T for acute myocardial infarction. Clin Chem 1995;41:
24 Cohen M, Demers C, Gurfinkel EP, et al. A comparision of low molecular weight heparin with unfractionated heparin 36 Leung FY, GriYth AP, Jablonsky G, et al. Comparison of the for unstable coronary artery disease. N Engl J Med diagnostic utility of timed serial (slope) creatinine kinase 1997;337:447–52.
measurements with conventional serum tests in the early 25 Gibler WB, Runyon JP, Levy RC, et al. A rapid diagnostic protocol and treatment centre for patients with chest pain in the emergency department. Ann Emerg Med 1995;25:1–8.
26 Gaspoz JM, Lee TH, Cook EF, et al. Outcome of patients 37 Lindsey J Jr, Bonnet YD, Pinnow EE. Routine stress testing who were admitted to a new short stay unit to rule out for triage of patients with chest pain: Is it worth the candle? myocardial infarction. Am J Cardiol 1991;68:145–9.
Ann Emerg Med 1998;32:600–3.
27 De Leon AC, Farmer CA, King G, et al. Chest pain evalua- 38 Lewis WR, Amsterdam EA. Evaluation of the patient with tion unit: A cost eVective approach for ruling out acute rule out myocardial infarction. Arch Intern Med 1996;156:
myocardial infarction. Scott Med J 1989;82:1083–9.
Melanoma, Parkinson’s disease and levodopa:causal or spurious link? A review of the literatureRoberto Zanettia, Dora Loriab and Stefano RossoaSince the early 1970s, a number of case reports havecorrelation between social class and melanoma risk; (5)suggested that levodopa therapy for Parkinson’s diseasethe relationship between the risk of Parkinson’s diseaseincreases the risk of cutaneo