USING THE GUIDEThe purpose of the document is to provide advice and explanations for colleagues who may not have clinicale...
INDEX TO GLOSSARY                                                             Cardiac facilityAcute coronary syndromes    ...
•    The Department of Health             •    Strategic Health Authorities             •    Cardiac Networks, and via the...
Is it worthwhile to collect data on all patients? Information on length of stay is of considerable interest tomanagement; ...
•   Troponin (T or I), or trop. T and I are two forms of troponin giving the same                              information...
o   If thrombolytic treatment has been given on the basis of either a pre-hospital ECG or the            admission ECG the...
o   If patient went elsewhere for primary angioplasty the details will be recorded at the other            hospital.•   If...
     The time of the arrest                     The cardiac rhythm (see cardiac arrhythmias )                     The o...
•   Final diagnosis. This is based on all available information, but might not be clear in the notes!       The discharge ...
INDEX TO GLOSSARYGetting about. Use Ctrl (control) + left click while over the subject of interest in order to move to the...
Acute coronary syndromes.              This term covers the spectrum of clinical, biochemical andelectrocardiographic feat...
Primary angioplasty The technique of reopening an occluded coronary artery as the primary        reperfusion strategy. Thi...
Asystole Complete cessation of all cardiac activity. Terminal, and with a bad prognosis even withall resuscitative techniq...
Calcium channel blockers          Primarily a group of anti-anginal and anti-hypertensive drugs.Verapamil is the only memb...
Thienopyridine inhibitor(s).        Clopidogrel. (Presently the only licensed drug in this class of        agents) Platele...
Cerebrovascular event. (syn CVA, stroke ) Loss of neurological function, sensory or motor following anischaemic insult to ...
ECG appearances The appearance of the electrocardiograph is one of the main diagnostic tools for    determining the presen...
Myocardial infarction (unconfirmed) please note this can only apply to patients dying (usually earlyafter admission) with ...
measurement of the degree of myocyte damage. The more cells that are broken down the greater thequantity of cellular conte...
Non ST elevation infarction. (Usually abbreviated to nSTE MI, non STE MI) The term describes all        infarctions where ...
Rehabilitation Term covering all aspects of support given to patients having ACS including physicalrehabilitation, and lif...
severity of angina, symptoms which may bring someone into hospital. The crucial test for you is to check ifthere was any t...
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  1. 1. USING THE GUIDEThe purpose of the document is to provide advice and explanations for colleagues who may not have clinicalexperience of acute coronary disease, and who may not be familiar with some of the clinical terms used todescribe it. There are two parts to this document. • A list of commonly used terms in alphabetical order. • How to go about entering a patient record into MINAP Getting about. When using the screen version terms appear in blue. By placing the cursor over the term, pressing on Control (Ctrl) and then left clicking the mouse you will be taken to the part of the glossary where this term is explained. To return to the index run the cursor over the blank spaces on the line immediately after the term. A small yellow box will appear. Follow the instruction to press Ctrl and left click the mouse. In the text ‘How to enter a patient into MINAP’ there are also links to the glossary which should be used in the same way. To return to the text run the cursor over the blank space at the end of the relevanr paragraph and the yellow box with instructions will appear. 1
  2. 2. INDEX TO GLOSSARY Cardiac facilityAcute coronary syndromes Cardiopulmonary resuscitation Classification of Acute Coronary CardioversionSyndromes Cerebrovascular event.Angiography CCUAngiographic facilities DatabaseAngioplasty Data set Facilitated angioplasty Discharge medication Primary angioplasty Electromechanical dissociation (EMD) see cardiac Rescue angioplasty arrhythmiasAtheroma Exercise testAtrial fibrillation (AF) see cardiac arrhythmias EchocardiographyAtrial tachycardia (SVT, PAT,AVNRT) see cardiac Ejection fractionarrhythmias Final diagnosisAsystole see cardiac arrhythmias Haemorrhagic risk Heart block, complete (CHB) see cardiacBiomarker arrhythmiasBleeding see haemorrhagic risk and Initial diagnosiscerebrovascular event (below) Ischaemic eventCardiac drugs Left bundle branch block ACE inhibitors Low molecular weight heparin Angiotensin receptor blockers Missing data Antiplatelet agents MRI magnetic resonance imaging Beta blockers (oral) Myocardial infarction Betablockers (intravenous) Definition Calcium channel blockers ST elevation infarction Diuretics Non ST elevation infarction Epleronone Occlusion Fondaparinux Plaque rupture 2b3a inhibitors Previous medical history Heparin Radionuclide study Nitrates Rehabilitation Spironolactone Re-infarction Thienopyridine inhibitor(s) Reperfusion Thrombolytic drugs Thrombolytic drugs Warfarin TroponinCardiac arrhythmias Unstable angina IntroductionMINAP, the national audit of myocardial infarction is a database based on the MINAP data set started with alimited number of data items with which to examine the response of hospitals to the requirements of theNSF. This was mainly concerned with delays in provision of thrombolytic treatment for patients with STelevation infarction, and use of secondary prevention medication. The data set has expanded so that it nowcovers all aspects of care of patients having acute coronary syndromes (ACS). Note that the data set hasterms that cover most if not all clinical eventualities. It follows that not every item has to be completed onevery patient. See section x, a guide to what items need to be completed in different cases.The purpose of MINAP. MINAP is a database which can be thought of as a national database, or a localhospital database. Analyses of records can be made at any level of aggregation in order to obtain a pictureof performance at any level from hospital up to the whole country. We provide data analyses in variousformats to 2
  3. 3. • The Department of Health • Strategic Health Authorities • Cardiac Networks, and via them to PCTs • Ambulance TrustsWe regard the analyses provided to hospitals to be of first and foremost importanceIt is vital to appreciate that MINAP is not simply a tool with which to produce annual data analyses related topatients who have had thrombolytic treatment. It is also designed to be a local tool with which you canexamine the process of care of all the patients with ACS admitted to your hospital. Many hospitals record alltheir patients with acute coronary syndromes and use the records for regular analysis of care. This isparticularly useful when patients are under the care of different consultants and clinical teams.Data collection is undoubtedly a chore. Some hospitals have suggested that as the ‘NSF targets’ have beenattained locally there is no point in continuing the exercise. This is a very narrow and incorrect interpretationof the purpose of data collection, and if it is performed only in order to prove that targets are being met then itis poor reward for the effort. The data are for use at local level, and those who do so find that they get moreand more out of it. We strongly recommend a MINAP data use group within hospitals who can use thedata to own support their practice. This will make data collection worthwhile, and if you share the analyseswith your management, they too will come to appreciate the value of MINAP. The sort of areas which are ofinterest to your management include length of stay, in relation to diagnosis, which is not accurately availablefrom hospital episode statistics, use of angiography, delays before transfer and much else. If your hospitalmakes use of the data it is much more likely to support data collection.The ultimate target should be for all patients admitted with an acute coronary syndrome (ACS) to berecorded in MINAP. Where all patients with acute coronary syndromes are admitted to the same ward orarea it is easy to identify patients. It is much harder where patients are not all cared for in one area, and arelooked after in several wards. [For the same reasons it is much harder to be sure that the care received is ofconsistent quality] Where this is the case it is necessary to make arrangements with ward clerical staff toidentify patients passing through their wards, based on a diagnosis of myocardial infarction or an acutecoronary syndrome, for subsequent logging. However, every hospital is different in how it deals with clinicalrecords, and arrangements for capture of data ultimately depend on local circumstances.This is a large task, and it is accepted that not all will have the facilities at present to log all patients.Nevertheless it was an NSF audit requirement that when it became possible to collect the data that a numberof additional areas of care should be examined for patients with myocardial infarction (any troponin positiveACS), In summary these included 30 day mortality following myocardial infarction, documentation ofassessment of left ventricular function, and assessment of need for intervention. 3
  4. 4. Is it worthwhile to collect data on all patients? Information on length of stay is of considerable interest tomanagement; MINAP can show that there is a more than twofold variation in length of stay for patients withnon ST elevation infarction between hospitals, and that more than 1 in 8 patients admitted with chest pain ofuncertain cause will be readmitted. These impose a considerable burden on hospitals, and MINAP can helphospitals to determine their own position, and whether it needs to be improved.Each hospital should plan a strategy to move towards inclusion of all patients with acute coronary syndromesinto MINAP. Identifying records for inclusionPatients having acute coronary syndromes and chest pain thought to be cardiac in nature represent a largeproportion of acute medical admissions, but are not necessarily easy to identify unless admitted to a cardiacward.Checking overall numbers. Your biochemistry department will be able to provide a list of patients who havehad troponin measured. Where patients with acute coronary disease are not all admitted to one clinical areasuch as a cardiac ward it is almost impossible to know how many admissions there are with acute coronarysyndrome. A list of patients who have been admitted who have an elevated troponin value, available fromfrom the biochemistry department, is a useful means of cross checking.admissions with ACSLooking at medical records. Look for evidence that the patient was admitted with an acute coronarysyndrome (ACS), or with a diagnosis of ACS that became apparent after admission. o Check the discharge slip or summary where present o Look at the early part of the admission notes for a (provisional) diagnosis. Medical acronyms and abbreviations often abound at this stage! o Terms such as ACS, AMI, infarct, or infarction might be accompanied by words like ‘probable’, ‘possible’, ‘exclude’ or ‘?’ (or lots of ‘??’). These all point to the same thought process somewhere in the doctors head that he or she might be dealing with an acute coronary syndrome. Have pity; it is often difficult to make a diagnosis until all the information is available, and as it is a bad diagnosis to miss doctors tend to err on the side of caution! [See Myocardial infarction and Classification of Acute Coronary Syndromes] o If in doubt there will be clues further into the notes.  Where was the patient admitted? If CCU or other cardiac facility it makes the working diagnosis more likely to be ACS  Look for the result of a troponin assay. This is a very sensitive test of cardiac damage, and is performed on every patient in whom the diagnosis is suspected. It can be performed as a laboratory test or as a bedside test. The result might be in with the biochemistry results, but when performed as a bedside test it is just as likely written in the clinical record. The words to look out for are; 4
  5. 5. • Troponin (T or I), or trop. T and I are two forms of troponin giving the same information. • The abbreviations TNI, or TNT o The troponin value is important, as it is a measure of the amount of cardiac damage. There is normally no troponin in blood, but this is not usually recorded as zero, but as a certain value beyond which the test (assay) is not sensitive enough to measure. It will be recorded a > (less than) a very small figure such as 0.015 ng/L. Please record this as 0 in MINAP. o An elevated troponin is (almost always) due to cardiac ischaemic damage, and the patient should be given an MINAP record. Deciding the initial diagnosis.Having concluded that the diagnosis is ACS, and that the record should be included in MINAP you nexthave to decide what type of ACS you are dealing with in order to decide the Initial diagnosis. ACS fallsinto two broad groups based on ECG appearances, those with ST segment elevation (syn definiteinfarction) appearances on the ECG, and those without. Treatment options and data entry depend onthis subdivision, and some of the NSF targets are based only on patients with ST segment elevation.MINAP uses the term Definite infarct for the Initial diagnosis when a diagnosis of ST elevation infarctionwas either made in an ambulance before arrival or on the first (admission) ECG. If ST elevationdevelops after arrival the Initial diagnosis is 2. Probable Infarction. o Look in the notes in the area of the admission diagnosis. Look for the term ECG (electrocardiogram). You may see ECG = MI or ST MI or STE MI These terms may be qualified by anterior, or inferior or lateral describing the anatomical site of the infarction. o The decision on how to treat the patient depends on these appearances, and so close by in the notes you should look for an indication of how the patient was treated. The treatment of ST elevation infarction is usually thrombolytic treatment or primary angioplasty. Sometimes a decision not to treat is made, and you should look to find the reason. Look for any indication that patient was referred immediately for primary angioplasty or that thrombolytic treatment was given  Look for terms such as STE MI ? suitable for pPCI or  ‘for lysis’, or thrombolysis, ‘for SK’, TnK (tenecteplase), RpA (Reteplase) etc,.  that thrombolytic treatment was actually given either in notes or the prescription chart  or look for any evidence that the patient was thought unsuitable for thrombolytic treatment, such as arriving too late, recent stroke (cerebrovascular event.), or severe hypertension. Usually the clinician will make it clear why a particular form of treatment was not used. o If there is no evidence in the notes that ST elevation was recorded on an ECG then the Initial diagnosis cannot be Definite infarction, and either Probable infarction or ACS should be used. It is unimportant at this stage which of these is used. 5
  6. 6. o If thrombolytic treatment has been given on the basis of either a pre-hospital ECG or the admission ECG then the admission diagnosis must be Definite infarction, whether the use of thrombolytic treatment was correct or not. Where there is a misdiagnosis and treatment is given inappropriately, the final diagnosis will make this clear. o Left bundle branch block (LBBB). Where there is LBBB and thrombolytic treatment is given the initial diagnosis is Definite infarction. Where there is LBBB and lytic treatment was not given the initial diagnosis should be Probable myocardial infarction, unless it is clear from the notes that the clinician thought reperfusion treatment was contraindicated for any reason. o There are three other points to note about the Initial Diagnosis.  When the initial hospital ECG (and any performed in an ambulance) do not show ST elevation, and then ST elevation changes subsequently develop, the initial diagnosis is not Definite infarction. Initial diagnosis is only based on initial hospital ECG (unless an ambulance ECG shows ST segment elevation) and so the diagnosis is Probable infarction.  There may be an occasional misdiagnosis of ST elevation infarction, with thrombolytic treatment given. Here you must stick with an admission diagnosis of Definite infarction, and then enter the correct diagnosis in the Final diagnosis. Do not exclude such a patient from MINAP. It is not possible to learn from hidden mistakes.  ST segment elevation can be quite transient. Where transient elevation occurs, and the subsequent ECG does not return to normal, the final diagnosis should be ST elevation infarction. o In summary  If there was ST segment elevation on the admission ECG, or the patient had thrombolytic treatment (pre-hospital or in hospital) then the Initial Diagnosis is Definite infarction.• If the initial diagnosis is Definite infarction you must record details of reperfusion (thrombolytic treatment or primary PCI) treatment, or the reason why it was not given or delayed. o It is necessary to know the time of onset of symptoms, the precise time of arrival in hospital and the precise time when lytic treatment was given. These times should be available from the notes, or in the case of treatment time, from the drug chart. Sometimes nursing and A&E records are informative. o If thrombolytic treatment was not given the reason should be stated. o If there has been a delay to treatment of those listed in 3.10 this should be recorded. The patient will not be counted towards any NSF target. o If primary angioplasty is performed in your hospital then the time of first balloon inflation during angioplasty should be recorded 6
  7. 7. o If patient went elsewhere for primary angioplasty the details will be recorded at the other hospital.• If ST elevation developed after first hospital ECG, and patient received thrombolytic treatment. o Record that lytic treatment or primary angioplasty was given o There is no need to enter a justified delay o Check that the initial diagnosis has not wrongly been recorded as Definite infarction, and alter if necessary.• If there was no ST elevation at any time the admission diagnosis cannot be definite infarction, and there is no reason to complete any details about thrombolytic treatment. Other data entry• Previous medical history These should be recorded in one place in the notes and are very important as some conditions independently predict survival.Tests and investigations. Cholesterol and blood sugar at admission are both routine investigations. Ifa result is not available do not enter 0, (zero), but leave blank. This must apply even if the value is part ofthe data completeness score. o The highest troponin value should be recorded, with assay type (troponin T or troponin I) o We ask ‘Were the enzymes / markers elevated?’ because assay values differ in each hospital, and this is a useful confirmation that there was at least one elevated value above the normal values for your hospital. Check if your hospital uses creatine kinase (CK), or CK_MB or CK mass as most have now gone over to troponin assays.• Left ventricular ejection fraction. May be checked in a variety of techniques, including echocardiography, angiography, radionuclide scanning, and magnetic resonance imaging. You will have to check which is the preferred technique in your hospital in order to record this. Focus on the term used, (normal, impaired etc) rather than the percentage.• Cardiac arrest If this occurs it is usually in the first few hours after the admission, most often in A&E, or as a terminal event. So the clinical record will have this at the beginning or the end of the admission. The MINAP default is ‘No arrest’. o If death occurs, ensure that this is also recorded in Discharge destination and Death in hospital field (done for you in MINAP), and the date of death (not entered automatically) o Where resuscitation succeeds and patient leaves hospital, check to see if there is any mention of neurological problems before discharge. Usually admission is prolonged, with transfer for in hospital rehabilitation where this is the case. o MINAP requires simple information. 7
  8. 8.  The time of the arrest  The cardiac rhythm (see cardiac arrhythmias )  The outcome• Bleeding complications (see haemorrhagic risk) The most important to record are intra-cerebral bleeding and retro-peritoneal haemorrhage.• Other tests and procedures. Including exercise test, echocardiography, radionuclide scanning, and rehabilitation. If there is no mention of any of these in the notes then record Unknown rather than No.• Procedures. (syn. interventions) Angiography and Angioplasty are probably indicated for a majority of patients following ACS unless there is a good reason not to. Often, in hospitals without angiographic facilities this may be delayed while a bed is found in an interventional hospital, and it is important to record this delay. It is useful to know why it was performed, and where. Locally means within your Trust, either with you or another hospital in the Trust. When angiography is perfomed in your Trust, the date must be recorded. If no intervention (angioplasty or CABG) took place this should be recorded.• Transfer dates. If the patient is transferred as a daycase, and expected back the same day, the patient is not discharged from you. If transferred but not as a day case then the patient is discharged from you and this must be recorded in date of discharge and discharge destination (other hospital). Done automatically in MINAP.• Re-infarction See glossary. There is usually detail of further symptoms starting after admission. Look for evidence of further marker tests, and repeat ECGs. Further pain alone does not necessarily mean re-infarction. There must be new ECG or marker evidence. May need a check with a clinician.• Discharge medication. Certain drugs prescribed on discharge are effective in reducing the risk of further infarction and complications such as heart failure. The groups of drugs which should be recorded are o Aspirin o Clopidogrel o Beta blockers (all end in –olol) o Statins (all end in –statin) o ACE inhibitors (all end in –april) or Angiotensin receptor blockers (ARBs) (all end in – sartan) o Any diabetic medication 8
  9. 9. • Final diagnosis. This is based on all available information, but might not be clear in the notes! The discharge slip or summary is the most reliable source of information. See the Application Notes for detail on Final Diagnoses. Other points appear below ACS troponin positive. There must be a record of an elevated troponin value. Conversely, if there is no evidence of elevated troponin, or the value is not elevated this cannot be the diagnosis! Consider troponin ACS negative, or Chest pain ? cause. Unknown is inconsistent with this diagnosis. ACS troponin negative. There cannot be elevation of troponin! Chest pain ? cause. There should not be elevation of troponin unless the cause for it is truly unknown, and clinicians are confident the elevation is not due to cardiac ischaemia. Other There must be a definite (usually non cardiac) diagnosis in order to be in this group. ACS troponin not recorded. This category is now obsolete as troponin is now used throughout the countryImportant data entry advice. If you are completing a field where the answer is unknown, such asAngiography – Not performed, never leave the field blank as this does not mean unknown. Alwaysenter an available option. All MINAP fields have options for not performed or not known; please usethem where appropriate. 9
  10. 10. INDEX TO GLOSSARYGetting about. Use Ctrl (control) + left click while over the subject of interest in order to move to the text.Use Ctrl + Home to return to index. Some items are cross referenced, allowing you to move from one item toanother linked item directly 10
  11. 11. Acute coronary syndromes. This term covers the spectrum of clinical, biochemical andelectrocardiographic features that follow a coronary plaque event. Refer to text books for more detail. Inessence, an area of atheromatous deposit lying within the coronary arterial wall becomes unstable, and theoverlying endothelium (very fine layer of cells) ruptures, allowing blood to come in contact with the interior orthe arterial wall. When blood comes in contact with the interior of the arterial wall the blood clots (clinical termthrombus). The clinical features of the syndrome depend on several factors. The extent of the thrombus. If the vessel where the event took place is completely occluded bythrombus blood flow downstream ceases and unless there is collateral flow (see below) all the heart musclesupplied by the vessel is at risk of death. Clearly the more rapidly the vessel is reopened (either naturally orusing a thrombolytic drug or angioplasty) the greater the chance of saving muscle in jeopardy When the vessel is only partially occluded, thrombus lying within the vessel may break off and passdownstream until it occludes in a smaller distal vessel, producing a local ‘microinfarction’. Troponin assays,which are able to pick up as little as a few grams of infarction are able to confirm the small amount ofdamage, whereas less sensitive assays such as CK and its sub forms may not. Collateral flow. If the vessel has had severe atheromatous deposits for some time, with chronicpartial occlusion, the greater the chance of collateral vessels developing and providing an (incomplete) backup circulation to the affected area. Site of the vessel. A major epicardial (surface) vessel occlusion will do more damage than a smallerbranch vessel occlusion. Generally epicardial vessel occlusion, involving the left, right or circumflex arterysystems results in ECG appearances of ST segment elevation infarction. The exception is that occlusion ofepicardial vessels supplying the back of the heart (from either the right coronary artery or the circumflex) mayproduce a different ECG pattern. Reactivity of the vessel. Coronary arteries respond to local trauma such as plaque rupture byconstricting, and making the local narrowing worse. Vasoconstriction may play a part in determining the typeof infarction.Angiography The investigative technique of injecting radiographic contrast into coronary arteries todetermine the presence and extent of disease. There is a strong case to be made for offering angiographyto a large proportion of patients who present with an acute coronary syndrome.Angiographic facilities. The radiographic facilities to perform coronary angiography. Many district generalhospitals have angiographic facilities with which they perform ‘cold’, non urgent angiography, and do notperform angiography on acute admissions which may be unstable. A number of larger DGHs do performangiography and percutaneous coronary interventions on emergency admissions.Angioplasty a technique for reopening occluded coronary arteries using a balloon tipped catheter. Nowcommonly performed in conjunction with stenting of the occluded section of artery. 11
  12. 12. Primary angioplasty The technique of reopening an occluded coronary artery as the primary reperfusion strategy. This has to be performed as quickly as possible after the onset of symptoms (the time of occlusion), but primary angioplasty is not as critically time dependent as thrombolytic treatment. Rescue angioplasty Following thrombolytic treatment there may be evidence that the occluded vessel has not re-opened. The strongest evidence is that the ST segment elevation pattern on the ECG has not resolved. Continuing pain is also suggestive. In this circumstance immediate ‘rescue’ angioplasty may be performed. The evidence suggests that this may be more effective than a conservative approach (ie doing nothing) Facilitated angioplasty The technique of using thrombolytic treatment followed immediately by angioplasty as a routine. The present evidence suggests no clinical benefit, with an excess of bleeding complications.Atheroma (Greek for porridge) Pathological term for a localised collection of gungy material whichdevelops within arterial walls. It consists of cholesterol rich fatty material, fibrous tissue, and cellular debris.It distorts the cross sectional shape of the vessel, thickening the wall, and compressing the lumen of thevessel. Where the vessel wall is compressed this is described as an atheromatous plaque.Biomarker. A generic term for a body protein, often an enzyme, which can be assayed, and whosepresence (above normal or expected values) indicates the existence of a pathological process.Cardiac arrest Very common early after coronary occlusion, and results from electrical instablility ofthe myocardium, and resulting loss of co-ordinated pumping activity. Deaths occurring before arrival inhospital may be 50% of the total mortality from AMI. The ‘massive’ heart attack causing sudden deathbeloved of the tabloids is usually not massive at all, in the sense of involving a lot of heart, but may be quitesmall in size, but still causing ventricular fibrillation and immediate death.Cardiac arrhythmias Common and potentially lethal complications of myocardial infarction. Ventricular fibrillation. (VF) Sudden and complete breakdown of the regular electrical activity ofthe ventricles into an irregular and chaotic activity. Accompanied by complete loss of pumping activity, lossof cardiac output, and immediate circulatory failure. Lethal unless cardiopulmonary resuscitation iscommenced within minutes. Ventricular tachycardia. (VT) Rapid and regular ventricular rhythm of sudden onset often > 200minute. Often the heart cannot sustain such a rapid rhythm and a significant fall of cardiac output results.Requires emergency treatment often using direct current (DC) cardioversion Atrial fibrillation (AF) Sudden and complete breakdown of regular electrical activity of the atria.Not lethal, but usually producing symptoms and needing either pharmacological treatment or DCcardioversion. Atrial tachycardia (PAT, SVT, AVNRT) Rapid heart rhythm, usually 150-250 / min usually needingdrug treatment 12
  13. 13. Asystole Complete cessation of all cardiac activity. Terminal, and with a bad prognosis even withall resuscitative techniques. Electro-mechanical dissociation EMD (syn pulseless electrical activity PES) Electrical activityevident on ECG, but not sustaining a cardiac output. Often a terminal event. Complete heart block a recognised early complication of (inferior) myocardial infarction. Heart ratefalls, sometimes suddenly, to around 25-40 beats / min with symptoms as a result of a fall of cardiac output.May need temporary pacemaker support.Cardiac drugs ACE inhibitors. (Angiotensin converting enzyme inhibitors) important group of agents which have significantly improved the outcome of patients with heart failure from all causes]. Act by effects on peripheral resistance, inhibition of the renin-angiotensin axis, and inhibition of various effects of aldosterone. Widely used as secondary prevention medication following infarction. [all end in –pril] Angiotensin receptor blockers. Group of drugs with broadly similar cardiovascular effects to ACE inhibitors. Used when ACE inhibitors cannot be tolerated. [all end in –sartan]. Antiplatelet agents Drugs which inhibit platelet aggregation (see clotting). Platelet aggregation is the second part of the clotting mechanism, and inhibition of platelet aggregation is the primary means of preventing propagation (extension) of clot. Aspirin is the most important platelet inhibitor, having an overall benefit in terms of mortality reduction following infarction which is about the same as thrombolytic drugs. Clopidogrel (Plavix) is a newer agent, with affects that are additive to aspirin. Sulphinpyrazone (persantin) is less often used. Antplatelet drugs act on platelets at the time of their development, and so existing platelets are not inhibited. The turnover of platelets is rapid, but it still takes several days for antiplatelet agents to reach full effect Beta blockers Beta (adrenergic receptor) blockers are a class of compounds mainly used orally which have been known since the early 1980s to reduce the risk of further coronary events following myocardial infarction. They inhibit the adverse effects of endogenous catechols (adrenaline and noradrenaline), and probably act mainly by reducing cardiac arrhythmias. Routine secondary prevention medication wherever tolerated. Also used for hypertension, but no longer first choice drugs. Intravenous betablockers In the context of myocardial infarction iv betablockers may be used very early because of theoretical benefit of reduction of infarction size, and proven benefit of reduction in lethal cardiac arrhythmia. There may be a downside of a higher frequency of cardiogenic shock if used injudiciously. [all end in –olol] 13
  14. 14. Calcium channel blockers Primarily a group of anti-anginal and anti-hypertensive drugs.Verapamil is the only member with significant anti-arrhythmic actions.Diuretics The two main groups, loop and thiazide diuretics, act on renal tubules to inhibitreabsorbtion of sodium back into the circulation after initial excretion via the glomerulus. Waterfollows the sodium, and produces the diuretic effect. Used in heart failure. Patients may be takingdiuretics at admission for previous heart failure or as part of the treatment of hypertensionFondaparinux A pentasaccharide composed increasingly used as an anticoagulant inacute coronary syndromes. By binding to thrombin, fondaparinux inhibits factor Xa. Fondaparinux isgiven subcutaneously daily. There is no need for haematological monitoringHeparin An anticoagulant drug used either subcutaneously or intravenously. Anticoagulantsinterfere with the clotting cascade (series of complex biochemical reactions which result in theformation of fibrin, the primary ingredient of a clot). Heparin is used as an adjunctive drug withtenecteplase and reteplase in the treatment of ST elevation infarction . [See re-infarction] Heparinn isalso used routinely in the management of non ST elevtion infarctionDosing with heparin is not easy, and requires very careful adjustment of dose using a heparininfusion and a pump. Dosing is adjusted according to the APTT (activated partial thromboplastintime). It is difficult to maintain a stable APTT within the recommended range. It is possible thatheparin will eventually be superseded by low molecular weight heparins or fondaparinux.Low molecular weight heparin LMWH a more recent development which specifically blocks factorXa (10a) in the clotting cascade. Has the huge advantage of not requiring major dose adjustmentsafter initial adjustment for body weight. Blood monitoring is not required in normal circumstancesCan be used IV for immediate effect or subcutaneously. Evidence suggests that it is more effectivein ACS, and is likely, when licensing issues are resolved to become the drug of choice with lyticagents. It is easier to use, and longer acting, which may be of crucial importance when used out ofhospital.Nitrates A group of orally active (well absorbed from the mucosa of the mouth as well asintestinally) short acting organic nitrate compounds which are powerful vasodilators. Used for therapid control of angina. They can be used intravenously.Potassium channel modulator(s) Nicorandil is the only licensed drug in this group. An anti-anginal agent.Spironolactone. Initially used ( >30 years ago ) as a diuretic with specific effects on the renin –angiotensin mechanism, it is now recognised that spironolactone has other potent effects within thevasculature, and has an important role in treatment of heart failure, where use has been shown toreduce mortality. Epleronone A new analogue of spironolactone, possibly with less side effects. 14
  15. 15. Thienopyridine inhibitor(s). Clopidogrel. (Presently the only licensed drug in this class of agents) Platelet inhibitor which is increasingly used in conjunction with aspirin following myocardial infarction to reduce frequency of further ischaemic events. Thrombolytic drugs. (syn lytic drugs, fibrinolytic drugs) A group of drugs used intravenously which can dissolve recently formed thrombus. Streptokinase is the original lytic drug, which can only be used by infusion (usually over 60 minutes)m and hence unsuitable for pre-hospital treatment. Tenecteplase and Reteplase are both made using recombinant technology. Both are bolus drugs, with reteplase given in two doses, 30 minutes apart Both have a short half life (duration of action) and both must be used in combination with unfractionated heparin or low molecular weight heparin (qv) in order that thrombus does not reform after it has been dissolved. Warfarin. The original orally active anticoagulant. It inhibits clotting factor production by the liver. Requires haematological control using the INR test. Shown to reduce frequency of re-infarction and improves mortality following infarction, but not used for this purpose because of the logistical problems of anticoagulant control for very large numbers. Other secondary prevention drugs are used instead. Very commonly used for patients with atrial fibrillation, especially when other risk factors such as heart failure, diabetes exist, or where there is evidence of cerebrovascular disease. 2b3a inhibitors (syn 2b3a glycoprotein inhibitors) A group of drugs which inhibit platelet aggregation. They are always used in conjunction with aspirin, and or Clopidogrel. The agents presently in use are tirofiban, and abciximab. Both are used intravenously, typically in unstable patients who are about to have an intervention.Cardiac facility. A ward or section of a ward specifically used for patients with acute cardiac conditions.The CCU may be part of it. The nursing staff will have a specific expertise in cardiological conditions.CCU The ‘traditional‘ coronary or cardiac care unit, usually with 4-8 beds, which are monitored andconnected to a central monitoring station. Increasingly CCU is part of a larger cardiological facilityCardiopulmonary resuscitation CPR. Applied collectively to the techniques of cardiac massage andassisted ventilation, which are used to maintain a cardiac output of oxygenated blood in the absence of aneffective cardiac rhythm, or during respiratory arrest. Combined with pharmacological interventions anddirect current countershock to restore normal cardiac electrical activity.Cardioversion - or direct current cardioversion (syn DC shock, countershock) used in treatment ofcardiac tachyarrthymias. Performed with patient unconscious. A high energy, short duration direct currentelectric shock is applied over the left chest with the intended effect of producing transient asystole, followingwhich normal cardiac activity may resume. Essential part of cardiopulmonary resuscitation. 15
  16. 16. Cerebrovascular event. (syn CVA, stroke ) Loss of neurological function, sensory or motor following anischaemic insult to part of the brain. This can result from intracerebral bleeding, an embolic event, or from acerebral thrombosis. Following any treatment that interferes with the clotting mechanism intracerebralbleeding can occur, and is seen in ~ 0.7% of patients having thrombolytic treatment. It is commoner inpatients of low body weight, females, and the elderly hypertensive. Cerebral embolism may occur followingangiography or angioplasty, with thrombus arising from atheromatous plaques in the aorta which aredislodged / disrupted by passage of the catheter. Cerebral thrombosis may occur on a background of severepre-existing cerebrovascular disease, with occlusion of a cerebral vessel. Overall the frequency of allcerebrovascular events after thrombolytic treatment is ~1.8%. It is much less after angioplasty, but is notnegligible.Classification of Acute Coronary Syndromes Terminology is inconsistent. Below is a classificationshowing how acute coronary syndromes are properly classified according to ECG appearances and resultsof a biomarker assay (ie troponin) Acute coronary SyndromesBio - marker Troponin positive Troponin negative ECG ST elevation on No ST elevation on ECG No ST elevation on ECG ECG Name ST elevation Non ST elevation Troponin negative ACS infarction infarction Synonyms Definite MI in Partial thickness MI Unstable angina MINAP initial Subendocardial MI diagnosis (both out-dated terms)Coronary intervention is short for percutaneous coronary intervention. Usually means angioplasty, but canapply to coronary surgery (CABG).Clotting.Database. A set of records based on common definitions, the data set. Usually stored electronically.Data set. A set of generally agreed defined terms that can be used to record events, actions, or activities,such as care for patients treated for a particular condition, or the application of a treatment such asangioplasty.Echocardiography Ultrasound technique allowing immediate visualisation of cardiac structures. Usedwith various sophistications such as stress echo, and contrast echo, to determine cardiac function followinginfarction. 16
  17. 17. ECG appearances The appearance of the electrocardiograph is one of the main diagnostic tools for determining the presence of coronary heart disease in general and ACS in particular. AN ECG does not always provide yes/no answers, and often changes may be equivocal. Typical changes are very helpful but are not invariable. The term appearances here refers to the shape of the electrocardiographic complex, that is the electrical waveform that initiates each heart beat. The commonest terms recorded are • ST elevation. The appearances associated with occlusion of a large coronary artery. • T wave inversion • ST depression The last two are seen with non ST elevation infarction, but can be seen in other conditions, which is why additional information, such as troponin, is valuable in confirming a diagnosisEjection fraction (left ventricular ejection fraction). A numerical assessment of the quantity of bloodejected from the left ventricle. Measured as a percentage, with >50% being normal, 30 – 49% regarded asmoderate impairment, and < 30% as severe. Often measured by ‘eyeballing’ rather than precisemeasurement which can be technically difficult by echo, which is the commonly used technique. Some use35% as the cut off between impaired and severely impaired. If the reported conclusion is ‘severe’ then usethat category regardless of the number recorded. Also measured by angiography, radionuclide andmagnetic resonance imaging.Exercise test A graded exercise protocol performed using either a treadmill of bicycle ergometer whileelectrocardiographic monitoring and haemodynamic monitoring is recorded. Used in order to assesspresence and degree of coronary ischaemia, which is a crude measure of the degree of coronaryobstruction. Normally performed pre-discharge after an acute coronary syndrome. Now that coronaryangiography which gives an immediate view of the degree and extent of coronary disease is performed morefrequently, the need for exercise testing has reduced.Final diagnosis (discharge diagnosis) The diagnosis for this episode (or admission) based on all availableinformation. ST elevation infarction. This is defined within the dataset. If ST elevation occurs on any ECG duringthe admission, in association with troponin release then the final diagnosis is one of ST elevation infarction.Check that troponin value has been entered Non ST elevation infarction. Also defined within application notes. Non ST elevation infarction andtroponin positive acute coronary syndrome are synonymous. Both diagnoses are given for historical reasonsconcerning the redefinition of infarction. Most colleagues presently use non ST elevation infarction for thecombination of appropriate symptoms, cardiographic changes without ST elevation and troponin release.MINAP analyses both diagnosis as one. Chest pain of uncertain cause. This final diagnosis is inconsistent with any elevation of troponin orother cardiac marker. 17
  18. 18. Myocardial infarction (unconfirmed) please note this can only apply to patients dying (usually earlyafter admission) with a very strong presumption of a diagnosis of infarction for whom no marker confirmationis available. Acute coronary syndrome (troponin unspecified) use only where no troponin value is available.Haemorrhagic risk All drugs used in reperfusion treatment, (anticoagulants, antiplatelet drugs,antithrombotics and fibrinolytics) and in reducing the risk of further ischaemic events act by interfering withthe clotting mechanism. All will carry a risk of bleeding complications, of which intra-cerebral bleeding ismost feared. Retroperitoneal haemorrhage, bleeding into the space behind the peritoneum is a less commonbut serious bleeding complication which may cause renal failure. In using these agents a balance of risk andbenefit has to be weighed. The elderly, females, and poorly controlled hypertensives are most at risk ofbleeding, and doses of some drugs are adjusted to lessen the risk. Patients with low body weight also are athigher risk.Hypertension (syn high blood pressure) Common medical condition, seen in ~45% patients presentingwith ACS. Uncontrolled hypertension is associated with an increased risk of intra-cerebral bleeding withthrombolytic agents.Initial diagnosis (syn admission diagnosis). The diagnosis based only on the initial clinical history and theadmission ECG. The purpose of this is to divide patients into those suitable for immediate reperfusiontreatment, and those (without ST segment elevation on the ECG), who are not. The initial diagnosis is neveraltered on the basis of new or additional information.Ischaemic event. A loose term for an acute coronary event or syndrome.Left bundle branch block. (Usually recorded as LBBB ). This is an electrocardiographic finding, often butnot always unrelated to the acute infarction, which causes diagnostic difficulty. The present recommendationis to treat patients presenting with LBBB which is thought to be new (often it is not possible to tell) and withsymptoms consistent with acute infarction as if they had an ST elevation infarction. It may be a source ofdelay in treating patients with thrombolytic treatment while clinicians decide if the ECG appearances areindeed new.Missing data If you cannot find numeric data please do not enter 0. Leave blank. Why? Because blank, anull entry, and 0 are not the same thing. Statistical programs include 0 in calculations, and will ignore a nullentryMRI magnetic resonance imaging. Elegant non radiographic (no X rays) method of examining cardiacfunction.Myocardial infarction When a tissue loses its supply of nutrients and oxygen it dies (pathological term isinfarction), and this takes place over minutes or at the most, hours after occlusion of a coronary vessel. Themuscle cells (myocytes) cease to function, and cell walls break down. The release of cellular contents allows 18
  19. 19. measurement of the degree of myocyte damage. The more cells that are broken down the greater thequantity of cellular contents, cardiac intracellular enzymes, and troponin, that is subsequently found inserum. Troponin T and troponin I are highly specific to cardiac myocytes, whereas Creatine Kinase (CK),and its subforms CK MB and CK MB mass are not quite as sensitive. Troponin T and I are now the goldstandard for assessing myocardial necrosis, but values recorded must be understood in relation to assayperformance. See TroponinIn order to confirm a diagnosis of myocardial infarction there must be troponin release, as this impliesmyocyte death. No troponin elevation; no infarction! Definition of myocardial infarction. At its simplest a myocardial infarction requires some symptoms suggestive of myocardial infarction (chest pain is NOT essential and may be present in only 40% of infarctions coming to hospital. Women, the elderly and diabetics commonly have atypical symptoms), and an elevation of troponin which has a time course consistent with the symptoms. There are usually ECG changes, but not always where the extent infarction is very small, or the site is electrocardiographically remote. The ECG appearances are most commonly used to define the type of infarction. Was this ST or a non ST elevation infarction? This term refers to the typical appearance of part of the ECG complex, the ST segment, which is typical of the changes seen with occlusion of a major coronary vessel. The distribution of the changes on the ECG help define which vessel was involved, although in some cases this may not be accurate. Where infarction occurs (as proved by troponin elevation) without ST elevation this is referred to as a ‘non ST infarction’. The importance of the difference between ST elevation and non ST elevation infarction is that patients with ST elevation and eligible for immediate reperfusion treatment either with thrombolytic treatment of primary PCI, whereas non ST elevation infarctions do not benefit from reperfusion treatment and are treated differently. ST elevation infarction. (Usually abbreviated to ST MI or STE MI) The term describes the ECG appearances, and the site of the infarction is determined by the distribution of the changes on the ECG. Sometimes it is not possible to be precise beyond saying that ST elevation is present. ST elevation infarction is the immediate result of occlusion of a major epicardial artery. The commonest places for occlusion are in: the right coronary artery, which usually results in inferior or infero-lateral infarction, so called because the inferior surface or inferior and apical part of the heart is involved. The left anterior descending artery. Occlusion results in anterior infarction The circumflex artery. Occlusion depends on precise distribution of the vessel (it varies from person to person) but may produce inferior or true posterior infarction. 19
  20. 20. Non ST elevation infarction. (Usually abbreviated to nSTE MI, non STE MI) The term describes all infarctions where there is not ST segment elevation. There has to be troponin release, and a background of symptoms suggestive of infarction (something must have brought the patient to hospital!), and any ECG changes other than ST elevation. The commonest other changes are; ST depression, or T wave inversion. Rarely there may be no obvious ECG changes, but unless another reason for troponin release is found, such as a pulmonary embolus, this should be recorded as a non STE MI. Terms such as ‘Sub-endocardial’ and ‘partial thickness’ infarctions are now redundant and should be coded as non ST elevation infarction. • Site of infarction. Terms like Anterior, inferior, and infero-lateral refer to the distribution of the cardiographic changes on the 12 lead ECG MINAP does not record this at present • Size of infarction The peak troponin, normally recorded 12 hours or more after onset of symptoms, is a very broad measure of infarction size • Vessel involved. As angiography is increasingly used very early on following infarction the infarct is sometimes referred to in relation to the culprit vessel.Occlusion Term for blockage of a coronary arteryPrevious medical history (syn co-morbidity) These are pre-existing medical conditions which may have anindependent effect on outcome, such as heart failure, chronic renal failure, or diabetes. Other conditions,such as severe asthma, may influence management, by preventing use of a beta blocker for secondaryprevention. The following are important • Treated hyperlipidaemia • Treated hypertension • Previous myocardial infarction • Previous angina, that began > 2 weeks before this event • Diabetes • Heart failure • Renal failure, with a creatinine consistently greater than 200 micromol /L (see biochemistry results). Creatinine is a measure of renal function and not the same as creatine kinase. • Asthma / chronic obstructive pulmonary disease • Smoking historyPlaque rupture. (syn plaque event) The spontaneous rupture of the endothelium overlying a plaque.Results in further distortion of the vessel lumen. The initiating event for myocardial infarction. 20
  21. 21. Rehabilitation Term covering all aspects of support given to patients having ACS including physicalrehabilitation, and life style advice. Normally starts within fist days after admission and will continue afterdischarge.Re-infarction. following reperfusion of an occluded coronary artery there is a risk that further thrombus maydevelop after the effects of a thrombolytic drug have worn off. There may be further pain, new ECG changesin the area of the original damage, and new marker release. Associated with a poorer long term outcomeHeparin or Enoxaparin is used with reteplase or tenecteplase in order to prevent re-infarction. Re-infarctionis much less common after primary angioplasty.Reperfusion. The term used to describe the return of blood to myocardium which was starved of blood bysudden occlusion of a coronary vessel (myocardial infarction) Reopening an occluded coronary artery can beperformed either by angioplasty or by use of a thrombolytic drug. Reperfusion treatment means eitherthrombolytic treatment or primary angioplasty.Radionuclide study technique using radioactive tracer compounds, such as technetium, and sestamibi, toevaluate cardiac performance, and myocardial perfusion. Used in conjunction with stress testing it canprovide better information on cardiac performance and myocardial perfusion than a simple exercise test.Secondary prevention There are a number of complementary strategies which are used to reduce the riskof further ischaemic events which are correctly described as secondary prevention measures. These includeimprovement of life-style, such as diet, smoking cessation, and exercise. However the term is normally usedin the context of the medications which have been demonstrated to reduce frequency of further events.These are aspirin (and within the first year after ACS, Clopidogrel), statin drugs, beta blockers and, forpatients with any significant left ventricular impairment, ACE inhibitors or angiotensin receptor blockers.Troponin is a protein molecule almost 100% specific to cardiac myocytes (muscle cells). It is released intothe plasma with the irreversible rupture of myocyte cell membranes for which the usual cause is a cardiacischaemic event. Normally there is no troponin in plasma. Assays for troponin are very sensitive, but cannotdistinguish between no troponin, and infitesimally small amounts, which are at the extremes of the capabilityof the assay. In other words assays cannot distinguish between ‘background noise’ and very tiny amounts.Thus troponin assays may be reported as less than eg., 0.015 ng/L as this is the point at which the assay isno longer reliable. Even within the range in which the assay is thought to function satisfactorily , very lowvalues may be subject to wide variation (different results when the assay is repeated on the same sample).There are many assays for troponin I, and one for troponin T (owned by a pharmaceutical company) MINAPcannot distinguish between the lower ends of the functioning range for each assay . So we ask you,whenever a value is at or below the bottom of the range for your local assay to report the result as 0, zero.Unstable angina (Syn. Crescendo angina) This is a good descriptive term the definition of which haschanged with time, but not one which is used in MINAP. It refers to an acceleration in the frequency or 21
  22. 22. severity of angina, symptoms which may bring someone into hospital. The crucial test for you is to check ifthere was any troponin release. If present then this has to be coded an acute coronary syndrome (troponinpositive), and if absent acute coronary syndrome (troponin negative). 22

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