USING THE GUIDE

The purpose of the document is to provide advice and explanations for colleagues who may not have clinical

experience of acute coronary disease, and who may not be familiar with some of the clinical terms used to

describe 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.

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INDEX TO GLOSSARY

Acute coronary syndromes Classification of Acute Coronary

Syndromes AngiographyAngiographic facilitiesAngioplasty

Facilitated angioplasty Primary angioplasty Rescue angioplasty

Atheroma Atrial fibrillation (AF) see cardiac arrhythmiasAtrial tachycardia (SVT, PAT,AVNRT) see cardiac arrhythmiasAsystole see cardiac arrhythmias

Biomarker Bleeding see haemorrhagic risk and cerebrovascular event (below)Cardiac drugs

ACE inhibitors Angiotensin receptor blockers Antiplatelet agents Beta blockers (oral) Betablockers (intravenous) Calcium channel blockers Diuretics Epleronone Fondaparinux 2b3a inhibitors Heparin Nitrates SpironolactoneThienopyridine inhibitor(s) Thrombolytic drugs Warfarin

Cardiac arrhythmias

Cardiac facility Cardiopulmonary resuscitation Cardioversion Cerebrovascular event. CCU DatabaseData setDischarge medicationElectromechanical dissociation (EMD) see cardiac arrhythmiasExercise test Echocardiography Ejection fraction Final diagnosis Haemorrhagic risk Heart block, complete (CHB) see cardiac arrhythmiasInitial diagnosis Ischaemic eventLeft bundle branch blockLow molecular weight heparin Missing data MRI magnetic resonance imagingMyocardial infarction

DefinitionST elevation infarctionNon ST elevation infarction

OcclusionPlaque rupturePrevious medical history Radionuclide study Rehabilitation Re-infarction ReperfusionThrombolytic drugsTroponin Unstable angina

Introduction

MINAP, the national audit of myocardial infarction is a database based on the MINAP data set started with a

limited number of data items with which to examine the response of hospitals to the requirements of the

NSF. This was mainly concerned with delays in provision of thrombolytic treatment for patients with ST

elevation infarction, and use of secondary prevention medication. The data set has expanded so that it now

covers all aspects of care of patients having acute coronary syndromes (ACS). Note that the data set has

terms that cover most if not all clinical eventualities. It follows that not every item has to be completed on

every 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 local

hospital database. Analyses of records can be made at any level of aggregation in order to obtain a picture

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of performance at any level from hospital up to the whole country. We provide data analyses in various

formats to

The Department of Health

Strategic Health Authorities

Cardiac Networks, and via them to PCTs

Ambulance Trusts

We regard the analyses provided to hospitals to be of first and foremost importance

It is vital to appreciate that MINAP is not simply a tool with which to produce annual data analyses related to

patients who have had thrombolytic treatment. It is also designed to be a local tool with which you can

examine the process of care of all the patients with ACS admitted to your hospital. Many hospitals record all

their patients with acute coronary syndromes and use the records for regular analysis of care. This is

particularly 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 been

attained locally there is no point in continuing the exercise. This is a very narrow and incorrect interpretation

of the purpose of data collection, and if it is performed only in order to prove that targets are being met then it

is poor reward for the effort. The data are for use at local level, and those who do so find that they get more

and more out of it. We strongly recommend a MINAP data use group within hospitals who can use the

data to own support their practice. This will make data collection worthwhile, and if you share the analyses

with your management, they too will come to appreciate the value of MINAP. The sort of areas which are of

interest to your management include length of stay, in relation to diagnosis, which is not accurately available

from hospital episode statistics, use of angiography, delays before transfer and much else. If your hospital

makes 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 be

recorded in MINAP. Where all patients with acute coronary syndromes are admitted to the same ward or

area it is easy to identify patients. It is much harder where patients are not all cared for in one area, and are

looked after in several wards. [For the same reasons it is much harder to be sure that the care received is of

consistent quality] Where this is the case it is necessary to make arrangements with ward clerical staff to

identify patients passing through their wards, based on a diagnosis of myocardial infarction or an acute

coronary syndrome, for subsequent logging. However, every hospital is different in how it deals with clinical

records, 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 number

of additional areas of care should be examined for patients with myocardial infarction (any troponin positive

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ACS), In summary these included 30 day mortality following myocardial infarction, documentation of

assessment of left ventricular function, and assessment of need for intervention.

Is it worthwhile to collect data on all patients? Information on length of stay is of considerable interest to

management; MINAP can show that there is a more than twofold variation in length of stay for patients with

non ST elevation infarction between hospitals, and that more than 1 in 8 patients admitted with chest pain of

uncertain cause will be readmitted. These impose a considerable burden on hospitals, and MINAP can help

hospitals 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 syndromes

into MINAP.

Identifying records for inclusion

Patients having acute coronary syndromes and chest pain thought to be cardiac in nature represent a large

proportion of acute medical admissions, but are not necessarily easy to identify unless admitted to a cardiac

ward.

Checking overall numbers. Your biochemistry department will be able to provide a list of patients who have

had troponin measured. Where patients with acute coronary disease are not all admitted to one clinical area

such as a cardiac ward it is almost impossible to know how many admissions there are with acute coronary

syndrome. A list of patients who have been admitted who have an elevated troponin value, available from

from the biochemistry department, is a useful means of cross checking.admissions with ACS

Looking at medical records. Look for evidence that the patient was admitted with an acute coronary

syndrome (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

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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;

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 next

have to decide what type of ACS you are dealing with in order to decide the Initial diagnosis. ACS falls

into two broad groups based on ECG appearances, those with ST segment elevation (syn definite

infarction) appearances on the ECG, and those without. Treatment options and data entry depend on

this 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 infarction

was either made in an ambulance before arrival or on the first (admission) ECG. If ST elevation

develops 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.

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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.

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.

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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

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. If

a result is not available do not enter 0, (zero), but leave blank. This must apply even if the value is part of

the 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)

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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.

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)

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o ACE inhibitors (all end in –april) or Angiotensin receptor blockers (ARBs) (all end in – sartan)

o Any diabetic medication

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

country

Important data entry advice. If you are completing a field where the answer is unknown, such as Angiography – Not performed, never leave the field blank as this does not mean unknown. Always enter an available option. All MINAP fields have options for not performed or not known; please use them where appropriate.

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INDEX TO GLOSSARY

Getting 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 to another linked item directly

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Acute coronary syndromes. This term covers the spectrum of clinical, biochemical and

electrocardiographic features that follow a coronary plaque event. Refer to text books for more detail. In

essence, an area of atheromatous deposit lying within the coronary arterial wall becomes unstable, and the

overlying endothelium (very fine layer of cells) ruptures, allowing blood to come in contact with the interior or

the arterial wall. When blood comes in contact with the interior of the arterial wall the blood clots (clinical term

thrombus). 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 by

thrombus blood flow downstream ceases and unless there is collateral flow (see below) all the heart muscle

supplied by the vessel is at risk of death. Clearly the more rapidly the vessel is reopened (either naturally or

using 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 pass

downstream 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 of

damage, 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 chronic

partial occlusion, the greater the chance of collateral vessels developing and providing an (incomplete) back

up circulation to the affected area.

Site of the vessel. A major epicardial (surface) vessel occlusion will do more damage than a smaller

branch vessel occlusion. Generally epicardial vessel occlusion, involving the left, right or circumflex artery

systems results in ECG appearances of ST segment elevation infarction. The exception is that occlusion of

epicardial vessels supplying the back of the heart (from either the right coronary artery or the circumflex) may

produce a different ECG pattern.

Reactivity of the vessel. Coronary arteries respond to local trauma such as plaque rupture by

constricting, and making the local narrowing worse. Vasoconstriction may play a part in determining the type

of infarction.

Angiography The investigative technique of injecting radiographic contrast into coronary arteries to

determine the presence and extent of disease. There is a strong case to be made for offering angiography

to a large proportion of patients who present with an acute coronary syndrome.

Angiographic facilities. The radiographic facilities to perform coronary angiography. Many district general

hospitals have angiographic facilities with which they perform ‘cold’, non urgent angiography, and do not

perform angiography on acute admissions which may be unstable. A number of larger DGHs do perform

angiography and percutaneous coronary interventions on emergency admissions.

Angioplasty a technique for reopening occluded coronary arteries using a balloon tipped catheter. Now

commonly performed in conjunction with stenting of the occluded section of artery.

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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 which

develops 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 the

vessel. 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 whose

presence (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 of

the myocardium, and resulting loss of co-ordinated pumping activity. Deaths occurring before arrival in

hospital may be 50% of the total mortality from AMI. The ‘massive’ heart attack causing sudden death

beloved of the tabloids is usually not massive at all, in the sense of involving a lot of heart, but may be quite

small 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 of

the ventricles into an irregular and chaotic activity. Accompanied by complete loss of pumping activity, loss

of cardiac output, and immediate circulatory failure. Lethal unless cardiopulmonary resuscitation is

commenced within minutes.

Ventricular tachycardia. (VT) Rapid and regular ventricular rhythm of sudden onset often > 200

minute. 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 DC

cardioversion.

Atrial tachycardia (PAT, SVT, AVNRT) Rapid heart rhythm, usually 150-250 / min usually needing

drug treatment

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Asystole Complete cessation of all cardiac activity. Terminal, and with a bad prognosis even with

all resuscitative techniques.

Electro-mechanical dissociation EMD (syn pulseless electrical activity PES) Electrical activity

evident on ECG, but not sustaining a cardiac output. Often a terminal event.

Complete heart block a recognised early complication of (inferior) myocardial infarction. Heart rate

falls, 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]

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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 inhibit

reabsorbtion of sodium back into the circulation after initial excretion via the glomerulus. Water

follows the sodium, and produces the diuretic effect. Used in heart failure. Patients may be taking

diuretics at admission for previous heart failure or as part of the treatment of hypertension

Fondaparinux A pentasaccharide composed increasingly used as an anticoagulant in

acute coronary syndromes. By binding to thrombin, fondaparinux inhibits factor Xa. Fondaparinux is

given subcutaneously daily. There is no need for haematological monitoring

Heparin An anticoagulant drug used either subcutaneously or intravenously. Anticoagulants

interfere with the clotting cascade (series of complex biochemical reactions which result in the

formation of fibrin, the primary ingredient of a clot). Heparin is used as an adjunctive drug with

tenecteplase and reteplase in the treatment of ST elevation infarction . [See re-infarction] Heparinn is

also used routinely in the management of non ST elevtion infarction

Dosing with heparin is not easy, and requires very careful adjustment of dose using a heparin

infusion and a pump. Dosing is adjusted according to the APTT (activated partial thromboplastin

time). It is difficult to maintain a stable APTT within the recommended range. It is possible that

heparin will eventually be superseded by low molecular weight heparins or fondaparinux.

Low molecular weight heparin LMWH a more recent development which specifically blocks factor

Xa (10a) in the clotting cascade. Has the huge advantage of not requiring major dose adjustments

after initial adjustment for body weight. Blood monitoring is not required in normal circumstances

Can be used IV for immediate effect or subcutaneously. Evidence suggests that it is more effective

in ACS, and is likely, when licensing issues are resolved to become the drug of choice with lytic

agents. It is easier to use, and longer acting, which may be of crucial importance when used out of

hospital.

Nitrates A group of orally active (well absorbed from the mucosa of the mouth as well as

intestinally) short acting organic nitrate compounds which are powerful vasodilators. Used for the

rapid 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 the

vasculature, and has an important role in treatment of heart failure, where use has been shown to

reduce mortality. Epleronone A new analogue of spironolactone, possibly with less side effects.

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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 and

connected to a central monitoring station. Increasingly CCU is part of a larger cardiological facility

Cardiopulmonary resuscitation CPR. Applied collectively to the techniques of cardiac massage and

assisted ventilation, which are used to maintain a cardiac output of oxygenated blood in the absence of an

effective cardiac rhythm, or during respiratory arrest. Combined with pharmacological interventions and

direct current countershock to restore normal cardiac electrical activity.

Cardioversion - or direct current cardioversion (syn DC shock, countershock) used in treatment of

cardiac tachyarrthymias. Performed with patient unconscious. A high energy, short duration direct current

electric shock is applied over the left chest with the intended effect of producing transient asystole, following

which normal cardiac activity may resume. Essential part of cardiopulmonary resuscitation.

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Cerebrovascular event. (syn CVA, stroke ) Loss of neurological function, sensory or motor following an

ischaemic insult to part of the brain. This can result from intracerebral bleeding, an embolic event, or from a

cerebral thrombosis. Following any treatment that interferes with the clotting mechanism intracerebral

bleeding can occur, and is seen in ~ 0.7% of patients having thrombolytic treatment. It is commoner in

patients of low body weight, females, and the elderly hypertensive. Cerebral embolism may occur following

angiography or angioplasty, with thrombus arising from atheromatous plaques in the aorta which are

dislodged / disrupted by passage of the catheter. Cerebral thrombosis may occur on a background of severe

pre-existing cerebrovascular disease, with occlusion of a cerebral vessel. Overall the frequency of all

cerebrovascular events after thrombolytic treatment is ~1.8%. It is much less after angioplasty, but is not

negligible.

Classification of Acute Coronary Syndromes Terminology is inconsistent. Below is a classification

showing how acute coronary syndromes are properly classified according to ECG appearances and results

of a biomarker assay (ie troponin)

Acute coronary SyndromesBio - marker Troponin positive Troponin negative

ECG ST elevation on ECG

No ST elevation on ECG No ST elevation on ECG

Name ST elevation infarction

Non ST elevation infarction

Troponin negative ACS

Synonyms Definite MI in MINAP initial

diagnosis

Partial thickness MISubendocardial MI

(both out-dated terms)

Unstable angina

Coronary intervention is short for percutaneous coronary intervention. Usually means angioplasty, but can

apply 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 as

angioplasty.

Echocardiography Ultrasound technique allowing immediate visualisation of cardiac structures. Used

with various sophistications such as stress echo, and contrast echo, to determine cardiac function following

infarction.

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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 diagnosis

Ejection fraction (left ventricular ejection fraction). A numerical assessment of the quantity of blood

ejected from the left ventricle. Measured as a percentage, with >50% being normal, 30 – 49% regarded as

moderate impairment, and < 30% as severe. Often measured by ‘eyeballing’ rather than precise

measurement which can be technically difficult by echo, which is the commonly used technique. Some use

35% as the cut off between impaired and severely impaired. If the reported conclusion is ‘severe’ then use

that category regardless of the number recorded. Also measured by angiography, radionuclide and

magnetic resonance imaging.

Exercise test A graded exercise protocol performed using either a treadmill of bicycle ergometer while

electrocardiographic monitoring and haemodynamic monitoring is recorded. Used in order to assess

presence and degree of coronary ischaemia, which is a crude measure of the degree of coronary

obstruction. Normally performed pre-discharge after an acute coronary syndrome. Now that coronary

angiography which gives an immediate view of the degree and extent of coronary disease is performed more

frequently, the need for exercise testing has reduced.

Final diagnosis (discharge diagnosis) The diagnosis for this episode (or admission) based on all available

information.

ST elevation infarction. This is defined within the dataset. If ST elevation occurs on any ECG during

the 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 and

troponin positive acute coronary syndrome are synonymous. Both diagnoses are given for historical reasons

concerning the redefinition of infarction. Most colleagues presently use non ST elevation infarction for the

combination 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 or

other cardiac marker.

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Myocardial infarction (unconfirmed) please note this can only apply to patients dying (usually early

after admission) with a very strong presumption of a diagnosis of infarction for whom no marker confirmation

is 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 with

the clotting mechanism. All will carry a risk of bleeding complications, of which intra-cerebral bleeding is

most feared. Retroperitoneal haemorrhage, bleeding into the space behind the peritoneum is a less common

but serious bleeding complication which may cause renal failure. In using these agents a balance of risk and

benefit has to be weighed. The elderly, females, and poorly controlled hypertensives are most at risk of

bleeding, and doses of some drugs are adjusted to lessen the risk. Patients with low body weight also are at

higher risk.

Hypertension (syn high blood pressure) Common medical condition, seen in ~45% patients presenting

with ACS. Uncontrolled hypertension is associated with an increased risk of intra-cerebral bleeding with

thrombolytic agents.

Initial diagnosis (syn admission diagnosis). The diagnosis based only on the initial clinical history and the

admission ECG. The purpose of this is to divide patients into those suitable for immediate reperfusion

treatment, and those (without ST segment elevation on the ECG), who are not. The initial diagnosis is never

altered 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 but

not always unrelated to the acute infarction, which causes diagnostic difficulty. The present recommendation

is to treat patients presenting with LBBB which is thought to be new (often it is not possible to tell) and with

symptoms consistent with acute infarction as if they had an ST elevation infarction. It may be a source of

delay in treating patients with thrombolytic treatment while clinicians decide if the ECG appearances are

indeed new.

Missing data If you cannot find numeric data please do not enter 0. Leave blank. Why? Because blank, a

null entry, and 0 are not the same thing. Statistical programs include 0 in calculations, and will ignore a null

entry

MRI magnetic resonance imaging. Elegant non radiographic (no X rays) method of examining cardiac

function.

Myocardial infarction When a tissue loses its supply of nutrients and oxygen it dies (pathological term is

infarction), and this takes place over minutes or at the most, hours after occlusion of a coronary vessel. The

muscle cells (myocytes) cease to function, and cell walls break down. The release of cellular contents allows

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measurement of the degree of myocyte damage. The more cells that are broken down the greater the

quantity of cellular contents, cardiac intracellular enzymes, and troponin, that is subsequently found in

serum. 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 gold

standard for assessing myocardial necrosis, but values recorded must be understood in relation to assay

performance. See Troponin

In order to confirm a diagnosis of myocardial infarction there must be troponin release, as this implies

myocyte 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.

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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 artery

Previous medical history (syn co-morbidity) These are pre-existing medical conditions which may have an

independent 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 secondary

prevention.

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 history

Plaque 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.

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Rehabilitation Term covering all aspects of support given to patients having ACS including physical

rehabilitation, and life style advice. Normally starts within fist days after admission and will continue after

discharge.

Re-infarction. following reperfusion of an occluded coronary artery there is a risk that further thrombus may

develop after the effects of a thrombolytic drug have worn off. There may be further pain, new ECG changes

in the area of the original damage, and new marker release. Associated with a poorer long term outcome

Heparin or Enoxaparin is used with reteplase or tenecteplase in order to prevent re-infarction. Re-infarction

is much less common after primary angioplasty.

Reperfusion. The term used to describe the return of blood to myocardium which was starved of blood by

sudden occlusion of a coronary vessel (myocardial infarction) Reopening an occluded coronary artery can be

performed either by angioplasty or by use of a thrombolytic drug. Reperfusion treatment means either

thrombolytic treatment or primary angioplasty.

Radionuclide study technique using radioactive tracer compounds, such as technetium, and sestamibi, to

evaluate cardiac performance, and myocardial perfusion. Used in conjunction with stress testing it can

provide 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 risk

of further ischaemic events which are correctly described as secondary prevention measures. These include

improvement of life-style, such as diet, smoking cessation, and exercise. However the term is normally used

in 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, for

patients 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 into

the plasma with the irreversible rupture of myocyte cell membranes for which the usual cause is a cardiac

ischaemic event. Normally there is no troponin in plasma. Assays for troponin are very sensitive, but cannot

distinguish between no troponin, and infitesimally small amounts, which are at the extremes of the capability

of 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 is

no longer reliable. Even within the range in which the assay is thought to function satisfactorily , very low

values 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) MINAP

cannot 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 has

changed with time, but not one which is used in MINAP. It refers to an acceleration in the frequency or

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severity of angina, symptoms which may bring someone into hospital. The crucial test for you is to check if

there was any troponin release. If present then this has to be coded an acute coronary syndrome (troponin

positive), and if absent acute coronary syndrome (troponin negative).

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