Clinical
The use of primary PCI
for the treatment of STEMI
Diana Cooper, Senior Nurse, Cath Lab, Musgrove Park Hospital, Taunton. Email: Diana.Cooper@tst.nhs.uk
I
n Mending hearts and brains (Boyle, 2006), on
reorganising care for acute coronary events, Sir Roger
Boyle advocated treatment of acute myocardial
infarction (AMI) at specialist centres by percutaneous
coronary intervention (PCI). Following pilots across the
UK and publication of the National Infarct Angioplasty
Project (NIAP) report, the Department of Health (2008)
recommended primary percutaneous coronary
intervention (PPCI) as the treatment of choice for acute
STelevation myocardial infarction (STEMI).
Various studies have demonstrated the efficacy and
mortality benefits of this method of restoring blood flow
to the myocardium over thrombolysis, which was the pre-
vious standard (Keeley et al, 2003). PPCI services had also
been successfully developed in various European coun-
tries which had reported good outcomes with this proce-
dure (Nielsen et al, 2010).
As a result of changes in management, mortality follow-
ing acute coronary syndromes has reduced from 20% to
Abstract
Acute myocardial infarction (AMI) accounts for 1 in 5 male and 1 in 8
female deaths in the UK. Primary percutaneous coronary intervention
(PPCI) is the treatment of choice for ST elevation myocardial infarction
(STEMI). A network of PPCI centres across the UK provides a safe and
effective treatment for patients and prompt diagnosis and transfer to
a PPCI cardiac catheter laboratory provider is the key to a successful
outcome. Access is more commonly via the radial artery, rather than
the femoral artery, since this reduces access site complications.
Complications are rare (less than 1%), but serious, and require a
skilled multidisciplinary team approach for optimal management.
Hospitalisation is for 23days in uncomplicated cases, with secondary
prevention and cardiac rehabilitation being offered to all AMI patients.
The introduction of PPCI for STEMI across the UK has reduced patient
mortality and improved outcomes in comparison with fibrinolysis,
which was the previous standard. This article provides a review of
PPCI for the treatment of STEMI.
Key words
w Primary percutaneous coronary intervention (PPCI)
w Acute myocardial infarction (AMI) w Cardiac catheter laboratory
w Complications
Submitted for peer review: 8 May 2014. Accepted for publication: 18 May 2015.
Conflict of interest: None.
354
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5% over the past 30 years (National Institute for Health
and Care Excellence (NICE), 2013a). The incidence of
STEMI is around 1000 per 1 million population (NICE,
2013a) and 82000 deaths per year in the UK are attributed
to acute cardiac events accounting for one in five male and
one in eight female deaths (Heart Research Institute,
2015). Prevention is a key factor in reducing the incidence.
Mortality is reduced following PPCI in comparison with
intravenous thrombolytic therapy both in the short term
and at 12 months (Huynh et al, 2009). However, the
STREAM study suggests that modern fibrinolysis is safe
and effective (Sinnaeve et al, 2014).
Pathophysiology
Atheroma is the accumulation of debris between the
endothelium and medial layers of the arterial wall forming
plaques (Grech, 2003; Libby and Theroux, 2005). This
debris contains macrophage foam cells, lipid and fibrous
deposits. Calcium may also be deposited in these plaques
and the plaque is covered by a fibrous cap. This atheroscle-
rotic process takes place over years and is accelerated by
smoking, diabetes, hyperlipidaemia and hypertension.
The muscular (medial) layer of the artery remodels itself
to compensate for the changes in the arterial wall to main-
tain blood flow; however, over time, these plaques extend
as a result of further cholesterol deposition. Depending on
the thickness of the overlying fibrous cap, small ruptures
can occur, which may heal to form stenoses which narrow
the lumen of the artery and hence restrict blood flow. This
may lead to symptoms of angina. The fibrous cap can
become unstable owing to inflammatory changes and may
rupture abruptly releasing the contents of the plaque and
initiating the bodys platelet response and thrombus for-
mation. When this occurs in a coronary artery, the vessel
can block completely causing an acute myocardial infarc-
tion (AMI). A relatively small lesion can sometimes give
rise to a large thrombus and massive AMI, or a well estab-
lished lesion may only develop a relatively small blood clot
(Figure1).
In either scenario, although thrombolytic agents can
dissolve the clot, the underlying stenosis or inflamed
unstable lesion remains vulnerable to further closure.
Thygesen et al (2012) describe a universal definition of
myocardial infarction (MI) which identifies five types of
MI including STEMI. This article focuses on STelevation
myocardial infarction (STEMI) and does not discuss the
management of non-STelevation (NSTEMI) or other MIs.
British Journal of Cardiac Nursing July 2015 Vol 10 No 7
 Clinical

Diagnosis

Peter Lamb
AMI typically presents as crushing central chest pain
which is intense and unremitting for up to an hour (Steg
et al, 2012; Zafari, 2015). It may radiate to the neck, shoul-
der or jaw and down the left arm. Patients may describe a
substernal pressure, or weight on their chest, that may be
squeezing, aching or burning. Others describe a feeling of
indigestion, with repeated burping. Nausea, sweating, and
shortness of breath are common features. Patients may feel
associated anxiety and present with pallor, clamminess
and cold extremities. The latter may be a result of hypoten-
sion which may indicate reduced ventricular function.
Coughing, wheezing and sputum production may result
from acute pulmonary oedema. Alternatively, some peo-
ple do not complain of pain. However, vital signs may
reveal an increased heart rate and irregularities may indi-
cate secondary arrhythmias.
The heart receives its blood supply via three main coro-
nary arteries:
ww Right coronary artery (RCA)
ww Left anterior descending artery (LAD)
ww Left circumflex artery (Cx).
The two left coronary arteries are both supplied by the left
main stem (LMS). All of these arteries, however, have
branches coming off of them, providing the whole myo-
cardium with oxygenised blood (Figure2).
The depolarisation, and more particularly repolarisa-
tion, of cardiac cells is altered by changes in blood supply
and this can be identified using 12-lead electrocardiogram
(ECG) (Davey, 2008). Different leads of the ECG correlate
to different areas of the heart; therefore, by analysing Figure1. Development of atheromatous plaque in a coronary artery
changes which occur in association with clinical symp-
toms of AMI, diagnosis can be made by a health profes- (NICE, 2014a). There is a network of hospitals across the
sional trained in 12-lead ECG interpretation (Figure3a). UK providing this service. Because of the difficulty of
Broadly speaking, anterior changes are associated with timely delivery of PPCI, it may not be the preferred strat-
the LAD (front of the heart), lateral changes with the Cx egy for coronary reperfusion in all health communities
(side), and inferior (underside) changes with the RCA and local commissioners may decide on fibrinolysis for
(although in 30% of the population the Cx provides the management of STEMI. It is recommended that patients
inferior myocardium with blood). who have received fibrinolysis for STEMI but continue to
When the main arteries block completely owing to have ECG changes 6090minutes after administration be
thrombus, the first ECG change is usually STelevation in transferred to a PPCI centre.
the corresponding leads. For example, if the LAD blocks, Within a PPCI pathway collaboration, shared patient
STelevation will be seen in leads V2V4 with reciprocal pathways, appropriate training and equipment of para-
STdepression in other leads. In association with clinical medic service, and agreed responsibilities (Steg et al, 2012)
symptoms, an acute STEMI can be diagnosed (Figure3a ensure that the PPCI team can be activated by paramedics
and Figure3b). in the community. Patients may be received directly into
Blockage of smaller branch vessels or transient blockade the cardiac catheter laboratory to reduce delay (call-to-
of larger vessels by vasoconstriction or with thrombus that door time). Assessment on arrival to the PCI centre
subsequently dissolves or dislodges distally, may give rise includes ECG analysis, condensed medical history partic-
to NSTEMI. This is not normally treated as PPCI. PPCI is ularly noting stroke, recent surgery, bleeding and hyper-
the treatment of choice when this process occurs in the tension, drug therapy, allergies and examination of heart
context of an acute event. and lung fields. Renal function is important because of the
nephrotoxic effects of contrast medium and some centres
Acute STEMI use point-of-care creatinine testing. Intravenous cannula-
Patients in the UK should have access to a cardiac catheter tion of the patient allows rapid administration of any
laboratory within 120minutes of the time when fibrinoly- required drugs.
sis could have been administered (i.e. diagnosis by a On diagnosis of AMI, aspirin 300 mg should be given
health professional) so that PPCI can be performed orally, commonly by the paramedics at scene, along with

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 Clinical
Peter Lamb
Figure2. Anterior view of the heart
appropriate pain relief. In addition, loading dose of dual
antiplatelet therapy (DAPT) (ticagrelor180mg, clopidog-
rel 600 mg or prasugrel 60 mg) should be administered.
NICE (2011a) approves all three following technology
appraisal; Ticagrelor with aspirin as DAPT is recom-
mended in European Society of Cardiology (ESC) guide-
lines (Steg et al, 2012). The PLATO trial (James et al, 2009)
reported that relative risk of cardiovascular death, MI and
stroke were reduced by 16% in patients taking ticagrelor,
and the absolute risk at 12months was 10%. ticagrelor is
thought to work faster, have greater efficacy and a more
consistent effect on platelet inhibition (Steg et al, 2012).
Ticagrelor is associated with increased risk of bleeding
including cerebral haemorrhage and increased blood cre-
atinine and uric acid levels. Patient compliance may be of
concern owing to the twice daily maintenance dose
required and reports of troubling side effects such as dys-
pnoea. The drug choice will depend on centre protocol
and clinician preference.
The cardiologist will make the clinical decision to take
the patient into the catheter laboratory, supported by the
multidisciplinary team. In some instances, however, it
may not be in the patients best interest such as in patients
with other comorbidities or for whom revascularisation
attempts may be futile. Witnessed verbal consent includ-
ing the risks and benefits must be gained from the patient.
PCI is the opening of a coronary artery via a puncture
through the skin directly into an artery using X-ray fluor-
oscopic imaging. A fine wire is passed through the lesion
over which a balloon is passed and inflated. The inflation
pushes the plaque against the wall of the artery which can
be held open with a metal structure called a stent.
Traditionally, the femoral artery was used but access is
now more commonly via the radial artery (70% of all
PPCIs) (British Cardiovascular Intervention Society
(BCIS), 2014) since this is associated with a reduction in
arterial access complications (BCIS, 2014). Catheters,
which are long (150cm) hollow tubes, are directed by the
cardiologists through an access sheath in the chosen
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access site to the root of the aorta where the coronary
arteries are located. The catheters have different curves on
the end designed to cannulate the appropriate artery.
Radio-opaque contrast medium is injected directly into
the catheter and fluoroscopic images are taken in different
planes and viewed on an image intensifier. These images
can be recorded and stored. Staff in the laboratory should
wear lead-equivalent protection.
An appropriate guide catheter will also be selected.
Guide catheters have stiffer shafts, larger internal diame-
ter, re-enforced construction and shorter more angulated
tips than diagnostics and are used for PCI. The large inter-
nal diameter allows balloons, stents and wires to be
inserted within its lumen.
Once the blocked artery has been identified (Figure4a),
the clinician makes a rapid decision regarding the best
management for the individual patient. Disease in other
vessels, comorbidities and patient choice will affect the
decision to proceed to PPCI. The patient is monitored
throughout the procedure including arterial pressure
monitoring and ECG. Oxygen therapy and further pain
relief may be required. Reassurance and clear explanations
help reduce patient anxiety. Baseline bloods for full blood
count (FBC), renal function and electrolytes, cholesterol
and glucose should be obtained.
Prior to disturbance of the blocked lesion, unfraction-
ated heparin 100 U/kg bolus or bivalirudin (a direct
thrombin inhibitor) 0.75 mg/kg bolus plus 1.75 mg/kg/
hour infusion should be administered. NICE (2011b) rec-
ommends the use of bivalirudin following technology
appraisal of data from the HORIZONS-AMI trial (Mehran
et al, 2009). A recent meta-analysis (Cassese et al, 2014)
does not concede any benefits of bivalirudin over heparin
and found a considerable cost implication (Shahzad et al,
2014). Choice will be dependent on local protocol and
operator preference. A coronary guide wire (14/1000-inch
in diameter) is passed though the lesion which may itself
disrupt the blockage and often results in some return of
blood flow, as evidenced by flow of contrast within the
previously occluded vessel. Visible clot may be sucked out
using an aspiration catheter. The lesion may be stretched
with a small balloon. Balloon time is the time at which
the first device crosses the lesion (Figure4b).
Once blood flow has been restored, the lesion will be
sized and an appropriate stent will be deployed across it.
The choice of stent will be made by the clinician following
NICE (2008) recommendations and individual patient
assessment. Reperfusion arrhythmias may occur at this
time which are usually self-terminating but may require
treatment. It is common practice to manage only the cul-
prit lesion at this time, although control trials (Gershlick
et al, 2015) are currently in progress analysing the benefits
of treating bystander disease at the same time (Figure4c).
Where bivalirudin is not used, GPIIb/IIIa (platelet)
inhibitors may be administered intravenously to reduce
risk of clot reformation in selected patients including
those with the following conditions:
ww Complex disease
British Journal of Cardiac Nursing July 2015 Vol 10 No 7
 Clinical

ww Significant thrombus load reduced cerebral perfusion. Permanent pacing may be

ww Delay in accessing PPCI
ww Diabetes.
NICE-approved drugs are abciximab and tirofiban which
are both weight-adjusted doses.
All PCI procedures are recorded in the BCIS database.
Call-to-balloon and door-to-balloon times are measured
against the national target and data are published annually
in The Myocardial Ischaemia National Audit Project
(MINAP) (National Institute for Cardiovascular Outcomes
Research (NICOR), 2014).
PCI is associated with low but serious complications,
occurring in less than 1% of cases (BCIS, 2014). These
relate either to the AMI or as a direct consequence of the
procedure. Although mortality for AMI patients undergo-
ing PPCI is 4.9% (BCIS, 2014), it increases to 31% for
patients presenting in cardiogenic shock (BCIS, 2014).
AMI complications
Cardiogenic shock
Cardiogenic shock can occur as a result of the ischaemic
insult to the myocardium. The ventricular contractibility
is reduced resulting in symptoms of poor cardiac output
including low blood pressure, tachycardia, reduced
peripheral perfusion (slow capillary refill) and hypoxia.
Acute pulmonary oedema may be present. Depending on
the clinical condition of the patient, some form of positive
pressure ventilation assistance may also be required (e.g.
continuous positive airway pressure (CPAP) or mechani-
cal ventilation). Haemodynamic support such as intra-
aortic balloon pump (IABP) or catheter-based pump
device may reduce cardiac afterload and improve coro-
nary perfusion. Inotropic support may be required.
required if the AV block persists following reperfusion.
Arrhythmias
Arrhythmias are common following AMI and may occur
as a result of ischaemia or during reperfusion of the myo-
cardium. Ventricular fibrillation requires immediate car-
dioversion along the advanced life support algorithm.
Symptomatic ventricular tachycardia (VT) or supraven-
tricular tachycardia (SVT) may require urgent direct cur-
rent (DC) cardioversion. Amiodorone is the drug of
choice for acute chemical cardioversion in these circum-
stances (Resuscitation Council UK, 2010). Patients in
cardiac arrest require resuscitation with support of the
anaesthetic team as appropriate. Reperfusion of the
blocked vessel remains the priority.
Peri-procedural complications
Side-branch occlusion
These occur in 1% of all cases (BCIS, 2014). As a result of
opening a main coronary artery, a side branch may
become blocked either by the stent placed in the main ves-
sel or clot. A good analogy is that to keep the motorway

No-reflow
In some cases, despite having opened the culprit vessel,
blood does not flow down the artery (Harrison et al,
2013). This is known as no-reflow and is probably caused
by distal atherothrombic embolisation, ischaemia or
reperfusion injury. Treatment includes pharmacological
support to dilate the coronary artery using epinephrine Figure3a. 12-lead ECG showing areas of heart and corresponding leads
(Aksu et al, 2015), intra-coronary nitrates, adenosine or
phenylephrine depending on operator preference. This
effectively flushes any small thrombotic debris distally and
allows restoration of normal circulation. This may have
only limited effect however. It is a difficult situation to
recover from and can confer an adverse prognosis.
Additional attempts at thrombus extraction and further
stent deployment may be required.

Atrio-ventricular heart block

Atrio-ventricular heart block may occur as a result of
reduced blood supply to the sinoatrial (SA)/atrioventricu-
lar (AV) node. The incidence has reduced significantly
since the days of thrombolysis but remains a poor prog-
nostic indicator (Gang et al, 2012). Insertion of a tempo- Figure 3b. Acute anterior STEMI (Note: ST elevation in the anterior leads
rary pacing wire during the PPCI procedure may be indi- and reciprocal ST depression III and AVF
cated if the patient is compromised with hypotension and Used with kind permission from Deepak Naterajan

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Clinical
Figure4a. Fluoroscopic image Figure4b. Fluroscopic image
demonstrating blocked LAD demonstrating balloon inflation of LAD
open, a b-road may be compromised. Incidence is reduced
by awareness of this risk. The patient may develop signs of
AMI, including chest pain, and ECG changes, as well as
rising troponin may be observed. Studies (Kralev et al,
2006) do not suggest that side-branch occlusion confers
any additional risk to the PCI outcome.
Dissection
When the balloon inflates within the coronary artery, the
intimal layer is torn. Trauma to the medial layer can cause
dissection of the artery which can extend in either direc-
tion. Stenting the dissection is usually enough to contain
the tear but in rare cases, emergency coronary artery
bypass grafting (CABG) to restore coronary blood flow
may be indicated (Rogers and Lasala, 2004). The guide
catheter engages the coronary artery in the root of the
aorta and, in very rare cases, mechanical trauma to the
aorta may cause a dissection. Emergency surgical inter-
vention is often required.
Wire exit
Should the wire exit the coronary artery, blood can leak
into the pericardial sac causing tamponade. Initial treat-
ment is by inflating a balloon across the puncture to pre-
vent further leak and promote sealing. A pericardial drain
may be required and emergency echocardiography should
be available in an emergency catheter laboratory to facili-
tate diagnosis and treatment.
Emboli
Emboli, most commonly from atheroma along the arch of
the aorta, may be disturbed by the passage of the guide-
wire or catheter as it progresses up the aorta and travels to
the cerebral vessels. The patient may develop acute signs of
a cerebrovascular event.
Less commonly, haemorrhagic stroke can occur as a
result of a cerebral bleed associated with anti-thrombotic
agents. It is important to maintain communication with
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Figure4c. Fluroscopic image
demonstrating revascularised LAD
the conscious patient during the procedure in order that
signs can be recognised.
Aftercare
The patient should be transferred to an appropriate acute
cardiac care department with cardiac monitoring follow-
ing PPCI. Patients requiring ventilatory support will
require intensive care management. On completion of the
procedure, haemostasis is achieved in the arterial access
site. The anti-thrombotic drugs given can make manual
compression time-consuming and challenging for the
health professional. Radial haemostasis can be achieved
using a variety of wrist devices designed to apply pressure
over the puncture site.
Femoral punctures may be sealed using arterial closure
devices, which create a mechanical seal. In patients where
these devices are not suitable, such as those with periph-
eral vascular disease or side-branch puncture, compres-
sion either with a device or manual pressure is recom-
mended. It is advisable to delay sheath removal until the
activated clotting time has dropped to less than 150sec-
onds (Merriweather and Sulzbach-Hoke, 2012).
Access site complications occur in less than 1% of
patients, with radial access having lower incidence than
femoral access (BCIS, 2014), although some articles quote
a significant variation (Merriweather and Sulzbach-Hoke,
2012). In the initial few hours post PPCI, close monitoring
is recommended including blood pressure, heart rate, res-
piration and oxygen saturation. The arterial access site
should be monitored carefully for bleeding and distal limb
for signs of arterial occlusion including colour, warmth,
sensation and distal pulse. Bed rest is also recommended
for a couple of hours post procedure depending on patient
condition and progress.
Bleeding out from the puncture site is easily observed
and firm pressure should be applied for an appropriate
length of time (e.g. 10minutes) above the arterial puncture
site to allow elastic recoil of the artery and clot formation in
British Journal of Cardiac Nursing July 2015 Vol 10 No 7

the puncture site. There appears to be little evidence for
either the time recommended for manual compression or
extent of bed-rest post procedure. It is not uncommon for
the puncture site to ooze blood as a result of small vessels in
the capillary bed leaking. To differentiate whether a bleed is
arterial or capillary, the artery can be compressed; if bleed-
ing continues, it is not arterial (Merriweather and Sulzbach-
Hoke, 2012). A pressure dressing and use of a compression
device may be helpful.
Following femoral artery puncture, should the posterior
wall of the femoral artery be punctured or the closure
device fail to provide secure haemostasis, blood can leak
retro-peritoneally. Retro-peritoneal bleed presents with a
sudden drop in blood pressure and signs of vasovagal
including yawning, extreme pallor, clamminess and brady-
cardia, sometimes with back or abdominal pain. The beta-
blocked patient may not respond with an increase in heart
rate. Treatment consists of compression of the puncture,
administration of IV crystalloid, pain relief and reassurance
of the patient. FBC will reveal the extent of the blood loss
and blood may be cross-matched in case transfusion is
required. Monitoring of urine output gives indication of
renal perfusion in the case of prolonged hypotension. A
computerised tomography (CT) scan may help to diagnose
retro-peritoneal bleed but does not alter its management
and may delay treatment. Experience of the nursing team is
key in the recognition of these symptoms since patients do
not present in the same way as post-surgical haemorrhage.
A false aneurysm is a connection between the artery and
a haematoma in the surrounding tissuethe haematoma
forms a sort of capsule within which blood circulates from
the puncture site. This can lead to nerve compression
resulting in localised pain or severe haemorrhage and
blood loss should it burst. Assessment with ultrasound
and a surgical opinion is recommended. Some may heal
spontaneously but ultrasound-guided compression or
thrombin injection may be required (Merriweather and
Sulzbach-Hoke, 2012).
A rare complication of radial punctures is compartment
syndrome, where blood leaks from the puncture site com-
promising circulation to the limb. In this situation, urgent
surgical opinion is required. Distal embolism will mani-
fest as limb pallor and slow capillary refill, reduced or
absent pulse and cool extremity. Vascular opinion is rec-
ommended in this case.
Length of stay is commonly 3days post PPCI, though
some studies (Jones and Rathod, 2012) advocate safe dis-
charge of low-risk patients after 2days. Gradual return to
normal activities usually occurs during the hospital stay.
Echocardiography to assess left ventricular function is
recommended (NICE, 2013) prior to discharge or within
6weeks post event if this is not achievable. Patients with
left ventricular ejection fraction (LVEF) of less than 35%,
QRS complex of greater than 120seconds, and at risk of
sudden cardiac death may benefit from an implantable
cardiac defibrillator (ICD) or cardiac resynchronisation
therapy (CRT) (NICE, 2014). Referral for further angiog-
raphy to review or treat non-culprit lesions may be
British Journal of Cardiac Nursing July 2015 Vol 10 No 7
Clinical
Key Points
PPCI is gold standard treatment for acute STEMI
w
There is a network of centres providing PPCI across the UK
w
Where access to a PPCI is limited, there is a role for fibrinolysis
w
Complications are rare but may be serious
w
Patients need secondary prevention and cardiac rehabilitation
w
following their cardiac event and may require further intervention
required. Secondary prevention should be commenced
and referral to cardiac rehabilitation initiated.
Secondary prevention
All patients following AMI should be offered the following
drug therapy (NICE, 2013) as appropriate:
ww Angiotensin-converting enzyme inhibitor (ACEI)
ww DAPT
ww Beta-blocker
ww Statin.
The ACEI and beta-blocker should be titrated up to the
maximum/target dose. Some patients experience difficulty
in dealing with the speed of their diagnosis, admission and
treatment. Many require extensive information and sup-
port to come to terms with the significance of their cardiac
event. All patients should be offered and actively encour-
aged to participate in a cardiac rehabilitation programme
which should be available in a range of formats to meet the
needs of individuals (NICE, 2013).
Education includes smoking cessation, changing to a
Mediterranean-type diet, increasing physical activity,
weight management and safe alcohol consumption. Verbal
advice should also always be supported by written infor-
mation. Despite the improvements in patient outcome,
significant mortality remains at 30days and 1year which
depends on comorbidities, left ventricular dysfunction
and age (Halkin et al, 2005).
The MINAP Registry collects data manually entered by
each organisation from all patient admissions across the
UK following AMI. The data are used to monitor compli-
ance with NICE guidelines and ensure patients across the
country receive high quality, evidence-based care follow-
ing an MI aiming for a reduction in incidence and
improved outcomes.
PPCI provides a safe and effective treatment for patients
suffering acute STEMI. The specialty of cardiac catheter
laboratory nursing and working as part of the multi-pro-
fessional team provides a stimulating and rewarding
working environment. Research studies continue to bring
new advancements in treatment and patient management.
The challenge for catheter laboratory nurses, however, is
to ensure that practice continues to be current and evi-
dence-based. BJCN
Acknowledgements: The author would like to thank David
Beacock and Mike Seddon, consultant cardiologists,
359
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Clinical
Musgrove Park Hospital, Taunton and Somerset NHS
Foundation Trust
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