Yael MoussadjiAug 21, 2008

Diagnosis of ACS in the ED Risk Stratification

Cardiac markers ECG Risk Scores

Management UA/NSTEMI STEMI

Complications

54 y/o male with 2 hours of exertional retrosternal burning CP

No previous episodes of pain Feels slightly SOB VSS, exam normal ECG non-specific, TnT neg You ask CCU to see because you are

concerned re the possibility of an ACS (UA)

The CCU res asks, does he have any risk factors?

Are cardiac risk factors useful in evaluating the risk of ACS?

Post-hoc analysis of 10,806 ED visits for ACS using the i*trACS registry for ED visits for ACS

ACS defined as need for 30-day revascularization (PTCA or CABG), or death or AMI with positive cardiac enzymes at hospitalization

Cardiac RF were diabetes, HTN, dyslipidemia, smoking, + family history of CAD; cardiac RF burden defined as number of RF present

Analysis stratified by age; <40, 40-65, >65

In patients over 40, cardiac risk factor burden is of limited clinical value in the diagnosis of ACS

In patients under 40, cardiac RF useful if there are none (-LR 0.17) or if there are 4 or more (+LR 7.39)

61 y/o female with 45 minutes of sharp left sided pleuritic chest pain

Feels nauseated, slightly diaphoretic Pain is radiating to her left shoulder No PMHx, no DVT/PE risk factors Cardiac Risk factors: Who cares? Vital signs are normal, ECG nonspecific,

enzymes pending

How useful are clinical features in the diagnosis of acute, undifferentiated chest

pain?

Measured the predictive value and diagnostic performance of clinical features used to diagnose ACS in undifferentiated CP

Clinical features were prospectively recorded on a standard form for 893 patients presenting to the ED; 3.8% had an MI and 9.1% had ACS

Six month follow-up for adverse events Tested the power of each feature to predict

AMI (WHO criteria) and ACS (cardiac testing, AMI, death, or revascularization within 6 months

Features useful in the diagnosis of AMI were exertional pain (LR 2.35), pain radiating to the shoulder or both arms (LR 4.07), and chest wall tenderness (LR 0.3)

Features useful in the diagnosis of ACS were exertional pain (LR 2.06), pain radiating to the shoulder, left arm, or both arms (LR 1.62)

Location, quality, and presence of N/V or diaphoresis were not predictive

A 57 y/o male with no PMHx presents to the ED with CP

Pain has been intermittent for 2 weeks, and is described as pleuritic and exertional; occational nausea is noted

Physical exam is unremarkable Patient’s pain resolved spontaneously

prior to medical therapy, and he is pain free when you see him

Enzymes were negative Patient was discharged home with

instructions to return if worse, and referral to C-era.

24 hours later, the patient returns to emerg with ongoing chest discomfort, nausea, and diaphoresis

What is the predictive and prognostic value of the ECG in patients with ACS?

Non-specific ST and T wave changes ST segment depression or elevation of < 1mm

with or without an abnormal T wave T wave may have altered morphology and/or

blunted, flattened, or biphasic configuration without inversion or hyperacuity

Normal Absence of NSSTTW, AV block, intraventricular

conduction delay, repolarization changes, and rhythms other than NSR

In a study of adult CP patients in the ED, 1% of patients with a normal ECG had a final diagnosis of AMI, and 4% had a final diagnosis of UA

In another study, of patients with classic angina on history and a normal ECG, 3% had a final diagnosis of AMI

3-4% of patients with AMI and over 20% of patients with an ACS (NSTEMI/UA) have NSSTTW findings

Therefore, of all patients with ACS, one fifth will show a normal or non-specific ECG in the ED

Of 202 chest pain patients presenting to the ED with STE, 15% had an AMI

LVH was the most common cause of STE (25%), followed by LBBB (15%) and AMI (15%)

12% had BER, 5% had RBBB, and 5% had nonspecific BBB

Other less common diagnoses were LVA, pericarditis, and paced rhythm

A retrospective analysis of GUSTO-IIb trial Over 12,000 patients who had ACS confirmed on

ECG 22% had T wave inversion, 28% had STE, 35% had

STD, and 15% had a combination of the above 30 day incidence of death or MI was 5.5% in those

with T wave inversions, 9.4% in those with STE, 10.5% in those with STD, and 12.4% in those with a STE + STD

In another study of 205 consecutive patients with UA/NSTEMI, STE of > 0.5mm in aVR was found to be a strong predictor of 30-day mortality, even in patients with low TIMI risk scores

T-wave inversion

ST

ST

P 0.001

CM Gibson 2002

50% of patients with AMI will have a clearly diagnostic ECG at presentation (STE or STD)

ST segment elevation identifies those who benefit from reperfusion therapy (lytics)

Mortality increases with the number of leads showing STE

Other important predictors of mortality include LBBB and anterior location

Reciprocal changes are seen in 70% of inferior and 30% of anterior MIs, which demonstrates over 90% specificity and PPV for AMI

RV infarcts complicate 40% of inferior AMIs

So, if risk factors, clinical features, and ECG’s are not always helpful, how many patient’s with ACS are missed, and what

are their characteristics?

Analyzed clinical data from a multicentre prospective trial of over 10,000 patients with chest pain suggestive of ACS

17% ultimately met the criteria for ACS (8% had AMI and 9% had UA)

2.1% of those with AMI and 2.3% of those with UA were mistakenly discharged from the ED

Acute ischemia Women <55 Non-white SOB as chief

symptom Normal or non-

diagnostic ECG AMI

Non-white Normal or non-

diagnostic ECG

Percentage of patients who get discharged home is low, but discharge of these patients may be associated with increased mortality

Failure to make a diagnosis is related to race, gender, and lack of typical features on ECG

83 y/o male with known renal insufficiency, baseline Cr 150

Presents with vague intermittent CP of 2 days duration, no associated symptoms

PMhx significant for HTN, previous MI and PCTA 10 years ago

ECG non-diagnostic (no acute changes from baseline)

TnT 0.11 CCU res says “it’s elevated because of his

renal failure”

Can you diagnose ACS based on an elevated TnT in a patient with renal

failure?

Analyzed outcomes in over 7000 patients enrolled in the GUSTO IV trial

Assessed baseline TnT level (considered abnormal if >0.1 ng/mL) and Cr clearance

Primary end point was death or MI at 30 days

An elevated TnT level was predictive of death of MI, even among patients with a Cr clearance in the lowest quartile

Cardiac troponin is predictive of short term prognosis in patients with ACS regardless of their level of Cr clearance

Due to near absolute specificity for myocardial tissue and high sensitivity for microscopic zones of myocardial necrosis, cardiac troponins are the preferred biomarker for diagnosing MI

Onset 3-6 hours Peak 12-18 hours Elevated for 5-7 days

Time from onset of symptoms

Approximate sensitivity

6 hours 60%

8 hours 80%

10 hours 90%

Examined the TnT, CK-MB, and ECG abnormalities for risk stratification in patients with ACS within 12 hours on onset of symptoms

Use logistic regression to predict outcome Mortality was significantly higher in the group

with Tn >0.1 ng/mL (ARR 8%) TnT was the variable most strongly related to 30

day mortality, followed by ECG category and the CK-MB level

TnT is a powerful independent predictor of mortality in patients who present with ACS

Prospectively examined 733 patients with acute CP < 12 hours without STE; Tn was measured at least twice on arrival and 4-6 hours later so that one sample was taken at least 6 hours after the onset of pain

TnT was positive in 16% of patients, and 94% of patients who eventually evolved into an AMI

Among patients with UA, TnT was positive in 20%

TnT was a strong independent predictor of cardiac events

The event rate for patients with negative Tn T was 1.1%

2 questions What is the likelihood that the presenting

symptoms represent ACS? What is the likelihood of adverse outcome

Risk stratification process is challenging given then presence of risk factors is an unreliable determinant of ACS, and the ECG and Tn are not very sensitive for UA

2007 ACC/AHA Update to the guidelings for UA/NSTEMI are helpful

2002 Guidelines state that tools such as the TIMI Risk Score can be helpful adjuncts

Since 2002, data from a unselected ED chest pain population have validated its utility

Other recommended tools include the GRACE (Global Registry of Acute Coronary Events) Risk Score and the PURSUIT (Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy) risk model

A study comparing the 3 showed good predictive accuracy for death at 1 year and MI

However, these tools were developed using population based models and may not be reliable for individual patients; they do not replace clinical judgement

Two phase 3 international, randomized, double-blinded trials (TIMI 11B, ESSENCE)

A total of 1957 with UA/NSTMEI who were assigned to receive UFH in TIMI 11B(test cohort)

3 validation cohorts were the UFH group in ESSENCE and both enoxaparin groups (total of over 5000 patients)

Risk score was derived from test cohort using multivariate logistic regression, assinging a value of 1 when risk factor present, and 0 when absent

Outcomes were at least 1 component of the primary end point (mortality, MI, urgent revascularization)

TIMI Risk Score Age > or = 65 3 or more risk

factors for CAD Prior stenosis of 50%

or more ST segment

deviation at presentation

At least 2 anginal events in 24 hours

Use of ASA in prior 7 days

Elevated serum cardiac markers

ED based prospective observational cohort study in 3929 adult chest pain patients

TIMI risk scores determined at presentation; composite outcome of death, MI, revascularization within 30 days

TIMI risk score successfully stratified an unselected cohort of CP patients with respect to 30 day outcomes, with a range of 2.1% for a score of 0 to 100% for a score of 7

Highest correlated indicator for adverse outcome was positive cardiac biomarker at admission

Prospective observational cohort study evaluating the utility of the TIMI risk score in a broad ED CP population of 1481 patients

30 day outcomes were death, MI, revascularization

Incidence of composite outcome was: TIMI 0, 1.7%; TIMI 1, 8.2%; TIMI 3, 8.6%; TIMI 4, 24.6%; TIMI 5, 37.5%; TIMI 6, 33.3%

This relationship was highly significant Failed to stratify patients into discrete groups Patients with a score of 0 still have an incidence

of adverse events of 1.7%

2007 Guidelines make the following recommendations Nondiagnostic ECGs should be repeated every

15-30 minutes in patients with symptoms and a high clinical suspicion of ACS

Cardiac troponins are considered the preferred biomarker and should be repeated at 8-12 hours if negative at 6 hours

Algorithms and models may be useful in standardizing the approach, but should not replace clinical judgement

54 y/o female, arrives to the ED with 2 hours of exertional CP radiating to the Rt shoulder

No previous cardiac history, only risk factors if + family history

ECG demonstrates STD inferiorly Initial TnT comes back at 0.9 ng/mL The nurses have given ASA and nitro, and

ask you if you want to give plavix?

Should all patients with ACS (UA/NSTEMI/STEMI) get plavix?

ASA Multiple RCTs have demonstrated the benefits

of ASA ISIS-2 showed conclusively the efficacy of ASA

alone for the treatment of an MI, with an ARR for 35 day mortality of 2.4% (RRR 23%).

When combined with streptokinase, the ARR in mortality was 5.2% (RRR 42%)

There is a benefit if given early

Thienopyridine derivative that inhibits ADP action on platelet receptors, blocking platelet activation and aggregation

600 mg achieves irreversible platelet inhibition in 2 hours, 300 mg by 4-6 hours, and 75 mg by 3-4 days

CURE, CAPRIE, and COMMIT Trials have evaluated the use of clopidogrel in ACS

CAPRIE studied clopidogrel vs ASA in over 19,000 patienst with ACS; patients on plavix had a 9% RRR (NNT 196) over ASA, and may be used in lieu of ASA if needed

CURE trial Over 12,000 patients randomized to receive

plavix (300 mg loading dose + 75 mg daily) and ASA or ASA alone for a mean of 9 months

Patients were high risk for ACS/NSTEMI Primary composite outcome of death from

CV cause, MI, stroke Results: 20% RRR (2.1% ARR = NNT 48) for

combined primary end point Higher risk of major (non-fatal) bleeding with

plavix (NNH 100)

Benefit was seen within 24 hours (dose early)

Oral loading dose rapidly effective

A subset of the CURE trial of patients with NSTEMI undergoing PCI

Benefit of early treatment with plavix in patients undergoing PCI

ARR 3.8%, NNT 26 of composite end point (CV death, MI, need for revascularization)

RCT of over 45,000 patients seen within 24 hours of suspected MI (LBBB, STE, STD)

Randomized to plavix 75 mg daily or placebo (all patients received ASA); no loading dose

Primary composite outcome of death, MI, stroke

ARR of 0.9% and NNT 111 for composite end point

Small but significant risk of minor bleeding Benefits are independent of other standard

treatments (lytics) Plavix in the ED prevents about 10 deaths,

reinfarctions or strokes for every 1000 patients treated

Studies have demonstrated a benefit to an early loading dose

All patients enrolled have been high risk for ACS (TIMI > 4, positive markers, ECG changes)

Guidelines recommend 300mg plavix loading dose in ED if high risk ACS, or suspected ACS with contraindications to ASA

Best to hold if going to CABG, but studies are inconclusive for increased risk of major bleeding

Benefit of therapy outweighs likelihood of going to CABG in most cases

Should we give this patient (NSTEMI) UFH or LMWH? What if they are over 75 years of

age? Or have renal failure? Or have a STEMI?

Several studies have evaluated the role of heparin in STEMI and UA/NSTEMI and as an adjunct to revascularization

Although the evidence for heparin is weak (Cochrane review found only decreased risk of MI and similar risk of mortality or revascularization), it is the standard of care for ACS

In the last 10 years, many trials have tried to answer the question of which heparin to use, beginning with ESSENCE

ESSENCE demonstrated a benefit to enoxaparin over UFH in over 3000 patients with high likelihood ACS in reducing recurrent ischemic events, which was offset by an increase in the risk of minor bleeding

Compared UFH with enoxaparin for over 10,000 NSTEMI patients who were to be treated with an early invasive strategy

Patients with a Cr clearance of <30 mL/min were excluded

30 day composite end point of death or MI Primary efficacy endpoint failed to show superiority

of enoxaparin, although noninferiority criteria were satisfied

There was excess bleeding (not clinically significant) in the enoxaparin group, some of which was attributable to crossover from one to the other

Patients who received only enoxaparin (not intention to treat) had better outcomes at 6 months; at 12 months mortality between the groups was similar

To assess the effects of LMWH compared to UFH for ACS (UA/NSTEMI)

7 studies involving over 10,000 people No difference in overall mortality LMWH showed reduced recurrence of MI and

the need for revascularization procedures No difference in recurrent angina, major

bleeds, or minor bleeds; there was a decrease in the incidence of HIT

125 patients have to be treated with LMWH to prevent 1 MI, and 50 have to be treated to prevent 1 revascularization procedure

Cochrane Database of Systematic Reviews 2003

The ExTRACT-TIMI 25 trial (2006) was an international double blind comparison of enoxaparin vs UFH in over 20,000 patients with STEMI for whom lytics were planned

Dosing regimens were altered for those over 75 and those with reduced renal function

Primary endpoint of death or non-fatal MI occurred in 12% of those with UFH and 9.9% of those with LMWH; there was a small increase in major bleeding in the LMWH group, but not ICH (NNT = 48)

Among patients who underwent PCI within 30 days, the primary endpoint occurred in 10.7% of those receiving LMWH and 13.8% of those receiving UFH

A recent meta-analysis of UFH vs enoxaparin in over 49,000 patients across the ACS spectrum

Primary end point was death, MI, or major bleeding at 30 days

Death or MI was significantly reduced by enoxaparin (9.8% vs 11.4%)

Major bleeding was significantly higher with enoxaparin (4.3% vs 3.4%)

Net clinical end point was significantly lower with enoxaparin (12.5% vs 13.5%); ie. Increase in major bleeding was offset by decrease in death or MI

The net clinical endpoint was significant among STEMI trials but not NSTEACS trials, although there was a significant reduction in death or MI among NSTEACS

Heparin and enoxaparin continue to be I-A level recommendations for UA/NSTEMI, whether the patient is treated with an early invasive strategy or a selectively invasive strategy

Enoxaparin is now the recommended treatment for patients with STEMI receiving lytics (superior efficacy, no increased risk of ICH)

There is not enough data to make a recommendation for patients undergoing primary PCI, however that is the standard of practice here

New recommendations for dosing from the ExTRACT trial 30 mg IV bolus followed by 1 mg/kg Q 12 h If older than 75, omit bolus and administer 0.75 mg/kg Q

12h If Cr Clearance < 30 mL/min, change to Q 24 hours dosing

Should we give this patient (or all patients with ACS) beta blockers?

In the first few hours of onset of STEMI, beta-blockers may diminish myocardial oxygen demand, heart rate, BP, and myocardial contractility, augmenting perfusion to the ischemic myocardium by prolonging diastole

Large early trials (ISIS-2, TIMI-II) suggested a benefit of IV beta-blockers, particularly on recurrent MI and possibly on mortality

However, data from the recent COMMIT trial challenges these findings

Randomized over 45,000 patients within 24 hours of symptoms onset to receive up to three 5 mg doses of IV metoprolol within 15 minutes, followed by 60 mg PO Q 6 h

Primary outcome was all-cause mortality or composite of death, MI, cardiac arrest

Patients undergoing primary PCI excluded No improvement in primary outcome For every 1000 patients treated, there were 5 fewer

reinfarctions and 5 fewer episodes of VF at the expense of 11 additional episodes of cardiogenic shock

This was observed within the first 48 hours of treatment, in close temporal proximity to the IV treatment; reductions in MI and arrythmia occurred later

Relative increased risk of cardiogenic shock was 30%, and were higher in patients > 70, SBP <120, HR > 110 , Killip Class >I

Guidelines similar for STEMI and NSTEACS IV beta-blockers should only be considered ED

therapy in patients with hypertension +/- tachycardia, or in patients who have pain unrelieved by nitrates

Otherwise, oral beta-blockade therapy is recommended to be initiated within the first 24 hours

Contraindications to beta-blockers: Signs of heart failure of low-output state Increased risk of cardiogenic shock (age >70, SBP <120,

HR >110 or <60) Heart block (first through third degree) Reactive airway disease

54 y/o male with known CAD presents to the ED with 45 minutes of CP radiating to left arm

Feels SOB, slightly diaphoretic BP 155/82, HR 110, RR 22, SpO2 96% Exam otherwise normal

The cath lab has an unstable crashing patient on the table, and don’t think they can get to your patient for another hour

How do you want to manage this patient?

Expeditious restoration of flow in the obstructed artery is a key determinant of both short and long term outcomes, and is associated with improved survival

This effect is seen regardless of which method of reperfusion is chosen

Time from onset of symptoms is an important predictor of outcome

Fibrinolytics can dramatically reduce mortality if given within the first 2 hours from onset of symptoms; in some centres, pre-hospital fibrinolysis reduces treatment delays by 1 hour and reduces mortality by 17%

For PCI, time from symptoms onset to balloom inflation is significantly correlated with 1-year mortality; the RR equals 1.08 for each 30 minute delay

It is well established based on large controlled clinical trials that lytics provides a survival benefit

An overview of 9 trials of fibrinolytic therapy vs controls demonstrated a highly significant 18% risk reduction in 35-day mortality (9.6% for lytics vs 11.5% for controls), which corresponds to a reduction of 18 deaths per 1000 treated (NNT 52) when data from all groups are pooled (ICH risk 1% for tPA)

There is a decline of 1.6 lives per 1000 patients treated for every 1-hour delay

In patients with STD, the was an increased risk of mortality (7.4% vs 4.9% for conservative Tx)

The mortality benefit of fibrinolytic therapy diminishes as duration from symptom onset increases: 0-1 h: 65 lives saved

per 1000 pts Rx 1-2 h: 37 lives saved 2-3 h: 26 lives saved 2-6 h: 29 lives saved

Effect of fibrinolysis on 35 d mortality

Boersma et al. Lancet 1996;348:771

Adjusted probability of death or cerebral bleeding in patients >75

At 30 days, this was 23% vs 32% and at 1 year 26% vs 36% for those treated with lytics vs not

At 1 year, this is a RRR of 13% and an ARR of 4% (NNT = 25)

Class I In the absence of contraindications, fibrinolytic

therapy should be administered to STEMI patients with symptoms onset within the prior 12 hours and STE > 0.1 mV in at least 2 contiguous precordial leads or 2 adjacent limb leads

In the absence of contraindications, fibrinolytics should be administered to STEMI patients with symptom onset in the prior 12 hours and a new or presumed new LBBB

The 9 studies analyzed in the Fibrinolytic Therapy Trialists Collaborative Group defined STE as > 1mm STE in 2 or more limb leads and > 2mm STE in 2 or more precordial leads

Absolute Any prior ICH Known structural

cerebral vascular lesion Brain tumour Ischemic CVA within

the last 3 months (EXCEPT within 3 hours)

Suspected aortic dissection

Active bleeding diathesis (not menses)

Signigicant head or facial trauma within 3 months

Relative Hx of chronic, severe,

poorly controlled HTN SBP > 180, DBP > 110 Prior ischemic CVA > 3

months, dementia, or known intracranial pathology

Trauma, CPR (>10 min), or major surgery within 3 wk

Recent internal bleeding (2-4 weeks)

Pregnancy Active PUD Current use of

anticoagulents

Do you give this patient lytics, or do you wait an hour for the cath lab?

PCI is successful in achieving TIMI 3 flow in 70-90% of patients

Has been compared to fibrinolytics in 22 randomized clinical trials, plus the SHOCK trial

These studies demonstrated that PCI-treated patients have lower short-term mortality rates (5% vs 7%), less reinfarction (3% vs 7%), and less hemorrhagic stroke (0.05% vs 1%) than those treated with lytics; combine end point was better overall for PCI (8% vs 14%)

Much of the superiority of primary PCI is driven by a reduction in the rate of non-fatal MI

The mean time delay for primary PCI in the RCTs was 40 minutes

However, there is concern that routine policies of primary PCI may result in unacceptable delays to treatment

An analysis of the RCTs that compares PCI to lytics suggests that the mortality benefit with PCI exists only if treatment is delayed by no more than 60 minutes

In PRAGUE-2, in the subset of patients presenting within 3 hours of symptoms, there was no mortality benefit for PCI (although PCI was better overall)

In CAPTIM, patients treated within 2 hours of symptom onset had better outcomes with pre-hospital tPA vs transfer for primary PCI (trend toward reduced mortality)

Both studies showed that PCI was better than lytics if symptom duration was greater than 2-3 hours

Class I If immediately available, primary PCI should

be performed as quickly as possible with a goal of medical contact to balloon time of 90 minutes (vs goal door to needle time of 30 minutes)

If symptoms duration is within 3 hours and door to needle time is: Within 1 hour – primary PCI preferred > 1 hour – fibrinolytic therapy is preferred

If symptom duration time is > 3 hours, primary PCI is generally preferred

Just as you’re about to order TNK, the patient suddenly becomes hypotensive and appears to be in respiratory distress

BP is 74/50, HR 125,SpO2 86%, CXR demonstrates pulmonary edema

You cautiously intubate(!) and line this patient, judiciously provide fluids, and start him on dopamine

Will you give TNK now?

302 patients with STEMI and LV dysfunction randomized to emergency revascularization within 6 hours (angioplasty, CABG, +/- IABP) or medical stabilization (+/- lytics, +/- IABP)

There was a non-significant 9% ARR in 30 day mortality with revascularization overall

The benefit was larger and statistically significant for those < 75 (subgroup analysis)

The overall mortality was significantly reduced at 6 months in patients who underwent revascularization

Class I Primary PCI should be performed for patients

<75 with STEMI or LBBB who develop shock within 36 hours of MI

Primary PCI should be performed in patients with severe CHF (Killip class 3) and onset of symptoms within 12 hours

Class II Primary PCI should be considered for those

>75 and shock It is reasonable to perform primary PCI for

patients with onset of symptoms within 12-24 hours

Fibrinolysis is generally preferred if Early presentation

(<3 hours) and delay to PCI

PCI not available Delay to invasive

strategy [Door to balloon] –

[Door to needle] >1hr Presentation to balloon

time > 90 minutes

PCI generally preferred if Skilled PCI lab

available with surgical back-up

High-risk patient Cardiogenic shock Killip class 3 or

greater Contraindications to

fibrinolysis Late presentation Diagnosis in doubt

You are the REP on call and receive a call from Golden about a 57 y/o male with an anterior STEMI who “failed TNK”

His onset of symptoms was 10:00, and he was treated with fibrinolytics at 14:45 (within 30 minutes of presentation to hospital)

It is now 1600h and the patient is having ongoing symptoms with no resolution of his STE on the ECG

What is the definition of “failed fibrinolysis” and does this patient require “Rescue PCI”?

Fibrinolysis is successful in restoring TIMI 2/3 flow in 50-85% of patients

If ST segment elevation in the lead showing the greatest degree of STE has not resolved by at least 50% 90 minutes after administration of a lytic, fibrinolysis is considered to have failed

Resue (salvage) PCI is defined as PCI within 12 hours after failed fibrinolysis for patients with continuing or recurrent ischemia

The RESCUE trial demonstrated a reduction in in-hospital mortality in patients with anterior STEMI who failed fibrinolytic therapy, when PCI was performed within 8 hours of symptoms

Rescue PCI after fibrinolytic therapy is recommended in the following circumstances: Patients in cardiogenic shock < 75 Patients with severe heart failure Patients with hemodynamically compromising

ventricular dysrhythmias It is reasonable to perform resuce PCI if:

Patients in cardiogenic shock >75 Patients with persistent symptoms, or

hemodynamic or electrical instability Patients in whom lytics have failed and a moderate

to large area of myocardium is at risk

What are the complications of an MI?

CHF Cardiogenic shock Arrythmias Heart blocks Reperfusion arrythmias Acute MR Ventricular wall rupture and tamponade VSD LV aneurysm Thromboembolism Post-MI pericarditis

THE END!