Acute coronary syndromes
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Acute Coronary syndromes. Yael Moussadji Aug 21, 2008. Objectives. Diagnosis of ACS in the ED Risk Stratification Cardiac markers ECG Risk Scores Management UA/NSTEMI STEMI Complications. Pathophysiology. Definitions. Case 1.

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Acute Coronary syndromes

Yael Moussadji

Aug 21, 2008


Objectives

  • Diagnosis of ACS in the ED

  • Risk Stratification

    • Cardiac markers

    • ECG

    • Risk Scores

  • Management

    • UA/NSTEMI

    • STEMI

  • Complications


Pathophysiology


Definitions


Case 1

  • 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?


Question 1

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


Results


ROC


Conclusions

  • 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)


Case 2

  • 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


Question 2

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


AMI


ACS


Conclusions

  • 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


Case 3

  • 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


ECG


Case 3 continued

  • 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


ECG at 24 hours


Question 3

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


Definitions

  • 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


ECG Findings in ACS

  • In a study of adult CP patients in the ED, 1% of patients with anormal 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


ECG Changes


Causes of ST Elevation


  • 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


Prognostic Value of Admission ECG in ACS

  • 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


GUSTO 2B: ST DepressionA High Risk Finding

ST 

P  0.001

ST 

T-wave inversion

CM Gibson 2002


ECG Pearls

  • 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


Question 4

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


Missed diagnosis of ACS

  • Acute ischemia

    • Women <55

    • Non-white

    • SOB as chief symptom

    • Normal or non-diagnostic ECG

  • AMI

    • Non-white

    • Normal or non-diagnostic ECG


Conclusion

  • 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


Case 4

  • 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”


Question 5

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


Cardiac Troponin

  • 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


  • 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%


Other Causes of Elevated Tn


Risk Stratification

  • 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


Likelihood of ACS based on signs and symptoms


Predictors of Adverse Outcomes


Use of Risk Stratification Tools

  • 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)


Results

  • 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


Validation


Validation and Treatment Effect


Application of TIMI Risk Score for UA and STEMI ACS to an unselected ED chest pain population

  • 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%


Risk Scores for ACS


Final Comments

  • 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


Case 5

  • 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?


Question 6

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


Antiplatelet Agents

  • 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


ASA


Clopidogrel

  • 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)


CURE

  • Benefit was seen within 24 hours (dose early)

  • Oral loading dose rapidly effective


PCI-CURE

  • 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


Bottom Line

  • 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


Question 6

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?


Anticoagulents

  • 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


Low molecular weight heparins vsunfrctionated heparin for acute coronary syndromesMagee KD, Sevcik W, Moher D, Rowe BH

  • 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


LMWH and STEMI

  • 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


Death or nonfatal MI vs net clinical end point


Bottom Line

  • 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


Question 8

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


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


Bottom Line

  • 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


Case 6

  • 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


ECG


Question 9

  • 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?


Reperfusion in STEMI

  • 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


Fibrinolytics for STEMI

  • 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)


Time to Thrombolysis

Effect of fibrinolysis on 35 d mortality

  • 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

Boersma et al. Lancet 1996;348:771


Age > 75

  • 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)


If ICH risk >4% - PCI preferred


AHA/ACC Indications for Fibrinolytics

  • 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


Contraindications

  • 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


Question 10

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


Lytics Vs PCI

  • 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


Primary PCI

  • 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


Time to PCI


Primary PCI: Recommendations

  • 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


Case continued

  • 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


Primary PCI: Recommendations

  • 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


Bottom Line

  • 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


Case 7

  • 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”?


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: Guidelines

  • 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


Question 11

What are the complications of an MI?


Complications of 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!


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