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

Acute Coronary syndromes

Yael Moussadji

Aug 21, 2008


Objectives

Objectives

  • Diagnosis of ACS in the ED

  • Risk Stratification

    • Cardiac markers

    • ECG

    • Risk Scores

  • Management

    • UA/NSTEMI

    • STEMI

  • Complications


Pathophysiology

Pathophysiology


Definitions

Definitions


Case 1

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

Question 1

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


Acute coronary syndromes

  • 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

Results


Acute coronary syndromes

ROC


Conclusions

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

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

Question 2

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


Acute coronary syndromes

  • 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


Acute coronary syndromes

AMI


Acute coronary syndromes

ACS


Conclusions1

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

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


Acute coronary syndromes

ECG


Case 3 continued

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

ECG at 24 hours


Question 3

Question 3

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


Definitions1

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

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

ECG Changes


Causes of st elevation

Causes of ST Elevation


Acute coronary syndromes

  • 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

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 depression a high risk finding

GUSTO 2B: ST DepressionA High Risk Finding

ST 

P  0.001

ST 

T-wave inversion

CM Gibson 2002


Ecg pearls

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

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?


Acute coronary syndromes

  • 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

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

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

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

Question 5

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


Acute coronary syndromes

  • 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

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


Acute coronary syndromes

  • 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


Acute coronary syndromes

  • 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

Other Causes of Elevated Tn


Risk stratification

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

Likelihood of ACS based on signs and symptoms


Predictors of adverse outcomes

Predictors of Adverse Outcomes


Use of risk stratification tools

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


Acute coronary syndromes

  • 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)


Results1

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


Validation and treatment effect

Validation and Treatment Effect


Application of timi risk score for ua and stemi acs to an unselected ed chest pain population

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


Acute coronary syndromes

  • 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

Risk Scores for ACS


Final comments

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

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

Question 6

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


Antiplatelet agents

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


Acute coronary syndromes

ASA


Clopidogrel

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


Acute coronary syndromes

  • 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)


Acute coronary syndromes

CURE

  • Benefit was seen within 24 hours (dose early)

  • Oral loading dose rapidly effective


Pci cure

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)


Acute coronary syndromes

  • 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

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 61

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

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


Acute coronary syndromes

  • 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


Acute coronary syndromes

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

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


Acute coronary syndromes

  • 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

Death or nonfatal MI vs net clinical end point


Bottom line1

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

Question 8

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


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


Acute coronary syndromes

  • 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 line2

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

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


Acute coronary syndromes

ECG


Question 9

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

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

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

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

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

If ICH risk >4% - PCI preferred


Aha acc indications for fibrinolytics

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

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

Question 10

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


Lytics vs pci

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

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

Time to PCI


Primary pci recommendations

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

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?


Acute coronary syndromes

  • 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 recommendations1

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 line3

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

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

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: 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

Question 11

What are the complications of an MI?


Complications of 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


Acute coronary syndromes

THE END!


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