Dr . Ranjith MP

14-11-2011

Definition of MI

Risk stratification

Medical management

(Myocardial infarction redefined—a consensus document of The Joint European Society of Cardiology/American College of Cardiology committee for the redefinition of myocardial infarction:. J. Am. Coll. Cardiol. 2000;36;959-969)

Criteria for Acute, Evolving, or Recent MI Either of the following criteria satisfies

1. Typical rise &/or fall of biochemical markers of myocardial necrosis with at least one of the following:a) Ischemic symptoms

b) ECG changes indicative of new ischemia (new ST elevation ornew/presumed to be new LBBB)

c) Development of pathological Q waves in the ECG

d) Imaging e/o new loss of viable myocardium or new RWMA

2. Pathologic findings of an acute MI

(Myocardial infarction redefined—a consensus document of The Joint European Society of Cardiology/American College of Cardiology committee for the redefinition of myocardial infarction:. J. Am. Coll. Cardiol. 2000;36;959-969)

PCI periprocedural MI:

increases of biomarkers >3 x 99th percentile URL

CABG-related MI

Increases of biomarkers >5 x 99th percentile URLplus either new pathological Q waves or new LBBB,or angiographically documented new graft or nativecoronary artery occlusion, or imaging evidence ofnew loss of viable myocardium.

(Myocardial infarction redefined—a consensus document of The Joint European Society of Cardiology/American College of Cardiology committee for the redefinition of myocardial infarction:. J. Am. Coll. Cardiol. 2000;36;959-969)

Criteria for established MI.Either of the following criteria satisfies

1. Development of new pathologic Q waves on serial ECGs. The patient may or may not remember previous symptoms. Biochemical markers of myocardial necrosis may have normalized, depending on the length of time that has passed since the infarct developed.

2. Pathologic findings of a healed or healing MI.

There is risk stratification within STEMI,but in general, STEMI is high-risk

Important to select greater-risk patientswho warrant more aggressive strategiesfor prevention of future serious eventssuch as reinfarction or sudden death

Occurs in several stages

Initial presentation

In-hospital course (CCU, intermediate CU)

At the time of hospital discharge

Prior angina pectoris

Prior MI

Female gender

Hypertension

History of CHF

Hyperlipidemia

Diabetes

ECG Criteria

Markedly elevated cardiac enzymes

Elevated BUN

Complications

VSR/PMD-rupture

Myocardial rupture

Anterior MI/ Persisting ST elevation

Q waves in multiple leads

RVMI + IWMI

High sum of ST elevation

Reciprocal ( anterior ) ST depression

Persisting ST depression

Prolonged QT

Conduction defects/ heart block

Sinus tachycardia/atrial fibrillation

Killip Classification % patients Mortality (%)

I No CHF 30-50 5

II Rales, S3, Pulmonary venous hypertension 33 15-20

III Pulmonary edema 15 40

IV Cardiogenic shock 10 80-100

(Killip T, and Kimball JT: Treatment of myocardial infarction in a coronary care unit: a two year experience of 250 patients. American Journal of Cardiology 1967; 20: 457-464 )

Left ventricular dysfunction is the single most important predictor of mortality

TIMI

GRACE

PURSUIT

ACI-TIPI

Goldman

best used to supplement—not replace—clinical judgment

less useful in atypical presentations, but indeed validated in an ED population . . .

(David A et al. TIMI Risk Score for ………..: An Intravenous nPA for Treatment of Infarcting Myocardium Early II Trial Substudy. Circulation 2000, 102:2031-2037)

(David A et al. TIMI Risk Score for ………..: An Intravenous nPA for Treatment of Infarcting Myocardium Early II Trial Substudy. Circulation 2000, 102:2031-2037)

( Wiviott SD et al Performance of the TRI in the National Registry of Myocardial Infarction-3 and -4:. J Am Coll Cardiol

2004;44:783–9 )

Derived from In TIME II trial & validated in TIMI-9 trials

Based on age and vital signs, in predicting mortality among a large, community based, unselected, heterogeneous population

Heart rate [age/10 ]2 /systolic blood pressure

A strong and independent predictor of mortality at 24 h and at 30 days (p 0.0001)

Can be used to predict the cumulative risk of death and death or myocardial infarction in the period from admission to hospital to six months after discharge

The tool is simple and applicable to patients across the complete spectrum of acute coronary syndrome

Exercise Testing performed either in the hospital or early after discharge in

patients not selected for cardiac catheterization andwithout high-risk features to assess the presence andextent of inducible ischemia Class I (B)

Exercise testing might be considered before discharge ofpatients recovering from STEMI to guide the post dischargeexercise prescription or to evaluate the functionalsignificance of a coronary lesion previously identified atangiography Class IIb (C)

Sub maximal protocolTarget workload =5 METS, 70 % MPHR or symptom

limited

Predictors of poor outcome Ischemic ST depression > 1 mm is inconsistent

predictor of mortality

poor exercise tolerance < 3 minutes doubles one year mortality ( 7% to14%)

Inability to exercise or contra-indication to TMT identifies High Risk patient.

Late Risk Stratification - 4 to 8 weeks(Assessment of residual ischaemia)

TMT

Stress echocardiography

Adenosine/Dipyridamole Perfusion imaging Un-interpretable ECG

Equivocal TMT

Inability to exercise

Prehospital EMS providers …162 to 325 mgof aspirin (chewed) …non–enteric-coatedformulations.

(goal is to quickly block thromboxane A2 formation in platelets)

Previously on NTG take I tab S/L Not improving after 5 mts Seek medical help

EMS Transport

Onset of symptoms of

STEMI

EMSDispatch

EMS on-scene• Encourage 12-lead ECGs.• Consider prehospital fibrinolytic if

capable and EMS-to-needle within 30 min.

GOALS

PCIcapable

Not PCIcapable

Hospital fibrinolysis:

Door-to-Needle

within 30 min.

Inter-HospitalTransfer

Golden Hour = first 60 min. Total ischemic time: within 120 min.

Patient EMS Prehospital fibrinolysisEMS-to-needlewithin 30 min.

EMS transportEMS-to-balloon within 90 min.

Patient self-transportHospital door-to-balloon

within 90 min.Dispatch

1 min.

5 min.

8 min.

Early presentation (≤3 hr from symptom onset and delay to invasive strategy)

Invasive strategy is not an option Catheterization laboratory occupied or not available

Vascular access difficulties

Lack of access to a skilled PCI laboratory

Delay to invasive strategy Prolonged transport

(Door-to-balloon)–(door-to-needle) more than 1 hr

Medical contact-to-balloon or door-to-balloon more than90 min

Skilled PCI laboratory is available with surgical backup

Medical contact-to-balloon or door-to-balloon less than 90 min

High risk from STEMI

Cardiogenic shock

Killip class ≥ 3

Contraindications to fibrinolysis

Late presentation (> 3 hr)

Diagnosis of STEMI is in doubt

1. Airway, Breathing, Circulation (ABC)

2. Vital signs, general observation

3. Presence or absence of jugular venous distension

4. Pulmonary auscultation for rales

5. Cardiac auscultation for murmurs and gallops

6. Presence or absence of stroke

should be performed, but should not delay the implementation of reperfusion therapy.

Serum biomarkers for cardiac damage

Complete blood count (CBC) with platelets

International normalized ratio (INR)

Activated partial thromboplastin time (aPTT)

Electrolytes and magnesium

Blood urea nitrogen (BUN),creatinine

Glucose

Complete Lipid Profile

0 1 2 3 4 5 6 7 8

Cardiac troponin-no reperfusion

Days After Onset of STEMI

Mu

ltip

les

of

the

UR

L

Upper reference limit1

2

5

10

20

50

URL = 99th %tile of Reference Control Group

100

Cardiac troponin-reperfusion

CKMB- reperfusion

CKMB- no reperfusion

Pain contribute to the heightened sympathetic activity

Typically accomplished with combination of nitrates, analgesics, oxygen and β-blockers

Oxygen

Arterial oxygen desaturation (SaO2 < 90%) Class I(B)

Uncomplicated STEMI during the first 6 hours Class II(A)

Nitroglycerin Class I (C)

Patients with ongoing ischemic discomfort

0.4 mg every 5 minutes for a total of 3 doses

Intravenous NTG

Ongoing ischemic discomfort that responds to nitrate therapy

control of hypertension

management of pulmonary congestion.

Nitrates should not be administered to patients with:

systolic pressure < 90 mm Hg or ≥ to 30 mm Hg below baseline

severe bradycardia (< 50 bpm)

tachycardia (> 100 bpm)

suspected RV infarction.

who have received a phosphodiesterase

AnalgesiaMorphine sulfate (2 to 4 mg intravenously) Class I (C)

NSAIDS Increase risk of cardiovascular events so should be discontinued

[A sub study analysis from the ExTRACT TIMI-25 trial showed increased risk of death, reinfarction, heart failure, or shock among patients on NSAIDswithin 7 days of enrollment].

AspirinShould be chewed by patients who have not taken aspirin

before presentation with STEMI. The initial dose should be 162 mg Class I (A) to 325 mg. Class I (C)

The principal goal of fibrinolysis is prompt restoration of full IRA patency

Streptokinase , tPA,, TNK, rPA

TNK and rPA - bolus fibrinolytics

Promote conversion of plasminogen to plasmin, which subsequently lyses fibrin thrombi

Absolute Contraindications:Any prior intracranial hemorrhage

Known structural cerebral vascular lesion

Known malignant intracranial neoplasm

Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hours

Suspected aortic dissection

Active bleeding or bleeding diathesis (excluding menses)

Significant closed-head or facial trauma within 3 months

Note: Age restriction for fibrinolysis has been removed compared with prior guidelines.

Relative Contraindications:Severe uncontrolled hypertension on presentation (SBP > 180

or DBP > 110)

Prior ischemic stroke >3 months

Traumatic or prolonged (> 10 mt.) CPR or major surgery (< 3 weeks)

Recent (< 2 to 4 weeks) internal bleeding

Noncompressible vascular punctures

For streptokinase/anistreplase: prior exposure (> 5 days ago) or prior allergic reaction to these agents

Pregnancy, Active peptic ulcer

Current use of anticoagulants

(Antman EM et al: ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction. Circulation 110:e82, 2004.)

PARAMETER STREPTOKINASE ALTEPLASE RETEPLASE TNK t-PA

Dose 1.5 MU in 30-60 minUp to 100 mg in 90 min (based on weight)

10 U ? 2 (30 min apart) each over 2 min

30-50 mg based on weight

Bolus administration No No Yes Yes

Antigenic Yes No No No

Allergic reactions hypotension most common

Yes No No No

Systemic fibrinogen depletion

Marked Mild Moderate Minimal

90-min patency rates (%)

≈50 ≈75 ≈75 ≈75

TIMI grade 3 flow (%) 32 54 60 63

Cost per dose (Rs) 2500 39375 (50mg)

WP-4 hr. t-PA is the preferred treatment

streptokinase t-PA equivalent choices -risk of death is low , and increased risk of ICH .

WP-4 to 12 hr . streptokinase and t-PA are equivalent options, but streptokinase is probably preferable to t-PA because of cost considerations

LATE and EMERAS trials

Fibrinolytics between 12 and 24 hours

No mortality benefit

Increases risk of cardiac rupture

Noninvasive findings s/o reperfusion include:

Relief of symptoms

Maintenance and restoration of hemodynamicand/or electrical instability

Reduction of ≥ 50% of the initial STE pattern onfollow-up ECG 60 to 90 minutes after initiation oftherapy.

Class II(A)

Flow in the IRA angiographically

Gd. 0, compl. Occlussion

Gd. 1, some penetration

Gd.2, entire vessel with

Impaired flow

Gd.3, entire vessel with

Normal flow

Prevention of DVT, pulmonary embolism, ventricular thrombus, cerebral embolization.

Establishing & maintaining patency of IRA.

Trials shown that more prolonged anticoagulant therapy is beneficial (duration of index hospita-lization) in patients receiving thrombolytic therapay

IV Unfractionated Heparin Selective Fibrinolytic – Bolus of 60 U/kg (maximum 4000 U)

followed by an infusion of 12 U/kg/hr (maximum 1000 U)

(Level of Evidence: C)

Nonselective fibrinolytic agents- who are at high risk for systemic emboli (large or anterior MI, atrial fibrillation (AF), previous embolus, or known LV thrombus).

(Level of Evidence: B)

LMWH- 30mg iv followed by 1mg/kg every 12hr.

Aspirin should be given indefinitely to all STEMI pts. without a true aspirin allergy.

Class I (A)

Patients undergoing PCI are also given aspirin loading

Class I (B)

Patients not on aspirin therapy should be given nonenteric aspirin 325 mg before PCI.

Class I(B)

After PCI, use of aspirin should be continued indefinitely

Class I (A)

Addition of P2Y12 inhibitor to aspirin warranted for most patients with STEMI (COMMIT & CLARITY-TIMI22)

In patients for whom PCI is planned, clopidogrel should be started and continued: Class I (B)

Patients receiving a stent (BMS or DES) clopidogrel 75 mg daily or prasugrel 10 mg for at least 12 months;

If the risk of bleeding outweighs the anticipated benefit afforded by thienopyridine therapy, earlier discontinuation .

Continuation of thienopyridines beyond 15 months may be considered in patients undergoing DES placement

Prior history of stroke and TIA for whom primary PCI is planned, prasugrel is not recommended

CABG planned ?... the drug should be withheld for at least 5 days in patients receiving clopidogrel and at least 7 days in patients receiving prasugrel, Class I (B)

Probably indicated in patients receiving fibrinolytictherapy who are unable to take aspirin because ofhypersensitivity or GI intolerance Class I (C)

It is reasonable to start abciximab as early as possible before primary PCI (with or without stenting) in patients with STEMI.

Tirofiban or eptifibatide may be considered before primary PCI (with or without stenting) in patients with STEMI.

Relieve ischemic pain, reduce need for analgesics, reduce infarct size and life-threatening arrhythmias

Contra indications:

signs of heart failure

evidence of a low output state

increased risk for cardiogenic shock

other relative contraindications (PR interval > 0.24 S. 2nd or 3rd degree AV block, or reactive airway disease)

Favorable effects with metoprolol, atenolol,carvedilol and timolol,

Beta blockers with intrinsic sympathomimeticactivity probably should not be chosen.

Trial of esmolol in the presence of relativecontraindications.

Favorable impact on ventricular remodeling, improvement in hemodynamics, and reductions in congestive heart failure

Angiotensin-converting enzyme inhibitors

Angiotensin II receptor blockers

Aldosterone blockade

EPHESUS trial: Eplerenone, 25 mg/day titrated to 50 mg/day for high-risk patients following STEMI (EF ≤40%, clinical HF, DM)

Mean follow-up 16 months, there was a 15% reduction in the RR of mortality

Immediate-release preparation of nifedipine increased risk of in-hospital mortality

Verapamil & diltiazem can be given for relief of ongoing ischemia or slowing of a rapid ventricular response in AF in patients with contraindication to beta blockers.

INTERCEPT trial compared 300 mg of diltiazem with placebo and Diltiazem did not reduce cardiac death, nonfatal reinfarction, during a 6-month follow-up

It is reasonable to use an insulin based regimen toachieve and maintain glucose levels less than 180mg/dl while avoiding hypoglycemia for patientswith STEMI with either a complicated oruncomplicated course Class IIa(B)

In the absence of complications patients need not be confined to bed for more than 12 hours

Progression of activity should be individualized

first day and as late as 6 weeks after STEMI

Radiation of the pain to either trapezius ridge.

Treatment consists of aspirin doses of 650 mg orally every 4 to 6 hours may be necessary.

NSAIDs and steroids should be avoided

Anticoagulation- heparin to elevate the aPTT to 1.5 to 2 times that of control, followed by a minimum of 3 to 6 months of warfarin in the following clinical situations:

An embolic event has already occurred or

The patient has a large anterior infarction whether or not a thrombus is visualized echocardiographically

More in older patients, women , hypertensive

More frequently in the left than right ventricle

1 day and 3 weeks, most commonly 1 to 4 days

Near the junction of infarct and normal muscle

Most often in patients without previous infarcts

Fibrinolytic therapy more than PCI

CATEGORY ARRHYTHMIA OBJECTIVE OF TREATMENTTHERAPEUTIC OPTIONS

Electrical instability

Ventricular premature beats

Correction of electrolyte deficits and increased sympathetic tone

Potassium and magnesium solutions, beta blocker

Ventricular tachycardia

Prophylaxis against ventricular fibrillation, restoration of hemodynamic stability

Antiarrhythmic agents; cardioversion/defibrillation

Ventricular fibrillation

Urgent reversion to sinus rhythmDefibrillation; bretylium tosylate

Accelerated idioventricular rhythm

Observation unless hemodynamic function is compromised

Increase sinus rate (atropine, atrial pacing); antiarrhythmic agents

Nonparoxysmal atrioventricular junctional tachycardia

Search for precipitating causes (e.g., digitalis intoxication); suppress arrhythmia only if hemodynamic function is compromised

Atrial overdrive pacing; antiarrhythmic agents; cardioversion relatively contraindicated if digitalis intoxication present

CATEGORY ARRHYTHMIAOBJECTIVE OF TREATMENT

THERAPEUTIC OPTIONS

Pump failure, excessive sympathetic stimulation

Sinus tachycardia

Reduce heart rate to diminish myocardial oxygen demands

Antipyretics; analgesics; consider beta blocker unless congestive heart failure present; treat latter if present with anticongestive measures (diuretics, afterload reduction)

Atrial fibrillation and/or atrial flutter

Reduce ventricular rate; restore sinus rhythm

Verapamil, digitalis glycosides; anticongestive measures (diuretics, afterload reduction); cardioversion; rapid atrial pacing (for atrial flutter)

Paroxysmal supraventricular tachycardia

Reduce ventricular rate; restore sinus rhythm

Vagal maneuvers; verapamil, cardiac glycosides, beta-adrenergic blockers; cardioversion; rapid atrial pacing

CATEGORY ARRHYTHMIA OBJECTIVE OF TREATMENTTHERAPEUTIC OPTIONS

Bradyarrhythmias and conduction disturbances

Sinus bradycardia

Acceleration of heart rate only if hemodynamic function is compromised

Atropine; atrial pacing

Junctional escape rhythm

Acceleration of sinus rate only if loss of atrial “kick” causes hemodynamic compromise

Atropine; atrial pacing

Atrioventricular block and intraventricular block

Insertion of pacemaker

At time of discharge patient should be on:

ASA unless contra-indication

Clopidogrel if PCI/NSTEMI (duration minimum1 year)

Longer duration of clopidogrel if DES in critical location or complex lesion

-blocker unless contra-indication

ACE inhibitor for CHF or LV dysfunction

All for vascular protection?

Statin for LDL to < 70mg%(minimum 50% reduction)

High Risk extensive ECG changes

anterior/ infero-posterior/ prior MI

Residual ischaemia post MI angina

positive TMT/ perfusion scan

non-Q MI

ischaemia at a distance

Complicated MI CHF/ flash pulmonary

edema

shock

heart block

RBBB

sustained ventricular arrhythmias

Anxiety/ physical labor/ young age

Smoking Goal: Complete Cessation

With in 2yrs risk of nonfatal MI falls to normal

Blood pressure control:

Goal: < 140/90 mm Hg or <130/80 mm Hg if chronic kidney disease or diabetes

Physical activity:

Minimum goal: 30 minutes 3 to 4 days per week; Optimal daily

Weight management: Goal: BMI 18.5 to 24.9 kg/m2

Waist circumference: Women < 35 in. Men: < 40 in.

Diabetes management: Goal: HbA1c < 7%

Lipid management: Primary goal: LDL-C <70mg% Start dietary therapy in all patients (< 7% of total calories as

saturated fat and < 200 mg/d cholesterol). Promote physical activity and weight management. Encourage increased consumption of omega-3 fatty acids.

Assess fasting lipid profile in all patients, preferably within 24 hours of STEMI. Add drug therapy according to the following guide:

LDL-C < 100 mg/dL (baseline or on treatment): Statins should be used to lower LDL-C.

LDL-C ≥ 100 mg/dL (baseline or on treatment): Intensify LDL-C–lowering therapy with drug treatment, giving preference to statins.

If TGs are ≥ 150 mg/dL or HDL-C is < 40 mg/dL: Emphasize weight management and physical activity. Advise smoking cessation.

If TG is 200 to 499 mg/dL: After LDL-C–lowering therapy, consider adding fibrate or niacin.

If TG is ≥ 500 mg/dL: Consider fibrate or niacin before LDL-C–lowering therapy.

Consider omega-3 fatty acids as adjunct for high TG.

Hormone therapy: with estrogen plus progestin should not be given de novo to postmenopausal

women after STEMI for secondary prevention of coronary events. Class III (A)

Postmenopausal women who are already taking estrogen plus progestin at the time of STEMI should not continue hormone therapy. Class II (B)

However, women who are beyond 1 to 2 years after initiation of hormone therapy who wish to continue such therapy for another compelling indication should weigh the risks and benefits. Class III (A)

Antioxidant vitamins:

such as vitamin E and/or vitamin C supplements should not be prescribed to

patients recovering from STEMI to prevent cardiovascular disease

Psychosocial status of the patient should be evaluated, including inquiries regarding symptoms of depression, anxiety, or sleep disorders and the social support environment. Class I (C)

Treatment with cognitive-behavioral therapy and selective serotonin reuptake inhibitors can be useful for STEMI patients with depression that occurs in the year after hospital discharge. Class IIa (A)

RRR 2yr Event Rate

None 8%

ASA 25% 6%

-Blockers 25% 4.5%

Lipid lowering 30% 3.0%

ACE-inhibitors

25% 2.3%

( Yusuf, S. Two decades of progress in preventing vascular disease. Lancet 2002; 360: 2-3).

Cumulative relative risk reduction if all four drugs are used is about 75%