Approach to acute coronary syndrome

transcript

Approach to Acute Coronary

Syndrome

Sujood Hussien Khraisat

Hashemite University

Myocardial ischaemia :

• Reduced blood flow due to mechanical obstruction .

• Due to decreased oxygenated Hemoglobin.

• Increased demand for oxygen .

• Myocardial ischaemia most commonly occurs as a result of obstructive coronary artery disease (CAD) in the form of coronary atherosclerosis .

Pathogenesis Of Atherosclerosis

CAD can have the following clinical presentations:• Asymptomatic

• Stable angina pectoris

• Unstable angina pectoris

• Myocardial infarction (MI)—either NSTEMI

or STEMI

• Sudden cardiac death

Acute coronary syndromes

spectrum of clinical presentations ranging from those for ST-segment elevation myocardial infarction (STEMI) to presentations found in non–ST-segment elevation myocardial infarction (NSTEMI) or in unstable angina. In terms of pathology, ACS is almost always associated with rupture of an atherosclerotic plaque and partial or complete thrombosis of the infarct-related artery.

Unstable angina and NSTEMI

CRITERIA• The diagnosis of UA is based largely on the

clinical presentation. – (1) it occurs at rest (or with minimal exertion),

usually lasting >10 min; – (2) it is severe and of new onset (i.e., within the

prior 4–6 weeks); and/or – (3) it occurs with a crescendo pattern (i.e.,

distinctly more severe, prolonged, or frequent than previously).

• The diagnosis of NSTEMI requires clinicalfeatures of UA + elevated cardiac enzymes.

USA and non–ST segment

elevation MI are often considered

together because it

is very difficult to distinguish

the two based on patient

presentation. If cardiac

enzymes are elevated, then

the patient has non–ST segment

elevation MI

History

• The severity and duration of coronary artery obstruction, the volume of myocardium affected, the level of demand, and the ability of the rest of the heart to compensate are major determinants of a patient's clinical presentation and outcome. A patient may present to the ED because of a change in pattern or severity of symptoms.

History

• Palpitations• Pain, which is usually described as pressure,

squeezing, or a burning sensation across the precordium and may radiate to the neck, shoulder, jaw, back, upper abdomen, or either arm

• Exertional dyspnea that resolves with pain or rest• Diaphoresis from sympathetic discharge• Nausea from vagal stimulation• Decreased exercise tolerance

• Elderly !

• Diabetics !

• Women !

Cardiac vs Non-Cardiac chest pain

Causes of chest pain

Physical Examination • frequently normal.

• patient will usually lie quietly in bed and may appear anxious, diaphoretic, and pale.

• Hypotension - Indicates ventricular dysfunction due to myocardial ischemia, infarction, or acute valvulardysfunction

• Hypertension - May precipitate angina or reflect elevated catecholamine levels due to anxiety or to exogenous sympathomimetic stimulation

• Diaphoresis

• Pulmonary edema and other signs of left heart failure.

• (S3) , (S4), The latter is especially prevalent in patients with inferior-wall ischemia .

• A new murmur may reflect papillary muscle dysfunction. Rales on pulmonary examination may suggest LV dysfunction or mitral regurgitation.

• May be normal.

• ST depression and T wave inversion are highly

suggestive for an ACS. The ECG should be

repeated and continuous ST-segment monitoring

is recommended if the patient is in pain.

• Transient ST elevation is seen with coronary

vasospasm or Prinzmetal’s angina.

Workup

CARDIAC BIOCHEMICAL MARKERS

• Elevated CK-MB and troponin distinguish NSTEMI

from unstable angina.

• There is a direct relationship between the degree of

troponin elevation and mortality.

• In patients without a clear clinical history of ACS,

minor troponin elevations have been reported and

can be caused by CHF, myocarditis, or PE, or they

may be false-positive readings. Thus, in patients with

an unclear history, small troponin elevations may not

be diagnostic of an ACS.

Other Investigations ?!

• CBC

• Basic metabolic profile

• CXR

Early Risk Stratification

• The first step in evaluating patients with possible UA/NSTEMI is to

determine the likelihood that CAD is the cause of the presenting

symptoms.

DIAGNOSTIC EVALUATION

• For most patients, standard treadmill ECG stress testing is

used, but for patients with fixed abnormalities on the ECG

(e.g., left bundle branch block), perfusion or

echocardiographic imaging is used.

• For patients who cannot walk, pharmacologic stress is used.

• By demonstrating normal myocardial perfusion, sestamibi or

thallium imaging can reduce unnecessary hospitalizations by

excluding acute ischemia.

• CT angiography can also be used to exclude obstructive CAD

RISK STRATIFICATION AND PROGNOSIS

• Thrombolysis in Myocardial Infarction (TIMI)

score is useful both in predicting the risk of

recurrent cardiac events and in identifying

those patients who would derive the greatest

benefit from antithrombotic therapies more

potent than unfractionated heparin, such as

low-molecular-weight heparin (LMWH) and

glycoprotein (GP)IIb/IIIa inhibitors, and from

an early invasive strategy.

Used to estimate percent risk at 14

days of MI, or revascularization

RISK STRATIFICATION AND PROGNOSIS

• Other risk factors include DM, LV dysfunction,

and elevated levels of creatinine, ANP, and

• CRP and BNP, a marker of increased

myocardial wall tension, correlate

independently with increased mortality (and,

in some studies, recurrent cardiac events) in

patients presenting with UA/NSTEMI.

Management of ACS

• General Measures ECG , Nitroglycerine , Morphine , Beta-Blockers , ACE Inhibitors , Atropine

• Parenteral Anti-coagulation ( UFH , Enoxaparin , Fondaparinux )

and Anti-platelets (Aspirin , Clopidogerl , Abciximab )

• Fibrinolytic therapy

• Anti-arrhythmic drug

ANTI-ISCHEMIC DRUGS

Nitrates

• Should first be given sublingually or by buccal spray (0.3–0.6

mg) if the patient is experiencing ischemic pain.

• If pain persists after 3 doses given 5 min apart, i.v. GTN 50 mg

in 50 ml 0.9% saline at 2-10 ml/h.

• The only absolute contraindications to the use of nitrates are

hypotension or the use of sildenafil (Viagra) or other drugs in

that class within the previous 24 h.

ANTI-ISCHEMIC DRUGS

ß-blockers

• I.V. metoprolol (Lopressor) 5 mg infusion over 1-2 minuets. It

is repeated every 5 min for a total dose of 15 mg. Followed in

1–2 h by 25–50 mg by mouth every 6 h continue for 48 hours;

then administer a maintenance dose of 100 mg twice daily.

• I.V. esmolol (Brevibloc)

• I.V. atenolol (Tenormin) 5 mg slow I.V. over 5 minutes; may

repeat in 10 minutes. Follow I.V. dose with 100 mg/day or 50

mg twice daily for 6 to 9 days postmyocardial infarction.

ANTI-ISCHEMIC DRUGS

ß-blockers

• Contraindications:

– PR interval (ECG) >0.24 s, 2° or 3° atrioventricular block

– HR <60 beats/min, BP <90 mmHg

– Shock

– Left ventricular failure with congestive heart failure

– Severe reactive airway disease

ANTI-ISCHEMIC DRUGS

Morphine sulfate

• If pain persists despite intravenous nitroglycerin and beta blockade, morphine sulfate, 1–5 mg intravenously, can be administered every 5–30 min as needed.

ANTITHROMBOTIC DRUGS

Aspirin and clopidogrel

• Aspirin blocks the formation of thromboxane A2 and so prevents platelet aggregation. In ACS patients 150-300 mg initially; then 75–150 mg aspirin reduced the relative risk of death or myocardial infarction by about 35–50%.

Aspirin and clopidogrel

• Clopidogrel (Plavex), which blocks the platelet P2Y12

(adenosine) receptor (in combination with aspirin), was

shown in the CURE trial to confer a 20% relative reduction in

cardiovascular death, MI, or stroke, compared with aspirin

alone in both low- and high-risk patients with UA/NSTEMI, but

to be associated with a moderate (absolute 1%) increase in

major bleeding, which is more common in patients who

undergo coronary artery bypass grafting, so it is best avoided

if urgent CABG is likely.

• Clopidogrel should be given (preferably more than 6 hours)

after planned PCI, but may be omitted if coronary

angiography is planned immediately.

• Intravenous GP IIb/IIIa inhibitors (abciximab, tirofiban, and eptifibatide) reduce cardiac complications in patients undergoing percutaneous coronary intervention (PCI).

• Small molecule inhibitors eptifibatide and tirofibanshow benefit, while the monoclonal antibody abciximabappears not to be effective in patients treated conservatively, (i.e., in those not undergoing coronary angiography or PCI).

• Concomitant tirofban is particularly useful in diabetic patients.

• Patients receiving GP IIb/IIIa inhibitors should be monitored for 24 hours for bleeding and thrombocytopenia.

Anticoagulants

• Unfractionated heparin (UFH) is the mainstay of

therapy.

• The LMWH enoxaparin (Clexane ®) is superior to UFH

in reducing recurrent cardiac events, especially in

conservatively managed patients.

• The Factor Xa inhibitor fondaparinux is equivalent

with enoxaparin but appears to have a lower risk of

major bleeding and thus may have the best benefit

risk ratio.

Anticoagulants

• However, UFH, LMWH, or a direct thrombin

inhibitor such as bivalirudin should be used

during cardiac catheterization or PCI. • Bivalirudin is a direct thrombin inhibitor as effective as

heparin plus GPIIb/IIIa inhibitors in reducing ischaemicevents in patients pretreated with a thienopyridine and undergoing diagnostic angiography or percutaneous intervention, but with less bleeding.

INVASIVE THERAPY

• In high-risk patients, following treatment with anti-ischemic and antithrombotic agents, coronary arteriography is carried out within ~48 h of admission, followed by coronary revascularization (PCI or coronary artery bypass grafting), depending on the coronary anatomy.

LONG-TERM THERAPY

• Risk factor modification: smoking cessation, achieving optimal weight, daily exercise following an appropriate diet, blood pressure control, tight control of hyperglycemia, and lipid management.

• Beta blockers.

• Statins (at a high dose, e.g., atorvastatin 80 mg/d) and ACE inhibitors are recommended for long-term plaque stabilization.

• Antiplatelet therapy: combination of aspirin and clopidogrelfor at least 9–12 months, with aspirin continued thereafter.

• Primary PCI is generally more effective than fibrinolysis and is preferred, especially when diagnosis is in doubt, cardiogenic shock is present, bleeding risk is increased, or if symptoms have been present for >3 h.

Fibrinolytic drugs

• Proceed with IV fibrinolysis if PCI is not available or if logistics would delay PCI >1 h longer than fibrinolysis could be initiated.

• Door-to-needle time should be <30 min for maximum benefit.

• Those treated within 1–3 h benefit most; can still be useful up to 12 h if chest pain is persistent or ST remains elevated in leads that have not developed new Q waves.

• Complications include bleeding, reperfusion arrhythmias, and, in case of streptokinase (SK), allergic reactions.

INITIAL THERAPY

Fibrinolytic drugs

• Coadmnister enoxaparin or heparin and maintain activated partial thromboplastin time (aPTT) at 1.5–2.0 × control (~50–70 s).

• If chest pain or ST elevation persists >90 min after fibrinolysis, consider referral for rescue PCI.

• Later coronary angiography after fibrinolysis generally reserved for pts with recurrent angina or positive stress test.

Thank You !

Approach to acute coronary syndrome

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