Angina

1. UNSTABLE ANGINA & NON–ST ELEVATION MYOCARDIAL INFARCTION
Unstable angina (UA) and non–ST elevation myocardial infarction (NSTEMI) are clinical syndromes
characterized by myocardial ischemia without electrocardiographic ST elevation.Both syndromes are caused by
plaque rupture and associated nonocclusive thrombus.
Although UA and NSTEMI have a similar underlying pathophysiology, they differ in the degree of ischemia.
Although UA is not associated with a clinically detectable cardiac enzyme (creatine kinase myocardial
band, myoglobin, or troponin) leak, there can be electrocardiographic (EKG) changes consistent with ischemia.
In contrast, NSTEMI is characterized by a gradual rise and fall in biomarkers for myocardial necrosis
associated with anginal-like symptoms.
Thrombi in UA/NSTEMI are platelet rich and usually nonocclusive. In contrast, occluding thrombi are characteristic
of acute STEMI and typically comprised of fibrin and red blood cells.
• The disrupted plaque and associated thrombus reduces myocardial blood flow and impairs oxygen delivery to
cardiac myocytes. However, microembolization of platelet aggregates also occlude small arteriolar and capillary beds,
thus furthering ischemia. Indeed, microembolization is thought to be necessary to induce frank myocardial necrosis
and the parallel release of biomarkers (creatine phosphokinase [CPK] and troponins).
CLINICAL PRESENTATION:
• The classic symptoms of UA/NSTEMI are characterized
by poorly localizing chest or arm discomfort described as pressure-like or tightening. The discomfort typically
radiates to the jaw and arms.
Symptoms may be precipitated by emotional or physical exertion or may occur spontaneously at rest.
• Often the clinical presentation is atypical, especially
in the elderly (age >65), in women and in patients
with comorbid conditions (diabetes mellitus).
• Atypical symptoms of UA/NSTEMI include the following:
Epigastric pain
Unexplained fatigue
Dyspnea (at rest or with exertion)
Confusion
Nausea
Diaphoresis
• Certain clinical features are considered characteristic of Unstable Angina. These include:
Rest angina (particularly if prolonged or associated with transient ST changes),
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New onset angina after minimal exertion,
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Changes in the frequency of angina
..
• Features considered not characteristic, but often confused, with myocardial ischemia include the following:
-Pleuritic stabbing pain worse with respiration.
-Lower or midabdominal pain.
-Point tenderness, especially over the apex.
-Pain reproduced with chest wall palpation.
-Constant pain lasting for hours (especially in the absence of ST changes)
-Fleeting pain lasting only seconds.
-Pain radiating to the lower extremities.
Patients presenting with symptoms suggestive of an acute coronary syndrome (ACS) should undergo a
focused medical history and physical examination. An electrocardiogram (ECG) and biochemical marker
measurements (CPK and CPK myocardial bands, troponins) should be obtained.
After an initial evaluation, the clinician should estimate the likelihood of developing an adverse outcome.
Although, risk stratification may prove useful in predicting outcome (death or recurrent MI) and designing
the overall therapeutic strategy, almost all patients, regardless of risk, require coronary angiography.

2. The Thrombolysis in Myocardial Infarction (TIMI):The TIMI risk variables are as follows:
-Age older than 65 years
Presence of at least three risk factors for coronary heart disease
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Prior coronary stenosis of ≥ 50%
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Presence of ST segment deviation on admission ECG
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Two episodes of angina in the past 24 hours
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At least two angina episodes in the prior 24 hours
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-Elevated serum cardiac biomarkers
Use of aspirin in the prior 7 days
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• A focused history and physical examination coupled with a surface EKG and cardiac biomarkers, allow
patients to be grouped into one of the following clinical categories:
Noncardiac chest pain
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Chronic stable angina
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Possible ACS
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Definite ACS
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• Traditional risk factors are also helpful in predicting the likelihood of coronary artery disease. Traditional risk
factors for coronary artery disease include the following:
Family history of CAD
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Hypertension
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Hyperlipidemia
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Smoking
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Advancing age
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• Patients classified as possible ACS must have a normal or unchanged EKG and no elevation in cardiac biomarkers.
They should be pain free and their symptoms should have been mild and of short duration.
These patients should have a TIMI risk score of 2 or less.
TREATMENT
• The treatment of ACS is designed to decrease cardiacmyocardial oxygen demand and increase oxygen
delivery (eg, coronary flow).
OXYGEN
• Oxygen should be administered to patients with arterial saturations less than 90%.
NITROGLYCERINE
• Nitroglycerine dilates the venous bed, decreasing preload and thus myocardial oxygen demand.
• It also dilates the arterial bed (although it is much less potent) and reduces afterload (thus reducing oxygen
consumption).
• Promotes collateral flow by dilating precapillary sphincters of the coronary microvasculature.
• Dilates normal and atherosclerotic epicardial coronary arteries redistributing flow to ischemic areas of myocardium.
• Initially, 0.4 mg is administered sublingually to patients with ischemia. This dose may be repeated as needed for the
symptoms and signs of ischemia.
• If pain is not relieved with sublingual nitroglycerine, intravenous (IV) nitroglycerine should be administered at a rate
of 10 µg/min and increased by 5 to 10 µg/min every 3 to 5 minutes until relief of symptoms. Although 200 µg/min is
commonly considered the maximal dose, higher doses can be safely administered provided that the patients blood
pressure remains stable.
• The blood pressure must be monitored closely. A systolic blood pressure of >110 mm Hg should be maintained.
Large abrupt decreases in blood pressure should be avoided as they may aggravate cardiac ischemia or precipitate a
cerebrovascular event.
• Tolerance to nitroglycerine develops within 24 hours and generally necessitates an increase in dosage.
• After 12 to 24 hours of symptom control, the nitroglycerine is weaned and changed to an oral preparation
MORPHINE SULFATE
• Because morphine sulfate has analgesic, anxiolytic &vasodilatory effects, it decreases myocardial oxygen
demand.
• Administered in doses of 1 to 5 mg intravenously
• Must monitor closely for hypotension and respiratorydepression.
• Intravenous doses of naloxone 0.4 to 2.2 mg will antagonize
morphine’s effects.

3. β-BLOCKERS
• β-Blockers reduce blood pressure, heart rate, and contractility, decreasing myocardial oxygen demand.
• Considerable evidence supports the use of β-blockers in the management of all forms of coronary artery disease.
• Intravenous administration is recommended with protracted ischemia eg, metoprolol 5 mg intravenously every 5
minutes for three doses, then 25 to 50 mg by mouth every 6 hours.
• Bronchospasm, hypotension, and bradycardia can occur. Esmolol has a very short half-life and may prove especially
useful in patients with comorbid conditions that could be worsened by β-blocker therapy (COPD)..
CALCIUM CHANNEL ANTAGONISTS
• Calcium channel antagonists decrease myocardial oxygen demand and theoretically limit the extent and severity of
myocardial necrosis.
• Calcium channel antagonists have been used to control ischemia and treat hypertension in ACS. However, the
American College of Cardiology/American Heart Association (ACC/AHA) guidelines on NSTEMI (and STEMI),
emphasized that no calcium channel blocker has been shown to reduce mortality in acute MI and that in certain
patients they may be harmful.
• Short-acting dihydropyridine agents (nifedipine) are contraindicated in ACS in the absence of a β-blocker.Verapamil
and diltiazem are contraindicated in patients with significant left ventricular dysfunction, eg, ejections fraction <45%
because of their negative inotropic effect. In general, calcium channel blockers should only be used in patients in
whom β-blockers are contraindicated.
ANGIOTENSIN-CONVERTING
ENZYME INHIBITORS
• Angiotensin-converting enzyme (ACE) inhibitors have been shown to reduce mortality in patients with
an acute MI with ischemic left ventricular dysfunction as well as in nonischemic cardiomyopathy.
• The HOPE and EUROPA trials demonstrated beneficial effects of ACE inhibitors in diabetic patients or patients with
preexisting CAD and at least one additional risk factor but without left ventricular dysfunction.
Accordingly, most patients discharged after undergoing management for UA/NSTEMI will be treated with an ACE
inhibitor.
• The ACC/AHA also recommends the administration of ACE inhibitors in all postmyocardial infarct patients with left
ventricular dysfunction, diabetes mellitus, and hypertension not controlled by β-blockers.
ASPIRIN
• In multiple clinical trials, aspirin has demonstrated significant benefits in patients with coronary artery disease.
• Aspirin should be administered as soon as possible in all cases of suspected ACS (eg, in the emergency department
and continued daily).
• If the patient has not been receiving aspirin as an outpatient, 160 to 325 mg (chewed to maximize absorption) is
recommended, followed by a dose of 81 mg daily.
UNFRACTIONATED HEPARIN AND LOW-MOLECULAR-WEIGHT HEPARIN
• Heparin accelerates the action of circulating antithrombin III, which is a proteolytic enzyme that inactivates
thrombin as well as factor IXa and Xa. Heparin should be used in combination with aspirin in all patients presenting
with UA or NSTEMI.
• The usual dose of unfractionated heparin is 60 to 70 U/kg (maximum 5000 U) as a bolus with an infusion of 12 to 15
U/kg/min. The partial thromboplastin time (PTT) should be maintained between 1.5 to 2.5 times control. The optimal
length of treatment is not known, but most trials using unfractionated heparin (UFH) lasted 2 to 5 days.
• Low-molecular-weight heparin (LMWH) activates factor Xa. The anticoagulant effect of LMWH is more predictable
than with UFH, therefore PTT monitoring is not necessary.
• In a pooled study of clinical trials comparing UFH to LMWH, patients on LMWH experienced a lower 30-day event
rate without a significant increase in bleeding. This was especially evident in patients managed conservatively (eg, not
taken directly to the catheterization laboratory). Importantly, the SYNERGY trial demonstrated a statistically
significant risk of bleeding in patients who were switched from UFH to LMWH and vice versa.
• Serial complete blood counts and platelet counts should be obtained daily during heparin administration. Mild to
significant thrombocytopenia may occur with heparin; and autoimmune-induced thrombocytopenia (HIT) with
thrombosis is a rare but catastrophic complication. If a patient has a history of heparin-induced thrombocytopenia,
a direct thrombin inhibitor such as hirudin can be used. Hirudin is administered as a 0.4 mg/g IV bolus
over 15 to 20 seconds followed by a continuous infusion of 0.15 mg/kg/h. The PTT should be maintained
between 1.5 to 2.5 times control.