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Coronary Heart Disease
General Considerations
Acute Myocardial Infarction
Essentials of Diagnosis
• Sudden but not instantaneous development of prolonged (> 30 minutes) anterior chest discomfort
(sometimes felt as “gas” or pressure)
• Sometimes painless, masquerading as acute heart failure (HF), syncope, stroke, or shock
• ECG: ST-segment elevation myocardial infarction (STEMI) or left bundle branch block
• Immediate reperfusion treatment is warranted
– Primary percutaneous coronary intervention (PCI) within 90 minutes of first medical contact is
the goal and is superior to thrombolysis
– Thrombolysis within 30 minutes of hospital presentation and 6–12 hours of onset of symptoms
reduces mortality
• Results, in most cases, from an occlusive coronary thrombus at the site of a preexisting (though not
necessarily severe) atherosclerotic plaque
• More rarely, may result from prolonged vasospasm, inadequate myocardial blood flow (eg, hypotension),
or excessive metabolic demand
• Very rarely, may be caused by embolic occlusion, vasculitis, aortic root or coronary artery dissection, or
aortitis
• Cocaine use may cause infarction and should be considered in young individuals without risk factors
Clinical Findings
Symptoms and Signs
• Recent onset of angina or alteration in the pattern of angina or chest pressure, squeezing or “indigestion”
• Pain characteristics
– Similar to angina in location and radiation but more severe
– Usually occurs at rest, often in the early morning
– Builds rapidly
– Minimally responsive to sublingual nitroglycerin or oral opioids
• Associated symptoms
– Diaphoresis
– Weakness
– Apprehensiveness
– Aversion to lying quietly
– Light-headedness
– Syncope
– Dyspnea
– Orthopnea
– Cough
– Wheezing
– Nausea and vomiting
– Abdominal bloating
• 33% of patients do not experience chest pain, especially older patients, women, and patients with diabetes
• Of all deaths due to MI, ~50% occur before patient reaches the hospital, usually of ventricular fibrillation
• Marked bradycardia (inferior infarction) to tachycardia (increased sympathetic activity, low cardiac
output, or arrhythmia)
• Jugular venous distention indicates right atrial hypertension, often from RV infarction or elevated LV
filling pressures
• Soft heart sounds may indicate LV dysfunction
• S4 is common; S3 indicates significant LV dysfunction
• Mitral regurgitation murmur usually indicates papillary muscle dysfunction or, rarely, rupture
• Pericardial friction rubs are uncommon in the first 24 hours but may appear later
• Edema is usually not present
• Cyanosis and cold temperature indicate low output
• Peripheral pulses should be noted, since later shock or emboli may alter the examination
Differential Diagnosis
• Acute coronary syndrome without ST segment elevation
• Aortic dissection
• Pulmonary embolism
• Tension pneumothorax
• Pericarditis
• Esophageal rupture
• Stress cardiomyopathy (Tako-Tsubo cardiomyopathy or apical ballooning syndrome)
Diagnosis
Laboratory Tests
• Quantitative CK-MB, troponin I, and troponin T elevations as early as 4–6 h after onset; almost always
abnormal by 8–12 h
• Troponins
– May remain elevated for ≥ 5–7 days
– Therefore, not generally useful for evaluating suspected early reinfarction
• High-sensitivity troponin assays
– When positive, help enable myocardial infarction to be detected earlier
– Many conditions, including chronic heart failure are associated with elevated levels
– When negative, may be useful in excluding myocardial infarction in patients with chest pain
Imaging Studies
• Chest radiograph: signs of CHF, often lagging behind the clinical findings
• Echocardiography: assesses global and regional LV function, wall motion
• Doppler echocardiography: can diagnose postinfarction mitral regurgitation or ventricular septal defect
• Thallium-201 or technetium scintigraphy does not distinguish recent from old MI
Diagnostic Procedures
• Angiography: can demonstrate akinesis or dyskinesis and measures ejection fraction
• Swan-Ganz hemodynamic measurements: can be invaluable in managing suspected cardiogenic shock
• ECG
– Extent of abnormalities, especially the sum of the total amount of ST-segment deviation, is a
good indicator of extent of acute infarction and risk of subsequent adverse events
– The classic evolution of changes is from peaked (“hyperacute”) T waves, to ST-segment
elevation, to Q wave development, to T wave inversion; this may occur over a few hours to
several days
– The evolution of new Q waves (> 30 milliseconds in duration and 25% of the R wave amplitude)
is diagnostic, but Q waves do not occur in 30–50% of acute infarctions (non-Q wave infarctions)
Treatment
Medications
• Aspirin
– All patients with definite or suspected myocardial infarction should receive aspirin at a dose of
162 mg or 325 mg at once regardless of whether thrombolytic therapy is being considered or the
patient has been taking aspirin
– Chewable aspirin provides more rapid blood levels
• P2Y12 inhibitors (eg, prasugrel, ticagrelor, or clopidogrel)
– Given to patients with a definite aspirin allergy
– P2Y12 inhibitors, in combination with aspirin, have been shown to be beneficial to patients with
acute STEMI
– Guidelines call for a P2Y12 inhibitor to be added to aspirin to all patients with STEMI,
regardless of whether reperfusion is given, and continued for at least 14 days, and generally for 1
year
– Prasugrel and ticagrelor are preferred; both have shown superior outcomes compared to
clopidogrel
– Prasugrel
▪ Dose is 60 mg orally on day 1, then 10 mg daily
▪ In the TRITON study, prasugrel was shown to be of greater benefit than clopidogrel in reducing
thrombotic events in the subgroup of patients with STEMI, including a 50% reduction in stent thrombosis
▪ Contraindicated in patients with history of stroke or who are older than 75 years
– Ticagrelor
▪ Dose is 150 mg orally on day 1, then 90 mg twice daily
▪ In the PLATO trial, ticagrelor was shown to be of greater benefit than clopidogrel in reducing
cardiovascular death, myocardial infarction, and stroke as well as in reducing stent thrombosis
– Clopidogrel
▪ Loading dose of 600 mg orally (or 300 mg) results in faster onset of action than standard 75 mg
maintenance dose
• Nitroglycerin
– Agent of choice for continued or recurrent ischemic pain
– Useful in lowering BP or relieving pulmonary congestion
• Morphine sulfate, 4–8 mg intravenously, or meperidine, 50–75 mg intravenously, if nitroglycerin alone
does not relieve pain
• Enoxaparin reduced death and MI at day 30 (compared with unfractionated heparin) at the expense of a
modest increase in bleeding
– Give as a 30-mg intravenous bolus and 1 mg/kg every 12 hours for patients aged < 75 years
– Give with no bolus and 0.75 mg/kg intravenously every 12 hours for patients aged ≥ 75 years
• Fondaparinux reduced death and reinfarction (compared with unfractionated heparin when indicated,
otherwise placebo) with less bleeding
– Dose: 2.5 mg once daily subcutaneously
– Not recommended as sole anticoagulant during PCI due to risk of catheter thrombosis
• Thrombolytic therapy (see Table 10–11)
– Reduces mortality and limits infarct size in patients with acute myocardial infarction associated
with ST-segment elevation (defined as ≥ 0.1 mV in two inferior or lateral leads or two contiguous
precordial leads), or with left bundle branch block
– Greatest benefit occurs if initiated within the first 3 hours, when up to a 50% reduction in
mortality rate can be achieved
– The magnitude of benefit declines rapidly thereafter, but a 10% relative mortality reduction can
be achieved up to 12 hours after the onset of chest pain
• Glycoprotein IIb/IIIa inhibitors, specifically abciximab, have been shown to reduce major thrombotic
events, and possibly mortality, for patients undergoing primary PCI
Therapeutic Procedures
• ST elevation connotes an acute coronary occlusion and thus warrants immediate reperfusion therapy
• Primary PCI is the approach of choice in patients with absolute and many relative contraindications to
thrombolytic therapy
• In patients with cardiogenic shock, early catheterization and percutaneous or surgical revascularization
are the preferred management and has been shown to reduce mortality
• For patients who have received thrombolytic therapy but will undergo angiography in the first day or two,
the early benefits of a P2Y12 inhibitor need to be weighed against the necessary delay in bypass surgery for
approximately 5 days for those patients found to require surgical revascularization
Outcome
Follow-Up
• For nonhypotensive patients with low ejection fractions, large infarctions, or clinical evidence of heart
failure, start ACE inhibitor on first postinfarction day; titrate and continue long-term
• Diltiazem appears to prevent reinfarction and ischemia in patients with non–Q-wave infarctions
• Patients with recurrent ischemic pain prior to discharge should undergo catheterization and, if indicated,
revascularization
Complications
• Myocardial dysfunction, HF, and hypotension
• Postinfarction ischemia
• Sinus bradycardia, sinus tachycardia
• Supraventricular premature beats
• Atrial fibrillation, ventricular fibrillation
• Ventricular premature beats
• Ventricular tachycardia
• Accelerated idioventricular rhythm
• RBBB or LBBB or fascicular blocks
• Second- or third-degree AV block
• Rupture of a papillary muscle, interventricular septum, or LV free wall
• LV aneurysm
• Pericarditis, Dressler's syndrome
• Mural thrombi
Prevention
• Control LDL cholesterol and BP
• β-Blockers
• Antiplatelet agents
• Exercise training and cardiac rehabilitation programs
Prognosis
• Killip classification classifies heart failure in patients with acute MI and has powerful prognostic value
– Class I is absence of rales and S3
– Class II is rales that do not clear with coughing over one-third or less of the lung fields or
presence of an S3
– Class III is rales that do not clear with coughing over more than one-third of the lung fields
– Class IV is cardiogenic shock (rales, hypotension, and signs of hypoperfusion)
When to Refer
• All patients with acute myocardial infarction should be referred to a cardiologist
When to Admit
• All patients with possible MI to the CCU
Angina Pectoris: Stable, Unstable, Prinzmetal Variant III.
Angina Pectoris
Etiology
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Atherosclerotic stenosis of coronary arteries—most common.
Coronary artery spasm.
Congenital coronary artery anomalies.
Aortic stenosis (AS), regurgitation.
Hypertrophic cardiomyopathy.
Myocardial muscle bridge.
Pulmonary hypertension.
Severe systemic hypertension.
Collagen vascular disease.
Syndrome X (possible microvascular disease).
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Symptom complex of chest discomfort or equivalent secondary to myocardial ischemia because of
mis-match of supply and demand.
Classic stable angina—substernal pressure or heavi-ness sensation precipitated by exertion or
anxiety; relieved in a predictable pattern by rest.
Unstable angina—chest discomfort at rest, or new and severe (within 2 months and brought on
by minimal exertion), or has changed in pattern with increased frequency, duration, and
intensity.
Crescendo angina—angina occurring with increasing frequency.
Variant angina (Prinzmetal)—rest or nocturnal chest pain with ST segment elevation on ECG;
thought to be caused by coronary artery spasm.
Postprandial angina—angina occurring after meals.
Anginal equivalent—dyspnea on exertion caused by myocardial ischemia.
Pathology
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Syndrome X—typical exertional or stress-induced angina in the absence of coronary artery
stenosis on angiography.
 Silent ischemia—evidence of myocardial ischemia on stress ECG, thallium, or echocardiography
with chest discomfort; thought to be more common in patients with diabetes.
Risk Factors for Atherosclerosis
● Advancing age.
● Male gender (female begins to equal male after menopause).
● Smoking tobacco.
● Hypertension.
● Genetic (family history: CHD in male - first-degree relative <55 years; CHD in female - first-degree
relative <65 years).
● Increased total cholesterol and LDL-C, decreased HDL-C, increased apolipoprotein (a) (Lp(a)),
increased small, dense LDL particles, increased triglycerides.
● DM.
● Obesity.
● Sedentary lifestyle.
● Increased homocysteine.
● Increase C-reactive protein (inflammation).
● Low-glutathione peroxidase (antioxidant enzyme).
● Proteinuria.
Clinical Features
History
● Precordial pressure or heaviness radiating to back, neck, shoulders, arms, lower jaw, or teeth brought on
by exertion, eating large meal, cold air exposure, or emotional stress, and relieved by rest or NTG; usually
lasts minutes.
● May present as dyspnea on exertion.
● Levine sign—patient describes pain using clenched fist over his or her anterior chest (sternum).
● May be accompanied by dyspnea, dizziness, palpitations, and infrequently syncope.
Physical Exam Findings
● May be normal.
● Fourth heart sound (S4) and sometimes S3.
● Paradoxical splitting of S2 during angina episode.
● May have signs of atherosclerosis (e.g., xanthelasma, decreased peripheral pulses).
● May have signs of hypertension as risk factor (e.g., increased BP, retinopathy).
● Murmur of (AS) aortic stenosis or (AR) aortic regurgitation as etiology, or (MR) mitral regurgitation
from papillary muscle dysfunction.
● Signs of HF as complication.
Diagnostic Studies
● ECG—can frequently be normal or may show ST segment depression or T-wave inversion during
attack; Q waves seen in patients with previous MI.
● Cholesterol may be elevated with elevated LDL-C, increased Lp(a), decreased HDL-C, increased
triglycerides.
● C-reactive protein—increased.
● Homocysteine—increased. Ambulatory ECG may show transient ST segment depression with exertion.
● Stress testing is usually done as the second step after the resting ECG and can include the following:
● Stress or exercise ECG—may disclose temporary ST segment depression.
● Myocardial perfusion scintigraphy after exercise (or pharmacologic stress testing with IV
dipyri-damole or adenosine) with thallium-201, techne-tium-99m, tetrofosmin, or sestamibi using
planar or single-photon emission computed tomography imaging—may show reversible
perfusion defects.
● Stress echocardiography using exercise or pharma-cologic agents (dipyridamole, dobutamine,
adenos-ine)—may show stress-induced global or regional wall motion abnormalities.
● Stress gated blood-pool scintigraphy (technetium-99m) using exercise or pharmacologic
agents—may show stress-induced global or regional wall motion abnormalities.
● Positron emission tomography.
● Cardiac magnetic resonance imaging (MRI).
● Ultrafast electron-beam computed tomography scan for coronary artery calcification.
● Cardiac arteriography—cardiac catheterization with angiography is a definitive study to diagnose,
quan-tify, and anatomically define CAD (“gold standard”).
Management
● Smoking cessation.
● Weight reduction, low-fat/low-cholesterol diet.
● Cardiac rehabilitation or supervised exercise program to improve exercise capacity.
● Treat hypertension, diabetes, and hypercholesterol-emia (goal—LDL <100 mg per dL, ideal would be
<70 mg per dL).
Pharmacologic
● Aspirin—81 to 325 mg per day, or clopidogrel.
● Sublingual (SL) NTG spray or tablets—as needed or before exertion.
● Long-acting oral nitrates (e.g., isosorbide dinitrate and isosorbide 5-mononitrate) with 8- to 12-hour
nitrate-free period to avoid tolerance.
● Long-acting transdermal nitrates by way of paste or patches with 8-hour to 12-hour nitrate-free period to
avoid tolerance.
● IV NTG in unstable angina.
● IV heparin in unstable angina.
● b-Adrenergic blockers.
● Calcium channel blockers (i.e., diltiazem or verapamil). Avoid short-acting nifedipine as this may
increase the risk of cardiac event.
● Ranolazine (Ranexa)—can cause QT prolongation.
● Folic acid to decrease homocysteine. This has not been proved to yield absolute benefit.
● Statin to decrease LDL and C-reactive protein.
Invasive Revascularization Procedures (Percutaneous Coronary Interventions [PCI])
● Percutaneous transluminal coronary angioplasty (PTCA).
● Directional coronary atherectomy.
● Coronary laser angioplasty.
● Coronary stenting, including drug-eluting stents (used with PTCA).
Surgical Procedures
● Coronary artery bypass grafting surgery.
Others
● Mechanical extracorporeal counterpulsation— limited data.
Prinzmetal (variant) angina
 Coronary vasoconstriction
 Usually the right coronary artery with or without stenosis
 Also called “syndrome X”
 Usually causes ST elevation
 Usually women <50
 Occurs in the morning awakening from sleep