Management of a

patient with
cardialgia
.
The classical symptoms of different sources of acute chest
pain can be subjective and difficult for patients to
characterize. Care should be taken to maintain a low
threshold for referral. Both history and physical exam have
been shown to have a poor sensitivity and specificity to
distinguish benign from life-threatening causes of chest
pain.
Cardiovascular:
Ischemic cardiac causes:
ACS and stable angina: deep, poorly localized chest or arm
discomfort reproducibly associated with exertion and relieved with
rest or nitroglycerine. May be provoked by emotional distress,
associated with radiation, diaphoresis, dyspnea, nausea, syncope,
and hypotension. Expect variable characterization of symptoms, and
atypical (sometimes pain free) presentations in women, diabetic
patients, and the elderly.
If symptoms are new, changing, or progressive, urgent referral to
emergency department is appropriate.
Non-ischemic cardiac causes:
Heart failure: chest discomfort typically associated with dyspnea,
orthopnea, pulmonary edema and lower extremity edema.
Acute thoracic aortic dissection: severe chest or back pain which
can also radiate to the abdomen, classically with a ‘tearing’ quality.
Pericarditis: pleuritic chest pain improved by leaning forward. Also
associated with classic ECG changes (diffuse ST elevation, PR
depression, without T-wave inversion) and an audible friction rub.
Takotsubo/Stress Cardiomyopathy: substernal chest pain of
ischemic character with onset in the setting of acute emotional
distress, more common in female patients.
Pulmonary:
Pneumonia: presentation with fever, chills, productive cough, pleuritic pain.
Pulmonary embolism: acute onset dyspnea, tachycardia, pleuritic chest pain,
with or without extremity symptoms to suggest the presence of deep vein
thrombosis.
Chronic obstructive pulmonary disease: under-appreciated source of chest
tightness. Typically present with chest discomfort in the setting of dyspnea
related to asthma or COPD exacerbation.
Acute Chest Syndrome: infiltrate and fever, dyspnea, cough, and hypoxia in
patients with sickle cell anemia.
Sarcoidosis: chest pain often present in patients with either pulmonary or
cardiac sarcoidosis. Higher degree of concern for cardiac sarcoidosis if syncope,
dizziness, and ECG changes consistent with conduction disease.
Musculoskeletal:
Chest wall pain: localized muscle tension or tenderness,
pain reproducible by palpation, absence of cough.
Costochondritis: reproducible pain to palpation
specifically localized to the parasternal/chostochondral
joints
Injury or Trauma: Rib fractures, neoplasm, bruising of
the ribs
Gastrointestinal:
GERD: substernal burning with significant anginal character, acid
regurgitation, sour taste, can radiate and persist for many hours.
Often occurs after meals, lying down, or with emotional distress.
Esophagitis: burning retrosternal pain which can occur after pill-
associated injury, viral or fungal esophageal infection in
immunodeficiency, or via food allergen triggers in eosinophilic
esophagitis.
Esophageal Spasm: painful, self-resolving spasm of smooth muscle
of esophagus
Esophageal injury: severe pain, typically in the setting of vomiting or
dry heaving.
Psychological:
Anxiety and Panic Disorder: typically spontaneous and
rapid onset episodes associated with a discrete
triggering event, perpetuated by fear of ongoing panic
episode. Caution because hyperventilation can also
cause true demand ischemia in patients with
underlying CAD.
Cause Pathogenes Location Features of Precipitating, Selected
is pain exacerbating, accompanyin
and g signs or
alleviating symptoms
factors
Stable Transient Retrosternal, Crushing, Exercise, Dyspnea
ischemic myocardial may be burning, stress, cold
heart ischemia referred to squeezing; air, heavy
disease neck, jaw, persists for 2- meals;
scapulae, 10 min resolves soon
arms, elbows, after stopping
epigastrium activity or use
of
nitroglycerin
Cause Pathogenes Location Features of Precipitating, Selected
is pain exacerbating, accompanyin
and g signs or
alleviating symptoms
factors

Acute Prolonged As above As above but Not resolving Dyspnea,

coronary myocardial usually more after use of excessive
syndrom ischemia, severe; nitroglycerin sweating,
es myocardial persists for or stopping fatigue,
including necrosis >30 min in MI, activity nausea,
NSTEACS <20 min in vomiting
and angina
STEACS pectoris
Cause Pathogene Location Features Precipitating, Selected
sis of pain exacerbating, accompanyin
and alleviating g signs or
factors symptoms

Pericarditi Irritation Retrosternal Sharp, Exacerbated by Features of

s/ of or over apex, stabbing, deep inspiration, underlying
myoperic pericardial may be varying trunk turning, condition,
arditis layers or referred to intensity supine position, pericardial
part of neck and left cough; reduced rub, dyspnea
pleura shoulder when sitting and
adjacent leaning forward
to
pericardiu
m
Cause Pathogenesis Location Features of Precipitating, Selected
pain exacerbating, and accompanying
alleviating factors signs or
symptoms

Hypert Supply/ As in SIHD As in SIHD Physical activity, Dyspnea,

rophic demand dehydration, presyncope or
cardio mismatch due tachyarrhythmias, frank syncope,
myopa to decreased nitrates, and other SCD
thy coronary flow, preload- or
left ventricular afterload-reducing
hypertrophy; agents
left ventricular
outflow tract
obstruction.
Cause Pathogenesis Location Features of Precipitating, Selected
pain exacerbating, accompanyin
and g signs or
alleviating symptoms
factors

Takots Unknown but Similar as in Similar as in Emotional or Dyspnea,

ubo presumed due ACS ACS physical heart failure,
cardio to stress; strong cardiogenic
myopa catecholamin female shock
thy e-induced preponderanc
cardiotoxicity e
Cause Pathogenesis Location Features of Precipitating, Selected
pain exacerbating, accompanyin
and g signs or
alleviating symptoms
factors

Valvul Myocardial Similar as in Similar as in Physical Exertional

ar oxygen SIHD SIHD activity, dyspnea,
heart supply/deman resolves with exertional
diseas d mismatch rest presyncope/sy
e ncope in AS,
(AS/AI signs of heart
) failure
Cause Pathogenesis Location Features of Precipitating, Selected
pain exacerbating, accompanyin
and g signs or
alleviating symptoms
factors
Pulmo Impaired Similar as in Similar as in Similar to Dyspnea,
nary coronary SIHD SIHD SIHD fatigue, signs
hypert perfusion to of right heart
ension a dilated and failure, signs
hypertrophied and
RV symptoms of
underlying
cause of PH
Cause Pathogenesis Location Features of Precipitating, Selected
pain exacerbating, accompanyin
and g signs or
alleviating symptoms
factors

Aortic Distension of Anterior chest Extremely High BP Murmur of

dissectaortic wall wall, may be severe, mitral
ion referred to tearing, of regurgitation,
interscapular sudden onset asymmetric
or lumbar BP in
area extremities,
new-onset
neurologic
deficits
Cause Pathogenesis Location Features of Precipitating, Selected
pain exacerbating, accompanyin
and g signs or
alleviating symptoms
factors

Pleurit Inflammatory Usually Sharp, Exacerbated Features of

ic pain infiltration of unilateral, stabbing by deep underlying
pleura, may be inspiration, condition,
irritation of referred to cough, trunk usually
pleura in interscapular movement; dyspnea,
pulmonary area reduced after tachypnea
infarction, lying down on
pneumothora the side of
x pain
Cause Pathogenesis Location Features of Precipitating, Selected
pain exacerbating, accompanyin
and g signs or
alleviating symptoms
factors

Neural Neuritis (eg, Unilateral in Sharp, Exacerbated Rash typical

gia in herpes herpes zoster, shooting by palpation of herpes
zoster), nerve may be along nerve, zoster,
compression bilateral when sometimes tenderness of
by spinal caused by with very light thoracic
lesions spinal lesions touch vertebrae
(allodynia)
Cause Pathogenesis Location Features of Precipitating, Selected
pain exacerbating, accompanyin
and g signs or
alleviating symptoms
factors

Gastro Esophagitis Retrosternal, Usually Heavy meals, Upper

esoph may be burning or leaning abdominal
ageal referred to squeezing forward, lying pain,
reflux back down dyspepsia
diseas
e
Cause Pathogenesis Location Features of Precipitating, Selected
pain exacerbating, accompanyin
and g signs or
alleviating symptoms
factors

Esoph Disruption of Retrosternal Very severe, Forceful Vomiting

ageal esophageal burning, of vomiting
ruptur wall sudden onset
e
Cause Pathogenesis Location Features of Precipitating, Selected
pain exacerbating, accompanyin
and g signs or
alleviating symptoms
factors

Cholel Increased Right Severe pain Fatty meals; Nausea,

ithiasi pressure in hypochondriu with gradually alleviated by vomiting, loss
s gallbladder m or increasing lying down of appetite
epigastrium, intensity, still
may be resolves
referred to slowly,
right shoulder persists for
minutes to
hours
Cause Pathogenesis Location Features of Precipitating, Selected
pain exacerbating, accompanyin
and alleviating g signs or
factors symptoms

Peptic Gastric or Epigastrium, Dull, rarely Exacerbated by Dyspepsia

ulcer duodenal sometimes in sharp or meals (gastric
diseas mucosal lower chest burning ulcer) or fasting;
e injury meals alleviate
symptoms in
patients with
duodenal ulcer
Cause Pathogenesis Location Features of Precipitating, Selected
pain exacerbating, accompanyin
and g signs or
alleviating symptoms
factors

Bone Inflammation Local, anterior Sharp or Chest wall Tenderness

and of chest wall squeezing movement, (often
joint sternocostal particularly reproducible
pain and cough on palpation)
sternoclavicul
ar joints,
trauma, other
Cause Pathogenesis Location Features of Precipitating, Selected
pain exacerbating, accompanying
and signs or
alleviating symptoms
factors

NeurotUnclear Anterior chest Variable Stress Dyspnea,

ic pain wall palpitations,
anxiety
EVALUATION
The first decision point in evaluating patients with acute chest pain is
determining whether the pain is likely to reflect cardiac ischemia or
ACS. Any patient with chest pain that is exertional or with ECG
changes should be seen in an acute care setting for troponin levels
and cardiac stress testing.
History: History and physical exam not sensitive or specific for
diagnosing ACS in low-prevalence setting. The most specific
characteristics studied are: absence of chest wall tenderness on
palpation, diaphoresis, pain worse with exertion, radiation to the arm
or shoulder, and pressure-type pain.
Physical Exam:
o Early vital sign measurement is important for evidence of
hypotension, tachycardia, and hypoxia. If concern for dissection,
BP measurement in both arms. If concern for tamponade,
assessment of pulsus paradoxus.
o Auscultation for new third heart sound, friction rub, irregular
heart rhythm, pulmonary edema or wheezing.
o Skin exam for rashes, palpation over chest for evidence of
musculoskeletal pain source.
Red flags
Certain findings raise suspicion of a more serious etiology
of chest pain:
Abnormal vital signs (tachycardia, bradycardia, tachypnea,
hypotension)
Signs of hypoperfusion (eg, confusion, ashen color,
diaphoresis)
Shortness of breath
Hypoxemia on pulse oximetry
Asymmetric breath sounds or pulses
New heart murmurs
Pulsus paradoxus > 10 mm Hg
 Labs: if available, labs including serum troponin,
lactate, CBC and CMP. D-dimer, VBG as appropriate.
 Imaging: CXR appropriate in most patients. Can also
consider CT chest if concern for dissection, PE is
high.
 ECG: 12 lead ECG to assess for evidence of ST
segment changes, new left bundle branch block,
presence of Q waves or new onset T wave inversions.
TREATMENT
Treatment of chest pain involves addressing the underlying physiologic source. A
common list of treatments to the most frequent causes of chest pain below:
Acute Coronary Syndrome (ACS): These patients should be sent directly to the ED
or can be directly admitted to cardiology. Patients with STEMIs will go directly to
the cardiac catheterization. Initial oral medications can be given in the outpatient
setting:
o Aspirin 325 mg PO once
o Atorvastatin 80 mg PO once
o Metoprolol tartrate 12.5 mg PO (hold for a heart rate <60 BPM and/or the
presence of acute heart failure or cardiogenic shock)
o Nitroglycerin 0.4 mg sublingually (hold if signs of inferior or right-sided
myocardial infarction)
Costochondritis: Costochondritis is a self-limited
condition that resolves spontaneously over
weeks. Adjunct therapy can help alleviate
symptoms and may reduce the duration of
symptoms.
oHeat/Ice, stretching exercises, NSAIDS and/or
APAP, Muscle rubs (menthol or ASA-based
creams are most common)
Gastroesophageal reflux (GERD) In the absence of ‘red flag’ symptoms or signs,
H2 blocker or PPI can be effective. Pain is typically caused from esophagitis rather
than reflux itself.
o Famotidine (H2B) 20-40 mg QD or BID (favored over PPI if only occasional
symptoms or if relative contraindication to PPI such as recurrent C. difficile
infection)
o Omeprazole (PPI) 20-40 mg QD or BID (may be less effective if taken prn with
meals)
o Sucralfate or bismuth solutions
o Avoidance of potassium or iron supplementation or doxycycline if possible
(or these medications and all PO intake should occur with 30-60 minutes of
post-prandial upright posture)
Pneumonia: If CURB-65 and other subjective/objective
measures suggest safe outpatient treatment of infection, PO
antibiotics
oCephalosporin + doxycycline; levofloxacin, per IDSA
guidelines and local antibiogram
Pulmonary embolism: If the Pulmonary Embolism Severity
Index (PESI score) dictates a low risk of mortality, then these
patients can be treated as an outpatient with oral
anticoagulation.
oNOAC or DOAC initiation with close outpatient follow-up
Heart failure: Cardiac stretch and pulmonary edema are typically the
underlying cause of chest pain in these patients.
o Lasix, torsemide, or bumex, typically 1.5-2x prior dose for 3 days
Pericarditis: Low-risk patients can be treated in outpatient setting using
combination therapy for 7-14 days.
o NSAIDS: aspirin 625 mg – 1000 mg or ibuprofen 600 – 800 mg TID
o Colchicine 0.6 mg BID
o Activity restriction to reduce symptoms
Anxiety/Panic: In the acute setting, reasonable to use low-dose
benzodiazepine: long-term management is via SSRI and CBT.
o SSRI or SNRI other medication for treatment of anxiety (long-term
medication) with Cognitive behavioural therapy.
Management of a
patient with chronic
coronary syndrome .
Stable Angina Pectoris
Angina pectoris is a clinical syndrome characterized by chest pain (or its equivalent) due to
myocardial ischemia, usually developing on exertion or caused by stress and not
associated with necrosis of cardiomyocytes. In some patients the pain may be
spontaneous. Angina reflects an inadequate oxygen supply in relation to myocardial
demand. Stable angina pectoris is diagnosed in patients with symptoms of angina and no
worsening over the prior 2 months.
CLINICAL FEATURES AND NATURAL HISTORY
1. Symptoms: The clinical diagnosis of angina is based on history. Therefore, a detailed
characterization of the symptom complex is critical to the patient assessment.
Anginal chest pain is typically retrosternal in location and may radiate to the neck, jaw, left
shoulder, and/or left arm (and usually further along the ulnar nerve to the wrist and fingers),
to the epigastrium, or rarely to the interscapular region. The pain is caused by exertion
(threshold may vary from patient to patient) and emotional stress; it usually lasts a few
minutes and is relieved by rest or sometimes decreases in the course of continued exercise.
The pain is frequently more severe in the morning and may be exacerbated by cold air or
a heavy meal. Pain intensity is not related to body position or phase of the respiratory cycle; it
usually resolves within 1 to 3 minutes of sublingual administration of nitroglycerin (if it
resolves after 5-10 minutes, it is probably not related to myocardial ischemia and may be
caused, eg, by esophageal disease). The pain may be absent in patients with an anginal
“equivalent,” particularly exertional dyspnea; however, it may be challenging to distinguish
the anginal equivalent from a pulmonary cause.
Typical angina
(1) is substernal and referred in a typical way;
(2) is caused by exertion or emotional stress;
(3) resolves at rest or after sublingual
administration of a nitrate.
Atypical angina fulfills 2 of these criteria.
Nonanginal pain meets only 1 criterion.
Grade I: Ordinary physical activity (such as walking and climbing stairs) does not cause
angina. Angina occurs with strenuous, rapid, or prolonged exertion at work or recreation
Grade II: A slight limitation of ordinary activity. Angina occurs when:
– Walking or climbing stairs rapidly
– Walking uphill
– Walking or climbing stairs after meals, in cold, or in wind, or when under emotional stress,
or only during the few hours after awakening
– Walking >200 meters or climbing more than 1 flight of stairs at a normal pace and in
normal conditions

Grade III: Marked limitation of ordinary physical activity. Angina occurs when walking 100-
200 meters or climbing 1 flight of stairs at a normal pace in normal conditions
Grade IV: Inability to carry on any physical activity without discomfort; anginal syndrome
may be present at rest
Diagnostic Tests
1. Laboratory tests may reveal risk factors for atherosclerosis and
disorders that may trigger angina. Baseline tests in a patient with
stable coronary disease include:
1) Fasting lipid profile (total cholesterol [TC], low-density lipoprotein
cholesterol [LDL-C], high-density lipoprotein cholesterol [HDL-C], and
triglycerides [TG]).
2) Fasting blood glucose and glycated hemoglobin (HbA1c) (and oral
glucose tolerance test, when indicated.
3) Complete blood count (CBC).
4) Serum creatinine level and estimated glomerular filtration
rate (eGFR).
Moreover, in patients with clinical indications perform:
1) Measurement of cardiac troponin levels (in the case of
suspected acute coronary syndrome).
2) Thyroid function tests.
3) Liver function tests (after starting statin therapy).
4) Measurement of creatine kinase levels (in patients with
features of myopathy).
5) B-type natriuretic peptide (BNP)/N-terminal pro–B-type
natriuretic peptide (NT-proBNP) (in the case of suspected
heart failure).
2. Resting electrocardiography (ECG) should be performed in every patient with
suspected angina. Although the results are normal in the majority of patients,
some patients may have significant Q waves, indicating prior myocardial
infarction (MI) (even in the absence of a clinical history suggestive of prior MI) or
ECG features of myocardial ischemia, mainly ST-segment depression or T-wave
inversion.
3. Resting echocardiography is indicated in all patients to detect other diseases
that may cause angina, assess impaired myocardial contractility and diastolic
function, and measure left ventricular (LV) ejection fraction (LVEF), which is
necessary for risk stratification.
4. ECG Holter monitoring rarely provides significant diagnostic information and
therefore should not be performed routinely. It can be considered in the case of
suspected arrhythmia or vasospastic angina (Prinzmetal variant angina).
Noninvasive Imaging Diagnostic Tests for CAD
1. ECG stress testing is not recommended as a first-line diagnostic test but can be considered if
noninvasive imaging testing is unavailable. It is also used to assess event risk, exercise
tolerance, and symptom severity. The study is of limited diagnostic value in patients in whom
the baseline ECG features make it impossible to interpret the recordings during exercise (left
bundle branch block [LBBB], preexcitation syndromes, pacemaker rhythms).
2. ECG stress testing with imaging: The addition of imaging to stress testing improves
sensitivity, specificity, and prognostic information. Stress imaging is especially useful in
assessing patients who have uninterpretable ECG. The two common types of imaging are single-
photon emission computed tomography (SPECT) with sestamibi or thallium isotopes and stress
echocardiography. Imaging can be performed with pharmacologic stress (dipyridamol [trade
name Persantine] or dobutamine) in individuals who are not able to exercise. However, exercise
is always preferred whenever possible for the additional prognostic information that it
provides.
3. Coronary computed tomography angiography (CCTA) should be
considered as an alternative to stress testing with imaging and in
patients in whom stress testing yields equivocal results or is not
feasible (due to limited exercise capacity or uninterpretable ECG).
4. Cardiac magnetic resonance imaging (MRI) and positron
emission tomography (PET) are the emerging modalities for cardiac
imaging. They have value for the assessment of myocardial viability
and ventricular function; however, they are not widely used as
stress testing modalities.
5. Coronary angiography is the gold standard for demonstrating coronary
anatomy, establishing prognosis, and assessing the feasibility of invasive
treatment. Coronary angiography should be considered for the diagnosis
of CAD in the following situations:
1) A high PTP of CAD in patients with severe symptoms or clinical features
suggestive of high risk of cardiovascular events. In such cases it is justified to
proceed to early coronary angiography without prior noninvasive imaging with
the intention of revascularization.
2) Coexistence of typical angina and systolic LV dysfunction (LVEF <50%).
3) Equivocal diagnosis made on the basis of noninvasive tests or conflicting
results of various noninvasive tests (this is an indication for coronary angiography
with measurement of functional flow reserve [FFR], if necessary).
4) Unavailability of imaging stress testing, special legal requirements associated
with certain professions (eg, aircraft pilots).
TREATMENT
1. Control of the risk factors of atherosclerosis (secondary prevention)
2. Treatment of conditions worsening angina, such as anemia,
hyperthyroidism, rapid or excessive hormone replacement in
hypothyroidism, or tachyarrhythmias.
3. Increasing physical activity (below the threshold of angina): 30 minutes
daily ≥3 days a week.
4. Influenza vaccination: Annually.
5. Optimal medical therapy to improve prognosis and control the
symptoms of angina.
6. Invasive treatment (percutaneous coronary intervention [PCI], coronary
artery bypass grafting [CABG]): In eligible patients.
Optimal Medical Therapy: Treatment to Improve Prognosis
1) Antiplatelet agents: Acetylsalicylic acid (ASA) 75 mg once daily; in the case of adverse
gastrointestinal effects, add an antacid. In patients with contraindications to ASA (allergy,
aspirin-induced asthma), use clopidogrel 75 mg once daily; a combination therapy with ASA
and clopidogrel is not recommended in stable patients except after stenting (see below).
2) ­Low-dose oral anticoagulants: ASA in addition to a low-dose oral anticoagulant
(rivaroxaban 2.5 mg bid) may be considered as an added risk-reduction strategy in patients
who are at elevated risk of future coronary events compared with bleeding events.
3) Statins: Make attempts to lower LDL-C levels ≤1.8 mmol/L (<1.4 mmol/L according to the
European Society of Cardiology [ESC]), and if this cannot be achieved, to reduce them by
>50% compared with baseline levels. In cases of poor tolerance or ineffectiveness of statins,
the use of ezetimibe or proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors can be
considered.
4) Angiotensin-converting enzyme inhibitors (ACEIs) (or angiotensin-receptor
blockers [ARBs]) are indicated in patients with coexisting hypertension, diabetes mellitus,
heart failure, or LV systolic dysfunction.
Optimal Medical Therapy: Treatment to Control Symptoms
1. Acute symptom control and prevention prior to planned exercise: Use
a short-acting nitrate: nitroglycerin aerosol. Patients should be instructed to use
nitroglycerin 3 times at 5-minute intervals. If no relief is achieved, the patient
should call an ambulance and should be assessed by the medical personnel for
acute chest pain. Relative contraindications include hypertrophic
cardiomyopathy with outflow tract obstruction, severe aortic stenosis, use of
phosphodiesterase-5 (PDE-5) inhibitors (eg, sildenafil). Other drug interactions
include alpha-blockers (in male patients with benign prostatic hyperplasia, the
combined use of nitrates and a selective alpha-blocker [tamsulosin] is allowed).
Adverse effects: headache, facial flushing, dizziness, syncope.
2. Prevention of angina and increasing exercise tolerance:
1) Beta-blockers reduce heart rate, contractility, and atrioventricular (AV) conduction. They
are the first-line agents for treatment of angina. Physicians should titrate the dose on the
basis of heart rate and blood pressure with a goal to achieve the maximum recommended
dose. A beta-blocker may be considered in asymptomatic patients with extensive ischemia
(>10% of LV).
Absolute contraindications: symptomatic bradycardia, symptomatic hypotension, second-
degree or third-degree AV block, sick sinus syndrome, severe decompensated heart failure.
Adverse effects: bradycardia, AV block, bronchospasm, peripheral artery spasm, and
peripheral hypoperfusion in patients with severe peripheral artery disease; sexual dysfunction
and loss of libido; and particularly in the case of propranolol, fatigue, headache, sleep
disturbances, insomnia, vivid dreams, depression. Caution should be exercised in combining
beta-blockers with verapamil and diltiazem due to their additive effects on AV conduction and
heart rate.
2) Calcium channel blockers are smooth muscle vasodilators; they have a negative inotropic
effect. They can be used in patients who cannot take beta-blockers or do not respond to
monotherapy with a beta-blocker.
a) Diltiazem and verapamil lower the heart rate. They are of value in patients with
contraindications to or intolerance of beta-blockers. Contraindications: heart failure,
bradycardia, AV conduction disturbances, hypotension. Adverse effects: constipation,
bradycardia, AV block, hypotension.
b) Dihydropyridines are vasodilators. Their mechanism of action is complementary to beta-
blockers. They can be used in combination with a beta-blocker in patients not responding to
a beta-blocker alone. Adverse effects: facial flushing, headache, peripheral edema.
3) Long-acting nitrates are arterial and venous vasodilators; they reduce preload. Isosorbide
dinitrate, isosorbide mononitrate, or nitroglycerin are recommended as second-line agents;
When administered bid, ensure ~10-hour intervals between the doses. The onset of action of
nitroglycerin patches occurs a few minutes after they are attached; their antianginal effect is
maintained for 3 to 5 hours.
Percutaneous coronary intervention
Coronary artery bypass graft
Findings of invasive angiography (extent and complexity of CAD, LV dysfunction) as well as clinical factors (age,
comorbidities, history of diabetes mellitus) dictate the decision to perform revascularization and the choice of
the revascularization strategy. In patients with multivessel disease, the angiographic extent and complexity of
CAD can be quantified using the SYNTAX score (www.syntaxscore.com). Decisions about the revascularization
strategy are usually taken by an interventional cardiologist in consultation with a cardiovascular surgeon as part
of the heart team approach.
Choice of PCI vs CABG
1. PCI is the preferred treatment in patients with:
1) One-vessel disease (including the proximal section of the LAD) or 2-vessel disease that does not involve the
proximal LAD.
2) Anatomic features of a low-risk lesion.
3) Comorbidities increasing the risk of cardiac surgery.
2. CABG is preferred in patients with:
1) Three-vessel disease and a SYNTAX score >22 or reduced LV function.
2) Patients with diabetes mellitus and multivessel disease.
3) Left main coronary artery stenosis combined with 2-vessel or 3-vessel disease in patients with a SYNTAX score
>32.
Microvascular angina refers to angina pectoris with accompanying
ST-segment depression on the electrocardiography (ECG) stress test
(resting ECG is usually normal) and normal coronary angiography
(without epicardial coronary artery spasm on ergonovine or
acetylcholine challenge). Microvascular angina was formerly termed
cardiac syndrome X.
Symptoms: Chest pain is often atypical; it may be very severe and
usually develops on exertion but may also occur at rest. The pain
usually lasts >10 minutes (up to >30 minutes after the end of
exertion); it responds poorly to nitroglycerin. Symptoms of anxiety
disorders may occur. Acute coronary syndrome may occur despite
the absence of significant epicardial artery occlusion on angiography.
Diagnosis is based on the exclusion of significant (or dominant)
coronary artery disease and other diseases that may cause chest pain.

TREATMENT
Acetylsalicylic acid (ASA) and statins are recommended in all patients;
treatment of chest pain using beta-blockers (first-line agents), nitrates,
or calcium channel blockers. In patients not responding to these agents,
used either alone or in combination, administer imipramine 50 mg once
daily. Some studies have reported beneficial effects of angiotensin-
converting enzyme inhibitors (ACEIs), sildenafil, ranolazine, L-arginine,
and metformin. Behavioral interventions and physical exercise also may
be beneficial.
Vasospastic angina (Prinzmetal variant angina) is a type of angina in
which chest pain is caused by transient ischemia secondary to
spontaneous coronary artery spasm. Chest pain generally occurs at
rest and usually in the absence of flow-limiting coronary stenoses.
Symptoms include chest pain occurring at rest, commonly in the late
night or early morning hours, which is frequently transient and lasts
between 5 and 15 minutes. On occasion, it may also develop on
exertion, although this is less common. Other associated symptoms
may include nausea, diaphoresis, palpitations, dyspnea, and
lightheadedness.
Diagnosis is based on the occurrence of unprovoked chest pain at rest with accompanying ST-
segment elevation (less commonly depression) on electrocardiography (ECG) and absence of
significant coronary artery stenosis on coronary angiography. If an episode occurs during
coronary angiography, coronary spasm may be directly observed during the procedure.
Interventionalists can provoke coronary spasm via medications such as acetylcholine,
ergonovine, or via hyperventilation, but this is not done commonly and only performed when
the diagnosis is unclear.
In patients with recurrent pain, Holter monitoring may reveal ST-segment changes with pain.
Whether ST-segment elevation or ST-segment depression is seen depends on the severity of
spasms: full occlusion causes ST-segment elevation, while a less severe spasm may cause ST-
segment depression. Rises in the levels of biomarkers of ischemia depend on the duration of
the spasm. While most times the spasm is transient, a prolonged spasm may lead to actual
infarction and arrhythmia in up to 25% of patients.
Electrocardiography (ECG) of a patient with vasospastic angina in a pain-free state (A) and during a pain
episode (B).
Medical Treatment
1. Modification of risk factors, particularly smoking cessation.
2. Low-dose acetylsalicylic acid (ASA).
3. High-dose oral calcium channel blockers: Diltiazem 120 to 360
mg/d, verapamil 240 to 480 mg/d. If treatment with 1 calcium
channel blocker is not effective, add another calcium channel blocker
of a different group or a long-acting nitrate.
4. Nonselective beta-blockers are contraindicated as they may
exacerbate vasospasm.
Invasive Treatment
Percutaneous intervention is not recommended as the first-line therapy for
patients with coronary vasospasm and nonobstructive coronary disease.
Consideration may be given to percutaneous coronary intervention (PCI) if
a significant plaque (≥70%) is present and if the plaque is thought to be a trigger
for localized vasospasm with the patient developing pain at rest. Further, PCI of
a vasospastic segment may be of benefit in patients who are refractory to
medical therapy if the vasospastic segment is clearly visualized on the diagnostic
catheterization. Outcomes overall are variable as vasospasm may occur in
a different section of the artery, and thus medical therapy is considered the first-
line treatment. Vasospasm-associated severe arrhythmias may require treatment
with a pacemaker or implantable cardioverter-defibrillator (ICD).