• Stable angina is a clinical syndrome characterized by discomfort in the chest, jaw, shoulder, back, or arms, typically elicited by exertion or emotional stress and relieved by rest or nitroglycerin.
• Chronic angina
  • Does not increase in frequency or severity, and is predictable in nature.
  • May be associated with ST segment depression on ECG.
  • May occur in patients with seemingly normal coronary arteries subjected to acute or chronic increases in myocardial work.
• Coronary artery spasm can provoke pain in the absence of increased myocardial demands such as variant (Prinzmetal’s) angina and some cases of stable or unstable angina.

• The most frequent causes of angina are as follows: coronary atherosclerosis, coronary artery vasospasm, fibrosis, embolism, dissection, and arteritis.
• Nonmodifiable risk factors: Age, family history, and male gender.
• Modifiable risk factors: Cigarette smoking, hypertension, dyslipidemia, diabetes, chronic kidney disease, obesity, and physical inactivity.

• Myocardial ischemia is caused by an imbalance between myocardial oxygen supply and myocardial oxygen consumption.
• Myocardial oxygen supply is determined by arterial oxygen saturation and coronary flow that is dependent on the luminal cross-sectional area of the coronary artery and coronary arteriolar tone. Atherosclerotic plaques may dramatically decrease both the cross-sectional area and coronary artery tone. When combined with increased oxygen demand from tachycardia, increased myocardial contractility and wall stress, the oxygen supply may become inadequate.
• Ischemia reduces the formation of adenosine triphosphate (ATP), an oxygen-dependent process. This results in the development of lactic acidosis, loss of the normal Na⁺/K⁺ ATPase pump, impaired myocardial membrane integrity, and release of chemical substances that stimulate chemosensitive and mechanoreceptive receptors within cardiac muscle fibers and around the coronary vessel.
• The primary mediator of angina is adenosine, via stimulation of the A1 adenosine receptor.

• Preoperative assessment should assess current myocardial function and if there is myocardium at risk for ischemia; a relevant clinical history may warrant further testing (1).
• Ensure an adequate myocardial oxygen supply: Assess hemoglobin, diastolic perfusion pressure, oxygen saturation, and adequate diastolic time (low heart rate; HR).
• Avoid increases in myocardial oxygen demand: Assess HR, myocardial contractility, afterload, and preload.

• Characterized as a discomfort rather than pain, and may be difficult to describe.
• Location is most commonly felt beneath the sternum, but can vary. Radiation may occur to the left shoulder and down the inside of the left arm, even to the fingers; straight through to the back; into the throat, jaws, and teeth; and, occasionally, down the inside of the right arm. It may also be felt in the upper abdomen.
• Onset and offset is typically gradual; the intensity of the discomfort increases and decreases over several minutes.
• Provoking factors: Physical activity, cold, emotional stress, sexual intercourse, meals, or lying down (which results in an increase in venous return and increase in wall stress).
• Duration: Generally lasts for 2–5 minutes unless the patient is experiencing an acute coronary syndrome, especially MI.
• Relief: Symptoms usually subside with rest.
• Associated symptoms include shortness of breath, belching, nausea, indigestion, diaphoresis, dizziness, lightheadedness, clamminess, and fatigue.

• Coronary angiography
• Revascularization
• Percutaneous coronary intervention (PCI)
• Coronary artery bypass grafting (CABG)
• Implanted pacemakers and defibrillation devices

• Antianginal therapy
  • Nitrates: Anti-ischemic efficacy pertains to their ability to decrease myocardial oxygen demand as a result of systemic vasodilatation rather than as a coronary vasodilator.
  • Beta-blockers: Relieve anginal symptoms by reducing both HR and contractility.
  • Calcium channel blockers: Improve anginal symptomatology by coronary and peripheral vasodilatation and by reducing contractility.
• Additional treatment
  • ACE inhibitors: Recommended for patients with stable angina pectoris and coexisting hypertension, diabetes, heart failure, asymptomatic LV dysfunction, or post-MI.
  • Angiotensin receptor blockers (ARBs): Recommended for patients who have hypertension, heart failure; indications for, but an inability to tolerate ACE inhibitors; or have had an MI with LV ejection fraction 40%.
  • Statins
• Antiplatelet drugs
  • Aspirin: The optimal antithrombotic dosage of aspirin appears to be 75–162 mg/day.
  • Clopidogrel: An alternative for patients who are allergic to aspirin.

• Congestive heart failure
• Arrhythmias

• ST segment changes on ECG
• Symptoms of worsened, or decompensated heart failure
• Symptoms of increased activation of the adrenergic system: Elevated BP and increased HR
• Supraventricular or ventricular arrhythmias with hemodynamic instability

• Canadian Cardiovascular Society Angina Classification
  • Class 0: Asymptomatic
  • Class 1: Angina with strenuous exercise
  • Class 2: Angina with moderate exertion
  • Class 3: Angina with mild exertion
    • Walking 1–2 level blocks at normal pace
    • Climbing 1 flight of stairs at normal pace
  • Class 4: Angina at any level of physical exertion

• Vigilance for chest pain, arrhythmias, and hemodynamic instability
• Consider supplemental oxygen (nasal cannula, face mask)
• Good pain control
• Normothermia

• Perioperative ischemia and/or MI.
• Patients with symptomatic MI after surgery have a marked increase in the risk of death (40–70%).
  • Postoperative troponin measurement is recommended in patients with ECG changes or chest pain typical of acute coronary syndrome.
• Perioperative arrhythmias and conduction disorders

• Coronary Arteries
• Myocardial Oxygen Demand

• 411.1 Intermediate coronary syndrome
• 413.1 Prinzmetal angina
• 413.9 Other and unspecified angina pectoris

• I20.0 Unstable angina
• I20.1 Angina pectoris with documented spasm
• I20.9 Angina pectoris, unspecified

Piotr K. Janicki , MD, PhD

Marek Postula , MD, PhD