Also known as: Chest Pain, Angina Pectoris
Related conditions: Chest Pain, Acute Coronary Syndrome, Myocardial Infarction
1. Description of the problem
Stable angina is a chronic pattern of transient chest pain that is precipitated by activity and relieved with rest. No permanent myocardial injury occurs.
During stable angina, there is a transient imbalance between myocardial oxygen supply and demand; as a result, during periods of exertion, demand outweighs the coronary blood supply, resulting in symptoms that can include chest pain and shortness of breath. Because of fixed coronary artery disease, chronic stable angina is manifested as a pattern of predictable chest discomfort. With greater degrees of coronary stenosis, less exertion is required to elicit anginal symptoms. Normally, angina occurs when the coronary artery lumen is reduced by approximately 70%. In addition, there is often endothelial dysfunction associated with coronary atherosclerosis that can result in inappropriate vasoconstriction that may exacerbate anginal symptoms.
Angina is often described as “chest pressure”, “discomfort”, “tightness” or “heaviness.” The discomfort does not usually vary with respiration. It is generally diffuse, located in the retrosternal area or left precordium, and can radiate across the chest, neck, arms/shoulders, and upper abdomen. Anginal symptoms usually last for several minutes, and are often relieved with cessation of activity.
The primary management goals are to decrease the frequency and intensity of anginal symptoms. This may be accomplished with pharmacologic and/or invasive therapies. Stress testing or coronary angiography should be considered to define the extent of myocardial ischemia and the underlying coronary anatomy. Medical therapy should focus on decreasing myocardial oxygen demand, while increasing myocardial oxygen supply.
2. Emergency Management
Chronic stable angina is rarely a medical emergency. An EKG should always be performed in cases in which patients seek medical attention – signs of coronary ischemia may include ST-segment depression and T-wave inversion; occasionally ST-segment elevation is seen, particularly when associated with coronary vasospasm. If electrocardiographic abnormalities fail to resolve, however, one should consider the possibility that this represents a true acute coronary syndrome.
Pharmacologic therapies (including nitrates, beta blockers, and calcium channel blockers) can be employed for both acute and chronic symptom relief for patients with stable angina. In cases refractory to medical treatment, coronary angiography and percutaneous coronary revascularization should be entertained for symptom resolution.
Medical and behavioral therapies should also focus on risk factor modification. Such treatments include tobacco cessation counseling, lipid-lowering therapies, antihypertensive medications, and diabetes control.
Diagnosis is often made by careful history and physical examination. Confirmatory studies, including stress testing and/or coronary angiography, can help define the pathologic substrate for chronic angina. Examples of stress tests include exercise treadmill testing, nuclear imaging studies, exercise or pharmacologic echocardiographic studies, and cardiac computed tomography.
Normal lab values
Patients with chronic, stable angina should have no elevation in cardiac biomarkers; in particular, CK-MB and cardiac troponins should be within the normal reference range for each specific assay. Any elevation in cardiac biomarkers could suggest the presence of myocardial infarction.
How do I know this is what the patient has?
With a typical history and examination, one can be fairly certain of a diagnosis of stable angina. If pain relief occurs with the addition of vasodilators, such as nitrate therapy, a diagnosis of stable angina is likely. Confirmatory testing that reveals myocardial ischemia during pharmacologic or exercise stress also supports this diagnosis. The gold-standard diagnostic tool is the coronary angiogram; if there is evidence of coronary stenosis of at least 70%, this is diagnostic of stable angina.
Other conditions can mimic stable angina; these include acute myocardial infarction, unstable angina, acute pericarditis, acute pulmonary embolism, and pneumonia, to name a few.
Confirmatory tests include the use of stress testing and/or coronary angiography. Diagnostic tests include the exercise treadmill test, pharmacologic and exercise echocardiography, pharmacologic and exercise nuclear imaging, and coronary computed tomography. Coronary angiography is the only definitive way to define the coronary anatomy and to evalute for the presence of fixed, obstructive coronary artery disease.
4. Specific Treatment
Nitrates (e.g. nitroglycerin) – these drugs will decrease myocardial oxygen demand through venodilatation; they also will increase oxygen supply by reducing vasospasm and increasing coronary perfusion
Beta Blockers – these drugs decrease myocardial oxygen demand by decreasing myocardial contractility and heart rate
Calcium Channel Blockers – these drugs decrease myocardial oxygen demand by reducing blood pressure (i.e. decreasing wall tension), contractility, and heart rate; through venodilatation, calcium channel blockers will also increase myocardial oxygen supply
Ranolazine – this drug decreases late-phase inward sodium currents; it has been shown to decrease the frequency of anginal episodes and improve functional capacity; its exact mechanism of action is incompletely understood
Aspirin – potent inhibitor of platelet aggregation; helps to prevent acute cardiac events in patients with chronic, stable angina
HMG-CoA Reductase Inhibitors – “statins”; lower MI rates and mortality for patients with established coronary artery disease through lipid-lowering and other pleiotropic mechanisms
Percutaneous Coronary Intervention – this includes percutaneous transluminal coronary angioplasty (PTCA) or coronary stenting, and is useful for the reduction in anginal symptoms in patients refractory to medical therapy
Drugs and dosages
Nitroglcyerin (sublingual) – 0.4mg under the tongue every 5 minutes up to 3 doses
Isosorbide Dinitrate – sustained release: 5-40 mg orally every 8-12 hrs
Isosorbide Mononitrate – sustained release: 30-60 mg daily, titrated up to 240 mg daily
Metoprolol – 100-400 mg in two divided doses orally
Atenolol – 50-200 mg daily
Calcium channel blockers
Amlodipine – 5-10 mg daily
Verapamil – 180-480 mg daily
Diltiazem – 180-360 mg divided in 3 or 4 doses daily
500-1000 mg twice daily
HMG-COA reductase inhibitors
Simvastatin – 5-40 mg daily
Atorvastatin – 10-80 mg daily
Rosuvastatin – 5-40 mg daily
Lovastatin – 10-80 mg daily
Pravastatin – 10-80 mg daily
Aspirin – 81-325 mg daily
For cases of stable angina refractory to medical therapy, consideration should be given to coronary revascularization. When coronary revascularization is not an option, alternative therapies include enhanced external counterpulsation (EECP).
5. Disease monitoring, follow-up and disposition
Expected response to treatment
A good response to pharmacologic therapy should include a decrease in the frequency of anginal episodes as well as the intensity of anginal symptoms. Coronary revascularization, if the target lesion is appropriately addressed, should significantly reduce anginal symptoms and the need for anti-anginal medical therapies.
When patients present with atypical signs and symptoms, and for those that fail to respond to aggressive anti-anginal therapies, an alternative diagnosis should be considered.
Patients should follow up closely with a primary care physician or cardiologist. Careful attention should be paid to interval changes in anginal frequency and intensity. Furthermore, aggressive modification of risk factors – including hypertension, hyperlipidemia, diabetes, obesity, and tobacco abuse – should be the focus of subsequent clinical visits.
Angina is, in its simplest form, the result of an imbalance between myocardial oxygen supply and demand. Factors that increase myocardial demand include increased wall stress, increased heart rate, and increased myocardial contractility. Wall stress is inversely proportional to the ventricular wall thickness; as a result, a hypertrophied heart will have lower wall stress and oxygen consumption than a thin-walled heart. Anything that increases the left ventricular cavity, however, will increase wall stress – conditions, therefore, that increase ventricular filling (e.g. aortic or mitral regurgitation) will increase wall stress and myocardial oxygen demand.
Any conditions that increase heart rate (e.g. physical exertion, stress) will increase oxygen demand, and conditions that increase contractility (e.g. use of positive inotropic drugs, circulating catecholamines) will also increase oxygen demand. Myocardial oxygen supply is affected by alterations in coronary arterial tone and vascular resistance.
Patients with chronic, stable angina have fixed coronary vessel narrowing due to stenoses. Associated with fixed vessel stenosis is endothelial dysfunction. Endothelial dysfunction contributes to ischemia through inappropriate coronary vasoconstriction and through loss of normal antithrombotic properties (i.e. impaired release of nitric oxide and prostacyclin).
Stable angina remains the most common manifestation of ischemic heart disease, and it is estimated that over 6 million people in the United States alone suffer from angina. The risk of developing angina increases with age and is associated with a number of risk factors, including diabetes mellitus, hypertension, tobacco abuse, and hyperlipidemia. Men with stable angina are more likely to develop future acute coronary syndromes than women and are more likely to succumb to coronary artery disease-related death.
The natural history of chronic, stable angina is somewhat unpredictable. Some patients may have no change in their stable pattern of ischemia over years to decades. Other patients, however, may have their stable angina punctuated by unstable episodes of acute coronary syndromes, acute myocardial infarction, and even sudden death. The mortality associated with coronary artery disease has decreased somewhat over time, likely the result of improvements in therapeutic agents that treat common risk factors. Nonetheless, ischemic heart diseases remain the most common cause of death worldwide.
What's the evidence?
Abrams, J. “Chronic stable angina”. NEJM. vol. 352. 2005. pp. 2524-33. (Good review on chronic angina.)
Fraker, TD. “2007 chronic angina focused update of the ACC/AHA 2002 guidelines for the management of patients with chronic stable angina: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Writing Group to develop the focused update of the 2002 guidelines for the management of patients with chronic stable angina”. J Am Coll Cardiol. vol. 50. 2007. pp. 2264-74. (Focused guidelines on the management of the patient with chronic angina.)
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- 1. Description of the problem
- 2. Emergency Management
- 3. Diagnosis
- 4. Specific Treatment
- 5. Disease monitoring, follow-up and disposition
- What's the evidence?