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Stable angina

Updated : January 1, 2024





Background

Stable angina, also referred to as typical angina or angina pectoris, serves as an indicator of myocardial ischemia. It presents chest discomfort or an anginal equivalent triggered by exertion and relieved either at rest or through the use of nitroglycerin. Frequently, it stands out as an initial manifestation or warning signal of underlying coronary disease.

The prevalence of angina is notable, affecting approximately 10 million individuals in the United States. Consequently, it is crucial not only to identify the signs and symptoms but also to assess the risk and manage individuals experiencing these manifestations appropriately. 

Epidemiology

Coronary heart disease has a substantial impact on more than 17 million adults in the United States. Among the affected population, 55% are male, and the condition contributes to an annual death toll exceeding 500,000 in the U.S. By the age of 40, the risk of developing coronary disease is estimated at 48% for men and 30% for women.

While the incidence of coronary events rises with age, the initially higher prevalence in males diminishes gradually with advancing years. It is important to note that coronary heart disease, or ischemic heart disease, is a global concern, standing as the leading cause of death among adults across low, middle, and high-income countries.

The repercussions of coronary heart disease extend beyond mortality, often resulting in significant debility. One notable manifestation of this debility is angina, impacting over 10 million individuals in the U.S., with more than 500,000 new cases diagnosed annually. 

Anatomy

Pathophysiology

Stable angina, also known as angina pectoris, is a manifestation of myocardial ischemia, which occurs when the blood supply to the heart muscle is insufficient to meet its metabolic demands. The pathophysiology of stable angina is primarily rooted in coronary artery atherosclerosis. During periods of increased demand, such as physical exertion or stress, the compromised coronary blood flow becomes insufficient to meet the heightened oxygen requirements of the heart muscle.

This imbalance between oxygen supply and demand results in ischemia, leading to the characteristic symptoms of stable angina. The pathophysiology of stable angina involves not only the mechanical obstruction caused by atherosclerosis but also the dynamic component of coronary vasospasm.

In addition to fixed atherosclerotic lesions, the coronary arteries may undergo transient constriction, further compromising blood flow and exacerbating ischemia. These episodes of vasospasm can be triggered by various factors, including emotional stress, exposure to cold, or the release of vasoactive substances. 

Etiology

The origin of stable angina lies in a discrepancy between myocardial oxygen supply and demand. This occurs when the transient demand for myocardial oxygen surpasses its supply, often giving rise to symptomatic manifestations. Various factors contribute to stable angina, with the predominant cause being coronary artery stenosis. 

Genetics

Prognostic Factors

The prognosis of stable angina is contingent upon its underlying cause. Regardless of the specific etiology, it is crucial to prioritize aggressive risk factor modification. Individuals with stable angina should undergo regular screening to detect any escalation in symptom frequency or progression to unstable angina. 

Clinical History

Individuals experiencing stable angina often exhibit a subacute rather than chronic presentation. Assessing the patient’s medical history and conducting a thorough physical examination serves as a valuable screening tool for identifying high-risk individuals. Incorporating routine screening measures for blood pressure, sleep patterns, weight, stress levels, exercise tolerance, and substance use (including alcohol, tobacco, and illicit drugs) is essential.

Typical angina manifests as chest discomfort or an anginal equivalent triggered by exertion and relieved by rest or nitroglycerin. Anginal equivalents may vary but often include symptoms such as shortness of breath, nausea, or fatigue that exceeds the expected level of exertion.

Differentiating between cardiac and non-cardiac chest discomfort is crucial. A detailed discussion of the patient’s symptoms, considering factors such as the location, quality, influencing factors, duration of pain, and timing, is instrumental in guiding this differentiation process. 

Physical Examination

Typical angina is commonly characterized by sensations of pressure, heaviness, tightness, or squeezing in the chest. It typically affects a diffuse area of the chest rather than a specific spot, and the pain may radiate depending on the affected dermatomes. Symptoms tend to intensify during periods of heightened demand, such as walking, lifting, or emotional stress.

The duration of symptoms generally spans two to five minutes, with relief experienced upon cessation of the provoking activity or through the use of nitroglycerin. During a physical examination, findings are typically unremarkable, as active ischemia is not expected in the context of typical angina, resulting in nonspecific exam results. 

Age group

Associated comorbidity

Associated activity

Acuity of presentation

Differential Diagnoses

  • Acute coronary syndrome 
  • Esophageal spasm 
  • Chronic obstructive pulmonary disease 
  • Costochondritis 

Laboratory Studies

Imaging Studies

Procedures

Histologic Findings

Staging

Treatment Paradigm

The treatment paradigm for stable angina focuses on alleviating symptoms, reducing the frequency of angina episodes, and improving the overall quality of life for individuals with this condition. Lifestyle modifications are often the initial approach and include recommendations such as smoking cessation, adopting a heart-healthy diet, regular exercise, and weight management.

Medications play a crucial role in managing stable angina, with antiplatelet agents, beta-blockers, calcium channel blockers, and nitroglycerin commonly prescribed. Antiplatelet drugs like aspirin help prevent blood clot formation, while beta-blockers and calcium channel blockers reduce the workload on the heart by lowering heart rate and blood pressure.

Long-acting nitroglycerin helps dilate coronary arteries, improving blood flow to the heart. In cases where symptoms persist despite optimal medical therapy or in patients with high-risk features, invasive interventions such as coronary artery revascularization may be considered. This can involve procedures like percutaneous coronary intervention (PCI) with stent placement or coronary artery bypass grafting (CABG) to improve blood flow to the heart muscle.

Overall, the treatment paradigm for stable angina is tailored to individual patient characteristics, emphasizing a comprehensive approach that addresses lifestyle factors, employs pharmacological management, and considers invasive interventions when necessary. Regular follow-up and ongoing adjustments to the treatment plan are crucial to ensure optimal symptom control and prevent disease progression. 

by Stage

by Modality

Chemotherapy

Radiation Therapy

Surgical Interventions

Hormone Therapy

Immunotherapy

Hyperthermia

Photodynamic Therapy

Stem Cell Transplant

Targeted Therapy

Palliative Care

Lifestyle Modifications

  • Smoking Cessation 

Cigarette smoking stands as the primary preventable contributor to premature mortality. Current smokers face a cardiovascular mortality risk approximately twice that of nonsmokers.

Notably, the risk of cardiovascular mortality in former smokers aligns closely with that of individuals who have never smoked. Therefore, it remains crucial to consistently advocate for smoking cessation, irrespective of age or the duration of an individual’s smoking history. 

  • Obesity 

Obesity ranks as the second major modifiable factor contributing to premature mortality. Tailoring weight-loss regimens to individual patients is essential, encompassing discussions on lifestyle modifications and, where suitable, exploring surgical options. 

  • Blood pressure control 

The 2017 AHA/ACC guidelines establish hypertension as having a systolic blood pressure ≥130 mmHg or diastolic pressure ≥80 mmHg. While individualized goal blood pressure targets are essential, it is crucial to recognize that every 20/10 mmHg rise in systolic/diastolic blood pressure corresponds to a twofold increased risk of mortality related to coronary heart disease and stroke, as supported by evidence. 

 

Administration of a pharmaceutical agent

  • Use of Aspirin 

Evaluate the coronary heart disease risk in each patient. For individuals classified as low-risk, the utilization of aspirin for primary prevention has been shown to decrease the risk of nonfatal myocardial infarction without demonstrating significant benefits in terms of all-cause mortality or nonfatal stroke.

Given the elevated risk of major bleeding associated with aspirin use, particularly extracranial bleeding, and an increased albeit less common risk of intracranial hemorrhage, risk stratification becomes crucial.

In cases where there is no evidence supporting a mortality benefit from aspirin use in low-risk individuals, the potential risk of bleeding may outweigh the anticipated advantages.

Therefore, the decision to prescribe aspirin in such cases should be made on an individual basis. Conversely, high-risk individuals or those with known cardiovascular disease experience benefits from the use of low-dose aspirin on a daily basis. 

  • Use of HMG-CoA reductase inhibitor 

The use of statin therapy in individuals without clinical evidence of coronary disease, categorized as high, moderate, or low risk for primary prevention, has shown efficacy in reducing the incidence of myocardial infarction, stroke, cardiovascular death, and overall mortality. 

Medication

 

felodipine

initial dose:

5

mg

Orally 

once a day


Maintenance dose: 10 mg orally once a day after 2 to 4 weeks of the initial dose



ranolazine

Chronic:

500

mg

Tablet

Oral

twice a day


increase to 1000 mg tablet twice a day only if needed



pindolol 

(Off-label)
indicated for Chronic Stable Angina:

15 - 40

mg/day

Orally 

dose divided every 4 hours



verapamil 


Indicated for Angina

Immediate release-80 mg orally three times a day initially, usual dose range 80-120 mg orally three times a day. It should not exceed 480 mg daily.
Extended-release(Covera-HS)- 180 mg every day orally at bedtime as an initial dose.
Maintenance dose-180-540 mg every day orally at bedtime.

Paroxysmal Supraventricular Tachycardia and Chronic Atrial Fibrillation

Immediate release-240-480 mg every day orally in divided doses three-four times a day.
Atrial Fibrillation or Flutter and Supraventricular Arrhythmia
2.5-5 mg intravenously over 2 min; after 15-30 min, 5-10 mg dose may be repeated.
Or

0.075-0.15mg/kg (should not exceed 10 mg) intravenously over 2 min; after 30 min, the dose may be repeated.
Tardive Dyskinesia
40 mg orally three times a day may enhance the dose up to 120 mg three times a day.
Migraine as off-label
As prophylaxis 160-320 mg orally three-four times a day.
Hypertension
Immediate release
Initial dose:80 mg orally three times a day.
Maintenance dose: 80-320 mg orally two times a day.
Extended-release
Isoptin SR, Calan-180 mg every day orally in the morning (if the patient is elderly,120 mg every day); for desired therapeutic response, the dose may enhance to 240 mg every day and then 360 mg every day (i.e., 180 mg two times a day or 240 mg at morning time and 120 mg at evening time)
Verelan-180 mg every day orally in the morning (if the patient is elderly,120 mg every day); for desired therapeutic response, the dose may enhance to 240 mg every day and then 120 mg every day at weekly intervals, should not exceed 480 mg every day.
Covera-HS-180 mg every day orally at bedtime (if the patient is elderly,120 mg every day); for desired therapeutic response, the dose may enhance to 240 mg every day and then 120 mg every day at weekly intervals, should not exceed 480 mg every day.
Verelan PM-200 mg every day orally at bedtime (if the patient is elderly,100 mg every day); the dose may be enhanced by 100 mg every day at weekly intervals, and should not exceed 400 mg every day.



nicardipine 

Take 20 to 40 mg orally every 8 hours
Start at 20 mg, and allow three days between dose raise to achieve steady-state plasma drug concentration
General daily dose range be 60 to 120 mg
Dosing Modifications
Renal impairment
Take a dose of 20 mg as immediate release orally every 8 hour initially and titrated in every three days
Take a dose of 30 mg as extended release orally every 12 hours initially and titrated in every three days
Use cautiously as intravenously
Hepatic impairment
Take a dose of 20 mg as immediate release orally every 12 hour initially and titrated in every three days
Daily immediate-release dose, may be not equivalent to daily extended-release dose
Use cautiously as intravenously
Pitt-Hopkins Syndrome (Orphan)
Orphan designation for treatment of Pitt-Hopkins Syndrome



perhexiline 


Indicated for chronic stable angina
100 mg orally every day
Depending on the plasma levels, adjust the dosage at two to four weeks intervals
The Maximum dosage is 300 mg to 400 mg in a day in divided doses



trimetazidine 

for conventional tab:
Take a dose of 20 mg orally three times a day
for modified-release tab:
Take a dose of 35 mg orally two times a day



 
 

verapamil 


Indicated for Angina

Immediate release-80 mg orally three times a day initially, usual dose range 80-120 mg orally three times a day. It should not exceed 480 mg daily.
Extended-release (Covera-HS)- 180 mg every day orally at bedtime as an initial dose.
Maintenance dose-180-540 mg every day orally at bedtime.
Hypertension
Immediate release
Initial dose:80 mg orally three times a day.
Maintenance dose: 80-320 mg orally two times a day.
Extended-release
Verelan PM-100 mg every day orally at bed time.
Covera-HS-180 mg every day orally at bed time.
Isoptin SR, Calan SR, Verelan-120 mg every day orally in the morning.
Note:
Generally, low doses are warranted, and based on clinical response dose may be adjusted.



Media Gallary

References

Stable angina

Updated : January 1, 2024




Stable angina, also referred to as typical angina or angina pectoris, serves as an indicator of myocardial ischemia. It presents chest discomfort or an anginal equivalent triggered by exertion and relieved either at rest or through the use of nitroglycerin. Frequently, it stands out as an initial manifestation or warning signal of underlying coronary disease.

The prevalence of angina is notable, affecting approximately 10 million individuals in the United States. Consequently, it is crucial not only to identify the signs and symptoms but also to assess the risk and manage individuals experiencing these manifestations appropriately. 

Coronary heart disease has a substantial impact on more than 17 million adults in the United States. Among the affected population, 55% are male, and the condition contributes to an annual death toll exceeding 500,000 in the U.S. By the age of 40, the risk of developing coronary disease is estimated at 48% for men and 30% for women.

While the incidence of coronary events rises with age, the initially higher prevalence in males diminishes gradually with advancing years. It is important to note that coronary heart disease, or ischemic heart disease, is a global concern, standing as the leading cause of death among adults across low, middle, and high-income countries.

The repercussions of coronary heart disease extend beyond mortality, often resulting in significant debility. One notable manifestation of this debility is angina, impacting over 10 million individuals in the U.S., with more than 500,000 new cases diagnosed annually. 

Stable angina, also known as angina pectoris, is a manifestation of myocardial ischemia, which occurs when the blood supply to the heart muscle is insufficient to meet its metabolic demands. The pathophysiology of stable angina is primarily rooted in coronary artery atherosclerosis. During periods of increased demand, such as physical exertion or stress, the compromised coronary blood flow becomes insufficient to meet the heightened oxygen requirements of the heart muscle.

This imbalance between oxygen supply and demand results in ischemia, leading to the characteristic symptoms of stable angina. The pathophysiology of stable angina involves not only the mechanical obstruction caused by atherosclerosis but also the dynamic component of coronary vasospasm.

In addition to fixed atherosclerotic lesions, the coronary arteries may undergo transient constriction, further compromising blood flow and exacerbating ischemia. These episodes of vasospasm can be triggered by various factors, including emotional stress, exposure to cold, or the release of vasoactive substances. 

The origin of stable angina lies in a discrepancy between myocardial oxygen supply and demand. This occurs when the transient demand for myocardial oxygen surpasses its supply, often giving rise to symptomatic manifestations. Various factors contribute to stable angina, with the predominant cause being coronary artery stenosis. 

The prognosis of stable angina is contingent upon its underlying cause. Regardless of the specific etiology, it is crucial to prioritize aggressive risk factor modification. Individuals with stable angina should undergo regular screening to detect any escalation in symptom frequency or progression to unstable angina. 

Individuals experiencing stable angina often exhibit a subacute rather than chronic presentation. Assessing the patient’s medical history and conducting a thorough physical examination serves as a valuable screening tool for identifying high-risk individuals. Incorporating routine screening measures for blood pressure, sleep patterns, weight, stress levels, exercise tolerance, and substance use (including alcohol, tobacco, and illicit drugs) is essential.

Typical angina manifests as chest discomfort or an anginal equivalent triggered by exertion and relieved by rest or nitroglycerin. Anginal equivalents may vary but often include symptoms such as shortness of breath, nausea, or fatigue that exceeds the expected level of exertion.

Differentiating between cardiac and non-cardiac chest discomfort is crucial. A detailed discussion of the patient’s symptoms, considering factors such as the location, quality, influencing factors, duration of pain, and timing, is instrumental in guiding this differentiation process. 

Typical angina is commonly characterized by sensations of pressure, heaviness, tightness, or squeezing in the chest. It typically affects a diffuse area of the chest rather than a specific spot, and the pain may radiate depending on the affected dermatomes. Symptoms tend to intensify during periods of heightened demand, such as walking, lifting, or emotional stress.

The duration of symptoms generally spans two to five minutes, with relief experienced upon cessation of the provoking activity or through the use of nitroglycerin. During a physical examination, findings are typically unremarkable, as active ischemia is not expected in the context of typical angina, resulting in nonspecific exam results. 

  • Acute coronary syndrome 
  • Esophageal spasm 
  • Chronic obstructive pulmonary disease 
  • Costochondritis 

The treatment paradigm for stable angina focuses on alleviating symptoms, reducing the frequency of angina episodes, and improving the overall quality of life for individuals with this condition. Lifestyle modifications are often the initial approach and include recommendations such as smoking cessation, adopting a heart-healthy diet, regular exercise, and weight management.

Medications play a crucial role in managing stable angina, with antiplatelet agents, beta-blockers, calcium channel blockers, and nitroglycerin commonly prescribed. Antiplatelet drugs like aspirin help prevent blood clot formation, while beta-blockers and calcium channel blockers reduce the workload on the heart by lowering heart rate and blood pressure.

Long-acting nitroglycerin helps dilate coronary arteries, improving blood flow to the heart. In cases where symptoms persist despite optimal medical therapy or in patients with high-risk features, invasive interventions such as coronary artery revascularization may be considered. This can involve procedures like percutaneous coronary intervention (PCI) with stent placement or coronary artery bypass grafting (CABG) to improve blood flow to the heart muscle.

Overall, the treatment paradigm for stable angina is tailored to individual patient characteristics, emphasizing a comprehensive approach that addresses lifestyle factors, employs pharmacological management, and considers invasive interventions when necessary. Regular follow-up and ongoing adjustments to the treatment plan are crucial to ensure optimal symptom control and prevent disease progression. 

  • Smoking Cessation 

Cigarette smoking stands as the primary preventable contributor to premature mortality. Current smokers face a cardiovascular mortality risk approximately twice that of nonsmokers.

Notably, the risk of cardiovascular mortality in former smokers aligns closely with that of individuals who have never smoked. Therefore, it remains crucial to consistently advocate for smoking cessation, irrespective of age or the duration of an individual’s smoking history. 

  • Obesity 

Obesity ranks as the second major modifiable factor contributing to premature mortality. Tailoring weight-loss regimens to individual patients is essential, encompassing discussions on lifestyle modifications and, where suitable, exploring surgical options. 

  • Blood pressure control 

The 2017 AHA/ACC guidelines establish hypertension as having a systolic blood pressure ≥130 mmHg or diastolic pressure ≥80 mmHg. While individualized goal blood pressure targets are essential, it is crucial to recognize that every 20/10 mmHg rise in systolic/diastolic blood pressure corresponds to a twofold increased risk of mortality related to coronary heart disease and stroke, as supported by evidence. 

 

  • Use of Aspirin 

Evaluate the coronary heart disease risk in each patient. For individuals classified as low-risk, the utilization of aspirin for primary prevention has been shown to decrease the risk of nonfatal myocardial infarction without demonstrating significant benefits in terms of all-cause mortality or nonfatal stroke.

Given the elevated risk of major bleeding associated with aspirin use, particularly extracranial bleeding, and an increased albeit less common risk of intracranial hemorrhage, risk stratification becomes crucial.

In cases where there is no evidence supporting a mortality benefit from aspirin use in low-risk individuals, the potential risk of bleeding may outweigh the anticipated advantages.

Therefore, the decision to prescribe aspirin in such cases should be made on an individual basis. Conversely, high-risk individuals or those with known cardiovascular disease experience benefits from the use of low-dose aspirin on a daily basis. 

  • Use of HMG-CoA reductase inhibitor 

The use of statin therapy in individuals without clinical evidence of coronary disease, categorized as high, moderate, or low risk for primary prevention, has shown efficacy in reducing the incidence of myocardial infarction, stroke, cardiovascular death, and overall mortality. 

felodipine

initial dose:

5

mg

Orally 

once a day


Maintenance dose: 10 mg orally once a day after 2 to 4 weeks of the initial dose



ranolazine

Chronic:

500

mg

Tablet

Oral

twice a day


increase to 1000 mg tablet twice a day only if needed



pindolol 

(Off-label)
indicated for Chronic Stable Angina:

15 - 40

mg/day

Orally 

dose divided every 4 hours



verapamil 


Indicated for Angina

Immediate release-80 mg orally three times a day initially, usual dose range 80-120 mg orally three times a day. It should not exceed 480 mg daily.
Extended-release(Covera-HS)- 180 mg every day orally at bedtime as an initial dose.
Maintenance dose-180-540 mg every day orally at bedtime.

Paroxysmal Supraventricular Tachycardia and Chronic Atrial Fibrillation

Immediate release-240-480 mg every day orally in divided doses three-four times a day.
Atrial Fibrillation or Flutter and Supraventricular Arrhythmia
2.5-5 mg intravenously over 2 min; after 15-30 min, 5-10 mg dose may be repeated.
Or

0.075-0.15mg/kg (should not exceed 10 mg) intravenously over 2 min; after 30 min, the dose may be repeated.
Tardive Dyskinesia
40 mg orally three times a day may enhance the dose up to 120 mg three times a day.
Migraine as off-label
As prophylaxis 160-320 mg orally three-four times a day.
Hypertension
Immediate release
Initial dose:80 mg orally three times a day.
Maintenance dose: 80-320 mg orally two times a day.
Extended-release
Isoptin SR, Calan-180 mg every day orally in the morning (if the patient is elderly,120 mg every day); for desired therapeutic response, the dose may enhance to 240 mg every day and then 360 mg every day (i.e., 180 mg two times a day or 240 mg at morning time and 120 mg at evening time)
Verelan-180 mg every day orally in the morning (if the patient is elderly,120 mg every day); for desired therapeutic response, the dose may enhance to 240 mg every day and then 120 mg every day at weekly intervals, should not exceed 480 mg every day.
Covera-HS-180 mg every day orally at bedtime (if the patient is elderly,120 mg every day); for desired therapeutic response, the dose may enhance to 240 mg every day and then 120 mg every day at weekly intervals, should not exceed 480 mg every day.
Verelan PM-200 mg every day orally at bedtime (if the patient is elderly,100 mg every day); the dose may be enhanced by 100 mg every day at weekly intervals, and should not exceed 400 mg every day.



nicardipine 

Take 20 to 40 mg orally every 8 hours
Start at 20 mg, and allow three days between dose raise to achieve steady-state plasma drug concentration
General daily dose range be 60 to 120 mg
Dosing Modifications
Renal impairment
Take a dose of 20 mg as immediate release orally every 8 hour initially and titrated in every three days
Take a dose of 30 mg as extended release orally every 12 hours initially and titrated in every three days
Use cautiously as intravenously
Hepatic impairment
Take a dose of 20 mg as immediate release orally every 12 hour initially and titrated in every three days
Daily immediate-release dose, may be not equivalent to daily extended-release dose
Use cautiously as intravenously
Pitt-Hopkins Syndrome (Orphan)
Orphan designation for treatment of Pitt-Hopkins Syndrome



perhexiline 


Indicated for chronic stable angina
100 mg orally every day
Depending on the plasma levels, adjust the dosage at two to four weeks intervals
The Maximum dosage is 300 mg to 400 mg in a day in divided doses



trimetazidine 

for conventional tab:
Take a dose of 20 mg orally three times a day
for modified-release tab:
Take a dose of 35 mg orally two times a day



verapamil 


Indicated for Angina

Immediate release-80 mg orally three times a day initially, usual dose range 80-120 mg orally three times a day. It should not exceed 480 mg daily.
Extended-release (Covera-HS)- 180 mg every day orally at bedtime as an initial dose.
Maintenance dose-180-540 mg every day orally at bedtime.
Hypertension
Immediate release
Initial dose:80 mg orally three times a day.
Maintenance dose: 80-320 mg orally two times a day.
Extended-release
Verelan PM-100 mg every day orally at bed time.
Covera-HS-180 mg every day orally at bed time.
Isoptin SR, Calan SR, Verelan-120 mg every day orally in the morning.
Note:
Generally, low doses are warranted, and based on clinical response dose may be adjusted.



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