The Navigation Model of Therapy: Why Awareness Changes Everything
November 16, 2025
Background
Angina pectoris, also known as typical angina or stabilized angina, is a sign of myocardial ischemia. It is partial chest pain provoked by effort and relieved by rest or nitrogylcerin. It is the first complaint or sign of underlying coronary artery disease. In the United States, angina affects ten million people. It is not only important to recognize signs and symptoms, but management of the condition considerably manages the individuals.Â
Epidemiology
Coronary disease affects more than 17 million adults in the US. Among the 17 million Americans influenced, 55 percent are men. Every year, this leads to more than 500,000 deaths in the United States. At 40 years old, men have a 49% likelihood of developing heart disease in their lifetime whereas women have 32%. Although occurrences of coronary events rise as individuals get older; there is a gradual decrease of males with these incidents due to their advanced age.Â
The countries that have the highest rates of death from ischemic heart diseases are low, middle, and high income countries which means that they are not unique to the U.S. adults.Â
Anatomy
Pathophysiology
Angina is due to a lack of balance in the supply and demand factors for myocardial oxygen. Vascular tone regulation and anti-thrombotic activity of coronary artery endothelial cells may be disrupted by stress, hypertension hypercholesterolemia, viruses, bacteria or immune complexes. The commonest cause of myocardial ischemia is stenosis of the coronary arteries which prevents sufficient oxygen delivery during periods when requirements are high. Myocardial supply depends on many things including size and tone of the coronary vessels, collateral blood flow pressure difference between aortic diastolic and ventricular endocardial perfusion per minute heart rate.  Mechanoreceptive and chemo sensitive receptors may get stimulated in the fibers of cardiac muscle when the myocardial demand for oxygen increases than supply. Understanding the exact cause of angina is important for medical treatment and management of risks.Â
Etiology
The mechanism behind stable angina is the result of supply-demand mismatch. The myocardial oxygen demand transiently exceeds the myocardial supply of oxygen, which often leads to the manifestation of symptoms. There are various factors that contribute to stable angina, and the most common one is coronary artery stenosis.Â
Genetics
Prognostic Factors
The probability of diagnosis varies with the type of stable angina that a person has. This makes it an absolute necessary to control risk factors in all cases. It is important to always look for an increase in frequency of symptoms or development to an unstable angina.Â
Clinical History
Stable angina often presents as subacute, requiring a thorough medical history and physical examination to identify high-risk individuals. Regular screening measures include blood pressure, sleep patterns, weight, stress levels, exercise tolerance, and substance use. Typical symptoms include chest discomfort or anginal equivalents, and distinguishing between cardiac and non-cardiac chest discomfort is crucial. Â
Physical Examination
Occasionally, patients may have stable angina or equivalent symptoms and yet have entirely normal findings on physical examination. However, in the presence of a compatible clinical syndrome, angina pectoris can be diagnosed with reasonable reliability if the Levine sign is positive. Third or fourth heart sound may be heard during anginal attack which is caused due to LV dysfunction and mitral regurgitation may occur due to dysfunction of papillary muscle.Â
Common angina is felt as feeling of pressure, squeezing or pain in the chest. Instead of a specific place, a broad area of the chest is generally affected, and the pain can move depending on which dermatomes are being touched. Symptoms are known to increase when there is a lot of demand like walking for long distances or carrying heavy loads up stairs along with emotional stress.Â
Usually, symptoms last for about less than five minutes and are relieved by stopping an activity that causes them or else taking nitroglycerin. There will not be any noticeable findings during physical examinations.  Â
Typical angina can be manifested by heaviness, tightness, pressure-like, or squeezing. It is crucial to identify the differences between non-cardiac and cardiac chest discomfort.Â
Age group
Associated comorbidity
Acute coronary syndromeÂ
Associated activity
Acuity of presentation
Differential Diagnoses
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Stable angina consists of modifications of lifestyle such as cessation of smoking, intake of diet healthy for heart, exercise and management of weight. Medications like antiplatelet agents, beta-blockers, calcium channel blockers and nitrogylcerin would be prescribed for this condition. In cases where symptoms persist or high- risk features occur, invasive interventions like coronary artery revascularization may be considered. The treatment varies among patients based on lifestyle, pharmacological management etc.Â
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
lifestyle-modifications
Cessation of smokingÂ
Smoking cigarettes is the primary contributor to premature moratlity. Cardiovascular mortality risk is higher in smokers than non-smokers. Hence, it is important to educate people to stop smoking irrespective of age.Â
A healthy weight is necessary for a healthy heart. This is the second modifiable factor that contributes to mortality. Based on individual response, weight loss methods should be designed for each patient.Â
Control of blood pressureÂ
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.Â
Use of antiplatelet agents
Aspirin: It prevents the aggregation of platelets by irreversible inhibition of cyclooxygenase following suppression of thromboxane A2. Its antiplatelet activity lasts for 7 days.Â
Clopidogrel: This drug selectively inhibits the binding of ADP to platelet receptors after activation of GPIIb/IIIa complex which further inhibits the aggregation of platelets.Â
Use of beta-adrenergic blockers
Metoprolol: It is a selective blocker of beta-1 adrenergic receptor and reduces the automaticity of contractions. Being lipophilic, it is capable of penetrating into CNS.Â
Atenolol: This blocks the β-1 adrenergic receptors selectively with no or little effect on β-2 receptor. Â
Propranolol: It is a non-selective beta-blocker which is lipophilic.Â
Use of calcium channel blockers
Amlodipine: It inhibits the entry of calcium ions into slow channels and voltage-sensitive parts of myocardium and vascular smooth muscle during depolarization.Â
Diltiazem: It inhibits the entry of calcium ions into slow channels and voltage-sensitive parts of myocardium and vascular smooth muscle during depolarization.Â
Verapamil: It inhibits the entry of calcium ions into slow channels and voltage-sensitive parts of myocardium and vascular smooth muscle during depolarization.Â
Use of short-acting nitroglycerins
Nitroglycerin IV: This drug leads to the relaxation of smooth muscles by stimulating the production of intracellular cyclic GMP.Â
Use of long acting nitroglycerins
Isosorbide: It causes relaxation of vascular smooth muscles via stimulation of intracellular cGMP. It also decreases the preload (LV pressure) and after load (arterial resistance).Â
Use of ACE inhibitors
Ramipril: This medication prevents the conversion of angiotensin I to a potent vasoconstrictor, angiotensin II that results in the reduced secretion of aldosterone.Â
Use of anti-ischemic agents
Ranolazine: It is a cardioselective anti-ischemic agent which inhibits the oxidation of fatty acids partially. It also prolongs the QT interval by inhibiting late sodium current into the myocardial cells. It is employed in treating chronic angina that is not responsive to other antianginal drugs.Â
use-of-phases-of-management-in-treating-stable-angina
Coronary artery disease is the cause of most deaths in the United States. Teaching people about the signs and symptoms of heart attack, unstable angina, and stable angina is important. People must be educated about the preventive measures like modification of risk factor and following healthy lifestyle.Â
Medication
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
Chronic:
500
mg
Tablet
Oral
twice a day
increase to 1000 mg tablet twice a day only if needed
(Off-label)
indicated for Chronic Stable Angina:
15 - 40
mg/day
Orally 
dose divided every 4 hours
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.
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
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
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
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.
Future Trends
Angina pectoris, also known as typical angina or stabilized angina, is a sign of myocardial ischemia. It is partial chest pain provoked by effort and relieved by rest or nitrogylcerin. It is the first complaint or sign of underlying coronary artery disease. In the United States, angina affects ten million people. It is not only important to recognize signs and symptoms, but management of the condition considerably manages the individuals.Â
Coronary disease affects more than 17 million adults in the US. Among the 17 million Americans influenced, 55 percent are men. Every year, this leads to more than 500,000 deaths in the United States. At 40 years old, men have a 49% likelihood of developing heart disease in their lifetime whereas women have 32%. Although occurrences of coronary events rise as individuals get older; there is a gradual decrease of males with these incidents due to their advanced age.Â
The countries that have the highest rates of death from ischemic heart diseases are low, middle, and high income countries which means that they are not unique to the U.S. adults.Â
Angina is due to a lack of balance in the supply and demand factors for myocardial oxygen. Vascular tone regulation and anti-thrombotic activity of coronary artery endothelial cells may be disrupted by stress, hypertension hypercholesterolemia, viruses, bacteria or immune complexes. The commonest cause of myocardial ischemia is stenosis of the coronary arteries which prevents sufficient oxygen delivery during periods when requirements are high. Myocardial supply depends on many things including size and tone of the coronary vessels, collateral blood flow pressure difference between aortic diastolic and ventricular endocardial perfusion per minute heart rate.  Mechanoreceptive and chemo sensitive receptors may get stimulated in the fibers of cardiac muscle when the myocardial demand for oxygen increases than supply. Understanding the exact cause of angina is important for medical treatment and management of risks.Â
The mechanism behind stable angina is the result of supply-demand mismatch. The myocardial oxygen demand transiently exceeds the myocardial supply of oxygen, which often leads to the manifestation of symptoms. There are various factors that contribute to stable angina, and the most common one is coronary artery stenosis.Â
The probability of diagnosis varies with the type of stable angina that a person has. This makes it an absolute necessary to control risk factors in all cases. It is important to always look for an increase in frequency of symptoms or development to an unstable angina.Â
Stable angina often presents as subacute, requiring a thorough medical history and physical examination to identify high-risk individuals. Regular screening measures include blood pressure, sleep patterns, weight, stress levels, exercise tolerance, and substance use. Typical symptoms include chest discomfort or anginal equivalents, and distinguishing between cardiac and non-cardiac chest discomfort is crucial. Â
Occasionally, patients may have stable angina or equivalent symptoms and yet have entirely normal findings on physical examination. However, in the presence of a compatible clinical syndrome, angina pectoris can be diagnosed with reasonable reliability if the Levine sign is positive. Third or fourth heart sound may be heard during anginal attack which is caused due to LV dysfunction and mitral regurgitation may occur due to dysfunction of papillary muscle.Â
Common angina is felt as feeling of pressure, squeezing or pain in the chest. Instead of a specific place, a broad area of the chest is generally affected, and the pain can move depending on which dermatomes are being touched. Symptoms are known to increase when there is a lot of demand like walking for long distances or carrying heavy loads up stairs along with emotional stress.Â
Usually, symptoms last for about less than five minutes and are relieved by stopping an activity that causes them or else taking nitroglycerin. There will not be any noticeable findings during physical examinations.  Â
Typical angina can be manifested by heaviness, tightness, pressure-like, or squeezing. It is crucial to identify the differences between non-cardiac and cardiac chest discomfort.Â
Acute coronary syndromeÂ
Stable angina consists of modifications of lifestyle such as cessation of smoking, intake of diet healthy for heart, exercise and management of weight. Medications like antiplatelet agents, beta-blockers, calcium channel blockers and nitrogylcerin would be prescribed for this condition. In cases where symptoms persist or high- risk features occur, invasive interventions like coronary artery revascularization may be considered. The treatment varies among patients based on lifestyle, pharmacological management etc.Â
Cardiology, General
Cessation of smokingÂ
Smoking cigarettes is the primary contributor to premature moratlity. Cardiovascular mortality risk is higher in smokers than non-smokers. Hence, it is important to educate people to stop smoking irrespective of age.Â
A healthy weight is necessary for a healthy heart. This is the second modifiable factor that contributes to mortality. Based on individual response, weight loss methods should be designed for each patient.Â
Control of blood pressureÂ
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.Â
Cardiology, General
Aspirin: It prevents the aggregation of platelets by irreversible inhibition of cyclooxygenase following suppression of thromboxane A2. Its antiplatelet activity lasts for 7 days.Â
Clopidogrel: This drug selectively inhibits the binding of ADP to platelet receptors after activation of GPIIb/IIIa complex which further inhibits the aggregation of platelets.Â
Cardiology, General
Metoprolol: It is a selective blocker of beta-1 adrenergic receptor and reduces the automaticity of contractions. Being lipophilic, it is capable of penetrating into CNS.Â
Atenolol: This blocks the β-1 adrenergic receptors selectively with no or little effect on β-2 receptor. Â
Propranolol: It is a non-selective beta-blocker which is lipophilic.Â
Amlodipine: It inhibits the entry of calcium ions into slow channels and voltage-sensitive parts of myocardium and vascular smooth muscle during depolarization.Â
Diltiazem: It inhibits the entry of calcium ions into slow channels and voltage-sensitive parts of myocardium and vascular smooth muscle during depolarization.Â
Verapamil: It inhibits the entry of calcium ions into slow channels and voltage-sensitive parts of myocardium and vascular smooth muscle during depolarization.Â
Cardiology, General
Nitroglycerin IV: This drug leads to the relaxation of smooth muscles by stimulating the production of intracellular cyclic GMP.Â
Cardiology, General
Isosorbide: It causes relaxation of vascular smooth muscles via stimulation of intracellular cGMP. It also decreases the preload (LV pressure) and after load (arterial resistance).Â
Cardiology, General
Ramipril: This medication prevents the conversion of angiotensin I to a potent vasoconstrictor, angiotensin II that results in the reduced secretion of aldosterone.Â
Cardiology, General
Ranolazine: It is a cardioselective anti-ischemic agent which inhibits the oxidation of fatty acids partially. It also prolongs the QT interval by inhibiting late sodium current into the myocardial cells. It is employed in treating chronic angina that is not responsive to other antianginal drugs.Â
Cardiology, General
Coronary artery disease is the cause of most deaths in the United States. Teaching people about the signs and symptoms of heart attack, unstable angina, and stable angina is important. People must be educated about the preventive measures like modification of risk factor and following healthy lifestyle.Â
Angina pectoris, also known as typical angina or stabilized angina, is a sign of myocardial ischemia. It is partial chest pain provoked by effort and relieved by rest or nitrogylcerin. It is the first complaint or sign of underlying coronary artery disease. In the United States, angina affects ten million people. It is not only important to recognize signs and symptoms, but management of the condition considerably manages the individuals.Â
Coronary disease affects more than 17 million adults in the US. Among the 17 million Americans influenced, 55 percent are men. Every year, this leads to more than 500,000 deaths in the United States. At 40 years old, men have a 49% likelihood of developing heart disease in their lifetime whereas women have 32%. Although occurrences of coronary events rise as individuals get older; there is a gradual decrease of males with these incidents due to their advanced age.Â
The countries that have the highest rates of death from ischemic heart diseases are low, middle, and high income countries which means that they are not unique to the U.S. adults.Â
Angina is due to a lack of balance in the supply and demand factors for myocardial oxygen. Vascular tone regulation and anti-thrombotic activity of coronary artery endothelial cells may be disrupted by stress, hypertension hypercholesterolemia, viruses, bacteria or immune complexes. The commonest cause of myocardial ischemia is stenosis of the coronary arteries which prevents sufficient oxygen delivery during periods when requirements are high. Myocardial supply depends on many things including size and tone of the coronary vessels, collateral blood flow pressure difference between aortic diastolic and ventricular endocardial perfusion per minute heart rate.  Mechanoreceptive and chemo sensitive receptors may get stimulated in the fibers of cardiac muscle when the myocardial demand for oxygen increases than supply. Understanding the exact cause of angina is important for medical treatment and management of risks.Â
The mechanism behind stable angina is the result of supply-demand mismatch. The myocardial oxygen demand transiently exceeds the myocardial supply of oxygen, which often leads to the manifestation of symptoms. There are various factors that contribute to stable angina, and the most common one is coronary artery stenosis.Â
The probability of diagnosis varies with the type of stable angina that a person has. This makes it an absolute necessary to control risk factors in all cases. It is important to always look for an increase in frequency of symptoms or development to an unstable angina.Â
Stable angina often presents as subacute, requiring a thorough medical history and physical examination to identify high-risk individuals. Regular screening measures include blood pressure, sleep patterns, weight, stress levels, exercise tolerance, and substance use. Typical symptoms include chest discomfort or anginal equivalents, and distinguishing between cardiac and non-cardiac chest discomfort is crucial. Â
Occasionally, patients may have stable angina or equivalent symptoms and yet have entirely normal findings on physical examination. However, in the presence of a compatible clinical syndrome, angina pectoris can be diagnosed with reasonable reliability if the Levine sign is positive. Third or fourth heart sound may be heard during anginal attack which is caused due to LV dysfunction and mitral regurgitation may occur due to dysfunction of papillary muscle.Â
Common angina is felt as feeling of pressure, squeezing or pain in the chest. Instead of a specific place, a broad area of the chest is generally affected, and the pain can move depending on which dermatomes are being touched. Symptoms are known to increase when there is a lot of demand like walking for long distances or carrying heavy loads up stairs along with emotional stress.Â
Usually, symptoms last for about less than five minutes and are relieved by stopping an activity that causes them or else taking nitroglycerin. There will not be any noticeable findings during physical examinations.  Â
Typical angina can be manifested by heaviness, tightness, pressure-like, or squeezing. It is crucial to identify the differences between non-cardiac and cardiac chest discomfort.Â
Acute coronary syndromeÂ
Stable angina consists of modifications of lifestyle such as cessation of smoking, intake of diet healthy for heart, exercise and management of weight. Medications like antiplatelet agents, beta-blockers, calcium channel blockers and nitrogylcerin would be prescribed for this condition. In cases where symptoms persist or high- risk features occur, invasive interventions like coronary artery revascularization may be considered. The treatment varies among patients based on lifestyle, pharmacological management etc.Â
Cardiology, General
Cessation of smokingÂ
Smoking cigarettes is the primary contributor to premature moratlity. Cardiovascular mortality risk is higher in smokers than non-smokers. Hence, it is important to educate people to stop smoking irrespective of age.Â
A healthy weight is necessary for a healthy heart. This is the second modifiable factor that contributes to mortality. Based on individual response, weight loss methods should be designed for each patient.Â
Control of blood pressureÂ
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.Â
Cardiology, General
Aspirin: It prevents the aggregation of platelets by irreversible inhibition of cyclooxygenase following suppression of thromboxane A2. Its antiplatelet activity lasts for 7 days.Â
Clopidogrel: This drug selectively inhibits the binding of ADP to platelet receptors after activation of GPIIb/IIIa complex which further inhibits the aggregation of platelets.Â
Cardiology, General
Metoprolol: It is a selective blocker of beta-1 adrenergic receptor and reduces the automaticity of contractions. Being lipophilic, it is capable of penetrating into CNS.Â
Atenolol: This blocks the β-1 adrenergic receptors selectively with no or little effect on β-2 receptor. Â
Propranolol: It is a non-selective beta-blocker which is lipophilic.Â
Amlodipine: It inhibits the entry of calcium ions into slow channels and voltage-sensitive parts of myocardium and vascular smooth muscle during depolarization.Â
Diltiazem: It inhibits the entry of calcium ions into slow channels and voltage-sensitive parts of myocardium and vascular smooth muscle during depolarization.Â
Verapamil: It inhibits the entry of calcium ions into slow channels and voltage-sensitive parts of myocardium and vascular smooth muscle during depolarization.Â
Cardiology, General
Nitroglycerin IV: This drug leads to the relaxation of smooth muscles by stimulating the production of intracellular cyclic GMP.Â
Cardiology, General
Isosorbide: It causes relaxation of vascular smooth muscles via stimulation of intracellular cGMP. It also decreases the preload (LV pressure) and after load (arterial resistance).Â
Cardiology, General
Ramipril: This medication prevents the conversion of angiotensin I to a potent vasoconstrictor, angiotensin II that results in the reduced secretion of aldosterone.Â
Cardiology, General
Ranolazine: It is a cardioselective anti-ischemic agent which inhibits the oxidation of fatty acids partially. It also prolongs the QT interval by inhibiting late sodium current into the myocardial cells. It is employed in treating chronic angina that is not responsive to other antianginal drugs.Â
Cardiology, General
Coronary artery disease is the cause of most deaths in the United States. Teaching people about the signs and symptoms of heart attack, unstable angina, and stable angina is important. People must be educated about the preventive measures like modification of risk factor and following healthy lifestyle.Â

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