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Unstable angina

Updated : January 1, 2024





Background

Unstable angina is situated within the spectrum of conditions collectively termed acute coronary syndrome, a pervasive public health concern impacting a substantial portion of the global population and standing as the foremost cause of mortality worldwide. It is imperative to discern between unstable angina and other sources of chest pain, including stable angina, as this differentiation significantly influences the therapeutic approach and subsequent patient management.

Recognizing the signs and symptoms of acute coronary syndrome is crucial, and patients rely on healthcare professionals to make accurate distinctions from alternative causes of chest pain. While individuals frequently present to the emergency room with such symptoms, it is noteworthy that acute coronary syndrome may also manifest in an outpatient setting.

Substantial research efforts have been directed toward identifying optimal treatment modalities and diagnostic tools for evaluating unstable angina and other variations of acute coronary syndrome throughout the years. 

Epidemiology

Coronary artery disease exerts a significant impact on a considerable segment of the population, with estimates indicating that it is responsible for more than one-third of fatalities in individuals aged 35 and above. Within this age demographic, it stands as the predominant cause of death.

In the United States alone, approximately 18 million people are believed to be affected by this condition. While the incidence is higher in men, particularly in the age group under consideration, as individuals surpass the age of 75, the occurrence becomes more comparable between males and females.

Various risk factors contribute to the prevalence of coronary artery disease, encompassing obesity, diabetes, hypertension, elevated cholesterol levels, a history of smoking, substance abuse involving cocaine or amphetamines, family predisposition, chronic kidney disease, HIV infection, autoimmune disorders, and anemia.

The average age at which individuals present with symptoms is 62, with women typically presenting at an older age than men. Notably, African Americans tend to manifest symptoms at a younger age compared to other racial groups. 

Anatomy

Pathophysiology

Unstable angina arises from impediments in blood flow, leading to inadequate perfusion of the myocardium. Initially perfusion originates from the heart, coursing through the aorta and later into the coronary arteries, each supplying distinct regions of the heart. The left coronary artery bifurcates into the left anterior descending artery and circumflex, further branching into smaller arteries.

Similarly, the right coronary artery undergoes division into smaller branches. The occurrence of unstable angina is a consequence of compromised blood flow to the myocardium. This obstruction is commonly attributed to factors such as vasospasm, intraluminal thrombosis, plaque formation, and elevated blood pressure. Often, a combination of these factors serves as the precipitating cause. 

Etiology

  • Plaque Rupture: 

The rupture of atherosclerotic plaques in the coronary arteries can expose the underlying tissue to the bloodstream, triggering the formation of blood clots. These clots can partially or completely obstruct the coronary arteries, leading to unstable angina. 

  • Intraluminal Thrombosis: 

Formation of blood clots within the coronary arteries, either due to plaque rupture or other factors, can contribute to the sudden development of unstable angina. Thrombosis further narrows or blocks the blood vessels, leading to ischemia and angina symptoms. 

  • Hypertension: 

Hypertension can strain the coronary arteries, making them more susceptible to damage and promoting atherosclerosis. Elevated blood pressure also increases the workload on the heart, potentially triggering episodes of unstable angina. 

Genetics

Prognostic Factors

Clinical History

Patients commonly present with symptoms such as chest pain and shortness of breath when experiencing unstable angina. The chest pain is often characterized as pressure-like, though it can also be described as tightness, sharpness, or burning; some patients may report discomfort rather than explicit pain. The pain often radiates to the jaw or arms, affecting both the left and right sides.

Constitutional symptoms like nausea, vomiting, dizziness, diaphoresis, and palpitations may accompany these symptoms. Exertion can exacerbate the pain, while rest may alleviate it. Administration of nitroglycerin and aspirin may improve the symptoms; however, a distinguishing feature of unstable angina is that the pain may not completely resolve with these interventions. 

Notably, many patients already have coronary artery disease, either as an established condition or based on symptoms they have experienced over time. Such individuals may be familiar with their symptoms and may report an increase in the frequency and duration of chest pain episodes, as well as heightened symptom severity.

These factors suggest a higher likelihood of unstable angina compared to stable angina or other causes of chest pain. Recognizing these differences is crucial because they may signify the potential for impending myocardial infarction and ST-elevation myocardial infarction (STEMI). Prompt evaluation is essential, as the risk of morbidity and mortality is elevated in this scenario compared to stable angina. 

Physical Examination

  • Cardiac Sounds: 

Auscultation of the heart may reveal abnormal sounds, including the presence of a third heart sound (S3) or a fourth heart sound (S4), which can indicate issues with ventricular function. 

  • Jugular Venous Pressure (JVP): 

Elevated jugular venous pressure may be indicative of fluid overload or heart failure. It is often assessed by observing the pulsations of the internal jugular vein in the neck. 

  • Rales and Crackles: 

Abnormal lung sounds such as rales (crackles) may be auscultated, indicating the presence of pulmonary edema or congestion. 

  • Blood Pressure: 

Hypotension may be present in severe cases and can be an ominous sign of cardiovascular compromise. 

  • Dyskinetic Apex: 

Dyskinesia of the apex refers to abnormal movement of the heart’s apex, which may be observed during examination and could suggest myocardial dysfunction. 

Age group

Associated comorbidity

Associated activity

Acuity of presentation

Differential Diagnoses

  • Aortic dissection 
  • Pneumothorax 
  • Pulmonary embolism 
  • Pericarditis 
  • Peptic ulcer disease 

 

Laboratory Studies

Imaging Studies

Procedures

Histologic Findings

Staging

Treatment Paradigm

In the treatment paradigm for unstable angina, the immediate administration of aspirin, typically orally or rectally for patients unable to swallow, serves as a crucial antiplatelet therapy to prevent blood clot formation. Simultaneously, nitroglycerin, available in various forms, is employed to induce vasodilation of coronary arteries, improving blood flow, reducing blood pressure, and alleviating the heart’s workload.

Supplemental oxygen, delivered via nasal cannula, is promptly administered to maintain optimal oxygen saturation. For those unable to tolerate aspirin, alternative antiplatelet agents such as clopidogrel, prasugrel, or the recently approved ticagrelor in combination with aspirin may reduce the risk of thrombotic cardiac events.

Additionally, anticoagulation with low or high molecular weight heparin and beta-blockers to lower blood pressure and heart rate may be incorporated into the treatment plan. Monitoring and evaluating the patient’s response is essential, particularly in cases of persistent pain or prolonged recovery, as these individuals face an increased risk of myocardial infarction.

Ranolazine, showing promise in reducing recurrent ischemia, emerges as a potential adjunctive therapy in the management of unstable angina. Overall, this comprehensive approach aims to alleviate symptoms, improve coronary perfusion, and mitigate the risk of adverse cardiovascular events. 

by Stage

by Modality

Chemotherapy

Radiation Therapy

Surgical Interventions

Hormone Therapy

Immunotherapy

Hyperthermia

Photodynamic Therapy

Stem Cell Transplant

Targeted Therapy

Palliative Care

Administration of a pharmaceutical agent

Patients are commonly prescribed aspirin as part of antiplatelet therapy, typically in doses ranging from 162 to 325 mg orally or 300 mg rectally for those who cannot swallow. Administering aspirin is critical and should commence within 30 minutes of presentation, as it functions as an antiplatelet agent, preventing the formation of blood clots. 

Nitroglycerin, available in various forms (intravenous, sublingual, transdermal, and orally), enhances perfusion by inducing vasodilation of the coronary arteries. This vasodilation improves blood flow, reduces blood pressure, and consequently lessens the workload on the heart, lowering its energy demand. 

For patients unable to tolerate aspirin, clopidogrel is an alternative. Prasugrel, although more potent than clopidogrel, is associated with a higher risk of bleeding. The recently approved ticagrelor can be used in conjunction with aspirin to reduce the incidence of thrombotic cardiac events. 

The prompt administration of supplemental oxygen, delivered via nasal cannula, is essential for maintaining adequate oxygen saturation. These actions—administration of aspirin, nitroglycerin, and supplemental oxygen—are crucial and represent the primary interventions for evaluating and treating unstable angina.

In cases where patients experience persistent pain or prolonged recovery, close monitoring is necessary as they are at a heightened risk for myocardial infarction. 

Additional therapeutic options may include anticoagulation using either low or high-molecular-weight heparin. Beta-blockers are another class of medications that can decrease the heart’s energy demand by reducing blood pressure and heart rate. 

Ranolazine, has shown a significant reduction in the endpoint of recurrent ischemia in the ranolazine group. This suggests its potential role in managing unstable angina. 

 

Medication

 

dalteparin 


Non-Q-wave myocardial infarction and unstable angina:


120 IU/kg total body weight subcutaneously every 12 hours in combination with aspirin therapy (75-165mg everyday) for 5-8 days
Do not exceed 10000 IU every 12 hours

Dosing based on the weight
<50kg:5500 IU subcutaneous every 12 hours
50-59kg: 6500 IU subcutaneous every 12 hours
60-69kg: 7500 IU subcutaneous every 12 hours
70-79kg: 9000 IU subcutaneous every 12 hours
≥80kg:10000 IU subcutaneous every 12 hours



 
 

dalteparin 


Indicated for Non-Q-wave myocardial infarction and unstable angina:


120 IU/kg subcutaneous every 12 hours for 5-8 days in combination with aspirin therapy



Media Gallary

References

Unstable angina

Updated : January 1, 2024




Unstable angina is situated within the spectrum of conditions collectively termed acute coronary syndrome, a pervasive public health concern impacting a substantial portion of the global population and standing as the foremost cause of mortality worldwide. It is imperative to discern between unstable angina and other sources of chest pain, including stable angina, as this differentiation significantly influences the therapeutic approach and subsequent patient management.

Recognizing the signs and symptoms of acute coronary syndrome is crucial, and patients rely on healthcare professionals to make accurate distinctions from alternative causes of chest pain. While individuals frequently present to the emergency room with such symptoms, it is noteworthy that acute coronary syndrome may also manifest in an outpatient setting.

Substantial research efforts have been directed toward identifying optimal treatment modalities and diagnostic tools for evaluating unstable angina and other variations of acute coronary syndrome throughout the years. 

Coronary artery disease exerts a significant impact on a considerable segment of the population, with estimates indicating that it is responsible for more than one-third of fatalities in individuals aged 35 and above. Within this age demographic, it stands as the predominant cause of death.

In the United States alone, approximately 18 million people are believed to be affected by this condition. While the incidence is higher in men, particularly in the age group under consideration, as individuals surpass the age of 75, the occurrence becomes more comparable between males and females.

Various risk factors contribute to the prevalence of coronary artery disease, encompassing obesity, diabetes, hypertension, elevated cholesterol levels, a history of smoking, substance abuse involving cocaine or amphetamines, family predisposition, chronic kidney disease, HIV infection, autoimmune disorders, and anemia.

The average age at which individuals present with symptoms is 62, with women typically presenting at an older age than men. Notably, African Americans tend to manifest symptoms at a younger age compared to other racial groups. 

Unstable angina arises from impediments in blood flow, leading to inadequate perfusion of the myocardium. Initially perfusion originates from the heart, coursing through the aorta and later into the coronary arteries, each supplying distinct regions of the heart. The left coronary artery bifurcates into the left anterior descending artery and circumflex, further branching into smaller arteries.

Similarly, the right coronary artery undergoes division into smaller branches. The occurrence of unstable angina is a consequence of compromised blood flow to the myocardium. This obstruction is commonly attributed to factors such as vasospasm, intraluminal thrombosis, plaque formation, and elevated blood pressure. Often, a combination of these factors serves as the precipitating cause. 

  • Plaque Rupture: 

The rupture of atherosclerotic plaques in the coronary arteries can expose the underlying tissue to the bloodstream, triggering the formation of blood clots. These clots can partially or completely obstruct the coronary arteries, leading to unstable angina. 

  • Intraluminal Thrombosis: 

Formation of blood clots within the coronary arteries, either due to plaque rupture or other factors, can contribute to the sudden development of unstable angina. Thrombosis further narrows or blocks the blood vessels, leading to ischemia and angina symptoms. 

  • Hypertension: 

Hypertension can strain the coronary arteries, making them more susceptible to damage and promoting atherosclerosis. Elevated blood pressure also increases the workload on the heart, potentially triggering episodes of unstable angina. 

Patients commonly present with symptoms such as chest pain and shortness of breath when experiencing unstable angina. The chest pain is often characterized as pressure-like, though it can also be described as tightness, sharpness, or burning; some patients may report discomfort rather than explicit pain. The pain often radiates to the jaw or arms, affecting both the left and right sides.

Constitutional symptoms like nausea, vomiting, dizziness, diaphoresis, and palpitations may accompany these symptoms. Exertion can exacerbate the pain, while rest may alleviate it. Administration of nitroglycerin and aspirin may improve the symptoms; however, a distinguishing feature of unstable angina is that the pain may not completely resolve with these interventions. 

Notably, many patients already have coronary artery disease, either as an established condition or based on symptoms they have experienced over time. Such individuals may be familiar with their symptoms and may report an increase in the frequency and duration of chest pain episodes, as well as heightened symptom severity.

These factors suggest a higher likelihood of unstable angina compared to stable angina or other causes of chest pain. Recognizing these differences is crucial because they may signify the potential for impending myocardial infarction and ST-elevation myocardial infarction (STEMI). Prompt evaluation is essential, as the risk of morbidity and mortality is elevated in this scenario compared to stable angina. 

  • Cardiac Sounds: 

Auscultation of the heart may reveal abnormal sounds, including the presence of a third heart sound (S3) or a fourth heart sound (S4), which can indicate issues with ventricular function. 

  • Jugular Venous Pressure (JVP): 

Elevated jugular venous pressure may be indicative of fluid overload or heart failure. It is often assessed by observing the pulsations of the internal jugular vein in the neck. 

  • Rales and Crackles: 

Abnormal lung sounds such as rales (crackles) may be auscultated, indicating the presence of pulmonary edema or congestion. 

  • Blood Pressure: 

Hypotension may be present in severe cases and can be an ominous sign of cardiovascular compromise. 

  • Dyskinetic Apex: 

Dyskinesia of the apex refers to abnormal movement of the heart’s apex, which may be observed during examination and could suggest myocardial dysfunction. 

  • Aortic dissection 
  • Pneumothorax 
  • Pulmonary embolism 
  • Pericarditis 
  • Peptic ulcer disease 

 

In the treatment paradigm for unstable angina, the immediate administration of aspirin, typically orally or rectally for patients unable to swallow, serves as a crucial antiplatelet therapy to prevent blood clot formation. Simultaneously, nitroglycerin, available in various forms, is employed to induce vasodilation of coronary arteries, improving blood flow, reducing blood pressure, and alleviating the heart’s workload.

Supplemental oxygen, delivered via nasal cannula, is promptly administered to maintain optimal oxygen saturation. For those unable to tolerate aspirin, alternative antiplatelet agents such as clopidogrel, prasugrel, or the recently approved ticagrelor in combination with aspirin may reduce the risk of thrombotic cardiac events.

Additionally, anticoagulation with low or high molecular weight heparin and beta-blockers to lower blood pressure and heart rate may be incorporated into the treatment plan. Monitoring and evaluating the patient’s response is essential, particularly in cases of persistent pain or prolonged recovery, as these individuals face an increased risk of myocardial infarction.

Ranolazine, showing promise in reducing recurrent ischemia, emerges as a potential adjunctive therapy in the management of unstable angina. Overall, this comprehensive approach aims to alleviate symptoms, improve coronary perfusion, and mitigate the risk of adverse cardiovascular events. 

Patients are commonly prescribed aspirin as part of antiplatelet therapy, typically in doses ranging from 162 to 325 mg orally or 300 mg rectally for those who cannot swallow. Administering aspirin is critical and should commence within 30 minutes of presentation, as it functions as an antiplatelet agent, preventing the formation of blood clots. 

Nitroglycerin, available in various forms (intravenous, sublingual, transdermal, and orally), enhances perfusion by inducing vasodilation of the coronary arteries. This vasodilation improves blood flow, reduces blood pressure, and consequently lessens the workload on the heart, lowering its energy demand. 

For patients unable to tolerate aspirin, clopidogrel is an alternative. Prasugrel, although more potent than clopidogrel, is associated with a higher risk of bleeding. The recently approved ticagrelor can be used in conjunction with aspirin to reduce the incidence of thrombotic cardiac events. 

The prompt administration of supplemental oxygen, delivered via nasal cannula, is essential for maintaining adequate oxygen saturation. These actions—administration of aspirin, nitroglycerin, and supplemental oxygen—are crucial and represent the primary interventions for evaluating and treating unstable angina.

In cases where patients experience persistent pain or prolonged recovery, close monitoring is necessary as they are at a heightened risk for myocardial infarction. 

Additional therapeutic options may include anticoagulation using either low or high-molecular-weight heparin. Beta-blockers are another class of medications that can decrease the heart’s energy demand by reducing blood pressure and heart rate. 

Ranolazine, has shown a significant reduction in the endpoint of recurrent ischemia in the ranolazine group. This suggests its potential role in managing unstable angina. 

 

dalteparin 


Non-Q-wave myocardial infarction and unstable angina:


120 IU/kg total body weight subcutaneously every 12 hours in combination with aspirin therapy (75-165mg everyday) for 5-8 days
Do not exceed 10000 IU every 12 hours

Dosing based on the weight
<50kg:5500 IU subcutaneous every 12 hours
50-59kg: 6500 IU subcutaneous every 12 hours
60-69kg: 7500 IU subcutaneous every 12 hours
70-79kg: 9000 IU subcutaneous every 12 hours
≥80kg:10000 IU subcutaneous every 12 hours



dalteparin 


Indicated for Non-Q-wave myocardial infarction and unstable angina:


120 IU/kg subcutaneous every 12 hours for 5-8 days in combination with aspirin therapy