Angina pectoris, commonly known as angina, is a frequent symptom of ischemic heart disease, a leading cause of morbidity and mortality globally. In the United States alone, approximately 9 million individuals experience angina symptoms, highlighting the significant challenge it poses in healthcare. Effectively evaluating and managing angina is crucial for improving patient outcomes. This article aims to provide a detailed overview of angina, focusing on its differential diagnosis, evaluation, and management, emphasizing the vital role of an interprofessional healthcare team in patient care.
Understanding Angina Pectoris
Angina manifests as chest pain or discomfort, but it’s essential to recognize that chest pain can originate from various cardiac and non-cardiac conditions. A thorough medical history and physical examination are paramount in distinguishing between these causes, particularly in identifying patients experiencing acute coronary syndrome (ACS). Angina itself is a key indicator of ACS and is further categorized into stable and unstable forms. Stable angina is characterized by symptoms triggered by exertion, while unstable angina, or angina occurring at rest, necessitates immediate medical attention and evaluation. Prompt recognition of angina symptoms is critical in enhancing patient outcomes and preventing severe cardiac events.
Etiology of Angina and Related Chest Pain
Chest pain, a primary symptom related to angina, can stem from a broad spectrum of causes, categorized into non-cardiac, non-ischemic cardiac, and ischemic cardiac origins. Non-cardiac causes encompass conditions such as gastroesophageal reflux disease (GERD), pulmonary diseases, musculoskeletal issues, and anxiety or panic attacks. Non-ischemic cardiac causes primarily include pericardial diseases. However, the predominant cause of chest pain related to angina is cardiac ischemia, largely attributed to atherosclerosis of the coronary arteries and coronary vasospasm.
This underlying pathology leads to an imbalance between myocardial oxygen supply and demand. In stable angina, this oxygen demand mismatch is typically triggered by physical exertion. In contrast, unstable angina can occur even at rest, indicating a more severe and unpredictable condition. Myocardial oxygen demand is significantly influenced by factors such as heart rate, blood pressure, and myocardial contractility, all of which increase during exercise. Under normal physiological conditions, increased oxygen demand during exertion is met by coronary vasodilation. However, in the presence of coronary artery atherosclerosis, this compensatory vasodilation is impaired, leading to ischemia and the characteristic chest pain of angina.
Vasospastic angina, also known as variant angina or Prinzmetal angina, shares the characteristic of occurring at rest but differs from stable angina by not being directly linked to coronary atherosclerosis. Instead, it results from spasms of the coronary arteries, further complicating the differential diagnosis of angina pectoris.
Epidemiology of Angina
Chronic stable angina is a prevalent condition, affecting approximately 30,000 to 40,000 individuals per million in Western countries. The prevalence of angina increases with age in both genders. For individuals aged 45 to 64, the estimated prevalence ranges from 4% to 7% in men and 5% to 7% in women. In older adults aged 65 to 84, the prevalence rises significantly, reaching 14% to 15% in men and 10% to 12% in women. These figures underscore the substantial public health impact of angina, particularly in aging populations.
Several modifiable risk factors contribute to the development of angina, including hyperlipidemia, hypertension, current or past tobacco use, diabetes mellitus, and obesity or metabolic syndrome. Notably, an increasing Body Mass Index (BMI) is recognized as an independent risk factor for coronary artery disease (CAD). Non-modifiable risk factors include advancing age, male sex, a family history of CAD, and ethnic origin. Understanding these epidemiological factors is crucial for risk stratification and targeted preventive strategies.
Pathophysiology of Angina Pectoris
The heart muscle relies on a continuous and adequate supply of oxygen for energy production, essential for its contractile function. At a cellular level, ischemia triggers anaerobic glycolysis, leading to an increase in hydrogen, potassium, and lactate levels in the venous blood draining the ischemic myocardial area. The elevated hydrogen ions interfere with calcium ions, causing regional hypokinesia or akinesia. In stable angina, this oxygen supply-demand imbalance is typically provoked by triggers that increase metabolic demand, such as exercise, emotional stress, or exposure to cold temperatures.
History and Physical Examination in Angina Diagnosis
Patients experiencing ACS commonly present with angina, which they often describe as pain, pressure, tightness, or a heavy sensation in the chest. This discomfort may radiate to the jaw or left arm and can be accompanied by shortness of breath, diaphoresis, nausea, or a combination of these symptoms. In stable angina, chest pain is typically precipitated by exertion and relieved by rest and/or nitroglycerin. However, in unstable angina or myocardial infarction (MI), including non-ST segment elevation MI (NSTEMI) and ST-segment elevation MI (STEMI), the chest pain is less likely to resolve completely with rest or nitroglycerin. Stable angina symptoms usually subside within 5 minutes of rest or nitroglycerin use.
While these are considered classic angina symptoms, atypical presentations are not uncommon, particularly in patients with diabetes. Therefore, a high degree of clinical suspicion is necessary when evaluating patients with significant cardiac risk factors, even if their symptoms do not perfectly align with classic angina.
During a physical examination, patients may appear uncomfortable or anxious. They might be diaphoretic or clutching their chest. Vital signs can be normal, but tachycardia and tachypnea are common findings. However, it’s important to note that physical examination findings are often non-specific in angina, emphasizing the need for comprehensive evaluation.
Evaluation and Diagnostic Testing for Angina
In patients presenting with symptoms suggestive of angina, the utility of cardiac testing is largely determined by the patient’s pretest probability of ACS. This pretest probability is assessed based on the patient’s clinical presentation and existing cardiac risk factors. In patients with very high or very low pretest probability, diagnostic tests may be less informative as they are less likely to alter the immediate management strategy.
Initial diagnostic evaluation typically includes a 12-lead electrocardiogram (ECG), a chest X-ray, and basic laboratory tests, including a complete blood count (CBC), basic metabolic profile (BMP), and serial troponin levels if ACS is suspected. In cases of stable angina, unstable angina, or NSTEMI, the initial ECG may not show any abnormalities. ECG indicators of myocardial ischemia include T-wave flattening or inversions, or ST-segment depressions. Further diagnostic testing may involve exercise or pharmacological stress testing, potentially with nuclear perfusion imaging, and diagnostic heart catheterization. ECG changes indicative of STEMI necessitate immediate coronary revascularization.
Treatment and Management Strategies for Angina
The primary goals in treating chronic stable angina are to alleviate symptoms and to slow the progression of the underlying cardiac disease, thereby preventing future cardiac events. Management is multifaceted, encompassing lifestyle modifications, risk factor management, and medical therapy as essential components. In cases where symptoms remain refractory to medical therapy, revascularization procedures may be considered. However, while revascularization can effectively control symptoms, it has not been consistently shown to reduce major cardiovascular events compared to optimal medical therapy alone.
Lifestyle modifications are crucial and include regular exercise, weight management, and smoking cessation. Patients should be strongly encouraged to adopt these changes. Risk factor modification involves managing conditions like hypertension, hyperlipidemia, and diabetes. Medications aimed at risk factor modification and disease progression prevention include aspirin, statins, angiotensin-converting enzyme inhibitors, or angiotensin receptor blockers.
Medical therapy plays a central role in both controlling angina symptoms and reducing the risk of atherosclerosis progression and subsequent cardiac events. Antianginal medications can be categorized based on their mechanism of action in relieving angina symptoms. Generally, symptomatic relief is achieved by reducing myocardial oxygen consumption.
Heart rate is a major determinant of myocardial oxygen consumption. Consequently, many anginal episodes are triggered by an increase in heart rate. Three classes of drugs reduce angina symptoms by heart rate reduction: beta-blockers, ivabradine, and non-dihydropyridine calcium channel blockers. However, calcium channel blockers should be avoided in patients with left ventricular dysfunction and reduced ejection fraction.
Another mechanism for treating angina symptoms is through vascular smooth muscle relaxation, leading to coronary artery dilatation and improved myocardial perfusion. Drugs acting via this mechanism include dihydropyridine calcium channel blockers, nitrates, and nicorandil.
Ranolazine, another medication used for chronic stable angina, works by inhibiting the late sodium current in ventricular myocardial cells, which reduces diastolic contractile dysfunction.
Treatment for unstable angina focuses on pain relief, minimizing myocardial damage, and reducing morbidity and mortality.
Nitrates are used for immediate chest pain relief by causing vasodilation, reducing preload and left ventricular end-diastolic volume, thus decreasing myocardial oxygen consumption. They do not provide mortality benefit and are contraindicated in hypotension and recent use of phosphodiesterase inhibitors.
Morphine is used for pain relief when nitrates are insufficient. It also provides some vasodilation but has no mortality benefit.
Beta-blockers are crucial in reducing mortality in unstable angina. They decrease heart rate, contractility, and blood pressure, thereby lowering myocardial oxygen demand.
Antiplatelet agents, specifically dual therapy with aspirin and clopidogrel, ticagrelor, or prasugrel, significantly reduce the risk of cardiovascular events in ACS patients.
Anticoagulants, used intravenously in acute settings, reduce mortality by preventing re-infarction when used with antiplatelet agents.
Anatomic assessment of coronary arteries and consideration for revascularization are essential for high-risk patients, who should be identified through risk stratification and considered for urgent revascularization.
Angina Pectoris Differential Diagnosis
The differential diagnosis of angina pectoris is broad and spans multiple body systems. It’s crucial to consider and rule out other conditions that can mimic angina symptoms. Accurate differential diagnosis is paramount to ensure appropriate management and avoid misdiagnosis.
Gastrointestinal Causes:
- Gastroesophageal Reflux Disease (GERD): Heartburn and chest discomfort from acid reflux can often be mistaken for angina.
- Hiatal Hernia: Can cause chest pain and discomfort due to stomach acid reflux or esophageal spasm.
- Peptic Ulcer Disease: Epigastric pain may radiate to the chest and mimic angina, especially if the ulcer is posterior.
- Esophageal Spasm: Painful spasms of the esophagus can present as chest pain similar to angina.
- Gallbladder Disease (Biliary Colic): Pain can sometimes radiate to the chest.
- Pancreatitis: Upper abdominal pain can sometimes be felt in the chest.
Pulmonary Causes:
- Pneumothorax: Sudden chest pain and shortness of breath can mimic unstable angina.
- Pneumonia and Pleurisy: Infections of the lung and pleura can cause chest pain that worsens with breathing.
- Pulmonary Embolism (PE): Can present with acute chest pain and shortness of breath, mimicking ACS.
- Asthma and COPD Exacerbation: Chest tightness and shortness of breath can be confused with angina.
- Pulmonary Hypertension: Can cause chest pain, especially with exertion.
Musculoskeletal Causes:
- Costochondritis: Inflammation of the cartilage in the rib cage, causing localized chest wall pain that can be sharp and mimic angina.
- Rib Injury and Fractures: Trauma to the ribs can cause chest pain.
- Muscle Spasm and Strain: Chest wall muscle strains or spasms can cause pain that is positional and reproducible on palpation.
- Fibromyalgia: Widespread musculoskeletal pain, including chest wall pain.
- Thoracic Outlet Syndrome: Compression of nerves and blood vessels in the thoracic outlet can cause chest and arm pain.
Psychiatric Causes:
- Panic Attack: Can cause sudden onset chest pain, palpitations, shortness of breath, and anxiety, mimicking unstable angina.
- Generalized Anxiety Disorder: Chronic anxiety can manifest as chest tightness and discomfort.
- Somatization Disorder: Psychological distress manifesting as physical symptoms, including chest pain.
Cardiac Non-Ischemic Causes:
- Pericarditis: Inflammation of the pericardium causing sharp, often pleuritic chest pain that can be positional and may improve when leaning forward.
- Myocarditis: Inflammation of the heart muscle, which can cause chest pain, fatigue, and shortness of breath.
- Hypertrophic Cardiomyopathy: Can cause angina-like chest pain due to myocardial ischemia from increased oxygen demand and supply mismatch.
- Mitral Valve Prolapse: Can sometimes cause atypical chest pain.
- Aortic Stenosis: Can cause angina due to reduced coronary perfusion and increased myocardial oxygen demand.
Vascular Causes:
- Aortic Dissection: A life-threatening condition presenting with sudden, severe tearing chest pain that radiates to the back.
- Pulmonary Hypertension: Can lead to chest pain due to right ventricular strain.
- Thoracic Aneurysm: Can cause chest pain as it expands and presses on surrounding structures.
Differentiating angina from these conditions requires a detailed clinical history, thorough physical examination, and appropriate use of diagnostic tests. Understanding the nuances of each condition is essential for accurate diagnosis and effective management.
Prognosis of Angina Pectoris
The prognosis for patients with chronic stable angina is variable and depends on several factors, including the presence of cardiovascular comorbidities and adherence to lifestyle modifications and medical treatment plans. Long-term prognosis is also significantly influenced by left ventricular systolic function, exercise tolerance, and the extent of coronary artery disease.
Risk factors associated with a poorer prognosis include diabetes mellitus, previous myocardial infarction, hypertension, increasing age, and male sex. Interestingly, the use of nitrates has also been identified as a negative prognostic indicator for mortality, likely because their use often signifies more advanced and severe disease.
Complications of Angina
Angina itself is often the initial symptom of underlying coronary artery disease. The primary complication of angina is the risk of future cardiac events, most notably myocardial infarction. Studies estimate that the 10-year risk of MI can exceed 10% in women with chronic stable angina from the time they start using nitrates for symptom management.
Beyond the life-threatening complication of MI, chronic stable angina significantly impacts patients’ quality of life and has broader societal implications. Reduced ability to perform daily activities leads to a lower quality of life. Furthermore, angina imposes a substantial burden on society through indirect costs, such as early retirement and disability. Effective angina treatment should aim not only to improve survival but also to alleviate symptoms, enabling patients to maintain a more active and fulfilling life.
Deterrence and Patient Education for Angina
For individuals with cardiac risk factors, proactive monitoring for angina symptoms and comprehensive patient education are crucial. Education should focus on recognizing alarming symptoms, such as angina occurring at rest or symptoms not relieved by nitrates. Emphasizing risk factor modification as a cornerstone of treatment is essential to slow disease progression. Dietary and exercise counseling, along with smoking cessation support, are vital components of patient education. Furthermore, stressing medication adherence is paramount to ensure treatment effectiveness and prevent disease progression.
Enhancing Healthcare Team Outcomes in Angina Management
Recognizing angina symptoms is the first critical step in diagnosing coronary artery disease. However, the similarity of angina symptoms to those of other conditions necessitates a collaborative interprofessional team approach. The team must be adept at differentiating cardiac from non-cardiac chest pain, understanding that symptom quality alone may not always provide a definitive diagnosis. In specific populations, such as patients with diabetes, angina presentation may be atypical and less obvious. A thorough understanding of the patient’s medical and family history is crucial for accurate diagnosis. In the presence of cardiac risk factors, clinicians must maintain a high index of suspicion for a cardiac etiology and pursue further investigation.
While cardiologists often lead the management of angina patients, primary care physicians play a vital role in initial workup and diagnosis. Effective communication and collaboration between physicians, nurses, and pharmacists are essential to avoid missed diagnoses, which can lead to increased morbidity and mortality due to delayed treatment.
Cardiology nurses are instrumental in monitoring patients, assessing treatment adherence, and promoting lifestyle modifications. Pharmacists contribute by optimizing medication regimens, checking for drug interactions, and ensuring appropriate dosing. This interprofessional collaboration is essential for improving the quality of life for patients with angina and preventing adverse outcomes.
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