Chest pain overview
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After injuries, chest pain is the second most common cause of seeking medical attention in emergency department (ED) in the United States and responsible for >6.5 million visits, which is 4.7% of all ED visits. Chest pain also is the cause of nearly 4 million outpatient visits every year in the United States. Chest pain remains a diagnostic challenge in the ED and outpatiet setting and needs thorough clinical evaluation. Causes of chest pain include noncardiac,and cardiac in which noncardiac chest pain is responsible for more than half of ED visits and only 5.1% will have an acute coronary syndrome. Coronary artery disease (CAD) is the leading cause of death for men and women. Distinguishing between serious and benign causes of chest pain is important. Chest pain is the most symptom of CAD in both men and women.
The first recorded description of chest pain was given by Benivieni, a Florentine physician in the early 1500s. The first concise account of angina pectoris was given by the then Earl of Clarendon when he described his father's illness. Angina pectoris was described by a medical practitioner when Dr. William Heberden read his paper to the College of Physicians in London on 21 July 1768.
Chest pain traditionally has been classified into typical and atypical types. Chest pain that is more likely associated with ischemia includes substernal chest discomfort aggravated by exertion or emotional stress and relieved by rest or nitroglycerin. Ischemic chest discomfort can be described based on quality, location, radiation, and provoking and relieving factors. Using the term of atypical chest pain is problematic. Although the term of atypical chest pain was intended to describe angina without typical chest symptoms, it is more often used to consider that the symptom is noncardiac in origin. Then, it is discouraged using the term of atypical chest pain. Notably, chest pain is a broadly term to define referred pain in the shoulders, arms, jaw, neck, and upper abdomen. So, using the terms of cardiac, possible cardiac, and noncardiac are encouraged to describe the suspected causes of chest pain.
The cardiovascular system, respiratory system, part of the gastrointestinal system, and the great vessels give off afferent visceral input via common thoracic autonomic ganglia. Painful stimuli in any of the aforementioned systems are usually sensed as originating from the chest. However, due to the fact that afferent nerve fibers overlap in the dorsal ganglia, pain in the thorax may be experienced at any point between the umbilicus and the ear, as well as in the upper limbs.
There are many organ systems, that when affected, can lead to the symptoms of chest pain.The most common organs involved are the heart, lungs, and the digestive system. Psychiatric disorders, can also lead to the perception of chest pain. The most important facet of diagnosis is distinguishing the life-threatening causes of chest pain, to the more benign causes. Life-threatening causes of chest pain include myocardial infarction, aortic dissection, pulmonary embolism, tension pneumothorax, and esophageal rupture. Other common causes of chest pain include GERD, chest wall tenderness, achalasia, pneumonia, and anxiety.
Differentiating Chest pain from Other Diseases
There are several life-threatening causes of chest pain which need to be evaluated for first, which include; myocardial infarction, aortic dissection, esophageal rupture, pulmonary embolism, and tension pneumothorax. The other possible causes of chest pain can be evaluated for by carefully assessing the nature of the pain, and obtaining a thorough patient history.
Epidemiology and Demographics
There is a significant difference in the epidemiology of chest pain in the outpatient and emergency settings. The incidence of chest pain is approximately 1,500 per 100,000 individuals worldwide. According to a study conducted in Belgium, the prevalence of chest pain is approximately 2000-5000 per 100,000 individuals worldwide. The incidence of patients presenting with chest pain increases with age and men are more likely to present with chest pain than women.
Common risk factors in the development of chest pain may be associated with the cardiac, respiratory, or gastrointestinal systems. Other risk factors include smoking, obesity, drug abuse, and psychiatric disorders.
There is insufficient evidence to recommend routine screening for chest pain
Natural History, Complications, and Prognosis
Angina pectoris is defined as a retrosternal chest discomfort that increases gradually in intensity (over several minutes). Percipitant factors are physical or emotional stress. In ACS, chest pain may occur during rest. Chest pain is characterized by radiation (left arm, neck, jaw) and its associated symptoms (dyspnea, nausea, lightheadedness). When actively treated or spontaneously resolving, it disappears over a few minutes. Relief with nitroglycerin is not necessarily a diagnostic criterion of myocardial ischemia, especially because other causes such as esophageal spasm may have respons to nitroglycerin. Associated symptoms such as shortness of breath, nausea or vomiting, lightheadedness, confusion, presyncope or syncope, or vague abdominal symptoms are more frequently seen among patients with diabetes, women, and the elderly. A detailed assessment of cardiovascular risk factors, review of systems, past medical history, and family and social history should be done in patients with chest pain. It is pivotal to identify and triage the patients presented with chest pain within 10 minutes of arrival to the hospital. Patients diagnosed with STEMI should be scheduled for primary PCI. Early recognition of STEMI may improve outcomes. Stable angina and non-cardiac chest pain should be evaluated in outpaient setting. Common complications of chest pain include arrythmia, heart failure and Death. Depending on the etiology at the time of presentation, the prognosis may vary. However, the prognosis is generally regarded as good.
Causes of chest pain in pregnancy are similar to those in the general population. Acute life-threatening causes include myocardial infarction, aortic dissection, tension pneumothorax, as well as thromboembolic diseases that are more common in pregnancy such as pulmonary embolism and amniotic fluid embolism. Occasionally, chest pain in pregnant women is caused by physiological changes in pregnancy, namely chest expansion and breast tenderness.
Diagnostic Study of Choice
Chest pain or chest pain equivalent may be referred as chest pain. Diagnosis of nontraumatic chest pain is frequent challenge for physicians. Initial evaluation is considered for life-threatening conditions such as ACS, aortic dissection, and pulmonary embolism , as well as nonvascular syndromes (eg, esophageal rupture, tension pneumothorax). So, therapy for those with less critical illnesses is reasonable. Although there are several life-threatening causes, chest pain usually reflects a more benign condition. The initial work-up is taking ECG, but exact history, physical examination, biomarkers, and other tests are necessary. There is no association between the intensity of symptoms and seriousness of disease and general similarity of symptoms among different causes of chest pain. A comprehensive history with all characteristics of chest pain including nature; 2) onset and duration, 3) location and radiation, 4) precipitating factors, 5) relieving factors, and 6) associated symptoms should be obtained to identify the underlying causes of chest pain.
History and Symptoms
The patient's history must be thoroughly investigated to exclude the life-threatening causes of chest pain, such as the cardiovascular ones: acute coronary syndrome, aortic dissection, pulmonary embolism but also the non-cardiac such as tension pneumothorax and esophageal rupture. Chest pain in myocardial ischemia presented as deep, difficult to localization, and diffuse. Point tenderness is less likely to be symptom of myocardial ischemia. Chest pain characterized by duration, provoking factors, relieving factors, age, cardiac risk factors. Patient history is the most important basis of defining myocardial ischemia. Because of complexity of cardiac symptoms and variable expression of chest pain, ischemic chest pain may be present as non-cardiac chest pain.Characteristic of chest pain with high likelihood of myocardial ischemia including: central, pressure, squeezing, gripping, heaviness, tighness, exertional, stress related, retrosternal, left-sided, dull, aching, Characteristic of chest pain with less likelihood of myocardial ischemia include right-sided, tearing, ripping, burning, sharp, fleeting, shifting, pleuritic, positional.
Physical examination should focus on evaluating for the life-threatening causes of chest pain first. A complete physical exam should be done, which includes a thorough cardiac, lung, and abdominal exam.
The key findings to look for on an ECG is the ST elevation which is characteristic of myocardial infarction. However, The major challenge is the differential between NSTE-ACS and non-cardiac chest pain. Diffuse ST elevation may point to the diagnosis of pericarditis. A serial ECG should be obtained to evaluate for continued or progression of myocardial injury over time.
Chest X-ray can be useful in the initial evaluation of the patient to ascertain if there is cardiomegaly, pulmonary edema and aortic dissection. CT scanning may be better for visualizing the etiology of chest pain depending on the patient history and their symptoms.
Echocardiography and Ultrasound
Transthoracic echocardiography (TTE) can be helpful for diagnosis the causes of acute chest pain such as acute aortic dissection, pericardial effusion, stress cardiomyopathy, and hypertrophic cardiomyopathy. In addition, TTE does provide information for patients with acute chest pain and suspected ACS about left and right ventricular function and regional wall motion abnormalities. Stress echocardiography can be used to define ischemia severity and for risk stratification purposes when ≥2 contiguous segments of wall motion abnormalities in coronary territories are visualized.
Coronary CT angiography (CCTA) can be helpful to diagnose the extent and severity of nonobstructive and obstructive CAD, as well as high-risk features of atherosclerotic plaque (positive remodeling, low attenuation plaque). Fractional flow reserve with CT (FFR-CT) provides additional information about ischemia related to lesion. Dosimetry is low for CCTA, with effective doses for most patients in the 3 to 5 mSv range.
Cardiovascular magnetic resonance imaging (CMR) is helpful to accurately determin global and regional left and right ventricular function, localized myocardial ischemia and infarction, and detection of myocardial viability. Myocardial edema and microvascular obstruction can be determined by CMR to differentiate acute versus chronic MI, as well as other causes of acute chest pain, including myocarditis.
Other Imaging Findings
After ruling out of ACS, rest/stress positron emission tomography (PET) or single-photon emission computed tomography (SPECT) myocardial perfusion imag-ing (MPI) are helpful for detection of perfusion abnormalities, measures of left ventricular function, and high-risk findings, such as transient ischemic dilation. For PET, calculation of myocardial blood flow reserve (MBFR, the ratio of peak hyperemia to resting myocardial blood flow) adds diagnostic and prognostic information over MPI. Radiation exposure dose is ∼3 mSv for rest/stress PET with Rb-82 and ∼10 mSv for Tc-99m SPECT.
Other Diagnostic Studies
Invasive Coronary Angiography (ICA) is used to determine the presence and severity of a luminal obstruction of an epicardial coronary artery, including its location, length, and diameter, as well as coronary blood flow. ICA provides the characterization of high-grade obstructive stenosis and possibility for percutaneous or surgical revascularization. (IFR and FFR) provide physiologic characteristic of stenosis. Radiation exposure to the patient during an interventional procedure varied 4 to 10 mSv and is dependent on procedural duration and complexity. The spatial resolution of ICA is 0.3 mm, so, visualization of arterioles (diameter of 0.1 mm) that regulate myocardial blood flow is impossible. Coronary vascular functional studies can be performed during coronary angiography. In normal coronary angiography there may be evident abnormal coronary vascular function. Assessment of coronary microcirculation and coronary vasomotion by coronary function testing are reasonable.
A correct diagnosis of the underlying cause of the chest pain should be obtained prior to deciding on an appropriate treatment strategy. The most dangerous causes should be evaluated first. If myocardial infarction or ischemia is suspected, the immediate pharmacotherapies including morphine, oxygen, nitrate, aspirin, ACE inhibitors should be initiated.
Common indications of coronary angiography in high risk ACS patients include new ischemic changes on the ECG, troponin-confirmed acute myocardial injury, new-onset left ventricular systolic dysfunction (ejection fraction <40%), and newly diagnosed moderate-severe ischemia on stress imaging. For high-risk patients presented with documented AMI and normal epicardial coronary arteries on CCTA or invasive coronary angiography, or nonobstructive CAD, CMR and echocardiography are useful for evaluation of nonischemic cardiomyopathy or myocarditis. Among high risk patients, invasive coronary angiography provides a comprehensive assessment of the extent and severity of obstructive CAD. The determination of the severity of anatomic CAD is critical to guide the use of coronary revascularization. Approximately 6% to 15% of troponin-positive ACS occurs in the absence of obstructive CAD. Additional testing may be helpful to determine the strategy of treatment. Evidence supports that CMR can identify wall motion abnormalities and myocardial edema and distinguish infarct-related scar from non-CAD causes such as myocarditis and nonischemic cardiomyopathy. Performing CMR within 2 weeks of ACS, can be useful to identify MI with nonobstructive CAD (MINOCA) from other causes. The term obstructive CAD indicates CAD with ≥50% stenosis. Nonobstructive CAD is used if CAD <50% stenosis. High risk CAD is defined in the presence of obstructive stenosis with left main stenosis ≥50% or anatomically significant 3-vessel disease (≥70% stenosis).
Common causes of acute chest pain in the months after CABG include musculoskeletal pain from sternotomy( the most common cause), myocardial ischemia from acute graft stenosis or occlusion, pericarditis, pulmonary embolism, sternal wound infection , nonunion. Post-sternotomy pain syndrome is defined as discomfort after thoracic surgery, persisting for at least 2 months, and without apparent cause. The incidence of post-sternotomy pain syndrome is varied 7%-66% with a higher prevalence in women compared with men within the first 3 months of thoracic surgery but, after 3 months, postoperative sex difference in prevalence was not seen. Causes of Graft failure within the first year post-CABG using saphenous venous grafts are technical issues, intimal hyperplasia, thrombosis. Internal mammary artery graft failure within the first-year post-CABG is most commonly attributable to issues with the anastomotic site of the graft. Causes of acute chest pain several years after CABG include graft stenosis, occlusion or progression of disease in a non-bypassed vessel. One year after CABG, about 10%-20% of saphenous vein grafts fail. By 10 years, about half of saphenous vein grafts are patent. The internal mammary artery has patency rates of 90% to 95% 10 to 15 years after CABG. The use of radial artery grafts for CABG has a higher patency rate at 5 years of follow-up, compared with the use of saphenous vein grafts.
Make healthy lifestyle choices to prevent chest pain from heart disease: Achieve and maintain normal weight, Control high blood pressure, high cholesterol, and diabetes, avoid cigarette smoking and secondhand smoke, eat a diet low in saturated and hydrogenated fats and cholesterol, and high in starches, fiber, fruits, and vegetables, get at least 30 minutes of moderate intensity exercise on most days of the week, Reduce stress.
Secondary prevention of chest pain depends on the cause for instance, risk factor modification remains essential part of the secondary prevention strategy in chronic stable angina. Secondary prevention of chest pain caused by GERD is avoiding food that worsens the symptoms, smoking cessation, weight loss, eating frequent meals, and head raising of the bed while sleeping.