Case 1: Diagnostic Evaluation of Chest Pain
A 65-year-old man presented to the emergency department with a complaint of left-sided chest pain radiating to his left arm. There were no alleviating factors. His past medical history included hypertension, uncontrolled diabetes mellitus, and hyperlipidemia. He denied any toxic habits. His baseline exercise tolerance is 2 city blocks limited by fatigue. Upon presentation, vital signs were stable and the physical examination was unremarkable. The chest pain was partially relieved by sublingual nitroglycerin. The 12-lead ECG showed nonspecific T-wave inversions in the inferolateral leads. He was administered aspirin, and the chest pain resolved shortly thereafter. Subsequently, he was admitted to the telemetry floor for further evaluation and observation. His serial cardiac biomarkers were negative. He did not have any recurrent chest pain and remained hemodynamically stable throughout the hospital stay. How would you manage this case?
In this clinical scenario, the patient does not fit the complete picture of anginal symptoms. However, the key here is the presence of risk factors and subtle 12-lead ECG changes, which place him at an elevated risk for coronary artery disease. He can be further evaluated by stress testing for risk stratification.
Angina consists of retrosternal chest pain increased by activity or emotional stress and generally relieved by rest or administration of nitroglycerin. The evaluation of chest pain begins with a thorough history and physical examination to delineate the etiology. The list of differential diagnoses is vast, and a detailed review of systems about pertinent diagnoses can narrow down the list. The presence of comorbid conditions and risk factors might hint toward a diagnosis of coronary artery disease. Both serial 12-lead ECG and highly sensitive cardiac troponin T testing should be performed before excluding ongoing ischemic coronary artery disease. Prior to stress testing, the patient should be chest pain free for 24 hours, without dynamic 12-lead ECG changes, and the highly sensitive cardiac troponin T level should be negative or trending downward.
The differential diagnosis of chest pain includes the following:
Coronary artery disease
Peptic ulcer disease
Chest pain should be classified as anginal or nonanginal based on the history.
Anginal symptoms can be considered in the setting of risk factors and should be evaluated by an appropriate stress modality if the symptoms are vague.
Serial 12-lead ECG and highly sensitive cardiac troponin T should be performed to exclude ongoing ischemic coronary artery disease before stress testing is performed.
Case 2: Diagnosis of Acute Coronary Syndrome
A 56-year-old obese man presented to the emergency department with a complaint of central chest pain awakening him from sleep. He has a past medical history of hypertension and bronchial asthma. In addition, he is an active smoker and works full time as an office secretary. He self-administered acetaminophen, but it did not alleviate the discomfort. Upon arrival, he continued to have chest pain, which was not relieved by nitroglycerin. He appeared to be in mild distress; otherwise, the vital signs and physical examination were unremarkable. The 12-lead ECG showed ST-segment depressions in the anterior and lateral precordial leads (as shown in Figure 1.2.1). Treatment with aspirin, clopidogrel, and an unfractionated heparin infusion was begun. The highly sensitive cardiac troponin T level was elevated. Subsequently, he was admitted to the telemetry unit for further care, including a discussion about cardiac catheterization. The chest pain improved, and his decision was to defer an invasive strategy. The 12-lead ECG changes resolved, and the highly sensitive cardiac troponin T level trended downward. How would you manage this case further?
Acute coronary syndrome consists of ST-segment elevation myocardial infarction (STEMI), non–ST-segment myocardial infarction (NSTEMI), and unstable angina (UA). In this clinical scenario, the patient was diagnosed with NSTEMI based on the clinical criteria of the 12-lead ECG changes and elevated highly sensitive cardiac troponin T level. The Thrombolysis in Myocardial Infarction (TIMI) risk score can be used to guide management (Table 1.2.1). A TIMI risk score of 3 is considered intermediate, and hence, a conservative strategy can be adopted, instead of an invasive strategy.
|Score||Incidence of Mortality (%)|
|Age ≥65 years||1||4.7|
|≥3 coronary artery disease risk factors||2||8.3|
|Prior coronary stenosis >50%||3||13|
|Presence of ST- segment deviation||4||20|
|≥2 episodes of angina within 24 hours||5||26|
|Elevated cardiac biomarkers||6||41|
|Prior use of aspirin in past 7 days||7||41|
NSTEMI/UA may present as a new-onset or worsening of anginal symptoms with 12-lead ECG changes such as ST-segment depression, transient ST-segment elevation, or dynamic T-wave inversions with the presence of cardiac biomarkers (NSTEMI) or with absent cardiac biomarkers (UA) (Table 1.2.2). Plaque rupture, thrombus formation, and vasospasm can be the underlying mechanisms of occurrence.
|ST-segment elevation myocardial infarction||Angina and ST-segment elevation with positive troponin|
|Non–ST-segment elevation myocardial infarction||Angina, ST-segment deviation, T-wave inversion, and positive troponin|
|Unstable angina||New or worsening angina, ST-segment nonspecific changes, and negative troponin|
Ongoing chest pain, heart failure symptoms, and syncope are signs of potentially worse outcomes.
Initial management consists of nitrates, dual antiplatelet agents, anticoagulation, β-adrenergic blockers, and angiotensin-converting enzyme inhibitors (in the presence of left ventricular dysfunction). High-intensity 3-hydroxy-3-methylglutaryl–coenzyme A (HMG-CoA) reductase inhibitors (statins) should be initiated early during the hospital course. Patients with active symptoms and hemodynamic instability should be considered for early invasive therapy with cardiac catheterization. The TIMI risk score and/or Global Registry of Acute Coronary Events (GRACE) score can be used to guide both prognosis and management. Low- or intermediate-risk patients can be managed with optimal medical therapy. Stress testing should be performed before discharge or within 72 hours. High-risk candidates should go for early invasive therapy. For the conservative strategy, a patient continuing to have symptoms or high risk of adverse events should undergo an invasive strategy. Low-risk candidates or patients with active chest pain with low probability of coronary artery disease can be managed with medical therapy.
Clinical symptoms, 12-lead ECG changes, and cardiac biomarkers are the cornerstone elements for the diagnosis of acute coronary syndrome. Serial 12-lead ECG and highly sensitive cardiac troponin T levels should be performed.
The TIMI risk score can guide the management and prognosis.
Dual antiplatelet agents, anticoagulation, and nitrates should be initiated regardless of the management strategy. Furthermore, β-adrenergic blockers should be started early in the hospital course.
If a conservative strategy is adopted, then stress testing should be performed once the clinical symptoms have resolved.
Case 3: Diagnosis of Anginal Variants
A 46-year-old man was evaluated by the emergency medical services with a complaint of chest pain. The on-site 12-lead ECG showed ST-segment elevation in the anterior precordial leads with ST-segment depression in the inferior leads (as shown in Figure 1.3.1). The local hospital ST-segment elevation myocardial infarction (STEMI) protocol was activated, and the patient was brought directly to the cardiac catheterization laboratory. The coronary artery anatomy demonstrated severe vasospasm, which improved with intracoronary nitroglycerin. The chest pain resolved, and he was admitted to the telemetry floor. He denied any medical conditions, and there was no family history of premature coronary artery disease. However, he is an active smoker and admitted intranasal cocaine use 1 night prior to the onset of his symptoms. Serial 12-lead ECG showed resolution of the ST-segment and T-wave changes. How would you manage this case?
Prinzmetal or variant angina is in the differential diagnosis of acute coronary syndrome. Although the initial management is similar to that for acute coronary syndrome, it should be considered when the pretest probability of coronary artery disease is low. In this clinical scenario, the patient should be advised about smoking cessation and abstinence from recreational drug abuse.
Prinzmetal or variant angina is defined as recurrent anginal symptoms that start at rest with transient 12-lead ECG changes and that are relieved by nitroglycerin. Decubitus angina with nocturnal awakening, syncope, and angina not associated with exertion are the components in the history. Cold exposure can be a trigger. The underlying mechanism is coronary vasospasm. The diagnosis can be made by clinical and angiographic evidence for vasospasm. Provocative testing is no longer suggested in the guidelines. The first-line treatment includes smoking cessation and avoidance of triggers. Vasodilators such as nitrates and calcium channel antagonists are used for symptomatic relief. β-Blockers should be avoided in these patients. Although it can be associated with sudden cardiac death due to the occurrence of malignant arrhythmias, long-term prognosis with early detection is generally favorable. The presence of underlying coronary artery disease should also be considered in the setting of traditional risk factors because mixed patterns can also be found.
Prinzmetal or variant angina is a differential for acute coronary syndrome.
Angina at rest with transient 12-lead ECG changes relieved by nitrates and angiographic features of vasospasm are the key in diagnosis.
Smoking cessation and use of vasodilators are the components of treatment. β-Blockers should be avoided.
A mixed pattern with underlying coronary artery disease should also be considered.
Case 4: Diagnosis of Musculoskeletal Chest Pain
A 35-year-old woman was evaluated in the emergency department for ongoing chest pain over the past week. She denied any shortness of breath, palpitation, nausea, vomiting, or pyrosis. She has no past medical or surgical history and is not receiving treatment with medication. There is no family history of coronary artery disease. The vital signs were stable. The cardiopulmonary examination revealed tenderness to palpation over the left parasternal region. The 12-lead ECG showed normal sinus rhythm, and chest radiography demonstrated no abnormalities. Cardiac biomarkers are pending in the chemistry laboratory. Pregnancy test was negative. What is the most likely diagnosis, and how would you manage this condition?
In this clinical secnario, the young woman without risk factors for coronary artery disease should be evaluated for other causes of chest pain.
Costochondritis, or Tietze syndrome (also called chondropathia tuberosa or costochondral junction syndrome), is an inflammation of the costochondral junctions of ribs of the chondrosternal joints. The exact cause of costochondritis is unknown. However, it can be caused by trauma, physical strain, arthritis, tumor in the costosternal region, and in some cases, infections.
Pain and tenderness usually occur on the sides of the sternum and are often worsened with cough, deep breathing, or strenuous physical activity.
In most cases, a thorough history and physical examination are enough to consider the diagnosis. However, 12-lead ECG, chest radiography, and cardiac biomarkers must be performed to exclude other causes of chest pain.
Costochondritis usually resolves on its own or with rest. Patient with mild to moderate symptoms can be treated with nonsteroidal anti-inflammatory drugs (NSAIDs), analgesics, or in some cases, tricyclic antidepressants, including amitriptyline and corticosteroid injections.
It is important to assess the pretest probability for the diagnosis before initiation of the workup. A consideration of risk factors for coronary artery disease is an important key to guide the approach.