A 37-year-old man with chest pain, ECG changes, and elevated cardiac enzymes
WHAT IS THE CAUSE OF HIS CHEST PAIN?
1. Which is the most likely cause of this patient’s chest pain?
- Acute myocardial infarction
- Acute pericarditis
- Myocarditis
- Pulmonary embolism
- Aortic dissection
- Pneumonia
Acute myocardial infarction. This is a young man with chest pain, ST-segment elevation, and elevated cardiac enzymes. Acute myocardial infarction should always be included in the differential diagnosis of such a patient, as recognizing it early and making an effort to rapidly restore blood flow to the myocardium can greatly improve the clinical outcome. However, particular features in his electrocardiogram and the duration and nature of his chest pain suggest another diagnosis.
Acute pericarditis causes pleuritic chest pain with diffuse ST-segment elevation, and its electrocardiographic changes may be difficult to distinguish from those of ischemia. The features in our patient’s electrocardiogram that point to pericarditis are1:
- ST-segment elevation that is concave upward, occurring in all leads except aVR
- T waves concordant with ST-segment deviation
- PR-segment depression, sparing V1 and aVR
- PR-segment elevation and ST depression in aVR.
Pleuritic chest pain is the most common symptom in acute pericarditis. A prodrome of fever, myalgia, and malaise is also common, especially in younger patients.2 On physical examination, a pericardial friction rub is pathognomonic.
Our patient has most if not all of the classic features of acute pericarditis. Elevated cardiac enzymes, which this patient has, are not a classic feature of pericarditis and are generally considered a marker of cardiac ischemia. However, because the myocardium is adjacent to the pericardium, the acute inflammatory process of acute pericarditis may also result in myocardial injury, resulting in release of creatine kinase-MB.3
An increase in cardiac troponin is also frequently observed in acute pericarditis, reflecting biochemical evidence of inflammatory myocardial cell damage.4 Furthermore, cardiac troponin can be elevated in several other medical conditions,5 such as ischemic heart disease, congestive heart failure, myocarditis, pulmonary embolism, severe pulmonary hypertension, significant left ventricular hypertrophy, renal failure, sepsis, critical illness, and subarachnoid hemorrhage. Therefore, cardiac enzymes are not good markers to distinguish between acute myocardial infarction and acute pericarditis. However, echocardiography is an effective way to help differentiate pericarditis from myocardial ischemia in the setting of elevated troponins and electrocardiographic changes, by determining if wall-motion abnormalities are present or absent.
Hence, the diagnosis of acute pericarditis should take into account the combination of the clinical picture, electrocardiographic findings, and laboratory values. Overreliance on any of these in isolation can lead to misdiagnosis.
Pulmonary embolism is another common cause of acute-onset pleuritic chest pain and dyspnea. Electrocardiographic changes can include ST-segment elevation, and cardiac enzymes can be elevated, although this is uncommon.
Myocarditis is commonly due to infections, collagen vascular diseases, or medications. Hallmarks of this disease are elevated cardiac enzymes and myocardial damage that results in reduction in heart function.
Aortic dissection typically causes a sharp, tearing chest pain that radiates to the back. This diagnosis is unlikely in this patient.
Pneumonia. Although our patient did not have a cough and no crackles were heard on lung examination to suggest pneumonia, his fever, pleuritic chest pain, and leukocytosis with a left shift warrant a workup for it. A parapneumonic effusion could manifest with fevers and pleuritic chest pain. However, the acuity of the symptoms and the characteristic electrocardiographic changes and elevated cardiac enzymes are better explained by the other diagnoses, notably acute pericarditis.
