A Young Woman with Chest Pain and Tachycardia
A 32-year-old woman presents with chest pain that began 48 hours ago. The pain is pleuritic, sharp, and substernal. She initially noticed it 2 days prior but it has become more definite, severe, and constant over the next 48 hours. She is not short of breath, but notes that the pain is worse lying down and eases somewhat with sitting forward.
Prior to this incident, her health had been excellent with nothing more than episodic orthopedic issues related to her active lifestyle. She is currently not on any medications, is a nonsmoker, and uses barrier contraception.
The patient was afebrile. She has a tachycardia of 106 beats per minute, which is regular. Her blood pressure is 105/75 mm Hg in both arms without changes with respirations. Chest is totally clear to percussion and auscultation. The heart has a regular rhythm and strong heart sounds, but a 2-component scratchy sound is audible along the left sternal border and axilla. All peripheral pulses are present and bilaterally equal.
Tests reveal an oxygen saturation on room air of 97%. The complete blood count, metabolic panels, and prothrombin time/partial thromboplastin time are normal, including white blood count and differential. Chest radiograph reveals normal cardiac silhouette and lung fields. An electrocardiogram (EKG) reveals 5T segment elevation in leads I, II, III, AVF, and V1–V4. Cardiac troponins are minimally elevated to just above normal.
Which of the following is the most appropriate next option in the management of this patient?
A. An NSAID, such as ibuprofen and colchicine, should be initiated.
B. Anticoagulant therapy with low molecular weight heparin should be empirically started and a CT angiogram performed.
C. Aggressive anticoagulant and antiplatelet therapy should be started and an urgent cardiac catheterization performed.
D. The diagnosis should be confirmed using CT scanning and cardiac MRI prior to initiating therapy.
(Answer and discussion on next page)
Correct Answer: A. An NSAID, such as ibuprofen and colchicine, should be initiated.
Chest pain remains one of the most common and frantic situations encountered in emergency rooms and urgent care centers. Patients very frequently are “plugged into” a protocol for diagnosing and treating several of the serious and acutely life-threatening diagnoses, such as pulmonary embolism and acute myocardial infarction (AMI). But there are other diagnoses that are important in their own right and can and should be diagnosed quickly and easily without the use of heavy technical and procedural ordinance.
One such diagnosis is acute pericarditis, as is the case for our aforementioned patient. A strong body of data has led to the creation of a set of guidelines to establish the diagnosis of acute pericarditis.
• Does the patient complain of a clinical, pleuritic, predominantly left-sided chest pain that is relieved by sitting forward.
• Note: What is not present in pericarditis helps exclude other causes. This includes a temperature >38.5°C, leukocytosis >13,000 L (eg, pneumonia), or significant hypoxemia (eg, acute pulmonary embolism).
• When coupled with chest pain, acute pericarditis is confirmed by the presence of at least 1 of the following: pericardial friction rub on auscultation, typical EKG changes (eg, diffuse ST segment elevations that would involve multiple coronary artery distributions in the case of AMI), and demonstration of the presence of pericardial effusion.
Our patient has a confirmed diagnosis based on typical pain and rub.
Imaging and Testing
Typically, pericardial effusion is demonstrated by echocardiography and is done in all cases, even in patients who demonstrate 2 criteria—typical chest pain and friction rub (such as our case). This is because even small effusions that are not demonstrable by routine chest x-rays and cardiac silhouette or current signs of tamponade physiology on exam (eg, hypotension and paradoxical pulse) can subsequently deteriorate into tamponade in a small percentage of cases.1,2
An echocardiogram would essentially always be the first imaging study. More refined testing, such as MRI or CT scanning, are more sensitive to pericardial thickening and inflammation, but are reserved for cases where diagnosis is difficult and not confirmed. Since this was not required in our case, Answer D is incorrect.
The next step is to determine the specific causation of pericarditis or whether the condition is idiopathic.
In the United States today, the idiopathic (presumed viral) etiology is by far most common and presents in about 80% of cases.1,2 The remainder 20% of cases are attributed to specific causes, including post-cardiac injury, AMI (although this is much less common now that modern emergency procedures address AMI so effectively), connective tissue disorders, and rarely neoplasm-related. The underlying disorder’s signs or symptoms usually dominate the presentation with corroborating studies making the diagnosis relatively easy.1,2
Once acute pericarditis is confirmed and clinical data and evaluation suggest the etiology is idiopathic, management issues are next to be addressed. The prognosis of idiopathic is excellent with an associated mortality risk of 1%. Large complicating effusions are uncommon (risk of 3%) with tamponade even less so. This should be monitored but in most cases pericardiocentesis is not part of usual management. Thus, the core of therapy is symptom relief and resolution of the inflammatory process.
Established therapies include the use of NSAIDs (ibuprofen, indomethacin, and aspirin).3 Additionally, well-performed recent trials have reported additional efficacy when colchicine is added to the NSAIDs as initial therapy.4,5 Thus, Answer A is correct. Such regimens can be expected to yield an 80% efficacy rate with side effects, which in turn causes discontinuation of the drugs in 10% of cases that are generally attributed to GI complications. Proton pump inhibitors are helpful in the latter regard and should be part of any of these regimens.4,5
Corticosteroids, once commonly used in idiopathic pericarditis, have fallen out of favor due to the frequency of relapse and recurrence with their withdrawal.1 Empirical data from randomized trials suggests 1 to 2 weeks of full doses, followed by a taper of the NSAIDs while maintaining colchicine for 3 months.
Answers B and C address other chest pain diagnoses that are very unlikely here. The patient does not manifest any shortness of breath and is not hypoxic; there were strong negatives for acute pulmonary embolism. Her chest pain is not typical of cardiac ischemia and an EKG such as hers would suggest a massive infarct, which would be expected to manifest much more dramatic clinical and lab abnormalities associated with that diagnosis. Further, both answers suggest the use of full anticoagulation in a patient with pericarditis, which is also problematic as regards to any effusion becoming hemorrhagic. Thus, both Answers B and C are not the optimal answers here.
Outcome of the Case
The patient was started on therapy consisting of ibuprofen 600 mg every 8 hours and colchicine 0.5 mg twice daily. A proton pump inhibitor was also prescribed. There was prompt improvement within 72 hours. The ibuprofen was continued for 10 days and gradually tapered. The colchicine was continued for 3 months and then stopped. At the 3- and 4-month follow-ups, all therapy had been stopped. The patient was clinically well and had no symptoms or signs. Her C-reactive protein levels and EKG was normal.
In most cases, such as when typical chest pain accompanied by 1 or more of a pericardial friction rub, typical electrocardiogram changes, and/or demonstration of pericardial effusion, acute pericarditis can be diagnosed clinically. About 85% of cases will be idiopathic and the cases with specific causes will often display clinical or laboratory features related to the underlying causative illness. Recent quality trials demonstrate therapy with NSAIDs and colchicine are effective in a vast majority (approximately 80%) of cases.
Ronald Rubin, MD, is a professor of medicine at Temple University School of Medicine and chief of clinical hematology in the department of medicine at Temple University Hospital, both in Philadelphia, PA.
- LeWinter MM. Clinical practice. Acute pericarditis. N Eng J Med. 2014;371(25):2410-2415.
- Kytö V, Siplä J, Rautava P. Clinical profile and influences on outcomes in patients hospitalized for acute pericarditis. Circulation. 2014;130(18):1601-1606.
- Lilly LS. Treatment of acute and recurrent idiopathic pericarditis. Circulation. 2013;127(16):1723-1726.
- Imazio M, Brucato A, Cemin R, et al. A randomized trial of colchicine for acute pericarditis. N Eng J Med. 2013;369:1522-1528.
- Imazio M, Bell R, Brucato A, et al. Efficacy and safety of colchicine for multiple recurrences of pericarditis (CORP-2): a multicenter, double-blind, placebo-controlled, randomized trial. Lancet. 2014;383(9936):2232-2237.