Prolonged Chest Pain Case Reports

CLINICAL CASE REPORTS and as Letters to the Editor will be published if suitable, space permits. They should not exceed 1,000 words (double in lengt...
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Letters to the Editor will be published if suitable, space permits. They should not exceed 1,000 words (double in length, and may be subject to editing or abridgment.


Acute Myocarditis Versus Myocardial Infarction: Evaluation and Management of the Young Patient with Prolonged Chest Pain—Case Reports Henry G. Stratmann, M.D., F.A.C.A. ST. LOUIS, MISSOURI

Abstract Both acute myocarditis and myocardial infarction must be considered in the differential diagnosis of the young patient with angina-like chest pain. Initial assessment may be difficult, since both diseases may produce similar clinical presentations, electrocardiographic changes, and elevations in cardiac enzymes. Early differentiation is important, however, since myocarditis and myocardial infarction differ greatly in their management and prognosis. These difficulties are illustrated by the 2 cases presented, and guidelines for diagnosis and treatment are

given. Introduction

Prolonged angina-like chest pain in a young patient can be due to either acute myocarditis or myocardial infarction. While uncommon, acute myocardial infarction does occur in young patients and must always be considered in the differential diagnosis.’ Acute myocarditis usually produces few or no symptoms but may present dramatically with severe chest pain, electrocardiograms (ECG), and laboratory tests indistinguishable from acute myocardial infarction.’-’ Because these two entities differ greatly in their treatment and prognosis, differentiation is important. The following cases illustrate these difficulties and suggest guidelines for diagnosis and management. Case Reports Case No. 1 A

twenty-eight-year-old white male presented with a two-hour history of severe, continuous substernal &dquo;aching&dquo; pain with radiation down the inner aspects of both upper extremities. It was accompanied by nausea, vomiting, shortness of breath, and diaphoresis. Prior to the sudden onset of these symptoms the patient had been in his usual state of good health with no From the Department of Cardiology, St. Louis Veterans Administration Medical Center and St. Louis University, St. Louis, Missouri



FIG. 1. Patient No. 1. ECG obtained shortly after admission, leads.

marked ST elevation in the anterior and inferior ,... f



previous history of chest pain and no recent symptoms suggestive of a viral infection. Significant risk factors for coronary artery disease included positive smoking and family histories. Initial cardiopulmonary examination was unremarkable, with no pericardial friction rub heard. The admission electrocardiogram demonstrated marked ST elevation in the anterior and inferior leads (Figure 1). Findings from admission chest x-ray and laboratory tests were unremarkable, with a total creatine phosphokinase (CPK) of 188 U/L and negative MB fraction, and lactic dehydrogenase (LDH) of 207 U/L. Over the next twenty-four hours chest pain recurred despite treatment with intravenous nitroglycerin and morphine sulfate and oral propranolol. Blood samples drawn at six-hour intervals over this period showed sequential elevations of CPK and LDH to peak values of 2,153 U/L and 476 U/L respectively with positive MB fraction and the LDH-1 isoenzyme exceeding LDH-2. M-mode and two-dimensional echocardiography showed normal left ventricular size and good contractility in all segments; no pericardial effusion or other abnormalities were seen. Technetium 99m pyrophosphate and thallium 201 myocardial scans revealed (Figure 2) avid diffuse uptake of technetium 99m but normal distribution of thallium 201. On the basis of these findings the patient was reassessed as having probable myopericarditis, and antianginal medications were gradually discontinued. He was started on oral indomethicin and had rapid and sustained relief of his chest pain. Serial electrocardiograms over the next several days showed gradual return of ST segments to baseline and prominent T wave inversion but no development of Q waves. Cardiac catheterization done ten days after admission showed akinesis of the apex but otherwise normal left ventricular function and normal coronary arteries. A repeat two-dimensional echocardiogram done the next day confirmed the presence of an akinetic left ventricular.apex. An endomyocardial biopsy done at the same time as catheterization showed lymphocytic infiltration and fibrosis on both light and electron microscopy, consistent with resolving myocarditis. The patient remained asymptomatic, and a


FIG. 2. Patient No. 1. A. Technetium 99m pyrophosphate scan. B. Thallium 201 perfusion scan. Both studies obtained several days after admission. ANT=anterior; 45 LAO=45 degree left anterior oblique; LAT=lateral.


repeat two-dimensional echocardiogram done three months after hospital discharge showed normal left ventricular function, with no segmental abnormalities. Case No. 2 A thirty-two-year-old white male presented with sudden onset of substernal pressure lasting thirty minutes and associated with shortness of breath and diaphoresis. The patient had no history of any previous medical problems or risk factors for coronary artery disease. He had, however, noted similar chest pains at rest lasting up to five minutes at a time starting several days prior to admission. Physical examination on admission showed nothing remarkable; blood pressure was 120/70 mmHg. The ECG on admission was within normal limits except for minimal nonspecific ST elevation in the anterior precordial leads (Figure 3). Admission laboratory tests were also normal except for a mild leukocytosis; serum cholesterol was 190 mg/dl. Initial CPK was 144 U/L, rising to a peak value of 350 U/L at six hours after admission. The LDH rose to only 145 U/L but with LDH-1 greater than LDH-2. Over the next forty-eight hours the patient had recurrent episodes of chest pain despite treatment with aspirin, intravenous nitroglycerin, and oral diltiazem. A technetium 99m pyrophosphate scan performed approximately forty-eight hours after his initial onset of chest paid showed no definite uptake. The patient subsequently underwent cardiac catheterization, which revealed proximal occlusion of the left anterior descending artery and a 50 % lesion of the right coronary artery. ’


FIG. 3. Patient No. 2. ECG obtained 18 hours after admission, anterolateral leads..


ST elevation and T


inversions in the

Moderate hypokinesis of the anterior wall of the left ventricle was also present. Based on their findings, a diagnosis of acute myocardial infarction due to atherosclerotic coronary artery disease was made. The patient’s chest pain improved with addition of oral isosorbide dinitrate and atenolol to his antianginal regimen. Discussion As these cases show, acute myocarditis may produce an initial clinical presentation difficult to distinguish from acute myocardial infarction, especially when it is associated with pericardial involvement (myopericarditis) . 2-1 In 34 patients with myopericarditis reported in one series,2 21 % had &dquo;coronary mimicking&dquo; chest pain and 71 % lacked a pericardial friction rub. Severe substernal chest pain &dquo;strongly suggestive of myocardial infarction&dquo; was also seen in another group of 24 patients with myocarditis.4 Although uncommon, myocardial infarction associated with atherosclerotic coronary artery disease does occur in young patients, especially cigarette smokers,’ and may occur from other causes, such as coronary artery spasm, arteritis, or emboli to the coronary arteries. While a history of preceding viral syndrome favors the diagnosis of myocarditis, and the presence of significant risk factors for atherosclerotic coronary artery disease or a long history of typical angina preceding the acute presentation suggests myocardial infarction, absence of these factors does not exclude either diagnosis. ECG abnormalities seen during acute myocarditis may simulate those associated with myocardial infarction and can include complex ventricular arrhythmias, ST and T wave changes, and even development of Q waves .2,4 Elevations in total CPK and LDH (including CPK-MB and LDH-1 isoenzymes) due to myocardial necrosis can also be seen in both diseases, with similar times of release of these enzymes relative to the onset of chest pain .2 ’

257 When the clinical presentation, ECG, and cardiac enzymes are ambiguous, a variety of cardiac imaging techniques may be employed to help clarify the diagnosis. Two-dimensional echocardiography has proved useful for early diagnosis of acute myocardial infarction. In one series 31 of 33 patients (94 % ) with chest pain and subsequent diagnosis of acute myocardial infarction had regional left ventricular wall abnormalities on an admission two-dimensional echocardiogram, while 27 of 32 similar patients in whom myocardial infarction was later ruled out did not.6 Similar wall motion abnormalities are also seen at various times during the course of myocarditis, however, and thus neither the presence nor absence of such abnormalities can be used to reliably distinguish between the two diseases . In acute transmural myocardial infarction, both technetium 99m pyrophosphate and thallium 201 scans usually yield abnormal findings, typically demonstrating focal rather than diffuse abnormalities.’ Conversely, in experimental myopericarditis, very strong, diffuse myocardial uptake of technetium 99m pyrophosphate, this tracer has been documented.9 This same pattern has also been reported in cases of clinical myocarditis in conjunction with normal thallium 201 perfusion scans,IO,1I reflecting myocardial necrosis in the presence of normal perfusion. However, while this pattern of strong, diffuse myocardial uptake of technetium 99m in conjunction with normal thallium scintigraphy may be relatively specific for myocarditis, its sensitivity is unclear. Acute myocarditis has been associated with absence of technetium 99m uptake’2 and also with focal perfusion defects on thallium 201 scintigraphy.’3 Thus, in the individual patient these scans may or may not be helpful. Both indium 111-labeled white blood cell and gallium 67 have been used to assess the presence of active myocardial inflammation. 14, &dquo; The value of gallium 67 is limited, however, by the long delay (usually seventy-two hours) required between injection of the tracer and imaging.’4 Although these imaging techniques may be useful for differentiating myocarditis from myocardial infarction, definitive evaluation requires cardiac catheterization. 12,14 The timing of cardiac catheterization should be based on the patient’s response to medical therapy. When the clinical presentation, ECG’s, and cardiac enzymes are compatible with either myocardial infarction or myocarditis, the patient should always be assumed to have a myocardial infarction until this diagnosis is excluded and be treated accordingly. Thus, recurrent or persistent chest pain should be treated initially with antianginal agents (eg, nitrates, calcium antagonists, betablockers, etc). If these do not produce adequate relief of chest pain, therapy for possible myopericarditis (aspirin or nonsteroidal antiinflammatory agents) may be added. Failure to respond to any of these measures indicates the need for early catheterization. Conversely, if empirical medical therapy results in good relief of chest pain, cardiac catheterization can be performed electively before hospital discharge. Prior to elective catheterization, cardiac imaging may be performed using the radioisotopes previously described and may provide information favoring a specific diagnosis. Even if these scans suggest the presence of myocarditis rather than myocardial infarction, however, their overall reliability is still unclear,10,12-IS and cardiac catheterization should still be recommended. The presence of significant coronary artery disease at catheterization strongly favors the diagnosis of acute myocardial infarction, especially if abnormal left ventricular segmental wall motion is associated with severe narrowing or occlusion of the vessel perfusing that segment. If the coronary vasculature is &dquo;normal,&dquo; however, endomyocardial biopsy should be performed to assess the presence of myocarditis.’6


If biopsy fails to demonstrate myocarditis, other potential etiologies for myocardial necrosis such as coronary artery spasm, should be considered and investigated.’4

Conclusions Standard methods of evaluating prolonged angina-like chest pain in a young patient may fail to distinguish between acute myocardial infarction and myocarditis. When the clinical presentation, ECG, and cardiac enzymes do not give a definitive answer, radionuclide cardiac imaging to assess myocardial perfusion (thallium 201 scintigraphy), the presence of active myocardial necrosis (technetium 99m scintigraphy), or inflammation (indium 111 or gallium 67 imaging) may be useful. If a definitive diagnosis has not yet been established, persistent or recurrent chest pain should initially be assumed to be ischemic and treated with appropriate antianginal agents. Antiinflammatory agents (such as aspirin) may be added for treatment of possible myopericarditis if antianginal therapy is ineffective. Early cardiac catheterization should be performed in patients whose chest pain does not respond satisfactory to these measures, and endomyocardial biopsy should be done in patients found to have normal coronary arteries.

Henry Stratmann, M.D., F.A. C. A. Department of Cardiology St. Louis Veterans Administration Medical Center St. Louis, Missouri 63125

References 1. Glover MU, Kuber MT, Warren SE, et al: Myocardial infarction before age 36: Risk factor and arteriographic analysis. Am J Cardiol 49:1600-1603, 1982. 2. Heikkila J, Karjalainen J: Evaluation of mild acute infectious myocarditis. Br Heart J 47:381-391, 1982. 3. Woodruff JF: Viral myocarditis. A review. Am J Pathol 101:427-484, 1980. 4. Gardiner AJS, Short D: Four faces of acute myopericarditis. Br Heart J 35:433-442, 1973. 5. Take M, Sakiguchi M, Hiroe M, et al: Early clinical profiles of cases with histopathologically proven acute idiopathic myocarditis and a proposal for diagnostic criteria. Jpn Circ J 45:1415-1420, 1981. 6. Horowitz RS, Morganroth J, Parrotto C, et al: Immediate diagnosis of acute myocardial infarction by twodimensional echocardiography. Circulation 65:323-329, 1982. 7. Nieminen MS, Heikkila J, Karjalainen J: Echocardiography in acute infectious myocarditis: Relation to clinical and electrocardiographic findings. Am J Cardiol 53 :1331-1337, 1984.


Henning H,

Schelbert HR,

Rignetti A,


al: Dual

myocardial imaging with technetium 99m pyrophosphate and thallium 201 for detecting, localizing and sizing acute myocardial infarction. Am J Cardiol 40:147-155, 1977. 9. Matsumori A, Kadota K, Kawai C: Technetium 99m pyrophosphate uptake in experimental viral peri-

myocarditis. Sequential study of myocardial uptake and pathologic correlates. Circulation 61:802-807, 1980. 10. Mitsutake A, Nakamura M, Inou T, et al: Intense, persistent myocardial avid technetium 99m pyrophosphate scintigraphy in acute myocarditis. Am Heart J 101:683-684, 1981. 11. Ahmad M, Duebiel JP: 99m Tc pyrophosphate myocardial imaging in perimyocarditis. J Nucl Med 22 :452454, 1981. 12. Chandraratna PAN, Nimalasuriya A, Reid CL, et al: Left ventricular asynergy in acute myocarditis. Simulation of acute myocardial infarction. JAMA 250:1428-1430, 1983. 13. Tamaki N, Yonekura Y, Kadota K, et al: Thallium-201 myocardial perfusion imaging in myocarditis. Clin Nucl Med 10:562-566, 1985. 14. Costanzo-Nordin MR, O’Connell JB, Subramanian R, et al: Myocarditis confirmed by biopsy presenting as acute myocardial infarction. Br Heart J 53:25-29, 1985. 15. O’Connell JB, Henkin RE, Robinson JA: Imaging techniques for myocardial inflammation. Ann Clin Lab Sci 16:146-154, 1986. 16. Fenoglio JJ, Ursell PC, Kellogg CF, et al: Diagnosis and classification of myocarditis by endomyocardial biopsy. N Engl J Med 308:12-18, 1983.