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Acute pericarditis presenting with sinus bradycardia: A case report
International Journal of Cardiology 60 (1997) 307–310
Acute pericarditis presenting with sinus bradycardia: A case report A.T. Marcel Gosselink*, Maarten P. van den Berg, Harry J.G.M. Crijns From the Department of Cardiology /Thoraxcenter, University Hospital Groningen, The Netherlands Received 19 March 1997; accepted 25 March 1997
Abstract Acute pericarditis is almost invariably associated with sinus tachycardia. Recent-onset chest pain in the presence of (sinus) bradycardia is considered to be associated with an acute ischemic syndrome rather than acute pericarditis. This report describes a patient with acute pericarditis initially presenting with sinus bradycardia, probably due to a vasovagal response to (chest) pain. 1997 Elsevier Science Ireland Ltd. Keywords: Acute pericarditis; Sinus bradycardia
1. Introduction
2. Case
Acute pericarditis may manifest electrocardiographically with abnormalities of the T-wave, S-T segment and the P-R segment [1]. In addition, acute pericarditis is almost invariably associated with sinus tachycardia [1] even in the absence of other contributing factors, such as fever or hemodynamic compromise [2]. Indeed, some suggest that the absence of tachycardia, and even more so the presence of bradycardia, may be a potential differentiating feature from an acute ischemic syndrome, in particular acute myocardial infarction (which may be associated with either sinus tachycardia or sinus bradycardia) [1]. In this paper, however, we report a patient with acute pericarditis presenting with marked sinus bradycardia.
A 46-year-old male with no previous medical history was admitted to our hospital with a severe, dull chest pain, radiating to both shoulders. A few days before, he had suffered a minor cold. The patient had smoked 15 cigarettes a day for several years. He did not use any medication. At hospital presentation, chest pain had been present continuously for approximately 2 h. The patient made a sick impression, looked pale, and was very tense. He perspired profusely and nearly fainted. The heart rate was 35 beats / min, with a marked respiratory arrhythmia, and his blood pressure was 100 / 70 mm Hg. Body temperature was 37.28C. Jugular venous pressure was normal. Cardiac examination showed a nondisplaced point of maximal intensity and normal S 1 and S 2 . There were no extra heart sounds or cardiac murmurs. Further physical examination was unremarkable.
*Corresponding author. Tel.: 131 50 3616161; fax: 131 50 3614391.
0167-5273 / 97 / $17.00 1997 Elsevier Science Ireland Ltd. All rights reserved PII S0167-5273( 97 )00084-3
308
A.T. .M. Gosselink et al. / International Journal of Cardiology 60 (1997) 307 – 310
The electrocardiogram (ECG) at hospital admission showed a marked sinus bradycardia with respiration associated sinus arrhythmia and minor non-specific ST-segments abnormalities (Fig. 1). Chest roentgenogram revealed no abnormalities. Admission laboratory data, including blood count, erythrocyte sedimentation rate, blood electrolytes and serum creatinine, cardiac enzymes (including creatine kinase (CK) and CK-MB isoenzyme), and arterial blood gas analysis, were all within normal limits. The differential diagnosis in this patient with recent-onset chest pain included ischemic heart disease (unstable angina or acute myocardial infarction), aortic dissection and acute pericarditis. A diagnostic work-up, including transthoracic and transesophageal echocardiography and cardiac catheterization was performed. Transthoracic echocardiography showed preserved left and right ventricular function without wall motion abnormalities. There was no valvular dysfunction or pericardial effusion. Transesophageal echocardiography also did not show any abnormalities, in particular no dissection of the thoracic aorta. Cardiac catheterization (including right and left heart catheterization as well as coronary angiog-
raphy) was unremarkable. In particular, there was no (epicardial) coronary artery disease. Also, left and right heart pressures were within normal limits. Thus, a diagnosis of coronary artery disease or thoracic aorta dissection was considered highly unlikely and rejected. On follow-up auscultation a pericardial friction rub was heard 4 h after admission, thereby confirming the diagnosis of acute pericarditis. The patient then also had a mild fever up to 38.38C. Blood pressure was 130 / 80 mm Hg. The ECG showed an increase in ST-segment elevation in several limb and precordial leads, compatible with acute pericarditis (Fig. 2). Sinus rate had increased significantly by then when compared to the admission ECG. Treatment with antiinflammatory drugs (ibuprofen 400 mg tid) had already been initiated and chest pain had been relieved almost completely. Cardiac enzymes remained within normal limits during follow-up. Further clinical course was uncomplicated and the patient was discharged in good clinical condition the next day. He visited the outpatient department 3 weeks after the event for routine follow-up. He had not suffered any complaints after hospital dismissal.
Fig. 1. The ECG at hospital admission, i.e. 2 h after beginning of chest complaints. A marked sinus bradycardia (mean heart rate 45 beats / min) and respiratory sinus arrhythmia is demonstrated. There are minor, non-specific ST-segment abnormalities in the right precordial (in particular lead V2 ) and inferior leads (II, III and AVF).
A.T. .M. Gosselink et al. / International Journal of Cardiology 60 (1997) 307 – 310
309
Fig. 2. The ECG 4 h after hospital admission (i.e. 6 h after start of complaints) showing a markedly increased heart rate (mean 90 beats / min) when compared to baseline. In addition, elevated concave-upward ST-segments as well as PR-segment depression, are present now in several leads.
The ECG had normalized by then (Fig. 3). Although acute and convalescent viral titers were not available, pericarditis was probably of viral origin.
3. Discussion Acute pericarditis is generally considered to be
Fig. 3. The ECG 3 weeks after the episode of acute pericarditis, showing normal sinus rhythm with normalized ST-segments and PR-segments.
310
A.T. .M. Gosselink et al. / International Journal of Cardiology 60 (1997) 307 – 310
almost invariable associated with sinus tachycardia [1]. Indeed, in a patient with chest pain, the presence of (sinus) bradycardia is more suggestive of an acute ischemic syndrome rather than acute pericarditis [1], and some even suggest that acute pericarditis can be practically ruled out in case of bradycardia. This report, however, demonstrates that acute pericarditis may, particularly in the early stage, present with marked sinus bradycardia. To our knowledge, this is the first case report describing this phenomenon. Obviously, our observation may be of clinical importance, since it implies that in the setting of (sub)acute-onset chest pain and bradycardia, acute pericarditis can not be ruled out with certainty. This may pose difficulties in differentiating between pericarditis and ischemia, particularly when medical history and additional ECG findings are not typical. Additional studies, in particular echocardiography and / or coronary angiography, may be necessary for final diagnosis. Several mechanisms may explain the generally observed sinus tachycardia in acute pericarditis, including (1) enhanced adrenergic drive due to pericarditis related chest pain, (2) pericarditis associated fever and (3) (mechanical) irritation of the myocardium and impulse generating tissues. This
case report does not clarify the precise mechanism by which pericarditis may induce sinus bradycardia. Nevertheless, a neurally-mediated bradycardia, initiated in higher central nervous system centres by severe (chest) pain and / or emotional stimuli (distress) appears most likely [3]. This is supported by the observation of a marked respiratory sinus arrhythmia and relatively low (systolic) blood pressure on admission. Moreover, after the initial stage, when chest pain had been treated adequately, sinus bradycardia was no longer present and blood pressure had increased. In conclusion, this case reported shows that the presence of marked sinus bradycardia in the setting of recent-onset chest pain, does not exclude the diagnosis of acute pericarditis.
References [1] Shamroth L, Pericarditis. In: Shamroth L, editor. The twelve lead electrocardiogram (Book 1). Oxford: Blackwell Scientific Publications, 1989:293. [2] Dressler N. Sinus tachycardia complicating and outlasting pericarditis. Am Heart J 1966;72:422–3. [3] Lurie KG, Benditt D. Syncope and the autonomic nervous system. J Cardiovasc Electrophysiol 1996;7:760–76.
Acute pericarditis presenting with sinus bradycardia: A case report A.T. Marcel Gosselink*, Maarten P. van den Berg, Harry J.G.M. Crijns From the Department of Cardiology /Thoraxcenter, University Hospital Groningen, The Netherlands Received 19 March 1997; accepted 25 March 1997
Abstract Acute pericarditis is almost invariably associated with sinus tachycardia. Recent-onset chest pain in the presence of (sinus) bradycardia is considered to be associated with an acute ischemic syndrome rather than acute pericarditis. This report describes a patient with acute pericarditis initially presenting with sinus bradycardia, probably due to a vasovagal response to (chest) pain. 1997 Elsevier Science Ireland Ltd. Keywords: Acute pericarditis; Sinus bradycardia
1. Introduction
2. Case
Acute pericarditis may manifest electrocardiographically with abnormalities of the T-wave, S-T segment and the P-R segment [1]. In addition, acute pericarditis is almost invariably associated with sinus tachycardia [1] even in the absence of other contributing factors, such as fever or hemodynamic compromise [2]. Indeed, some suggest that the absence of tachycardia, and even more so the presence of bradycardia, may be a potential differentiating feature from an acute ischemic syndrome, in particular acute myocardial infarction (which may be associated with either sinus tachycardia or sinus bradycardia) [1]. In this paper, however, we report a patient with acute pericarditis presenting with marked sinus bradycardia.
A 46-year-old male with no previous medical history was admitted to our hospital with a severe, dull chest pain, radiating to both shoulders. A few days before, he had suffered a minor cold. The patient had smoked 15 cigarettes a day for several years. He did not use any medication. At hospital presentation, chest pain had been present continuously for approximately 2 h. The patient made a sick impression, looked pale, and was very tense. He perspired profusely and nearly fainted. The heart rate was 35 beats / min, with a marked respiratory arrhythmia, and his blood pressure was 100 / 70 mm Hg. Body temperature was 37.28C. Jugular venous pressure was normal. Cardiac examination showed a nondisplaced point of maximal intensity and normal S 1 and S 2 . There were no extra heart sounds or cardiac murmurs. Further physical examination was unremarkable.
*Corresponding author. Tel.: 131 50 3616161; fax: 131 50 3614391.
0167-5273 / 97 / $17.00 1997 Elsevier Science Ireland Ltd. All rights reserved PII S0167-5273( 97 )00084-3
308
A.T. .M. Gosselink et al. / International Journal of Cardiology 60 (1997) 307 – 310
The electrocardiogram (ECG) at hospital admission showed a marked sinus bradycardia with respiration associated sinus arrhythmia and minor non-specific ST-segments abnormalities (Fig. 1). Chest roentgenogram revealed no abnormalities. Admission laboratory data, including blood count, erythrocyte sedimentation rate, blood electrolytes and serum creatinine, cardiac enzymes (including creatine kinase (CK) and CK-MB isoenzyme), and arterial blood gas analysis, were all within normal limits. The differential diagnosis in this patient with recent-onset chest pain included ischemic heart disease (unstable angina or acute myocardial infarction), aortic dissection and acute pericarditis. A diagnostic work-up, including transthoracic and transesophageal echocardiography and cardiac catheterization was performed. Transthoracic echocardiography showed preserved left and right ventricular function without wall motion abnormalities. There was no valvular dysfunction or pericardial effusion. Transesophageal echocardiography also did not show any abnormalities, in particular no dissection of the thoracic aorta. Cardiac catheterization (including right and left heart catheterization as well as coronary angiog-
raphy) was unremarkable. In particular, there was no (epicardial) coronary artery disease. Also, left and right heart pressures were within normal limits. Thus, a diagnosis of coronary artery disease or thoracic aorta dissection was considered highly unlikely and rejected. On follow-up auscultation a pericardial friction rub was heard 4 h after admission, thereby confirming the diagnosis of acute pericarditis. The patient then also had a mild fever up to 38.38C. Blood pressure was 130 / 80 mm Hg. The ECG showed an increase in ST-segment elevation in several limb and precordial leads, compatible with acute pericarditis (Fig. 2). Sinus rate had increased significantly by then when compared to the admission ECG. Treatment with antiinflammatory drugs (ibuprofen 400 mg tid) had already been initiated and chest pain had been relieved almost completely. Cardiac enzymes remained within normal limits during follow-up. Further clinical course was uncomplicated and the patient was discharged in good clinical condition the next day. He visited the outpatient department 3 weeks after the event for routine follow-up. He had not suffered any complaints after hospital dismissal.
Fig. 1. The ECG at hospital admission, i.e. 2 h after beginning of chest complaints. A marked sinus bradycardia (mean heart rate 45 beats / min) and respiratory sinus arrhythmia is demonstrated. There are minor, non-specific ST-segment abnormalities in the right precordial (in particular lead V2 ) and inferior leads (II, III and AVF).
A.T. .M. Gosselink et al. / International Journal of Cardiology 60 (1997) 307 – 310
309
Fig. 2. The ECG 4 h after hospital admission (i.e. 6 h after start of complaints) showing a markedly increased heart rate (mean 90 beats / min) when compared to baseline. In addition, elevated concave-upward ST-segments as well as PR-segment depression, are present now in several leads.
The ECG had normalized by then (Fig. 3). Although acute and convalescent viral titers were not available, pericarditis was probably of viral origin.
3. Discussion Acute pericarditis is generally considered to be
Fig. 3. The ECG 3 weeks after the episode of acute pericarditis, showing normal sinus rhythm with normalized ST-segments and PR-segments.
310
A.T. .M. Gosselink et al. / International Journal of Cardiology 60 (1997) 307 – 310
almost invariable associated with sinus tachycardia [1]. Indeed, in a patient with chest pain, the presence of (sinus) bradycardia is more suggestive of an acute ischemic syndrome rather than acute pericarditis [1], and some even suggest that acute pericarditis can be practically ruled out in case of bradycardia. This report, however, demonstrates that acute pericarditis may, particularly in the early stage, present with marked sinus bradycardia. To our knowledge, this is the first case report describing this phenomenon. Obviously, our observation may be of clinical importance, since it implies that in the setting of (sub)acute-onset chest pain and bradycardia, acute pericarditis can not be ruled out with certainty. This may pose difficulties in differentiating between pericarditis and ischemia, particularly when medical history and additional ECG findings are not typical. Additional studies, in particular echocardiography and / or coronary angiography, may be necessary for final diagnosis. Several mechanisms may explain the generally observed sinus tachycardia in acute pericarditis, including (1) enhanced adrenergic drive due to pericarditis related chest pain, (2) pericarditis associated fever and (3) (mechanical) irritation of the myocardium and impulse generating tissues. This
case report does not clarify the precise mechanism by which pericarditis may induce sinus bradycardia. Nevertheless, a neurally-mediated bradycardia, initiated in higher central nervous system centres by severe (chest) pain and / or emotional stimuli (distress) appears most likely [3]. This is supported by the observation of a marked respiratory sinus arrhythmia and relatively low (systolic) blood pressure on admission. Moreover, after the initial stage, when chest pain had been treated adequately, sinus bradycardia was no longer present and blood pressure had increased. In conclusion, this case reported shows that the presence of marked sinus bradycardia in the setting of recent-onset chest pain, does not exclude the diagnosis of acute pericarditis.
References [1] Shamroth L, Pericarditis. In: Shamroth L, editor. The twelve lead electrocardiogram (Book 1). Oxford: Blackwell Scientific Publications, 1989:293. [2] Dressler N. Sinus tachycardia complicating and outlasting pericarditis. Am Heart J 1966;72:422–3. [3] Lurie KG, Benditt D. Syncope and the autonomic nervous system. J Cardiovasc Electrophysiol 1996;7:760–76.