Introduction

Pericardial disease is encountered much less often in cardiac intensive care units (CICUs) than in cardiology clinics and inpatient services. Acute pericarditis is nevertheless an entity that sometimes must be considered in the population of patients hospitalized in a CICU. Patients who in reality do not have, or are unlikely to have, myocardial ischemic pain may be wrongly treated as though they were having a myocardial infarction or another acute coronary syndrome. Only after they have endured discomfort and have been exposed to the slight risk of harm, and after considerable expense, is the diagnosis of pericardial disease recognized and appropriate treatment begun whereas, in reality, many of these patients did not require hospitalization, still less admission to a CICU.

The possibility of acute pericarditis should be remembered by physicians who receive requests for admission of patients to the unit when the cause of chest pain has not been established.

The clinical picture of constrictive pericarditis is the same as that of right heart failure. Constrictive pericarditis and right heart failure of other etiology share some hemodynamic abnormalities, such as peripheral edema, pleural effusion and ascites, increased left and especially right ventricular diastolic pressure, and reduced cardiac output.

This chapter will focus on the issues outlined above. References that are to review papers are indicated as such in the text or citations. Physicians in charge of patients in a CICU must be aware of disorders of the pericardium because pericardial disease may simulate disease of the heart itself and lead to incorrect diagnosis and treatment. In the most extreme cases, this error may have fatal consequences. It remains as true today as when Osler ¹ first made the observation that pericardial disease is a frequently missed diagnosis. Especially in a CICU, pericardial disease is much less common than myocardial disease; therefore the best way to recognize pericardial disease is to maintain a high index of suspicion for this possibility when the cause of right heart failure or precordial pain is not readily apparent. The principal manifestations of pericardial disease simulating ischemic heart disease are listed in Table 30-1.

Table 30–1 Major Ways in Which Pericardial Disease May Simulate Ischemic Syndromes

Pericardial pain simulating ischemic pain

ST segment deviation suggesting myocardial ischemia

Dressler syndrome mistaken for reinfarction

Cardiac tamponade misinterpreted as heart failure

Severe tamponade mistaken for cardiogenic shock

Friction rub mistaken for murmur of acute mitral regurgitation

Friction rub mistaken for murmur of rupture of the ventricular septum

Pericardial Syndromes in Ischemic Heart Disease

Chest Pain

A significant proportion of patients experience some type of chest pain in the first day or so after acute myocardial infarction. The most important cause of recurring chest pain in patients in the CICU with a documented acute myocardial infarction is myocardial ischemia, which often demands therapeutic action; however, not all chest pain occurring under these circumstances is so ominous. Many episodes of such pain elude diagnosis, especially those that are the result of the patients’ natural apprehension and the understandable way in which they become sensitized to any abnormal sensations in the chest. Pulmonary infarction, embolism, or other conditions associated with pleuritic or substernal pain are included in the differential diagnosis. The cause of pleuritic chest pain can often be established from the clinical examination and the chest radiogram, but pleuritic pain may be a symptom of post–myocardial infarction pericarditis. Unfortunately, the pain of pericarditis is not always pleuritic in nature, but may simulate or be indistinguishable from pain of myocardial origin. The symptom may also have characteristics of both myocardial and pericardial pain; for instance, it may be a crushing sensation, yet be aggravated by inspiration, influenced by posture, or be referred to the trapezius ridge. It would be desirable to be able to rely on the electrocardiogram to distinguish with certainty between pericardial and myocardial pain, but the typical changes of acute pericarditis often are not recognizable against a background of the changes associated with acute myocardial infarction or active ischemia.²

A number of comprehensive reviews of this subject have been published in recent years.³^–⁹ Acute pericarditis most commonly is an acute infection of the pericardium and superficial myocardium (epicardium) that is adherent to the visceral pericardium. Acute viral pericarditis is a self-limiting relatively short disease that responds rapidly to anti-inflammatory treatment and therefore is classified as low risk for an early complication, most importantly cardiac tamponade, although tamponade does complicate about 1% to 2% and requires drainage to prevent a fatal outcome. In striking contrast is acute pericarditis of other etiologies, including infection with any living organism. Of special relevance to this chapter are pyogenic and tuberculous infection and acute pericardial injury of etiology other than that caused by viral infection. Examples include trauma including surgical or percutaneous intervention. The only common late complication is unpredictable recurrence that occurs at various intervals repeated over a highly variable period of time in 15% to 30% of patients (recent review papers).^8,⁹

Almost all patients complain chiefly of chest pain, but they may have few if any risk factors for coronary disease. They are often quite young and report a prodrome described as very like the flu. This prodromal event is febrile and very different from the feeling of general malaise that may precede acute myocardial infarction. Once the receiving physician considers it likely that a patient has acute pericarditis, evaluation and initial management should be done in a same-day unit,¹⁰ otherwise, hospital admission is necessary. The initial assessment can be completed in 24 hours and comprises enquiry about the details of the chief complaint (chest pain), any other symptoms, past medical history, standard biochemical laboratory tests, including C-reactive protein, and the erythrocyte sedimentation rate, and markers indicating myocardial inflammation.

Biomarkers

Acute pericarditis is associated with increased levels of serum biomarkers for myocardial injury, including modest elevations of creatine kinase (CK-MB) and serum cardiac troponin I (cTnI).¹¹^–¹³ Serum cTnI is detectable in 32% to 49% of patients and exceeds the threshold value of 1.5 ng/mL in 8% to 22%. Mild increases in cTnI often occur in the absence of elevations in CK-MB. The rise in serum cTnI in acute pericarditis is roughly related to the extent of concurrent myocardial inflammation and is transient, resolving within 1 week. Persistent cTnI elevation suggests ongoing epicardial inflammation. Patients with a rise in cTnI do not, however, have a higher incidence of complications. Laboratory signs of inflammation are diagnostic criteria for acute pericarditis. These include the elevated white blood cell count erythrocyte sedimentation rate and, most important, serum C-reactive protein concentration.

I believe that the initial evaluation, in addition to an ECG and chest radiogram, should include an echocardiogram, but some authorities state that echocardiography is not needed in straightforward cases. At the conclusion of this evaluation, most patients can be classified as either low or high risk for an early complication. Continued care of patients at low risk can be provided in an outpatient clinic. Patients considered to be at high risk or in whom the risk remains in doubt, should be admitted to the CICU or a medical ward, whichever is appropriate in individual cases, to determine the cause of the acute pericarditis, treat the cause and the pericarditis itself, a complication such as cardiac tamponade, or a large, slowly resolving pericardial effusion, if present.

Features suggesting high risk for an early complication are:

Viral, idiopathic, or acute pericarditis of various other causes is seldom an indication for admission to the CICU. Therefore most pericarditis encountered in the CICU is related to myocardial infarction and, less commonly, a cardiac or coronary intervention. Patients with acute pericarditis unrelated to ischemic heart disease may, however, also be placed in the CICU. When receiving physicians are unsure of the nature of the patients’ pain and/or suspect cardiac tamponade, they should admit them to the CICU. Rarely, acute pericarditis presents as severe cardiac tamponade. Patients with this presentation, or those who are clinically unstable for another reason, may also become CICU patients.

Two pericardiopathies may occur after an acute myocardial infarction. The more frequent but less ominous is acute pericarditis with or without a benign small effusion. This acute pericarditis occurs early in the course, the peak incidence being at 3 days. This is a manifestation of contiguous pericardial inflammation over the region of the infarction and is thus more a feature of Q-wave than non–Q-wave infarctions. Using clinical criteria, a pericardial friction rub used to be reported in about 10% of patients after acute myocardial infarction ² but is considerably more common in autopsy series. Pericardial friction rubs are most commonly detectable on the third day after the onset of infarction but sometimes are heard as early as the first day postinfarction. The rub has a tendency to be evanescent; therefore, if it is to be detected reliably, frequent careful auscultation focused on its detection is necessary.

The second pericardiopathy associated with acute myocardial infarction usually occurs considerably later. It is not caused by pericardial inflammation over the contiguous infarction, but is an autoimmune response to prior myocardial injury. The CICU is not the ideal milieu for auscultation, which doubtless is a reason for the underrecognition of pericardial friction rub. Rubs that first appear later than 1 week after an infarction suggest the onset of post–myocardial infarction syndrome, a subset of the pericardial injury syndrome and formerly known as Dressler syndrome.

Pericarditis may exaggerate the degree of ST segment elevation in acute myocardial infarction.^14,¹⁵ ST segment elevation in leads in which reciprocal depression would be anticipated is suggestive of complicating generalized pericarditis;¹⁶ thus ST elevation is concordant (Fig. 30-1). When pericarditis, with or without effusion, complicates myocardial infarction, evolution of the T-wave changes may be atypical, with the T wave remaining or becoming positive when T-wave inversion would be anticipated in an uncomplicated infarction.¹⁷

Figure 30-1 ECG of a patient with acute viral pericarditis. Characteristic features include ST segments elevated concave upward and not localized. T waves are upright in leads with ST segment elevation. Reciprocal repolarization changes are seen in aV_R and V₁. PR segments are depressed.

The standard treatment for acute pericarditis is administration of an anti-inflammatory agent, preferably nonsteroidal; corticosteroid treatment should be avoided, if at all possible. In the setting of acute myocardial infarction, however, the clinician should be aware that anti-inflammatory treatment, by inhibiting the normal healing process, may increase the risk of myocardial rupture.

Pericardial Effusion

Pericardial effusion after myocardial infarction, when specifically sought by serial echocardiography, is surprisingly common,¹⁸ occurring in about one fourth of the patients. Another unexpected feature of pericardial effusion as a sequel of myocardial infarction is that it persists for several weeks and bears no relation to pericardial friction rub. Pericarditis and pericardial effusion are associated with a worse prognosis, probably because they are more common after large infarctions, which tend to be anterior, and usually transmural.¹⁸^–²⁰ It is accepted practice to avoid administering anticoagulants or thrombolytic agents to patients with active or recent inflammatory pericarditis,²¹ but both the Gruppo Italiano per lo Studio della Streptochinasi nell’Infarcto Miocardio (GISSI)^20,²¹ and the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) trials²²