Myocarditis, Pericarditis and Other Pericardial Diseases

Home , Acute pericarditis, Carditis, Myocarditis, Pericarditis

Heart 2000;84:449–454

Diagnosis is easiest during epidemics of cox-

GENERAL CARDIOLOGY sackie infections but diYcult in isolated cases. Heart: first published as 10.1136/heart.84.4.449 on 1 October 2000. Downloaded from These are not seen by cardiologists unless they develop arrhythmia, collapse or suVer chest Myocarditis, pericarditis and other pain, the majority being dealt with in the primary care system. pericardial diseases Acute onset of chest pain is usual and may mimic myocardial infarction or be associated 449 Celia M Oakley with pericarditis. Arrhythmias or conduction Imperial College School of Medicine, Hammersmith Hospital, disturbances may be life threatening despite London, UK only mild focal injury, whereas more wide- spread inflammation is necessary before cardiac dysfunction is suYcient to cause symp- his article discusses the diagnosis and toms. management of myocarditis and peri- Tcarditis (both acute and recurrent), as Investigations well as other pericardial diseases. The ECG may show sinus tachycardia, focal or generalised abnormality, ST segment elevation, fascicular blocks or atrioventricular con- Myocarditis duction disturbances. Although the ECG abnormalities are non-specific, the ECG has Myocarditis is the term used to indicate acute the virtue of drawing attention to the heart and infective, toxic or autoimmune inflammation of leading to echocardiographic and other investi- the heart. Reversible toxic myocarditis occurs gations. Echocardiography may reveal segmen- in diphtheria and sometimes in infective endo- tal or generalised wall motion abnormalities or carditis when autoimmune mechanisms may a pericardial eVusion. Echocardiography allows also contribute. Persistent viral infection of the other causes of heart failure to be excluded but myocardium was first demonstrated a decade pronounced focal changes in wall motion may ago.1 Slow growing organisms such as chlamy- lead to confusion with myocardial infarction, especially if the ECG changes also suggest dia and trypanosomal infection in Chagas’ dis- 5 ease are causes of chronic myocarditis. Non- this. infective causes in sarcoidosis and the collagen The chest x ray may be normal, show cardiac vascular diseases need to be sought. enlargement, pulmonary venous congestion or Acute myocarditis and acute pericarditis are pleural eVusions. not always associated (likewise meningitis and Evidence of myocyte necrosis may be found encephalitis do not always occur together) and with an increase in creatine kinase or appear- the clinical emphasis is usually on one or the ance of troponin, indicating myocytolysis. The http://heart.bmj.com/ other. highest enzyme concentrations occur early and will probably have returned to normal by about Myocarditis can be caused by many diVerent 6 viruses and the microbial pathogenesis may be a week after onset. Cardiac autoantibodies can complex. Most cases of myocarditis with onset in be demonstrated only later in the disease proc- otherwise healthy people probably have an infec- ess. A viral origin of myocarditis can only be tious origin, although the pathogenesis is not yet proved if the virus is detected within an altered fully understood (such as the finding of a link myocardium. This has become possible between chlamydia and heart disease through on September 24, 2021 by guest. Protected copyright. through molecular analyses of necropsy, trans- antigenic mimicry). In western countries entero- plant, and endomyocardial biopsy specimens viruses, especially coxsackie B 1–6 serotypes, are using new techniques of viral gene amplifica- the most frequent, and the recent identification tion, which have shown persistence of viral of a common coxsackie virus B and adenovirus mRNA.1 The histological diagnosis of myocar- receptor has explained why these very diVerent ditis (fig 1) was clarified by the Dallas criteria,7 virus types both cause myocarditis.2–4 but these unfortunately did not include immu- nohistochemistry to demonstrate a T cell mediated immune response. Prevalence and clinical features The prevalence of acute myocarditis is unknown because most cases are not recognised on account of non-specific or no symptoms (but sudden death may occur). Myocarditis may develop as a complication of an upper res- piratory or gastrointestinal infection with general constitutional symptoms, particularly fever and skeletal myalgia, malaise, and ano- rexia. This systemic acute phase response Correspondence to: increases energy production but compromises Professor Celia performance. Since myocarditis may not de- Oakley, Hammersmith velop for several days or weeks after the symp- Hospital, Du Cane toms and after a return to normal work and lei- Road, London Figure 1. Acute myocarditis showing sheets of pale W12 0HS, UK sure activity, there is a risk of overexertion, staining myocytes. Lymphocytes are seen which were [email protected] which may be dangerous. identified as CD4 and CD8 cells on immunohistology.

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Myocardial failure in myocarditis Endocardial ﬁbroelastosis in infancy and

Contributory causes of myocardial dysfunction childhood, which was associated with persist- Heart: first published as 10.1136/heart.84.4.449 on 1 October 2000. Downloaded from include: ent mumps virus infection, has been almost (1) a direct cytotoxic eVect of the agent, be it eradicated by vaccination and the development viral, bacterial, etc; of vaccines against the other common viruses (2) a secondary immune response, which can may help reduce the incidence of myocarditis be triggered by any one of many diVerent in childhood. 450 agents including non-infective ones; (3) cytokine expression in the myocardium, which plays a crucial role—for example, Prognosis tumour necrosis factor á (TNF á) and Recovery from acute myocarditis often sur- nitric oxide synthase.4 prises and delights after life threatening illness. (4) aberrant induction of apoptosis, which Some recover seemingly normal ventricular may also play a part, particularly in function, but some cardiovascular reserve must individuals who go on to develop a chronic have been lost because biopsies during the cardiomyopathy.4 The proportion of pa- acute phase show myocytolysis. It is also tients who do this is completely unknown, uncertain how many will progress to dilated but a genetic predisposition to ongoing cardiomyopathy.13 inﬂammation, and possibly also to viral In a recent study 147 cases of myocarditis persistence, would explain the recognition were followed up for an average of 5.6 years. of a 25–30% familial incidence of dilated Out of 15 cases classed as fulminant, 93% were cardiomyopathy.8 alive without transplant 11 years after biopsy Detection of a causal agent is uncommon compared with 45% of 132 less severe cases. during the early phase (or even later). Demon- Left ventricular dilatation was not as great in stration of a viral origin is dependent upon the fulminant cases, who were more likely to gaining serial antibody titres against speciﬁc recover, as in the clinically milder cases who viruses and on showing a gradual fall in titre had bigger ventricles.14 during convalescence. Even if endomyocardial biopsy is carried out, persisting viral mRNA will be found in only 25–50% of patients with Other causes of acute myocarditis biopsy proven acute myocarditis.9 Lyme disease caused by Borrelia burgdorferi,a tick borne organism carried by deer, may cause an acute myocarditis, typically with a long PR Management interval as occurs with acute rheumatic fever. The treatment of acute myocarditis is largely Left ventricular dysfunction is usually transient supportive. EVective antiviral agents are but the organism has been cultured from

unavailable and usually inappropriate, but they endomyocardial biopsy material in a patient http://heart.bmj.com/ need to be more extensively investigated for with a dilated cardiomyopathy. clinical use. Immunosuppressive agents would Chagas’ disease, common in rural parts of be inappropriate if the myocarditis were caused Central and South America, results from infec- by the direct eVect of persisting virus but tion by Trypanosoma cruzi. Although best potentially useful to suppress an ongoing known as a cause of heart block and cardio- autoimmune inflammatory response. Discour- myopathy in the chronic phase, it can also aging results were obtained in a randomised cause a severe acute myocarditis and sudden controlled trial of the use of immunosuppres- death. During this phase, but not the chronic sive agents in the treatment of biopsy proven one, trypanosomes can be shown lying within on September 24, 2021 by guest. Protected copyright. acute myocarditis.10 The trial was weakened by the myocytes. failure to include immunohistochemical tech- Kawasaki disease (Japanese mucocutaneous niques in the biopsy criteria and by frequent lymph node syndrome) can cause a diVuse protocol violations. The use of steroids in an myocarditis in its first or second stages. Occlu- acutely ill patient therefore remains a sion of proximal coronary artery aneurysms is discretionary clinical option in addition to the the usual cause of death. Treatment with use of diuretics, angiotensin converting enzyme immunoglobulins during the early phases may (ACE) inhibitors, â adrenergic blocking help to prevent aneurysms from forming. The agents, and spironolactone. cause is still unknown but is probably It is recommended that whenever myocardi- infective. tis is suspected exercise should be avoided.11 Peripartum cardiomyopathy (PPCM) is a Interestingly, in a large Finnish epidemiologi- rare life threatening condition of unknown ori- cal study of myocarditis, which included nearly gin which occurs in women without known 700 000 healthy young men, there were 10 pre-existing heart disease. It is defined as the sudden unexpected deaths of which only one development of cardiac failure in the last was associated with acute myocarditis (and month of pregnancy or within five months of there were no cases of hypertrophic cardio- delivery, in the absence of an identifiable origin myopathy or arrhythmogenic right ventricular or recognisable heart disease before the last cardiomyopathy).5 month of pregnancy. The condition is rare and The future development of eVective treat- personal series are small. ment will depend on ability to make an early Recent work has shown evidence of acute diagnosis before establishment of a myopathic myocarditis in a majority of patients when process and on knowledge of whether the cause endomyocardial biopsy is carried out early is infective or autoimmune.12 in the illness.15 The onset is most often

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Clinical pericardial syndromes are: Some important causes of pericarditis Heart: first published as 10.1136/heart.84.4.449 on 1 October 2000. Downloaded from

x Acute pericarditis x Idiopathic

x Relapsing pericarditis x Infectious –viral x Cardiac tamponade –bacterial 451 –fungal x Chronic pericardial eVusion without –parasitic compression x Immunological x EVusive constrictive pericarditis –relapsing pericarditis –post-infarction (Dressler’s syndrome) x Constrictive pericarditis –post-cardiotomy syndrome associated with the connective tissue disorders postpartum and the origin probably immuno- –rheumatic fever logical without an infective precipitant. This –Still’s disease can be related to fetal–maternal incompatibil- –rheumatoid arthritis ity following the period of maternal immuno- –systemic lupus erythematosus (SLE) suppression during the pregnancy. A mortality –mixed connective tissue disease of up to 50% has been reported but PPCM –polyarteritis and the Churg-Strauss may not be as rare as is commonly thought, variant since subclinical cases may never be diagnosed. The use of immunosuppressive agents, x Neoplastic in addition to full treatment for the often Post-irradiation fulminating heart failure, is appropriate. Al- x though transplantation has been carried out, a x Traumatic large measure of recovery is common in survi- vors as in acute myocarditis outside preg- x Uraemic nancy. The use of ventricular assist devices as a bridge to recovery rather than transplanta- x Drug induced tion is indicated for the most seriously aVected patients. A genetic predisposition may exist in these Acute pericarditis patients and occasionally patients give a history The features of acute pericarditis are pericar- of relatives with dilated cardiomyopathy. Clini- dial pain, pericardial friction, and concordant http://heart.bmj.com/ cal recovery may be slow and delayed even up ST segment elevation on the ECG. to a year or more after the birth. Even when it As in acute myocarditis, there are numerous appears to be complete, a measure of cardio- causes but frequently none is found. Acute vascular reserve has been lost, as is indicated by idiopathic pericarditis is usually benign but the myocytolysis found on biopsy. Recurrence may rapidly constrict or pursue a relapsing in future pregnancies is not invariable but there course before burning out. Rarely it may be are few data. Pregnancy should therefore be associated with a clinically occult diVuse myo- discouraged in any patient with residual carditis (rather than the more usual epicarditis myocardial dysfunction and, if possible, de- which is responsible for the typical ECG on September 24, 2021 by guest. Protected copyright. layed for some years. changes). Pericardiocentesis in such cases may be followed by collapse and cardiogenic shock Summary and is ill-advised. Echo should prevent mis- Acute myocarditis has many diVerent clinical takes by checking ventricular contractile func- presentations but, most commonly by far, tion as well as the features of tamponade. mimics the onset of acute myocardial infarc- The patient is usually febrile and the pain tion. It may present with acute heart failure but may be mild or severe. It is typically exacer- only rarely as dilated cardiomyopathy of recent bated by inspiration and relieved by leaning onset. Subclinical myocarditis is common and forward. A friction rub may come and go. Signs strenuous exercise should be avoided during of tamponade are unusual. acute infections. The chest radiograph may be normal or the heart shadow may be slightly enlarged. There may be pleural eVusions but pulmonary Pericardial diseases congestion, if present, indicates associated myocarditis. Pericarditis is very much a part of general The ECG shows generalised ST segment medicine, developing as an acute illness or elevation. This is a current of injury from the complicating rheumatic renal and malignant superﬁcial layers of the myocardium. The disease or treatment with certain drugs. changes are usually generalised. The QRS is Echocardiography has done much to reveal normal unless there is a large pericardial pericardial (and myocardial) involvement eVusion. With resolution the ST segment in “non-cardiac” conditions and to demon- becomes isoelectric and there may be T wave strate the physiology of tamponade and inversion which sometimes persists. Arrhyth- constriction. mias may develop.

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Management

The ECG in acute pericarditis is Mild cases of relapsing pericarditis respond to Heart: first published as 10.1136/heart.84.4.449 on 1 October 2000. Downloaded from mimicked by: aspirin or other non-steroidal anti- inflammatory drugs. Steroids are dramatically x early repolarisation eVective but should be reserved for severe cases and used only to treat acute attacks, as mainte- acute early anterior myocardial infarction x nance steroids do not prevent relapses and cre- 452 x acute myocarditis ate a tendency to ever increasing dosage. Colchicine is the treatment of choice and can also provide eVective prophylaxis. It was intro- duced because of its eYcacy in familial The ECG changes of acute pericarditis may Mediterranean fever (polyserositis). Patients be mimicked by early repolarisation seen most who have been treated with steroids can be often in young males. Elevated concave upward weaned oV them and on to colchicine. The ST segments are located in the precordial leads dose for acute attacks is 1 mg followed by with reciprocal depression in AVR; T waves are 0.5 mg two or three hourly to a maximum of peaked and slightly asymmetrical with a notch 10 mg.17 The maintenance dose is 0.5 mg twice and a slur on the R wave. The axis is usually daily. If necessary, colchicine can be combined vertical with counter clockwise rotation, a short with indomethacin. and depressed PR interval, prominent U Pericardiectomy has been tried but fails to waves, and sinus bradycardia. The ST segment prevent relapses of pain. This is to be expected becomes isoelectric with exercise or adminis- as the inflammation may be a reaction to tration of isoprenaline. Early repolarisation is a epicardial (or viral) material recognised as for- benign condition. eign, so there is no reason why removal of the Both changes of early repolarisation and of fibrous pericardium should make a diVerence. acute pericarditis mimic those of early acute anterior myocardial infarction. Echocardio- Cardiac tamponade graphy provides the most rapid and certain Tamponade may occur in pericarditis of any means of diVerentiation in most cases but not cause but is uncommon in idiopathic and post- in all. Acute myocarditis also commonly mim- infarction pericarditis. It is usual in acute pyo- ics acute myocardial infarction. Enzyme release genic, tuberculous, and malignant pericarditis. is usual in those who show ST segment eleva- Acute haemopericardium may cause tampon- 16 tion on ECG and echo may show regional ade following cardiac rupture after myocardial akinesia. Coronary angiography diVerentiates, infarction, in dissection of the aortic root or and endomyocardial biopsy can be performed after cardiac surgery. Metastatic carcinoma, as at the same time. well as primary tumours, may present with Other investigations include exclusion of tamponade. http://heart.bmj.com/ known causes of acute pericarditis, particularly Patients with tamponade may complain of tuberculosis which may require pericardial shortness of breath, weakness, heaviness in the aspiration. In that case, the pericardium should chest, or present with hypotension or even car- be aspirated to dryness and all the fluid sent to diogenic shock. the laboratory so that it can be spun down and Examination reveals pulsus paradoxus, a the sediment stained for microbacteria. A high venous pressure in the neck, and a quiet tuberculin test may be negative in acute tuber- heart with faint heart sounds. It is readily diag- culous pericarditis, which is now being seen nosed in patients known to be at risk but often more commonly in immigrants and HIV posi- missed in a previously fit individual or, for on September 24, 2021 by guest. Protected copyright. tive patients and is increasingly found to be example, in a patient with septic shock where caused by variant and resistant forms of myco- the shock is actually caused by pericardial tam- bacteria. ponade rather than by septicaemia.18 Echocardiography is diagnostic, and has Relapsing pericarditis shown that inspiratory increase of blood flow Relapsing or recurrent pericarditis causes into the heart is accommodated in the right episodes of chest pain with or without a friction atrium and admitted to the right ventricle at rub, sometimes with pericardial and even pleu- the expense of left ventricular volume as the ral eVusions. Each episode may last several ventricular septum moves sharply towards the days and be accompanied by fever. Pericarditis left ventricle, reducing left ventricular stroke of any cause may be followed by this disabling volume. Diastolic collapse of the right atrium condition, which is frequently not diagnosed and right ventricular walls are seen when peri- especially if an initiating bout of acute pericar- cardial pressure rises to exceed the intracardiac ditis has not been documented. It may compli- pressure, terminating further flow into the cate recovery from acute myocardial infarction heart and thereby reducing or removing the Y (Dressler’s syndrome) or cardiac surgery (the descent of the venous pulse, which shows very postcardiotomy syndrome). Each may be small volume excursion and may therefore be followed by one or several recurrences but the diYcult to see. most recalcitrant cases tend to be idiopathic. Pericardiocentesis should be performed in The condition is benign and does not lead to the cardiac catheterisation laboratory under constriction. It can sometimes recur for several ultrasound guidance, in addition to fluoros- years before burning out and is then very copy and ECG, and preferably with simultane- debilitating, with a major impact on general ous cardiac pressure monitoring. The sub- well being, family life, and work. xiphoid approach is the safest. Pericardioscopy

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DiVerential diagnosis of constrictive Heart: first published as 10.1136/heart.84.4.449 on 1 October 2000. Downloaded from pericarditis

x Primary restrictive cardiomyopathy –pulmonary congestion –pulmonary hypertension and tricuspid regurgitation with large right (and left) 453 atrium

x Amyloid heart disease –absent third sound (until very advanced) –low ECG voltage –thickening of myocardium on echo

The heart is small and quiet with a sharp early third heart sound, which may be confused with Figure 2. Constrictive pericarditis caused by infection pulmonary closure (fig 2). presented 10 years after operation to relieve ileal atresia as a neonate. The patient had developed DiVerentiation from a restrictive cardio- septicaemia as an infant but purulent pericarditis had myopathy is not usually diYcult as in cardio- not been recognised. myopathy the left sided diastolic pressures are usually much higher than those on the right, has been used to facilitate diagnostic pericar- unless there is considerable tricuspid regurgita- dial biopsy. Triamcinolone can prevent recur- tion. The latter is rare in constrictive pericardi- rence of immunologically based eVusions and tis. cisplatin can deter re-accumulation of malig- In amyloid heart disease a left ventricular nant eVusions.19 third sound is not heard because slow ventricular filling continues through diastole, except in Chronic pericardial effusion without very advanced cases who develop a restrictive compression physiology. Echocardiography quickly diVeren- Large lax eVusions occasionally occur, may tiates. cause few symptoms, and are found acciden- Pericarditis is common in the connective tis- tally. It is unusual to find a cause. A very few sue diseases. Acute pericarditis is occasionally may be associated with myxoedema. the presenting manifestation in Still’s disease,

when the presence and persistence of severe http://heart.bmj.com/ constitutional symptoms and development of Effusive constrictive pericarditis arthritis make the diagnosis clear. Acute When pericardial eVusion is associated with pericarditis is common in systemic lupus, par- thickening of the visceral pericardium the ticularly during acute flares, and in the Churg- patient may have persistent cardiac compres- Strauss variant of polyarteritis, but is usually sion, even after pericardiocentesis. It may be painless in rheumatoid arthritis. Constriction seen in tuberculous pericarditis, rheumatoid may occur in any of these disorders but is most patients or after mediastinal irradiation. often seen in association with rheumatoid on September 24, 2021 by guest. Protected copyright. arthritis because of its greater prevalence. Constrictive pericarditis A number of drugs can induce a lupus When thickening and scarring of the parietal syndrome with pericarditis. The best known and/or visceral pericardium compresses the example is with hydralazine, but it may also be heart and restricts cardiac filling, stroke caused by procainamide, methyldopa, and volume becomes limited despite a considerable minoxidil. It is reversible on stopping the drug. rise in filling pressure. Constriction is usually generalised but rarely may be localised, owing 1. Kawai C. From myocarditis to cardiomyopathy: to constricting bands usually in the left or right mechanisms of inflammation and cell death in learning from the past for the future. Circulation 1999;99:1091–100. atrioventricular grooves or round the entry of • The molecular analysis of necropsy and endomyocardial the superior or inferior vena cava. biopsy specimens has clarified the causal link between myocarditis and dilated cardiomyopathy. A tuberculous origin is uncommon now in 2. Huber SA, Gauntt CJ, Sakkinen P. Enteroviruses and the west and most cases are idiopathic. A few myocarditis. Viral pathogenesis through replication, cytokine are associated with rheumatoid arthritis, colla- induction and immunopathogenicity. Adv Virus Res gen vascular disease or uraemia, or rarely 1998;51:35–80. 3. Bachmaier K, Neu N, de la Masa LM, et al. Chlamydia follow cardiac surgery or irradiation. infections and heart disease linked through antigenic The heart is small and pulmonary venous mimicry. Science 1999;283:1335–9. congestion rare. The diastolic pressures in the 4. Bowles NE, Towbin JA. Molecular aspects of myocarditis. Current Opinion in Cardiology 1998;13:179–84. four cardiac chambers will be similar and the • The pathogenesis of myocarditis remains elusive. The left atrial pressure is rarely high enough to crucial roles of cytokine expression and of aberrant cause pulmonary congestion. induction of apoptosis are being defined. 5. Karjalainen J, Heikkila J. Incidence of three The signs are predominantly right sided and presentations of acute myocarditis in young men in military congestive, a high jugular venous pressure with service: a 20 year experience. Eur Heart J 1999;20:1120–5. • The usual presentation mimics myocardial infarction (98 prominent X and Y descents, hepatomegaly, cases); only one presented with sudden death and nine as and peripheral oedema. There may be ascites. dilated cardiomyopathy of recent origin.

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6. Smith SC, Ladenson JH, Mason JW, et al. Elevations of 14. McCarthy RE, Boeehmer P, Hruban RH, et al. Long cardiac troponin I associated with myocarditis. Experimental term outlook of fulminant myocarditis as compared with and clinical correlations. Circulation 1997;95:163–8. acute (non-fulminant) myocarditis. N Engl J Med Heart: first published as 10.1136/heart.84.4.449 on 1 October 2000. Downloaded from • Many patients have elevated troponin or creatine kinase MB 2000;342:690–5. if studied during the first week of the disease. When found in a patient with chest pain and ECG ST segment elevation 15. Midei MG, De Ment SH, Feldman AM, et al. Peripartum on presentation, the clinical similarity with myocardial myocarditis and cardiomyopathy. Circulation 1990;81: infarction caused by coronary thrombosis may be complete. 922–8. 7. Aretz HT, Billingham ME, Edwards WD. Myocarditis: a • Changes of acute myocarditis are found in a high histopathological definition and classification. Am J proportion of cases if biopsies are obtained within a month 454 Cardiovasc Pathol 1987;1:3–14. of onset. 8. Mason JW. Myocarditis. Adv Intern Med 16. Karjalainen J, Heikkila J. “Acute pericarditis” 1999;44:293–310. myocardial enzyme release as evidence for myocarditis. Am Heart J 1986;111:546–52. 9. Brodison A, Swann JW. Myocarditis: a review. J • Myocardial enzyme release is uncommon without Infection 1998;37:99–103. simultaneous ST-segment elevation in suspected acute • Means of early identification are needed to prevent progression to chronic heart failure by more satisfactory myocarditis. therapies. 17. Adler Y, Finkelstein Y, Guindo J, et al. Colchicine 10. Mason JW, O’Connell JB, Herskowitz A, et al.A treatment for recurrent pericarditis. A decade of experience. clinical trial of immunosuppressive therapy of myocarditis. Circulation 1998;97:2183–5. The myocarditis treatment trial investigators. N Engl J Med • Colchicine is probably the treatment of first choice for 1995;333:269–75. recurrent pericarditis, especially when the origin is idiopathic. 11. Friman G, Ilback NG. Acute infection: metabolic responses, effects on performance, interaction with exercise 18. Arsura EL, Kilgore WB, Strategos E. Purulent and myocarditis. Int J Sports Med 1998;19(suppl 35):172–82. pericarditis misdiagnosed as septic shock. Southern Med J 12. Anandasabathy S, Frishman WH. Innovative drug 1992;92:285–8. treatments for viral and auto-immune myocarditis. J Clin • Failure to recognise purulent pericarditis and tamponade Pharmacol 1998;38:295–308. may be fatal in bacteraemic patients. In contrast to • Better means of distinguishing between viral and patients with septic shock, patients with tamponade have autoimmune causes are needed so that treatment can be high systemic vascular resistance and low cardiac output. appropriate. A useful review of treatments. 19. Maisch B, Pankuneit S, Brilla C, et al. Intrapericardial 13. Lieberman EB, Hutchins GM, Herskowitz A, et al. treatment of inflammatory and neoplastic pericarditis guided Clinico-pathological description of myocardititis. Am J Cardiol by pericardioscopy and epicardial biopsy results from a pilot 1991;18:1617–26. study. Clin Cardiol 1999;22(supp 1):117–22. http://heart.bmj.com/ on September 24, 2021 by guest. Protected copyright.