10. Myocarditis and pericardial disease.pptx

Gghbfhgg

1. CARDIOLOGY Cardiology lecture 10 :- Myocarditis and pericardial disease Date:- 15/12/2020 Prepared by Dr Guled Mohamud Nur (GMN@N ) MBBS

2. Myocarditis

3. Epidemiology Acute myocarditis is major cause of sudden death (15%–20% of cases) in adults <40 years of age.

4. Etiology Microbial pathogens Viruses Adenovirus (most common), group B coxsackieviruses, HIV, parvovirus B19, human herpesvirus 6 Parasites Trypanosoma cruzi (Chagas disease; Fig. 11-21A to C), Trichinella spiralis, and Toxoplasma gondii Bacteria Borrelia burgdorferi, Mycoplasma, and Rickettsia rickettsii Fungi Candida , Mucor, and Aspergillus N.B Viruses: MCC acute myocarditis

5. Etiology Myocarditis in acute RF (Toxins Examples—diphtheria, carbon monoxide, and venom from black widows and scorpions Drugs Examples—doxorubicin, cocaine, zidovudine, and sulfonamides Systemic and collagen vascular diseases Examples—SLE, systemic sclerosis, Kawasaki disease, and radiation Sarcoidosis

6. Pathology Global enlargement of the heart and dilation of all chambers Lymphocytic infiltrate with focal areas of necrosis is highly predictive of a viral myocarditis

7. Clinical findings Dyspnea ( most common symptom ) Fever (20% of cases) Chest pain (35% of cases) Arrhythmias:- Persistent tachycardia out of proportion to fever is a characteristic finding in myocarditis.

8. Clinical findings On examination Tachycardia Pericardial friction rub Biventricular heart failure with S3 and S4 heart sounds Heart murmurs MV regurgitation is the most common murmur and is due to stretching of the MV ring from volume overload in the left ventricle.

9. Investigations ECG findings are usually non-specific ST-T changes. Occasionally, ECG changes may mimic myocardial infarction or display arrhythmias or LBBB. Q waves or new LBBB are ominous prognostic signs.

10. Echocardiography may show global or segmental hypokinesia with or without pericardial effusion . Patients with fulminant myocarditis usually have small cardiac chambers and thickened walls, whereas in acute myocarditis there is marked left ventricular dilation and normal wall thickness. Diastolic filling patterns are abnormal in most patients, and the presence of right ventricular dysfunction is an ominous prognostic sign. Atrial dilatation with atrial wall thickening may suggest atrial giant cell myocarditis.

11. Cardiac biomarkers Cardiac biomarkers of myocardial injury are elevated in up to 35% patients with myocarditis. Increased serum concentrations of troponin T ( TnT ), and especially troponin I ( TnI ), are more common than increased levels of CK-MB in both adults and children with acute myocarditis.

12. Cardiac MRI Cardiac MRI provides information about tissue necrosis and fibrosis, hyperaemia , and interstitial oedema , and is a useful prognostic tool. MRI has sensitivity of 100% while specificity 90-100% in the diagnosis of acute myocarditis.

13. Cardiac MRI Increased troponin T and/or I (a normal value does not exclude myocarditis) Increased CK-MB (a normal value does not exclude myocarditis) Detection of antibodies of the suspected pathogen

14. Cardiac MRI Endomyocardial biopsy The usefulness of biopsy is limited by sampling error but is necessary in certain conditions, such as suspicion of giant cell or fulminant myocarditis. X-ray X-ray shows normal heart size initially and then cardiomegaly.

15. Therapy Because of the high incidence of LV dysfunction , standard therapy for heart failure is administered . Beta-blocker treatment should be avoided in the acute phase of decompensated heart failure and in the very early treatment of fulminant myocarditis. Physical activity is avoided in the acute phase.

16. Therapy Bed rest or limited activity as exertion increased viral replication. Standard heart failure therapy ( diuretics , ACE inhibitors ), and suppression of arrhythmia with beta blockers. As vasc ular spasm is a component of myocarditis, agents that precipitate or exacerbate vascular spasm should be avoided. Support with pressor such as dopamine and dobutamine and intra-aortic balloon c

17. Therapy Immunosuppressive therapy with intravenous immunoglobulin or corticosteroid proved no significant benefit and is not advised. Treatment of the cause if identified. Approximately 50% of patients will die within 5 years.

18. PERICARDIAL DISEASE

19. Acute Pericarditis Definition Inflammation of the pericardial lining around the heart.

20. Etiology Most cases are idiopathic (>40% of cases). Infectious (similar to the pathogens producing myocarditis) Examples—adenovirus, coxsackievirus, and HIV Drugs (similar to those listed for myocarditis) SLE (pericarditis with effusion is a common presentation), acute RF, post-MI pericarditis, autoimmune pericarditis post-MI, systemic sclerosis, uremia, metastasis (e.g., breast, lung, leukemia). Young woman with pericarditis and effusion most likely has SLE .

21. Clinical Manifestations Chest pain , often localized substernally or to the left of the sternum, is usually worsened by lying down , coughing , and deep inspiration (which helps in the differential diagnosis with MI) and is relieved by sitting up and leaning forward .

22. Diagnosis EKG may be diagnostic and reveals a diffuse ST-segment elevation with upright T waves at the onset of chest pain. PR segment depression is very specific . Differential Diagnosis The diffuseness of the ST-segment elevation , absence of reciprocal leads, and absence of the development of Q waves distinguish the characteristic pattern of acute pericarditis from the pattern seen in acute MI .

23. Treatment Treatment of the patient with acute pericarditis involves treating its etiology . In idiopathic pericarditis, treatment with anti-inflammatory medications ( NSAIDs , aspirin, corticosteroids ) is appropriate. Adding colchicine to an NSAID decreases recurrence.

24. Pericardial Effusion Etiology Fluid may accumulate in the pericardial cavity in virtually all forms of pericardial disease. The fluid may be a transudate , as are the serous cavity effusions that develop in patients with CHF , overhydration , or hypoproteinemia . More often, however, the pericardial effusion is an exudate , reflecting the presence of pericardial injury .

25. Clinical findings Normal heart sounds are muffled . Fluid surrounding the heart makes heart sounds difficult to hear. Cardiac output is decreased, because less blood is entering the right heart. Neck vein distention occurs on inspiration Blood cannot easily enter the RA on inspiration, because of fluid surrounding the heart. Some blood refluxes back into the jugular vein on inspiration, causing distention (this is called Kussmaul sign).

26. Clinical findings Hypotension is associated with pulsus paradoxus. On inspiration there is a further increase in pressure of blood in the RV, which displaces the IVS to the left, causing a decrease in the LV volume and a corresponding drop in SBP that is >10 mm Hg (called pulsus paradoxus). Serum CK-MB is usually normal. Troponins I and T are increased in 35% to 50% of cases. Usually indicates that a myocarditis is also present

27. Diagnosis Echocardiography is the most effective laboratory technique available. The presence of pericardial fluid is recorded as a relatively echo-free space between the posterior pericardium and the posterior left ventricular epicardium in patients with small effusions . In patients with large effusions , the heart may swing freely within the pericardial sac, and this motion may be associated with electrical alternans.

28. Chest x-ray may show a “ water-bottle ” configuration of the cardiac silhouette . ECG is useful in identifying changes that occur with the PR interval, ST wave, and T wave in different phases of pericarditis.

29. Treatment Fluid aspiration Management of acute pericarditis etiology

30. Reference By Clinical Cardiology Current Practice Guidelines And Short textbook of medical diagnosis & treatment. 11 th Edition