When An MI Is Not An MI. Morning Report July 30, 2003 Ryan Mattison, MD

Transcription

1 When An MI Is Not An MI Morning Report July 30, 2003 Ryan Mattison, MD

2 Confounding Factors In This Patient WPW Abnormality Dynamic EKG Changes With Symptoms

3 Myocarditis: Definition As the name implies, it is inflammation of the cardiac muscle caused by infectious agents, drug hypersensitivity, radiation, or chemicals. Of historic note, all cardiac muscle processes were termed myocarditis from the early 19 th century through the early 20 th century, when CAD became a recognized entity.

4 Myocarditis: Pathology Normal Borderline Active (Per Dallas Criteria Descriptions)

5 Clinical Features Symptoms range from none at all to fatigue, chest pain, shortness of breath, and (rarely) sudden cardiac death Exam findings can include tachycardia, extra heart sounds, and findings associated heart failure

6 Clinical Features (cont) Diagnostic tests Enzymes: Troponin T is more sensitive than CK- MB in one study of 80 patients (53% vs. 2%) EKG: ST changes, PAC s, PVC s, and NSVT s may be seen. Echo: Wall motion abnormalities and cardiac chamber dilation may be seen.

7 When To Think About Myocarditis New arrythmias Heart failure in the absence of ischemic, valvular, or congenital heart disease Absence of autoimmune causes Absence of substance-induced causes (i.e. cocaine, ethanol) Clinical features of MI in a patient who s pretest probability of CAD is very low

8 Prevalence There are a few studies which estimate as follows 5% prevalence in autopsy specimens in traumatic deaths of yo British men 0.4% prevalence in an AFIP study of 1402 noncardiac deaths Lack of a non-invasive gold standard makes knowing the true prevalence difficult

9 Etiology

10 Etiology (cont) In the United States, viral cause, especially coxsackie B virus, is the most common. In outbreaks of coxsackie infections, up to 5% of patients developed myocarditis.

11 Diagnosis The only definitive diagnosis is by endomyocardial biopsy. In a report of 38 cases, the sensitivity and specificity were 60% and 80%. The risk of perforation is 1/250, and the risk of death is 1/1000. Contrast-enhanced MRI is being investigated Cardiac catheterization is useful primarily to rule out other processes.

12 Diagnosis (cont) Biopsy should be performed when a patient is deteriorating despite optimal therapy. Biopsy should be performed when the results would modify therapy, such as in collagen vascular diseases, infiltrative processes, and in giant cell myocarditis

13 Natural History/Clinical Course There are four classifications Fulminant: Includes CV compromise over days Acute: Less severe dysfunction, quick onset Chronic active: Less distinct onset, can develop ventricular dysfunction Chronic persistent: No ventricular dysfunction, but can have symptoms of chest pain, palpitations

14 Natural History/Clinical Course (cont) Outcome depends on cause In viral myocarditis, fulminant type carries the best prognosis

15 Natural History/Clinical Course (cont)

16 Management/Treatment Look for treatable causes

17 Management/Treatment (cont) Ribavirin is being investigated for viral causes Immunosuppressant agents (steroids, azathioprine, cyclosporine) have been shown NOT to be useful for endpoints of death and transplantation In animal studies, NSAIDs have shown to make myocarditis worse

18 Management/Treatment (cont) Heavy exercise should be avoided for 4-6 weeks after diagnosis If ejection fraction is reduced and the patient has symptoms of heart failure, manage with conventional methods (i.e. diet, diuretics, ACE inhibitors) All newly diagnosed patients, even asymptomatic, should be followed up q 1-3 months, using EKG and echo

19 Our Patient His RMSF IFA titers were positive (1:320), though his latex agglutination test was negative He was discharged with a 14 day course of doxycycline and one month follow-up in the cardiology clinic At discharge, he showed no clinical or echocardiographic evidence of heart failure

20 References Feldman AM and McNamara D. Myocarditis. NEJM ; Fauci, Braunwald, et. al (Eds.) Harrison s Principles of Internal Medicine pp Cooper LT. UpToDate. Version