Pericarditis, Myocarditis.ppt

Myocarditis & Pericarditis Shorena Chumburidze MD, PhD Case 1 57 year old man Previously healthy No cardiac risk factors One week history of General malaise, fever/chills, myalgias, coryza Yesterday Gradual onset of 6/10 pleuritic chest pain  Worst lying dow...

Myocarditis & Pericarditis Shorena Chumburidze MD, PhD Case 1 57 year old man Previously healthy No cardiac risk factors One week history of General malaise, fever/chills, myalgias, coryza Yesterday Gradual onset of 6/10 pleuritic chest pain  Worst lying down  Better sitting forward  Not exacerbated by exertion  Slightly SOB Coryza catarrhal inflammation of the mucous membrane in the nose, caused especially by a cold or by hay fever. Physical exam HR 105 RR 20 BP 130/80 T 38.2 H&N – some palpable lymph nodes CVS – sounds like velcro Chest – Normal Abdo – Normal Velcro™-like crackles A popular term for dry or fine crackles— fancifully likened to the sound of a Velcroclosure being opened— which are heard posterolaterally at the lung bases and associated with interstitial lung disease.  Could this be a heart attack? Should I call the cath lab? What’s going on? Pericardial Disease  Chest Pain - Ischemic vs Pericarditis pericarditis ischemic pain Location Precordium, L Retrosternal, L trapezius ridge shoulder, arm Quality Pleuritic Pressure, tightness, burning Duration Hours to days 1-15 minutes Exacerbati Lying down, chest exertion on wall motion Relief Leaning forward Rest  Ischemic vs Pericarditis Pericarditis Ischemic Pain Associated SSx SOB, N/V, diaphoresis, no diaphoresis, N/V SOB Vital signs Often febrile High fever rare Pericardial Disease Pericarditis Non-specific inflammation of pericardium Rarely emergent Pericardial effusion Accumulation of fluid in pericardial space Serous, purulent, fibrinous, hemorrhagic Cardiac tamponade Impairment of ventricular filling due to fluid in pericardial space Emergent Pericardial physiology Parietal layer Thick, collagenous, stiff Adventitial attachments to sternum, diaphragm, mediastinum Visceral layer Thin Closely adherent to epicardial surface Pericardial fluid Potential space between layers Normally 15-60 cc fluid Functions Reduces friction Prevention of infection Augmentation of atrial filling Maintains normal pressure-volume relationship of chambers No physiological consequence to absent pericardium Pericardial innervation Parasympathetic Vagus Left-recurrent laryngeal nerve Sympathetic Stellate First thoracic ganglia Little somatic sensory innvervation Thus visceral nature of chest pain Pericarditis - etiology Viral Bacterial Traumatic Malignant Post-irradiation Post-MI Drug-induced Collagen vascular disease  Viral Pericarditis Most common cause Enteroviruses  Coxsackie A & B  Echovirus HIV Mechanism of injury Direct viral cytotoxicity Indirect auto-antibody mediated effects Viral Pericarditis - SSx Syndrome may be immediate or develop 2-4 weeks post viral illness Chest pain Pericardial friction rub  Heard with diaphragm over LLSB, leaning forward, breath held  Scratchy  Triphasic (presystolic, systolic, diastolic) Fever Tachycardia Tachypnea,dyspnea diaphoresis Bacterial Pericarditis Common in less developed countries More commonly associated with tamonade Higher mortality than viral Streptococcus, staphylococcus, gram negs, anaerobes TB Lyme disease Concomitant pneumonia / empyema Often not diagnosed until tamponade Definitive Dx requires pericardiocentesis Treatment Abx ICU admission indicated Uremic Pericarditis ESRD / Underdialysis Bloody pericardial effusions ECG often normal (little epicardial involvement) Cardiac tamponade common Often loculated - therapeutic pericardiocentesis difficult Treatment ICU admission NSAIDS (caution b/c bleeding diathesis of uremia) Post-MI Pericarditis May occur within days of MI Direct extension of myocardial inflammation Presents as “different” chest pain Must distinguish from reinfarction Incidence 7-16% Tx: NSAIDs Dressler’s syndrome Thought to be autoimmune Weeks to months Fever, chest pain, leukocytosis, pleuritis, pericardial/pleural effusions Tx: NSAIDs, steroids for resistant cases Collagen Vascular Disease Pericarditis Common in many CVDs RA  Incidence 30-50% - many clinically silent SLE  50% incidence Dx: CP, R CHF, echo ECG/CXR often normal Tx: steroids Commonly progress to constrictive pericarditis Malignant pericarditis Primary tumors rare Metastatic disease common Incidence 10% in cancer patients Lung, breast, lymphoma, leukemia, Metastatic Melanoma Children – Hodgkin’s, leukemia, lymphosarcoma Progress to tamponade in 50-85% Dx: pericardiocentesis / cytology Tx: symptomatic Post-Irradiation Pericarditis Early (days – months) Dose related pericardial effusion Must distinguish from malignant effusion SSx:  SOBOE  can mimic infectious pericarditis (fever, CP, friction rub) Tx:  Often resolves spontaneously  NSAIDs, steroids, pericardiocentesis Late (years) Constrictive pericarditis Tx:  Often requires pericardiectomy Drug-induced pericarditis SLE-like syndrome Methysergide Procainamide constrictive Hydralazine pericarditis / Isoniazid generalized mediastinal fibrosis Methyldopa Reserpine Doxorubicin Chemotherapy Hypersensitivity Pericarditis / reaction cardiomyopathy Penicillin Cromolyn sodium  Back to our case You order an ECG on your patient  His ECG STE – I, II, aVF, V2-V6 Reciprocal STD – aVR PR depression Pericarditis – ECG 4 Stages Evolution over 3-4 weeks Only 50% have all 4 phases Stage 1 Hours to days Diffuse ST elevation ventricular subepicardial injury I, II, III, aVL, aVF, V2 to V6  Concave upwards  No distinct J-point  No T-wave inversions Reciprocal ST depression aVR, V1 Diffuse PR depression atrial injury Stage 2 Variable timeline ECG transiently normal ST / PR return to baseline Some T-wave flattening Stage 3 Variable timeline T-wave inversion Deep, uniform Stage 4 Weeks to months Return to normal Some patients will have residual T- wave inversion  ECG – ECG vs Pericarditis Pericarditis Ischemia/ Infarction ST elevation Diffuse, concave Anatomical, convex ST changes few reciprocal Reciprocal changes changes PR segment Depression No depression Q-T Rarely without More commonly prolongation myocarditis seen Evolution Normalization in MI progression with stage 2 development of Q- waves Electrical Present with absent Alternans tamponade  What if your patient was an 18 year old male athlete with burning chest discomfort after one too many seven-layer burritos? His ECG Benign early repolarisation (BER) Benign early repolarisation (BER) is a ECG pattern most commonly seen in young, healthy patients < 50 years of age. It produces widespread ST segment elevation that may mimic pericarditis or acute MI. Benign early repolarisation (BER) Up to 10-15% of ED patients presenting with chest pain will have BER on their ECG, making it a common diagnostic challenge for clinicians. The physiological basis of BER is poorly understood. However, it is generally thought to be a normal variant that is not indicative of underlying cardiac disease. Benign early repolarisation (BER) BER is less common in the over 50s, in whom ST elevation is more likely to represent myocardial ischemia. It is rare in the over 70s. Avoid diagnosing BER in patients over the age of 50, especially those with risk factors for ischemic heart disease. BER vs Pericarditis Pericarditis – Ancillary tests Most useful for ruling out other diagnoses Troponin / CK-MB Normal to mildly elevated (damage of subepicardial myocardium) ESR – elevated or normal WBC – elevated or normal Echocardiogram Gold standard for pericarditis with effusion Can also evaluate Pericardial thickness Tamponade Tumours / cysts Constrictive pericarditis  Trans-thoracic echocardiogram Large pericardial effusion RV compressed  You suspect a viral pericarditis. How are you going to treat it? Viral Pericarditis - treatment All need to be followed to monitor for effusion Effusion suspected if:  Dyspnea, fatigue, findings of tamponade  Must distinguish between purulent & viral May need diagnostic pericardiocentesis NSAIDS – good relief of pain & fever Colchicine – 1-2mg po od Steroids – only if NSAID resistant Admit if: cannot rule out MI, pain control Pericardial Effusion Collection of fluid in indistensible pericardium Secondary to pericarditis infectious, uremic, malignant, post irradiation Secondary to hemorrhage / trauma aortic dissection, penetrating trauma Symptoms related to size and acuity of collection 80-100cc required before decompensation begins (15-60cc fluid normal) Chronic effusions rarely progress to tamponade Pericardial tamponade Physiologic decompensation due to pericardial effusion Acute surgical tamponade Penetrating injury aortic dissection Iatrogenic (central line insertion) Medical tamponade Due to pericardial effusions due to pericarditis Low-pressure tamponade Due to severe dehydration LV pressure lowered to equilibrate with RV pressure Pericardial tamponade Early 200cc,  CVP (unless hypovolemic),  BP,   cardiac output, +/- bradycardia Traumatic Tamponade 2% of penetrating thoracic trauma 80-90% of stab wounds to heart 20% of GSW to heart Large instruments cause exsanguination Foreign bodies, rib fractures Iatrogenic – cardiac catheterization, pacemaker insertion, pericardiocentesis, cardiac surgery Clinical features Beck’s triad: hypotension distended neck veins (>15mm H20 with hypotension is diagnostic) muffled heart sounds (unlikely to be heard in trauma room) pulsus paradoxus – difficult to measure during resuscitation no response to vigorous fluid resuscitation Diagnosis Echocardiography available at some centres, but difficult to perform during resuscitation TTE better than TEE 98.1% sensitive, 99.9% specific Also useful for evaluation of valves and wall motion Diagnosis Ultrasound Features include  fluid in pericardial sac  dilated IVC  Compression of RA  Collapse of RV during diastole Diagnosis ECG Generalized low voltage  R-wave height 200-250cc) Generally not useful for acute early tamponade as only a small amount of fluid is required to create significant hemodynamic compromise  Large Pericardial Effusion Loss of customary heart borders “water-bottle” heart Management Prehospital care Same as any trauma patient Consider tension pneumothorax and needle thoracostomy Management Emergency Department vigorous fluid resuscitation CVP monitoring Treat concomitant injuries Pericardiocentesis ED thoracotomy Pericardiocentesis Pericardiocentesis Diagnostic and therapeutic Many false positives / false negatives (clotted blood) Improvement possible with small volume of blood removed Complications Pericardial tamponade Laceration of coronary artery / lung Induction of dysrhythmia Continued deterioration may necessitate thoracotomy Pericardiocentesis Technique 18 gauge, 10 cm spinal needle, 20 cc syringe Continuous ECG monitoring Needle enters subxyphoid area Aim for left scapula Aspirate every 1-2 mm Stop if blood aspirated, cardiac pulsations felt, ECG changes NB: if more than 20 cc blood is removed easily you are probably in the RV (ooops!) Case 2 28 year old man previously healthy 8 day history Fever Fatigue Myalgias Progressive SOBOE (Shortness of breath on exertion) Vague chest discomfort Physical examination HR 140 RR 20 BP 100/70 T 38.3 SaO2 91% Diaphoretic H&N Some cervical lymphadenopathy Chest Coarse crackles in bases bilaterally CVS Apex inferolaterally displaced No murmurs No friction rub S4 ECG Sinus tachycardia Frequent premature atrial and ventricular beats Non-specific ST & T wave changes CXR Troponin 0.05 CBC WBC 13 Some atypical lymphocytes No left shift ESR 29 Echocardiogram Dilated chambers Global wall motion abnormalities Decreased LV and RV function Mild tricuspid and mitral insufficiency No pericardial effusion Cardiac Catheterization Totally normal coronary arteries What’s going on? Myocarditis Etiology Viral – most common Mostly enteroviruses – esp. Coxsackie B Adenovirus Influenza A/B CMV / EBV / VZV Bacterial S. aureus, Streptococcus Mycoplasma Diphtheria Spirochetal Lyme disease Mycotic Candida Aspergillus Rickettsial Rocky Mountain Spotted Fever Helminthic Trichinosis Schistosomiasis Protozoal Chagas disease most common cause worldwide Trypanosoma cruzi Insect vector Dx: Demonstration of serum parasites Tx: Nifurtimox (antitrypanosomal) HIV and myocarditis Myocarditis in 46% on autopsy Multifactorial HIV, CMV, toxoplasma, TB, aspergillus Kaposi’s sarcoma- may involve myocardium Cardiac B-cell lymphoma Treatment toxicity  Pentamidine, zidovudine, dideoxyinosine Drugs Cocaine Emetine Doxorubicin HIV treatment Systemic Diseases Collagen Vascular Disease SLE PAN (polyarteritis nodosa (PAN) RA Dermatomyositis Sarcoidosis Kawasaki’s Disease Pathophysiology Three major mechanisms 1. Myocardial necrosis from direct invasion 2. Autoimmune destruction Beta myosin chain & coxsackie B share 50% same amino acid sequences 3. Endotoxins produced by pathogens Clinical Features VERY NON-SPECIFIC! Wide spectrum of disease Subclinical (most)  overshadowed by other manifestations of illness Fulminant cardiac failure +/- death History Fever Fatigue Myalgias (**suggestics myotropic virus) Vomiting / diarrhea Chest pain May mimic ischemic or pericardial pain Physical Exam Cardiac exam may be normal Tachycardia disproportionate to fever Cardiomegaly Atrial or ventricular dysrhythmias S3, S4, TR/MR +/- pericardial rub CHF Usually biventricular SSx of RV dysfunction (JVD, edema, hepatic congestion, etc.) SSx of LV dysfunction if predominant LV involvement Children Respiratory distress (grunting respirations, intercostal retractions) Lungs clear / wheeze Ventricular dysrhythmias Infants Often fulminant syndrome  Fever, cyanosis, respiratory distress, tachycardia, cardiac failure ECG NON-SPECIFIC! Sinus tachycardia Low voltages Prolonged QTc AV block AMI patterns ST changes T wave inversions CXR Often normal Cardiomegaly +/- pulmonary congestion Depends on relative RV vs LV dysfunction Laboratory Cardiac enzymes May or may not be elevated Troponin  elevated in 34% of patients with biopsy proven myocarditis CK-MB  Elevated in 5.7% of patients with biopsy proven myocarditis Bottom Line …. Not really very helpful WBC Normal to elevated ESR Normal to elevated Viral titers May suggest a viral infection, but don’t confirm etiology of cardiac disease Echocardiography Non-specific May mimic AMI Usually multichamber dysfunction Reduced LVEF Global hypokinesis Wall motion abnormalities Can evaluate for thrombi and pericardial involvement That all sounds pretty non- specific… I’m confused When should I suspect myocarditis? Suspect myocarditis if … Systemic infection is associated with new cardiovascular problems. Young patient with few coronary RF’s Tachycardia out of proportion to fever Severe myalgias Suggests myotropic pathogen Non-anatomical ECG changes Continued pain with no ECG evolution Global (vs segmental) wall motion abnormalities on echo Unexplained CHF / dysrhythmias in previously healthy patient I suspect myocarditis. How do I confirm the diagnosis? MRI Contrast enhanced (gadopentate dimeglumine) shown to be useful Maybe the future? Antimyosin scintigraphy (Indium-111) Binds to exposed myosin in damaged myocardium Diffuse, faint uptake of antimyosin antibody (AMI typically has intense, localized uptake) Normal antimyosin scan excludes AMI and myocarditis Endomyocardial biopsy Gold standard One report … Sensitivity 79%, Specificity 63% Dallas criteria used to standardize diagnosis Histologic criteria for myocarditis  5-30% of patients with suspected myocarditis  41% of patients with acute dilated cardiomyopathy  63% of patients with chronic dilated cardiomyopathy Worse prognosis for patients with histological changes I’m pretty sure it’s myocarditis …. How do I treat it? Treatment ED treatment Bed rest Cardiac monitoring Management of arrhythmias  No treatment of PAC’s, PVC’s  Electrical cardioversion for supraventricular arrhythmias with rapid ventricular response  Drugs for serious ventricular ectopy / arrhythmias  Pacing for high grade conduction blocks CHF Treat very cautiously Aggressive preload or afterload reduction may cause cardiogenic shock Anticoagulation If intracardiac thrombi detected on echo Definitive Treatment Treat specific cause if possible Eg: Chagas disease, Lyme disease, etc. Anti-viral agents & immunosuppression are controversial IVIG (intravenous immunoglobulin) may be helpful in certain subsets Cardiac transplantation if fulminant Disposition Admission to monitored bed All patients with symptomatic suspected myocarditis ICU (Intensive care unit) / CCU (Coronary care unit) All hemodynamically unstable patients Prognosis Many cases subclinical and benign Wide spectrum Complete recovery to any of many permanent cardiac problems Dilated cardiomyopathy common sequelae NIH myocarditis trial 20% mortality at 1 year 56% mortality at 4.3 years LVEF & RV function 1 year after presentation best predictor of outcome The End