Pericarditis, Myocarditis and Endocarditis Flashcards
What is myocarditis? What are the main causes?
Myocarditis is an inflammatory disease of the myocardium diagnosed by specific histological, immunological and immunohistochemical criteria. Based on the WHO an endomyocardial biopsy is the key diagnostic tool.
The main causes are infections, immune mediated and toxin mediated. The immune mediated type is currently recognized as the primary cause.
Infectious agents—> bacteria such as Staphylococcus and streptococcus, fungal such as aspergillus, protozoan such as trypanosoma cruzi and viral such as coxsackie and influenza virus.
Immune mediated—> RA, SLE, Kawasaki, inflammatory bowel disease.
Toxin—> drugs like amphetamines and cocaine, heavy metals such as copper and iron, and physical agents such as radiation.
What are some immunohistochemical criteria to diagnose myocarditis?
> 14 leukocytes mm^2, > 4 monocytes mm^2, > 7 CD3+ T cells mm^2.
If any of these markers are positive then you can diagnose active phase myocarditis.
What is the Dallas criteria?
You look for any type of inflammatory infiltrate in the myocardium on the H&E assay. If there is damage or cardiac myocytes, it is very important to identify signs of necrosis.
What are the different types of histotypes of myocarditis?
Lymphocytic : most common, 90%, with H&E stain we can observe cluster of lymphocytes.
Eosinophilic : Not very common but associated with some other autoimmune disorder and with some tumors.
Granulomatous : causes SCD, arrhythmias and AV blocks. The sarcoid form is associated with systemic or cardiac isolated sarcoidosis and the giant cell form is characterized by the presence of numerous cells, particularly macrophages.
How can myocarditis evolve in a patient over time?
It can either heal completely, transform into chronic myocarditis or auto reactive myocarditis in which there is activation of auto reactive T cells and induction of autoantibodies.
Even when healed a scar can still cause disease at a later stage. Many scars can cause reentry circuit and vulnerability to arrhythmias.
Some patients even have recurring myocarditis due to genetic factors being involved.
What are the main differences between acute myocarditis and chronic inflammatory cardiomyopathy?
Acute myocarditis : onset of symptoms < 30 days, inflammatory infiltrate, release of cardiac biomarkers, potential fulminant presentation in need of hemodynamic support, LV normal or slightly dilated, necrosis but not much fibrosis.
Chronic : onset of symtoms > 30 days, fibrosis symptoms may be present or absent, LV dilated, hypertrophy, EF is typically reduced, not much infiltrate, slight elevation of biomarkers such as troponin.
What is the most common clinical presentation of myocarditis?
ACD-like presentation is the most common which includes acute chest pain, with absence of actual angiographic CAD, ST and T ECG changes, with or without increased troponins.
What is fulminant myocarditis?
Fulminant myocarditis, rather than being a distinct form of myocarditis, is instead a peculiar clinical presentation of the disease. It is characterized by sudden death from cardiogenic shock, ventricular arrhythmias or multi organ failure.
The main conclusion of is fulminant myocarditis may be due to different histotypes and aetiologies that can be diagnosed only by endomyocardial biopsy and managed by aetiology-directed treatment.
How do ECGs differ for different stages of myocarditis?
During active myocarditis there will be prevalence of irregular and polymorphic rhythms.
In a post inflammatory setting with mostly fibrosis and not much inflammation the ECG will be regular and monomorphic.
How is myocarditis treated?
Hemodynamically unstable patients should be treated according to current guidelines for HF.
In hemodynamically stable patients treatement varies depending on biopsy results. They may be treated with diuretics, ACEi and ARBs, immunosuppressive therapy, anti viral treatments and immunomodulatory treatments.
What is pericardial effusion?
A normal pericardial sac contains 10 to 50 ml of pericardial fluid which acts as a lubricant between the pericardial layers. Any condition increasing the amount of fluid around the heart is considered pericardial effusion. This fluid may be transudative, exudative, or sanguineous and may contain infectious organisms or malignant cells. It may be due to infection, inflammation, neoplasms, trauma, vascular injury and others.
What is the difference between transudates and exudates?
Transudates are clear, colorless, have less than 3 g/dL of proteins and less than 1000 uL cell count, and are common of CHF. Exudates are yellow, turbid and bloody with more than 3 g/dL, more than 1000 uL cell count and typical of infections and malignancies.
How is pericardial effusion classified?
Onset : acute, subacute or chronic (>3 months).
Size : mid <10mm, moderate 10-20mm, large >20mm.
Distribution : circumferential or loculated.
Composition : transudate or exudate.
What is the epidemiology of pericardial inflammatory syndromes?
They are the most common disease of the pericardium. Frequently benign disease, 5% of ER admissions, more frequent in males age 16-65 yr. Inhospital mortality is up to 1% often due to a systemic disease rather than the pericarditis itself. QoL of patient may be affected.
What are the main causes of pericarditis?
Viral such as enteroviruses (most common), bacterial such as mycobacterium tuberculosis (not common), autoimmune diseases (SLE or RA), neoplastic such as pericardial mesothelioma and secondary metastatic tumors, metabolic (myxoedema, anorexia nervosa), traumatic and iatrogenic (lesion).
What are the different types of pericarditis and their definitions?
Acute Pericarditis : a new-onset disease with acute presentation.
Chronic Pericarditis : >3 months symptoms and signs of pericarditis.
Recurrent Pericarditis : acute + symptom-free interval of 4-6 weeks subsequent recurrence of pericarditis. Overlap with known or clinically suspected concomitant myocardial involvement. In between pericarditis and myocarditis.
Myopericarditis: predominant pericarditis. In case it was purely pericarditis you would not see any change in troponin
(Tn), but in case there are any changes a potential overlap with myocarditis must be considered.
Perimyocarditis : predominant myocarditis, reduced LVEF, RWMA, stronger clinical presentation as there is involvement of myocardium.
Constrictive pericarditis : can occur after any pericardial disease process but mostly after bacterial pericarditis, causing severe impaired diastolic filling of the ventricles, peripheral edema and abdominal swelling. Advanced cases may also show pericardial thickening and calcification. Pericardiectomy is first line in chronic cases. In less severe cases anti inflammatory drugs may solve constriction within a few months.
What is the clinical presentation of pericarditis?
- Chest pain is typically sharp and pleuritic.
- Pain changes with breathing, increases during inspiration.
- Pain worsens in supine position and improves when sitting up.
- Pericardial friction rub, scratchy sound best heard over the left border (33% of cases).
- additional symptoms may reveal the underlying etiology e.g fever.
How is pericarditis diagnosed? How is it treated?
Pericarditic chest pain, pericardial rubs, new widespread ST elevation or PR depression on ECG and pericardial effusion, new or worsening.
To diagnosed pericarditis there must be at least 2 of the prior symptoms.
Additional diagnostic criteria : elevation of inflammation markers like C reactive protein, evidence of pericarditis by imaging technique (CT,CMR).
In patients with causes other than viral infection specific therapies may be appropriate based on the underlying condition.
Generally patients will giving aspirin or NSAIDs and recommended to stray away from physical activity for at least 3 months.
What is cardiac tamponade? Clinical presentation? Causes? Treatment?
It is compression of the heart due to pericardial accumulation of fluid, pus, blood, clots or gas. It is a life threatening condition.
It presents with tachycardia, hypotension, pulsus paradoxus, raises JVP, muffled heart sounds and low voltage on ECG.
Can be caused by most commonly : pericarditis, TB, invasive surgery related, trauma and malignancies. Less common causes include collagen vascular disease (SLE and RA), radiation induced, post MI, aortic dissection.
Treatment involves drainage of pericardial fluid preferably by needle pericardiocentesis with the use of echocardiographic guidance.
What are Kussmaul’s and Beck’s triad?
Both are used for Cardiac Tamponade.
- Kussmaul’s Sign : an increased jugular venous pressure with inspiration. As there is fluid compressing the heart, the excess is seen in the jugular vein pressure (usually seen and palpated).
- Beck’s Triad : a way to remember three main signs of cardiac tamponade; distention of jugular veins (Kussmaul’s Sign), low blood pressure and muffled heart sounds that are heard via stethoscope (this will show as low voltage on ECG).
ECG of acute pericarditis? ECG of cardiac tamponade?
ECG of acute pericarditis is characterized by ST elevation with no reciprocal signs, PQ depression, T wave inversionI in latter stages.
ECG of cardiac tamponade is characterized by low voltages and irregular HR. Because of the quantity of fluid there is continuous movement of the apex —> swinging heart.
What is endocarditis? Classification?
Endocarditis is an inflammation of the endocardium. It usually involves heart valves, but it can occur on the endocardium or intracardiac devices too.
Endocarditis can be classified based on different feature. Classification based on etiology : infective and non infective endocarditis.
Classification based on presentation : acute and subacute. Classification based on involved valves : native valve endocarditis or prosthetic valve endocarditis.
Classification based on site involved : right sided endocarditis and left sided endocarditis.
Infective endocarditis epidemiology, risk factors and causative agents?
Epidemiology : between 2.6-7 cases per 100.000 per year, M:F ratio is 1.7:1. More than 50% of patients are over 60.
Risk factors include : age>60, male gender, prior IE, poor dentition, prosthetic valve or intracardial device, history of valve disease, congenital heart disease, immunosuppression and injection drug use.
Causative agents : S.Aureus, 25-30%, most aggressive and destructive, often nosocomial in origin. Vivid as group streptococci 18%. Enterococci 11%. And other less common pathogens.
How is infective endocarditis diagnosed? Symptoms? Common findings?
To diagnose endocarditis, we need to see:
1. Positive blood culture showing presence of bacteria typical of endocarditis.
2. Presence of vegetations through imaging.
3. Signs and symptoms of infection→ fever, elevated CPR..
Symptoms and clinical findings :
- 90% of patients present with fever, often associated with systemic symptoms of chills, poor appetite and weight loss.
- Up to 25% of patients have embolic complications at the time of diagnosis. In fact, in many patients the first presentation is stroke due to vegetations and brain abscess. Therefore, IE has to be suspected in any patient presenting with fever and embolic phenomenon. Emboli are most common in brain, lung or spleen.
- Heart murmurs are found in up to 85% of patients.
- lab findings include leukocytosis/leucopenia, high CRP, procalcitonin, ESR, serum creatinine.
Imaging technique to find vegetations include : echocardiography, transesophageal echocardiography, cardiac CTA, MRI and PET.
