I) Infective endocarditis: Endocarditis refers to inflammation of the endocardium or innermost lining of the heart. It can be infective or non-infective. Virulent microbes like S.aureus cause acute endocarditis , which destroys previously healthy valves and has an acute presentation. Whereas, less virulent bacteria like S.viridans cause subacute endocarditis, which runs a longer course and infects previously damaged valves. Bacteria see endocardium during episodes of bacteremia caused by day-to-day tasks like brushing teeth, infections like pneumonia, periodontitis, invasive procedures like GIT, GUT, respiratory tract scopies, cardiac procedures, biopsies , surgeries and intravenous drug abuse. Individuals with congenital heart disorders like VSD, PDA, bicuspid aortic valve, Marfan’s syndrome, mitral valve prolapse, aortic stenosis; those with prosthetic valves, previous rheumatic heart disease and immunocompromised persons are at increased risk of endocarditis.
Turbulent blood flow damages the valves and favors the formation of platelet-fibrin thrombi which acts as a nidus to trap the bacteria circulating in the bloodstream. Several adhesion molecules such as integrins Mac 1(CD11b/18), ICAM 1-3, VCAM 1 and E selection are activated and lead to adhesion of bacteria to endocardium, which results in a local and systemic inflammatory response.
On gross examination, vegetations are seen, most commonly involving the mitral followed by the aortic valve. Right sided valves like tricuspid valve are more commonly involved in intravenous drug abuse. Vegetations in acute endocarditis (ABE) are bulkier than those with subacute endocarditis (SABE). Ulceration, perforation of the valve and perivalvular abscess may occur in ABE. Microscopically, vegetations show an eosinophilic, outer layer of fibrin and platelets, a middle, basophilic zone containing bacterial colonies and an inner zone of inflammation or repair.
Complications include valvular stenosis or insufficiency, valve or chordae tendinae rupture, perivalvular or myocardial abscess formation, pericarditis and heart failure.
II) Libman-Sacks or atypical verrucous endocarditis: It is seen in non-infectious, inflammatory conditions such as SLE, TTP and collagen diseases. It most commonly affects the mitral and tricuspid valves. It shows multiple, small, “mulberry -like”, sterile vegetations on both surfaces of the valves, chordae tendineae and adjoining endocardium. Microscopically, the vegetations show an outer exudative zone of fibrin, nuclear debris and haematoxylin-stained bodies; a middle zone of proliferating capillaries and fibroblasts and an inner zone of neovascularization which showed distinct, thin-walled junctional vessels.
III) Marantic or non-bacterial thrombotic endocarditis: It is a non-infectious endocarditis seen in hypercoagulable states like terminal cancers especially mucinous adenocarcinomas, pancreatic and colon cancers, sepsis etc. They commonly involve the mitral valve. Vegetations are small, friable, seen along the line of closure without any tissue destruction. Embolization can occur from vegetations in marantic endocarditis causing infarcts in the brain, spleen, lungs and kidneys. Secondary infections can occur causing infective endocarditis.
IV) Myocarditis: Myocarditis is inflammation of the heart muscle. It presents with chest pain, shortness of breath, fatigue, myalgia, arrhythmias, heart failure (in severe cases). Sudden cardiac death can occur. All four chambers of the heart are dilated. Microscopically, presence of edema, inflammatory infiltrate and necrosis is seen. CK-MB and troponins are elevated. ECG shows nonspecific ST-T changes or arrhythmias. Endomyocardial biopsy is the gold standard for diagnosis of myocarditis. Myocardial injury in myocarditis is caused due to various factors as follows:
V) Pericarditis: It is inflammation of the pericardium. It can be acute or chronic. Acute pericarditis may be serous, fibrinous, purulent or hemorrhagic. Almost all causes of myocarditis can also cause pericarditis. In serous type, a serous or thin, watery fluid accumulates in the pericardial sac and is seen in viral infections like Coxsackie virus (enterovirus), parvovirus B19, adenovirus, EBV, HHV 6, CMV; rheumatic fever, RA, SLE etc. Fibrinous type is seen in uraemia, AMI, rheumatic fever, trauma and bacterial infections. It is characterised by fibrinous exudate, the cardiac surface looks shaggy, with “bread and butter” appearance. It may heal by forming fibrous adhesions. Purulent type is seen in infections with pyogenic bacteria like S.aureus, Streptococci, etc. The exudate is pus and leads to chronic constrictive or adhesive pericarditis later on. Hemorrhagic pericarditis is characterised by the presence of blood in the pericardial sac and is caused by malignancies, tuberculosis or bleeding disorders.
Tuberculous pericarditis: Turbid, bloody exudate, tubercles seen on pericardium, tubercle granulomas seen on microscopy, heals by fibrosis and calcification
Chronic constrictive pericarditis: Thickened, fibrotic, scarred, calcified pericardium, sequelae of tuberculous, purulent or hemorrhagic pericarditis, previous history of cardiac surgery, normal or smaller sized heart, diastolic dysfunction, right heart failure
Chronic adhesive pericarditis: Follows any fibrinous, suppurative or hemorrhagic pericarditis; fibrous adhesions formed, cardiac hypertrophy and dilation
Patients suffering from pericarditis present with sharp, pleuritic chest pain, improved by sitting up and leaning forward; fever, pericardial friction rub can be auscultated and widespread, concave ST segment elevation is seen on ECG. Pericardial friction rub is best auscultated at the left sternal border, with the patient leaning forward, with the breath held. Pericardial effusion may be visualized on echocardiography. Large pericardial effusions may give the appearance of “water bottle shaped” cardiac silhouette on chest X ray.
VI) Pericardial effusion: It is an accumulation of fluid in the pericardial cavity. Most common type is serous seen in congestive heart failure, hepatic and renal failure etc; other types are sero-sanguinous in trauma; chylous in lymphatic obstruction or damage; cholesterol effusion in myxoedema.
Blood may accumulate in the pericardium following rupture of heart after AMI, dissecting aortic aneurysm, trauma or bleeding disorders. Massive amounts of blood may accumulate leading to cardiac tamponade.
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