I) Infective endocarditis: Endocarditis is inflammation of the endocardium (the innermost lining of the heart). It may be infective or non-infective. Virulent microbes like S. aureus cause acute endocarditis, which can destroy previously healthy valves and presents abruptly. Less virulent bacteria like S. viridans cause subacute endocarditis, which runs a longer course and typically infects previously damaged valves.
Bacteria reach the endocardium during episodes of bacteremia. This can happen with:
People at increased risk include those with congenital heart disorders (VSD, PDA, bicuspid aortic valve, Marfan’s syndrome, mitral valve prolapse, aortic stenosis), prosthetic valves, previous rheumatic heart disease, and immunocompromised states.
Turbulent blood flow damages valves and promotes formation of platelet-fibrin thrombi. These thrombi act as a nidus that traps bacteria circulating in the bloodstream. Adhesion molecules such as integrins Mac 1 (CD11b/18), ICAM 1-3, VCAM 1, and E selection are activated, allowing bacteria to adhere to the endocardium. This triggers both local and systemic inflammatory responses.
On gross examination, vegetations are seen, most commonly on the mitral valve, followed by the aortic valve. Right-sided valves (especially the tricuspid valve) are more commonly involved in intravenous drug abuse. Vegetations in acute bacterial endocarditis (ABE) are bulkier than those in subacute bacterial endocarditis (SABE). In ABE, ulceration, valve perforation, and perivalvular abscess may occur.
Microscopically, vegetations show:
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: This 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:
III) Marantic or non-bacterial thrombotic endocarditis: This is a non-infectious endocarditis seen in hypercoagulable states such as terminal cancers (especially mucinous adenocarcinomas), pancreatic and colon cancers, sepsis, etc. It commonly involves the mitral valve. Vegetations are small and friable, occur along the line of closure, and do not cause tissue destruction.
Embolization can occur from vegetations in marantic endocarditis, causing infarcts in the brain, spleen, lungs, and kidneys. Secondary infection of these vegetations can occur, leading to infective endocarditis.
IV) Myocarditis: Myocarditis is inflammation of the heart muscle. It presents with chest pain, shortness of breath, fatigue, myalgia, arrhythmias, and (in severe cases) heart failure. Sudden cardiac death can occur.
Grossly, all four chambers of the heart are dilated. Microscopically, edema, inflammatory infiltrate, and necrosis are 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: Pericarditis is inflammation of the pericardium. It may be acute or chronic. Acute pericarditis may be serous, fibrinous, purulent, or hemorrhagic. Almost all causes of myocarditis can also cause pericarditis.
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 with pericarditis typically present with sharp, pleuritic chest pain that improves on sitting up and leaning forward, and fever. A pericardial friction rub may be heard, and ECG may show widespread, concave ST segment elevation. The friction rub is best auscultated at the left sternal border with the patient leaning forward and holding their breath.
Pericardial effusion may be visualized on echocardiography. Large pericardial effusions may produce a “water bottle shaped” cardiac silhouette on chest X ray.
VI) Pericardial effusion: Pericardial effusion is accumulation of fluid in the pericardial cavity. The most common type is serous, seen in congestive heart failure, hepatic failure, renal failure, etc. Other types include sero-sanguinous (trauma), chylous (lymphatic obstruction or damage), and cholesterol effusion (myxoedema).
Blood may accumulate in the pericardium following rupture of the heart after AMI, dissecting aortic aneurysm, trauma, or bleeding disorders. Massive accumulation of blood can lead to cardiac tamponade.
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