VALVULAR HEART DISEASE Flashcards

1
Q

What are the two true-ism’s about calcium?

A

Calcium collects in various tissues as humans age

Calcium collects in various tissues that undergo damage, injury, or necrosis

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2
Q

What is Calcific aortic degeneration/stenosis?

A

Calcific aortic degeneration is the very/most common valvular abnormality that occurs with age, as repetitive motions of the delicate valves, combined with pressure gradient phenomena on either side, act to ever so slightly breakdown, remodel, or injure the valve structure; this agerelated, ‘wear and tear’ change can be arguably viewed as a ‘normal’ physiologic aging process, although it impacts only a small percentage of peoples (2-3%).

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3
Q

What is common pathology seen with calcific aortic degeneration/stenosis?

A
  • Calcific nodules (AKA: calcific degeneration) developing on valve
  • Aortic valvular thickening and narrowing, with impaired function
  • LVH developing as stenosis progressively increases
  • Chronic heart failure or chronic ischemic heart disease can finally evolve, leading to angina, syncope, and/or CHF findings
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4
Q

what are two common patient profiles of calcific aortic stenosis?

A
  • Senile calcific aortic stenosis – patients in their 70-80’s with a normal native valve
  • Calcific stenosis of congenital bicuspid valve – patients in their 50-60’s
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5
Q

Which valves are most at risk for developing aortic stenosis? What other things are they at risk for?

A

a bicuspid aortic valve (BAV) has less hemodynamic and structural stability than a tricuspid valve, because often 2 leaflets are fused and have a central raphe (thickened ridge or seam). BAV’s are most at risk for developing aortic stenosis, aortic dilation/insufficiency, endocarditis, and aortic dissection.

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6
Q

What is mitral annular calcifications? When is it clinically evident?

A

This is a variant on aortic calcifications, but with mitral valve involvement by nodular calcifications (also called generically calcific degeneration).

  • Patients with mitral valve prolapse are more at risk for developing symptoms (which can be regurgitation, stenosis, or arrhythmia issues)
  • Heavy calcific degeneration in any individual can lead to a ring of calcified tissue that is visible on chest radiographs
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7
Q

what is mitral valve prolapse?

A

The acquisition over time of grossly ‘floppy’ or ‘ballooning’ mitral valve leaflets, which also show myxomatous degeneration microscopically.
MVP typically evolves as increasing degeneration of the valve substance occurs. Excess extracellular matrix-like proteins, such as dermatan sulfate (a type of glycosaminoglycan or mucopolysaccharide), accumulate within the valve, causing it to weaken and appear somewhat thickened; recall that mucopolysaccharides readily bind water and, when in excess, the prefix ‘myxo-‘ will be used (myxomatous degeneration, myxedema, etc.). The valve leaflets eventually become redundant and floppy, and are displaced toward the left atrium.

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8
Q

what are some complications of mitral valve prolapse?

A
  • Mitral valve insufficiency that allows for systolic backflow; significant tension can cause chordae tendineae rupture
  • Infective endocarditis, which can occur on any valve with structure or function issues
  • Sterile thrombosis development and possible emboli, causing stroke or systemic infarction
  • Arrhythmia or conduction abnormalities
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9
Q

female to male ratio for mitral valve prolapse? what does mitral valve prolapse show on PE? more common in?

A
  • Female-to-male ration of 7:1
  • Typically asymptomatic; symptoms more likely to appear in older patients, males, and those with other heart issues (CAD, LVH for any reason, etc.)
  • Classic murmur: mid-systolic click followed by a late systolic murmur (as regurgitation occurs later in systole) • More common in Ehlers-Danlos syndrome, Marfan syndrome, polycystic kidney disease, and Graves disease
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10
Q

what is rheumatic fever? what is it triggered by?

A

Rheumatic fever (RF) is a systemic, recurrent inflammatory disease, classically occurring a few weeks later than, and triggered by, a pharyngeal infection with Group A β-hemolytic streptococci.

  • Rapid diagnosis and treatment for strep pharyngitis have dramatically decreased RF and RHD is the US
  • Acute and chronic cardiac involvement are well described.
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11
Q

what is the mechanism of rheumatic fever?

A

Mechanism: in genetically susceptible individuals, the infection results in production of antibodies that cross-react with cardiac antigens (type II hypersensitivity reaction), particularly antibodies and CD4+ T cells directed against streptococcal M proteins.

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12
Q

the acute carditis of Rheumatic fever may include?

A

The acute carditis of RF may include a series of inflammatory lesions involving any layer of the heart - the heart valves, endocardium, myocardium or pericardium/pericardial space. These can lead to clinical findings such as myocardial dysfunction or dilation, arrhythmia, pericardial effusions or friction rubs, or acute heart failure.

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13
Q

what is the classic pathology finding of Rheumatic fever? Valve leaflets may also develop?

A

the classic Aschoff body of RF – a collection of myocardial lymphocytes and macrophages; some references go on and on about Anitschkow cells (at arrow, maybe), which are the macrophages that may become binucleate or show chromatin changes.

• Valve leaflets can also develop verrucae composed of inflammatory cells and fibrin – an acute valvulitis.

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14
Q

what happens with Chronic rheumatic heart disease?

A

Chronic RHD doesn’t occur suddenly many years later, but slowly evolves from the acute changes above and eventually becomes clinically apparent. The delicate heart valves are most susceptible to chronic changes, and most of the long-term sequelae of RHD involves them. Valve leaflets, particularly the mitral valve, may thicken, fuse, and become stenotic; the same process can occur to the chordae tendineae.

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15
Q

All types of rheumatic heart disease can lead to?

A

All of these changes can lead to mitral stenosis, mitral regurgitation, left atrial enlargement, pulmonary vascular congestion, and right heart failure. The LV may appear fairly normal.

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16
Q

Explain papillary muscle rupture?

A

Three papillary muscles are present for the tricuspid valve, and two are present for the mitral valve. Recall that papillary muscles contract during systole, ‘firming up’ the valve leaflets and preventing backflow regurgitation during systole. Papillary muscles can undergo ischemia, necrosis, and rupture in a couple of characteristic settings:
• Following myocardial infarction
• Following states of general hypoperfusion (such as heart failure, shock, etc.)

17
Q

Explain chordae tendinae rupture?

A

Chordae rupture may present like acute mitral insufficiency/acute decompensation of CHF – SOB, pulmonary edema, orthopnea, and PND. Frank cardiovascular collapse (cardiogenic shock) can then further evolve. A holosystolic murmur and a third heart sound may also be present. Etiologies include:

  • Mitral valve prolapse that causes ballooning of the valve leaflets and increased tension placed upon chordae. In the image of a bisected heart, a floppy valve leaflet is protruding into the LA, and extending from one edge is a ruptured chordae tendineae.
  • Rheumatic heart disease – a variety of valve remodeling issues occur
  • Some types of endocarditis
18
Q

Explain infective endocarditis?

A

vegetations (thrombotic material forming a small mass) on heart valves characterize endocarditis. In IE, the vegetations have significant bacteria, which incite the process in the first place. As bacteremia occurs, the heart valves are a natural place where altered blood happens (recall Virchow’s triad of thrombosis – altered blood flow, endothelial injury, and/or hypercoagulability). Any heart valve that is altered in structure or function (RHD, MVP, BAV, congenital heart disease, etc.) is predisposed to developing endocarditis, particularly in the setting of bacteremia.

19
Q

Explain acute infective endocarditis?

A

• Acute IE is usually caused by high virulence organisms that have the ability to colonize an even normal valve, such as Staph. aureus; poor prognosis with high mortality (upwards of 40% in some series)

Acute IE will present as a very ‘sick’ patient with fever, chills, weight loss, and cardiac murmur. As vegetations are fundamentally thromboses, embolic phenomena may occur, affecting different systemic tissues:
• Roth spots: retinal emboli
• Osler nodes: painful, red subcutaneous nodules on the fingers and toes
• Janeway lesions: painless, erythematous lesions on palms & soles
• Splinter fingernail hemorrhages: tiny blood clots that run vertically under the nail

20
Q

Explain subacute infective endocarditis?

A

Subacute IE is usually caused by low virulence agents (oral cavity flora, can be acquired during dental procedures) that have a propensity to infect an altered valve, such as viridans streptococci; much more indolent disease course

21
Q

Endocarditis involving the tricuspid valve?

A

Endocarditis involving the tricuspid valve: IV drug use or central line bacteremia

22
Q

strep bovis endocarditis may occur due to?

A

Strep. bovis endocarditis may have occurred because of a colon carcinoma, and work-up should be done (colonoscopy) to confirm the diagnosis.

23
Q

What can happen with a vegetation?

A

A vegetation can break off and become a fragment of septic embolus, or spread to the endocardium, grow deeper, and form an abscess.

24
Q

what is non-bacterial thrombotic endocarditis? associations?

A

This condition typically arises in patients with severe debilitation, such as cancer or sepsis patients. Its historical name, marantic endocarditis, is derived from the word marasmus, meaning undernourishment or malnutrition. In NBTE, sterile (non-infective) vegetations arise on the heart valves, and produce very little inflammatory response. NBTE doesn’t usually produce clinically evident problems because of direct valvular damage, however, it can produce systemic emboli to various sites. Interesting associations exist between the incidence of NBTE and pro-thrombotic tendencies:

  • Hypercoagulable states – previous DVT, PE, etc. • Trauma or indwelling catheters – suggests some type of endothelial injury
  • Mucinous adenocarcinomas – well-associated cause of thrombosis/DIC due to prothrombotic circulating materials (mucin, tissue factor, etc.)
25
Q

What is libman-sacks endocarditis?

A

Much less commonly seen now that SLE is aggressively treated, LSE is composed of small (1-4 mm), tan-pink vegetations.
• Mitral or tricuspid valve locations
• Located on either surface of an affected valve
• Located on chordae tendineae
• Located on endothelium lining the atria or ventricles

26
Q

Explain carcinoid heart disease? General features? normally what happens? cardiac features correlate with?

A

This concept revolves around the cardiac manifestations of systemic carcinoid syndrome. Recall that low-grade neuroendocrine tumors are historically called carcinoid tumors, and that these tumors may become functional – the secretion of serotonin and other metabolically active tumor products into circulation.

Carcinoid syndrome general features:
• Skin flushing • Diarrhea • Cramping • Bronchospasm and wheezing • Telangiectasias

Normally the liver will breakdown the metabolically active components of carcinoid syndrome, such as serotonin, histamine, bradykinin, and various prostaglandins. However, in the setting of liver failure for any reason (such as abundant metastases of carcinoid tumor), these metabolites may create cardiac disease.

  • Plaque-like thickening (endocardial fibrosis) of the endocardium and valves, which is more prominent on the right side of the heart (the lungs provide some left-sided protection against the circulating components)
  • Cardiac findings may correlate well with urinary levels of 5-hydroxyindoleacetic acid (5-HIAA), which is a useful diagnostic assay
27
Q

What are the two types of replacement valves? Complications of any type of heart valve include?

A

Two general types of replacement valves are used:

1) tissue-based valves, secured from human or porcine sources, and
2) mechanical valves of various shapes/functions. Tissue breakdown complicates the former type, and thrombosis complicates the latter type.

Complications of any type of heart valve include:
• Endocarditis, particularly developing at the prosthesistissue interface
• Leakage, at the same interface
A heart valve undergoing degeneration with nodular calcifications.
Tearing is another potential complication. Eventually all tissue-based replacements will be expected to undergo structural deterioration

Thrombosis developing upon a mitral mechanical valve. The configuration of the mechanical components are largely not visible due to the thrombus. Of course, embolus could also result from such a process