Heart 2 Flashcards
Systemic (Left-Sided) Hypertensive Heart Disease
Criteria:
left ventricular hypertrophy
History of HTN or pathologic evidence of systemic hypertension in other organs
Pulmonary (Right-Sided) Hypertensive Heart Disease
Chronic Cor Pulmonale results from pulmonary disorders that cause chronic severe pulmonary hypertension
- thick and dilated RV & RA
Acute Cor Pulmonale occurs from massive pulmonary thromboembolism (saddle embolus, etc.)
- acutely dilated RV and RA
Disorders Predisposing to Cor Pulmonale
Diseasess of the pulmonary parenchyma
- of the pulmonary vessels
- affecting chest movement
- inducing pulmonary arterial constriction
Basic Types of Acquired Cardiac Valve Dysfunction
“Pure” when only stenosis or insufficiency present
“Mixed” when have stenosis and insufficiency in same valve
Stenosis: failure of valve to open
Virtually always a chronic disease
Almost always a cusp abnormality
Insufficiency (regurgitation or incompetence): failure of a valve to close
- Chronic disease or acute insufficiency syndromes may occur - Intrinsic disease of valve cusp or acquired abnormality of the supporting structures - - - Functional regurgitation – normal valve leaflets but problem with supporting structures (e.g. dilated annulus from ventricular dilatation)
Major etiology of mitral stenosis
postinflammatory scarring (rheumatic heart disease)
Major etiology of aortic stenosis
postinflammatory scarring (rheumatic heart disease) senile calcific aortic stenosis calcification of congenitally deformed valve
2/3 of all valvular disease
Acquired stenoses of the aortic and mitral valves
Most frequent causes of functional valvular lesions
aortic stenosis- calcification
aortic insufficiency- dilated ascending aorta
mitral stenosis- rheumatic valvular disease
mitral insufficiency- myxomatous degeneration
(Senile) Calcific Aortic Stenosis
Calcific Aortic Stenosis
Most common of all valvular abnormalities
Consequence of dystrophic calcification and ossification owing to chronic valve abuse (years of use)
Pathologic Features
Nodular masses of calcium are heaped up within the sinuses of Valsalva (arrow).
Clinical features
Clinical symptoms do not occur until 7th (60s) to 9th (80s) decades
Crescendo-decrescendo systolic murmur (crescendo with severe disease)
Pressure hypertrophy results from flow obstruction and patient develops significant left ventricular concentric hypertrophy
Left ventricular cardiac mass tends to be ischemic and leads to:
Congestive heart failure (die within 2 yrs)
Syncope (die within 3 years)
Angina pectoris (die within 5 yrs)
Calcific Stenosis of Congenitally Bicuspid Aortic Valve
Congenital bicuspid aortic valve occurs in ~ 2% population
Two cusps frequently not equal size: larger cusp may have a raphe” (seam) – result of incomplete separation during development
Bicuspid valves more susceptible to progressive degenerative calcification; develop significant calcification earlier
Develop clinical symptoms and signs of cardiac dysfunction earlier, 5th and 6th decades (7th to 9th decades with tricuspid aortic valves)
Mitral Annular Calcification Occurs in three types of patients
Women over 60 years of age
Individuals with myxomatous mitral valves
Patients with elevated left ventricular pressure
– e.g., hypertension
Generally does not affect valvular function
Occasionally associated with arrythmias
Myxomatous Degeneration of the Mitral Valve Pathologic Changes
Primary changes
Intercordal ballooning of mitral valve leaflets
Secondary changes:
Dilation of annulus
Jet lesions
Rheumatic Valvular Heart Disease (RHD)
Strep Pharyngitis →Acute Rheumatic Fever →Chronic Rheumatic Valvular Heart Disease (RHD)
Usually occurs 10 days to 6 weeks post strep throat.
Acute rheumatic fever: Acute systemic disease
Migratory polyarthritis of large joints (swollen, painful joints)
Acute carditis with cardiac enlargement and diminished function
Subcutaneous nodules
Erythema marginatum of skin
Sydenham chorea (involuntary, purposeless movements of extremities)
“Jones Criteria” for diagnosis
Evidence prior group A Strep infection plus
2 major system findings (from above list of 5)
Or 1 major system finding plus 2 minor manifestations
Fever
Arthralgia
Evidence of acute phase reactants
elevated sedimentation rate
elevated C-reactive protein
What we see in rheumatic carditis
Aschoff body - Collection of large activated histiocytes
Anitschkow cells – “mononuclear”
Aschoff cells - multinucleated forms
caterpillar” cells - unique linear chromatin pattern
MacCallum plaques – subendocardial fibrosis from regurgitant jets in RHD
Rheumatoid Heart Disease !!!
Cardiac involvement in 20-40% of cases of rheumatoid arthritis
Fibrinous pericarditis is most common presentation
Rheumatoid valvulitis
fibrous thickening and calcification of aortic valve cusps
Rheumatoid nodules
may be present in myocardium, endocardium, valves and aortic root
Infective Endocarditis
Destructive infection of heart valves or mural endocardium by pathogen
bacteria more often then fungi
S. viridans (50-60%) > S. aureus (20-30%) > HACEK (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
S. epidermidis #1 in artificial valves
S. aureus #1 in IV drug abusers
Usually involves left valves (except in IV drug abusers)
Bulky, friable vegetations
admixture of fibrin-platelet clot and organisms
Destruction of underlying cardiac structures, especially valves
Risk of systemic microemboli
lead to vascular infarcts and microabscesses (septic infarcts)
Acute Bacterial Endocarditis
Rapidly progressive destruction of infected cardiac valve
Infection by a highly virulent bacteria such as S. aureus (IV drug abusers)
Even with aggressive antibiotic therapy, 50% patients die in days or weeks of onset of symptoms.
Valve prior to infection is frequently normal
Subacute Bacterial Endocarditis
Insidious onset and protracted clinical course (weeks to months)
Infection by low virulence bacteria such as Streptococcus viridans
Most patients recover with antibiotic therapy
Involved valve usually deformed or abnormal
historically RHD, now mitral valve prolapse
. Diagnostic Criteria for Infective Endocarditis
GET 3 BLOOD CULTURES IN 24o!!!
the Duke Criteria, requires either pathologic or clinical criteria; if clinical criteria are used, 2 major, 1 major + 3 minor, or 5 minor criteria are required for diagnosis.
Noninfected Vegetations: Nonbacterial Thrombotic Endocarditis (NBTE)
Small (1-5 mm) along the line of closure of the valve leaflets or cusps
Valvular lesions are sterile
Major risk factor is hypercoagulable states
May produce systemic emboli to coronary arteries, brain, etc.
Once termed “Marantic Endocarditis” in debilitated
Noninfected Vegetations: Libman-Sacks Disease
Endocarditis of Systemic Lupus Erythematosus (SLE)
Small (1-4 mm) sterile verrucous “vegetations”
AV valve leaflets (mitral and tricuspid)
Valvular endocardium
Chordae tendineae
Ventricle or atrium subjacent to AV valves
Thrombotic vegetations associated with lupus anticoagulant (antiphospholipid antibody syndrome)
May be due to immune complex deposition with inflammation
Comparison of the four major forms of
vegetative endocarditis.
The acute rheumatic heart disease (RHD) is marked by small, warty verrucae along the lines of closure of the valve leaflets.
Infective endocarditis (IE) typically shows large, irregular masses on the valve cusps that can extend onto the chordae.
Nonbacterial thrombotic endocarditis (NBTE) typically exhibits small, bland vegetations, usually attached at the line of closure. One or many may be present.
Libman-Sacks endocarditis (LSE) has small or medium-sized vegetations on either or both sides of the valve leaflets, or elsewhere on the endocardial surface.
Carcinoid Heart Disease
Fibrous thickening of the endocardial surfaces accompanying carcinoid syndrome
Smooth muscle proliferation and acid mucopolysaccharide matrix
Usually involves right ventricle, tricuspid and pulmonic valves
except with pulmonary carcinoids or septal abnormalities
Metastatic carcinoid tumors produce serotonin (5HT)
Complications of Cardiac Valve Prostheses
Thrombosis/ thromboembolism
anticoagulant-related hemorrhage
prosthetic valve endocarditis
structural deterioration (intrinsic)- wear, fracture, poppet ailure in ball valves, cuspal tear, calcification
Other forms of dysfuntion: inadequate healing (paravalvular leak), exuerant healing (obstruction), hemolysis
