04.15 - Hypertensive and Related Heart Disease Flashcards
1
Q
What are the 4 major types of hypertrophic heart disease, and their epi?
A
- Hypertensive heart disease: left ventricular hyper-trophy (60% AA, 30% W w/HTN; 40% AA, 25% W have HTN in US)
- Hypertrophic cardiomyopathy: 0.2% of US pop (1 in 500)
- Aortic stenosis: 1% of pop
- Cor pulmonale: no good estimates (but lots)
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2
Q
How do patients with hypertrophic heart disease present?
A
- All present with dyspnea, angina, or sudden death
*Except: no angina with cor pulmonale
- All chronic
*Except cor pulmonale acute or chronic
- Clinico-pathologic correlations (structure & function)
3
Q
What are the differentiating characteristics of the hypertrophic heart diseases, i.e., for differential dx purposes?
A
- All occur in older people, except HC
- HHD, HC -> M = F; AS, CP -> M
- HHD more in AA
- All have LVH except cor pulmonale
- Only AS has a murmur (and sometimes HC)
- Treatment for HHD and CP is medical, AS surgical (or stent), and HC is variable
4
Q
What is going on here?
A
- Normal left ventricular wall thickness: 1.2-1.4cm
- Over time, HTN causes concentric left ventricular hypertrophy
- Diastolic dysfunction, impaired compliance, and ventricular filling are characteristic of hypertensive heart disease, but NOT specific
5
Q
What do you see in these 3 panels?
A
- Hypertrophied cardiac myocytes in first and last: expanded cytoplasm, and enlarged nuclei
- Compare them to the normal myocytes in the middle
6
Q
What do you see here?
A
- Nuclear enlargement in a hypertrophied cardiac myocyte
7
Q
What do you see (from left to right)? How does this affect compliance?
A
- Some pts w/hypertrophic heart diseases devo progressive myocardial fibrosis
- Driven by cytokine responses, including TGF-beta
- Leads to reduced arterial compliance
8
Q
What is the difference between right and left? Why is this important?
A
- Left: normal myocardium morphology
- Right: morphology of myocardium in pt with chronic renal failure
- Kidney disease causes HTN (and vice versa), so chronic renal failure pts highly prone to hypertensive heart disease
- Cardiomyocyte hypertrophy and myocardial interstitial fibrosis in uremia (urea in the blood) -> reduced compliance
- Myocardial fibrosis in HHD and other hypertrophic heart diseases tends to be INTERSTITIAL
9
Q
What is going on in the heart on the right?
A
- Hypertrophic cardiomyopathy (group of genetic conditions) is associated w/assymetric hypertrophy of the septum
- Normal at left for comparison
10
Q
What is HCOM?
A
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- Hypertrophic obstructive cardiomyopathy, a subset of hypertrophic cardiomyopathy
- About 1/3rd of pts w/hypertrophic cardiomyopathy have obstruction of outflow from left ventricle due to asymmetrically hypertrophied upper septum bulging into the outflow tract
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11
Q
What does this image show? When might you see this?
A
- Left ventricular outflow tract narrowed by septal hypertrophy -> point of coaptation of mitral leaflets in body of the leaflets, rather than at tips, as is normal
- Anterior leaflet beyond coaptation point carried anteriorly, superiorly by venturi drag forces, so mitral leaflet–septal contact, and subaortic obstruction
- Motion of anterior leaflet leads to coaptation failure of mitral leaflets and mitral regurgitation
- Can be seen in HCOM
12
Q
What is going on here?
A
- Contact of anterior leaflet of mitral valve & bulging upper septum injures both, causing repair response, fibrous thickening of mitral valve (asterisk in picture) and mirror image patch of fibrosis on the subaortic upper septum (arrows)
- May be a consequence of ventricular hypertrophy in HCOM
13
Q
Besides open heart surgery to resect obstructing upper septum in image shown (ventricular hypertrophy), what can you do?
A
- Inject poison (ethanol) into a septal coronary artery and infarct the inner part of the hypertrophied upper septum
14
Q
What are these examples of? When might you see this?
A
- Interstitial myocardial fibrosis, a feature of hyper-trophic cardiomyopathy (trichrome stain)
- In some cases, branching myocytes oriented out of normal parallel array, impairing their ability to all pull in the same direction as needed for most effective pumping of the blood
15
Q
What do you see here?
A
- Fibrosis: can be a prominent part of hypertrophic cardiomyopathy
- Anatomic substrate for reentrant ventricular tachycardia just like a patchy, old MI
16
Q
What do you see here?
A
- Aortic stenosis (bottom two)
- Usually causes nodular calcifications in sinuses of Valsalva (pockets b/t cusps of aortic valve and aorta)
- Correlate structure with function to see problem:
1. Systole: obstructed flow
2. Diastole (ventricular filling): stenotic aortic valve doesn’t close completely
17
Q
What are these three examples?
A
- Degenerative calcific aortic stenosis (elderly >70 y/o): formation of rocks in the sinus of Valsalva has gradually stenosed valve orifice
- Rheumatic aortic stenosis (young, middle aged adults): inflammation and fibrosis start at commissure and move inward (becoming rare in the US); aka, rheumatic valvulitis
- Bicuspid aortic stenosis (young, middle aged): in pts born w/bicuspid valve (1% US pop) due to fusion of two cusps (raphe on the right), aortic stenosis develops more rapidly
18
Q
What is a heart valve commissure?
A
Where the valve opening meets the valve annulus
19
Q
What is this?
A
- Typical degenerative calcific aortic stenosis with rocks in the sinuses of Valsalva
- Risk factors are nearly identical to those for atherosclerosis, but same therapies that work for athero have not proven to work for aortic stenosis
20
Q
What is this? How do these pts typically present?
A
- Bicuspid calcific aortic stenosis
- Older M with sudden death
21
Q
What is this? When might you use it?
A
- Stent: an alternative to open heart surgery to replace stenotic aortic valve
- Involves insertion of closed wire mesh stent through stenotic valve, then opening it and leaving it in place to keep the valve open
23
Q
What do you see here? What about the right ventricular wall?
A
- Normal heart (left) and hypertrophied heart (right; most likely from HTN -> common things are common)
- In both normal and hypertrophied hearts, thickness of right ventricular wall less than 1/3rd that of the left ventricle -> normal
24
Q
What is the diagnosis?
A
- Cor pulmonale -> note the sizes of the right and left ventricles
27
Q
What is this?
A
- Organizing small pulmonary thromboembolus, already partly converted to fibrous tissue thickening the arterial wall (to left of blue line)
- Partly composed of condensed fibrin infiltrated by fibroblasts, with small residual lumen (green arrow)
28
Q
What do you see here?
A
- Tumor embolism in small pulmonary artery, with wall thickening by organizing thrombus and probably some smooth muscle hyperplasia and hypertrophy, reacting to the associated pulmonary hypertension
29
Q
What do you see here?
A
- Foreign material from IV drug abuse -> under-recognized cause of pulmonary hypertension
