04.15 - Hypertensive and Related Heart Disease Flashcards Preview

Cardio > 04.15 - Hypertensive and Related Heart Disease > Flashcards

Flashcards in 04.15 - Hypertensive and Related Heart Disease Deck (29)
Loading flashcards...

What are the 4 major types of hypertrophic heart disease, and their epi?

1. Hypertensive heart disease: left ventricular hyper-trophy (60% AA, 30% W w/HTN; 40% AA, 25% W have HTN in US)

2. Hypertrophic cardiomyopathy: 0.2% of US pop (1 in 500)

3. Aortic stenosis: 1% of pop

4. Cor pulmonale: no good estimates (but lots)


How do patients with hypertrophic heart disease present?

- 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)


What are the differentiating characteristics of the hypertrophic heart diseases, i.e., for differential dx purposes?

- 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 


What is going on here? 

- 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 


What do you see in these 3 panels?

- Hypertrophied cardiac myocytes in first and last: expanded cytoplasm, and enlarged nuclei 

- Compare them to the normal myocytes in the middle



What do you see here?

- Nuclear enlargement in a hypertrophied cardiac myocyte 


What do you see (from left to right)? How does this affect compliance?

- Some pts w/hypertrophic heart diseases devo progressive myocardial fibrosis 

- Driven by cytokine responses, including TGF-beta

- Leads to reduced arterial compliance 


What is the difference between right and left? Why is this important?

- 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


What is going on in the heart on the right?

- Hypertrophic cardiomyopathy (group of genetic conditions) is associated w/assymetric hypertrophy of the septum 

- Normal at left for comparison 


What is HCOM?

- 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


What does this image show? When might you see this?

- 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


What is going on here?

- 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


Besides open heart surgery to resect obstructing upper septum in image shown (ventricular hypertrophy), what can you do?

- Inject poison (ethanol) into a septal coronary artery and infarct the inner part of the hypertrophied upper septum 


What are these examples of? When might you see this?

- 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


What do you see here?

- Fibrosis: can be a prominent part of hypertrophic cardiomyopathy 

- Anatomic substrate for reentrant ventricular tachycardia just like a patchy, old MI 



What do you see here?

- 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 


What are these three examples?

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 


What is a heart valve commissure?

Where the valve opening meets the valve annulus


What is this?

- 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 


What is this? How do these pts typically present?

- Bicuspid calcific aortic stenosis 

- Older M with sudden death


What is this? When might you use it?

- 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


What is cor pulmonale? Acute? Chronic?

- Stems from right ventricular pressure overload (aka, isolated pulmonary hypertensive heart disease) 

1. Normally (bc pulmonary circulation is low pressure) RV thinner, more compliant than LV

- Chronic: right ventricular hypertrophy, +/- dilation

1. Causes: lung disorders, esp chronic parenchymal diseases like emphysema, chronic PE w/many small (individually asymptomatic) PE composed of thrombi, foreign material from IV drug abuse, tumor or some combo of these and primary pulmonary HTN

- Acute: can follow massive PE, but pulmonary HTN most commonly a cx of left-sided heart disease

1. Dilation of right ventricle w/o hypertrophy

- NOTE: in chronic cor pulmonale, RV wall thickens, sometimes up to 1 cm or more; more subtle RV hypertrophy may be thickening muscle bundles in outflow tract immediately below pulmonary valve


What do you see here? What about the right ventricular wall?

- 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 



What is the diagnosis?

- Cor pulmonale -> note the sizes of the right and left ventricles 


How does acute vs. chronic cor pulmonale tend to affect the right ventricle?

- Acute = right ventricular dilatation

- Chronic = right ventricular hypertrophy 

- Acute-on-chronic = right ventricular dilatation + right ventricular hypertrophy 


Do most patients with cor pulmonale have heart failure?

- No -> mos pts w/cor pulmonale are compensated, and DO NOT have heart failure 

- Many more pts with right heart failure have it bc of left heart failure than cor pulmonale 

- Only a small group of pts with right heart failure due to cor pulmonale 


What is this?

- 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) 


What do you see here?

- 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


What do you see here?

- Foreign material from IV drug abuse -> under-recognized cause of pulmonary hypertension