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283 Aortic Valve Disease Flashcards

1
Q

dominant cause of valvular heart disease in developing and lowincome countries

A

Rheumatic fever

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2
Q

Prevalence of Rheumatic fever in costa rica and china?

A

as low as 1 per 100,000 school-age children in Costa Rica to as high as 150 per 100,000 in China.

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3
Q

Rheumatic heart disease accounts for which % of

hospital admissions related to cardiovascular disease and % of hospital discharges in some developing countries?

A

12–65%; 2–10%

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4
Q

Why does Rheumatic heart disease develop faster in developing countries?

A

This accelerated natural history may be due to repeated infections with more virulent strains of rheumatogenic streptococci.

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5
Q

Prevalence and Incidence of Rheumatic heart disease?

A

15 million to 20 million people live with rheumatic heart disease worldwide, an estimated prevalence characterized by 300,000 new cases and 233,000 case fatalities per year

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6
Q

left-sided valve disease affects what % of adults older than the age of 75?

A

12-13%

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7
Q

nr. hospital discharges with valvular heart disease in 2010 in the United States?

A

there were 85,000

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8
Q

Why is the prevalence of infective endocarditis increasing?

A

vascular grafts and intracardiac devices

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9
Q

Bicuspid aortic valve disease affects which % of the general population?

A

as many as 0.5–1.4%

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10
Q

% of all patients with chronic valvular heart disease that have aortic stenosis?

A

one-fourth

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11
Q

% of people with aortic stenosis that are male?

A

80% of adult patients with symptomatic, valvular AS are male

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12
Q

pathologic study of specimens removed at the time of aortic valve replacement for AS showed which % of bicuspid and unicuspid?

A

53% bicuspid and 4% unicuspid

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13
Q

risk factors for aortic stenosis?

A

vitamin D receptor, the estrogen receptor in postmenopausal women, interleukin 10, and apolipoprotein E4 and several traditional atherosclerotic risk factors

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14
Q

% of persons older than 65 years exhibit aortic valve

sclerosis, and % that exhibit frank stenosis.

A

30% and 2% respectively.

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15
Q

what is the most common congenital heart valve defect?

A

Bicuspid aortic valve disease

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16
Q

prevalence of Bicuspid aortic valve disease in first degree relatives?

A

10%

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17
Q

what is the male-to-female predominance?

A

2-4:1

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18
Q

single gene defect in bicuspid aortic valve disease?

A

NOTCH1 gene has been described in some families. Abnormalities in endothelial nitric oxide synthase and NKX2.5

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19
Q

When do patients with pure or predominant AS have symptoms? And patients with bicuspid aortic valve disease?

A

gradually increasing obstruction over years but do not become symptomatic until the sixth to eighth decades.
Adult patients with BAV disease, however, develop significant valve dysfunction and symptoms one to two
decades sooner.

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20
Q

three cardinal symptoms of Aortic Stenosis?

A

Exertional dyspnea, angina pectoris, and syncope

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21
Q

How is the pulse in Aortic Stenosis?

A

carotid arterial pulse rises slowly to a delayed peak (pulsus parvus et tardus).

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22
Q

Is there a thrill in Aortic Stenosis?

A

A thrill or anacrotic “shudder” may be palpable over the carotid arteries, more commonly the left. A systolic thrill may be present at the base of the heart to the right of the sternum when leaning forward or in the suprasternal
notch.

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23
Q

How is the venous jugular pulse in Aortic Stenosis?

A

In many patients, the a wave in the jugular venous pulse is accentuated.

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24
Q

How is the splitting in Aortic Stenosis?

A

There is paradoxical splitting of S2

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25
Q

How is the Aortic Stenosis Murmur?

A 
The murmur of AS is characteristically an ejection (mid) systolic murmur that commences shortly after the S1, increases in intensity to reach a peak toward the middle of ejection, and ends just before aortic valve closure. It is characteristically low-pitched, rough and rasping in character, and loudest at the base of the heart, most commonly in the second right intercostal space. It is transmitted upward along the carotid arteries. Occasionally it is transmitted downward and to the apex, where it may be confused with the systolic murmur of
mitral regurgitation (MR) (Gallavardin effect).
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26
Q

ECG in Aortic Stenosis?

A

severe AS, there is LV hypertrophy. In advanced cases, ST-segment depression and T-wave inversion (LV
“strain”) in standard leads I and aVL and in the left precordial leads are evident.

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27
Q

How is the aortic valve area measured?

A

The valve gradient and aortic valve area can be

estimated by Doppler measurement of the transaortic velocity.

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28
Q

How is defined the severity of the aortic stenosis?

A

Severe AS is defined by a valve area less than 1 cm2, whereas moderate AS is defined by a valve area of 1–1.5 cm2 and mild AS by a valve area of 1.5–2 cm2.
Aortic valve sclerosis, conversely, is accompanied by a jet velocity of less than 2.5 meters/s (peak gradient

29
Q

What is the Dobutamine stress echocardiography used for?

A

Dobutamine stress echocardiography is useful for the evaluation of patients with AS and severe LV systolic dysfunction (low-flow, low-gradient, severe AS with reduced EF), in whom the severity of the AS can often be difficult to judge.

30
Q

Catheterization is also useful in which patients:

A

(1) patients with multivalvular disease,(2) young, asymptomatic patients with noncalcific congenital AS for operation or percutaneous aortic balloon valvuloplasty
(PABV) (3) patients in whom it is suspected that the obstruction to LV outflow may not be at the level of
the aortic valve but rather at the sub- or supravalvular level.

31
Q

% of patients that need bypass ate wthe time of aotic valve replacement?

A

50% among adult patients.

32
Q

average time to death after the onset of various symptoms

A

angina pectoris, 3 years; syncope, 3 years; dyspnea,

2 years; congestive heart failure, 1.5–2 years

33
Q

% of adults dying with valvular AS, sudden death, which presumably resulted from an arrhythmia?

A

occurred in 10–20%

34
Q

Have statins shown benefit in reducing stenosis in aortic stenosis?

A

randomized prospective studies with either high-dose

atorvastatin or combination simvastatin/ezetimibe have failed to show a measurable effect on valve-related outcomes.

35
Q

Indications for surgery?

A

Severe AS (area 5.5 cm). Operation for aneurysm disease is recommended at smaller aortic diameters (4.5–5.0 cm) for patients with a family history of an aortic catastrophe and for patients who exhibit rapid aneurysm growth (>0.5 cm/year).

36
Q

Surgical risk por valve replacement in AS?

A

approximately 2%

37
Q

Relative indications for surgery in AS?

A

abnormal response to treadmill exercise; rapid progression of AS, especially when urgent access to medical care might be compromised; very severe AS, defined by an aortic valve jet velocity >5 meters/s or mean gradient >60 mmHg and low operative risk; and excessive LV hypertrophy in the absence of systemic hypertension

38
Q

Mortality risk in patients with low flow, low gradient?

A

15-20%

39
Q

survival rate at 10 years of patients with AVR?

A

60%

40
Q

Complications in bioprosthetic and mechanical valves?

A

Approximately 30% of bioprosthetic valves evidence primary valve failure in 10 years, requiring re-replacement, and an approximately equal percentage of patients with mechanical prostheses develop significant hemorrhagic complications as a consequence of treatmentwith vitamin K antagonists.

41
Q

Restenosis rate with PABV?

A

80% 1 year

42
Q

two available systems for TAVR?

A

a balloon-expandable valve and a selfexpanding

valve

43
Q

Benefits of TAVR compared with medical therapy and valve replacement in high risk surgery?

A

1- and 2-year survival rates are significantly higher with TAVR compared with medical therapy (including PABV)
(Fig. 283-4). One- and 2-year survival rates are essentially equal for high-surgical-risk patients treated with TAVR or surgical AVR (SAVR)

44
Q

What can be the two causes for aortic regurgitation?

A

AR may be caused by primary valve disease or by primary aortic root disease.

45
Q

Primary valve diseases that cause aortic regurgitation?

A

Rheumatic disease; Congenital fenestrations of the aortic
valve; Membranous subaortic stenosis with scarring of the aortic valve leaflets; Prolapse of an aortic cusp in patients with ventricular septal defect; myxomatous degeneration; infective endocarditis; syphilis or ankylosing spondylitis; traumatic rupture

46
Q

Two diseases that can cause AS and AR?

A

rheumatic or congenital AR

47
Q

Primary aortic root diseases that cause aortic regurgitation?

A

Marfan’s syndrome; idiopathic dilation of the aorta; annuloaortic ectasia; osteogenesis imperfecta; and severe, chronic hypertension; Syphilis and ankylosing spondylitis

48
Q

weight of hearts with AR?

A

the hearts of these patients may be among the largest encountered, sometimes weighing >1000 g.

49
Q

% of RA that are men?

A

3/4.

50
Q

How long do patients stay assymptomatic in chronic aortic regurgitation?

A

10-15 years

51
Q

First symptoms in aortic regurgitation?

A

palpitations and sinus tachycardia

52
Q

capillary pulsations?

A

flushing and paling of the skin at the root of the nail while pressure is applied to the tip of the nail (Quincke’s pulse), are characteriof chronic severe AR. A booming “pistol-shot” sound can be heard over the femoral arteries (Traube’s sign), and a to-and-fro murmur (Duroziez’s sign) is audible if the femoral artery is lightly compressed with a stethoscope.

53
Q

What happens to the pulse pressure in Aortic regurgitation?

A

The arterial pulse pressure is widened as a result of both systolic hypertension and a lowering of the diastolic pressure.

54
Q

Is there a thrill in AR?

A

A diastolic thrill may be palpable along the left sternal border in thin-chested individuals, and a prominent systolic thrill may be palpable in the suprasternal notch and transmitted upward along the carotid arteries.

55
Q

Besides Corrigan pulse, what other can AR patients have?

A

Bisferiens.

56
Q

In AR what happens with A2?

A

it is usually absent.

57
Q

In AR how is the murmur?

A

The murmur of chronic AR is typically a high-pitched, blowing, decrescendo diastolic murmur, heard best in the third intercostal space along the left sternal border (see Fig. 267-5B). In patients with mild AR, this murmur is brief, but as the severity increases, it generally becomes
louder and longer, indeed holodiastolic. However, when the murmur is heard best along the right sternal border, it suggests that the AR is caused by aneurysmal dilation of the aortic root.

58
Q

What is the Austin Flint murmur?

A

Austin Flint murmur, a soft, low-pitched, rumbling mid-to-late diastolic murmur. It is probably produced by
the diastolic displacement of the anterior leaflet of the mitral valve by the AR stream.

59
Q

What happens with S1 in acute Aortic Regurgitation? And with the pressure pulse and murmur?

A

In acute severe AR, the elevation of LV end-diastolic pressure may lead to early closure of the mitral valve, a soft S1, a pulse pressure that is not particularly wide, and a soft, short, early diastolic murmur of AR.

60
Q

ECG in Aortic Regurgitation

A

ST-segment depression and T-wave inversion in
leads I, aVL, V5, and V6 (“LV strain”). Left-axis deviation and/or QRS prolongation denote diffuse myocardial disease, generally associated with patchy fibrosis.

61
Q

Doppler imaging criteria for severe AR?

A

the central jet width assessed by color flow Doppler imaging exceeds 65% of the LV outflow tract, the regurgitant volume is ≥60 mL/beat, the regurgitant fraction is ≥50%, and there is diastolic flow reversal in the proximal descending thoracic aorta.

62
Q

What medical therapy is necessary in acute aortic regurgitation?

A

intravenous diuretics and vasodilators.

63
Q

In chronic aortic regurgitation what is the blood pressure goal?

A

less than 140 mmHg

64
Q

Are beta-blockers contraindicated in patients with AR?

A

More recent observational reports, however, suggest that beta blockers may provide functional benefit in patients with chronic AR.

65
Q

What is the optimal time for surgery in patients with chronic AR?

A

after the onset of LV dysfunction but prior to the development of severe symptoms.

66
Q

when is surgery performed in patients assymptomatic?

A

LVEF 50 mm, or an LV diastolic dimension >65 mm.

67
Q

When can one make primary surgical repair?

A

Trauma an infective endocarditis

68
Q

What types of surgery can be made when there is primary aortic root disease?

A

valve-sparing aortic root reconstruction; implanting a

composite valve-graft conduit

69
Q

surgery mortality for AVR?

A

2% low risk patients, 10% high risk patients; 5% a year in high risk

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