B P8 C72 Aortic Valve Stenosis Flashcards
Causes/etiology of AS
1.
2.
3.
A congenital bicuspid valve with superimposed calcification
Calcification of a normal trileaflet valve
Rheumatic disease
The most prevalent anatomy for a bicuspid valve is two cusps with a right-left systolic opening, consistent with congenital fusion of the____________________, seen in 70% to 80% of patients
Right and left coronary cusps
AVA ≤1.0 cm2 with resting aortic Vmax <4 m/s or mean ∆P <40 mm Hg
Dobutamine stress echocardiography shows AVA <1.0 cm2 with V max ≥4 m/s at any flow rate
Stage D2
ACC AHA Class 1 indications for treatment of AS
In adults with severe high-gradient AS (Stage D1) and symptoms of exertional dyspnea, HF, angina, syncope, or presyncope by history or on exercise testing, AVR is indicated
In asymptomatic patients with severe AS and an LVEF <50% (Stage C2), AVR is indicated
In asymptomatic patients with severe AS (Stage C1) who are undergoing cardiac surgery for other indications, AVR is indicated
In symptomatic patients with low-flow, lowgradient severe AS with reduced LVEF (Stage D2), AVR is recommended
In symptomatic patients with low-flow, lowgradient severe AS with normal LVEF (Stage D3), AVR is recommended if AS is the most likely cause of symptoms
Recommendations for Choice of SAVR Versus TAVI for Patients for Whom a Bioprosthetic AVR Is Appropriate
Recommendations for severe AS >80 years old
TAVR is Class 1
The most common clinical presentation in patients with a known diagnosis of AS who are followed prospectively is a _____.
Gradual decrease in exercise tolerance, fatigue,or dyspnea on exertion
The mechanism of exertional dyspnea may be _____, with an excessive rise in end-diastolic pressure leading to pulmonary congestion.
LV diastolic dysfunction
In patients without CAD, angina results from the combination of _____, which reduce the coronary perfusion pressure gradient and impair myocardial flow reserve.
(1) the increased O2 needs of hypertrophied myocardium and reduction of O2 delivery due to decreased myocardial capillary density
(2) endothelial cell loss
(3) increased LVEDP
Syncope most often is caused by the ______ that occurs during exertion when arterial pressure declines because of systemic vasodilation and an inadequate increase in cardiac out- put related to valvular stenosis
Reduced cerebral perfusion
Syncope also has been attributed to malfunction of the baroreceptor mechanism in severe AS, as well as to a _____ to a greatly elevated LV systolic pressure during exercise.
Vasodepressor response
Syncope at rest may be caused by _____ with loss of the atrial contribution to LV filling, which causes a precipitous decline in cardiac output, or to _____ caused by extension of the calcification of the valve into the conduction system.
Transient AF
Transient AV block
The prevalence of _____ without stenosis, defined as irregular thickening or calcification of the aortic valve leaflets, increases with age and ranges from 9% in populations with a mean age of 54 years to 42% in populations with a mean age of 81 years.
Aortic valve sclerosis
In population-based echocardiographic studies, _____% of persons aged 65 or older and _____% of persons 75 or older had calcific aortic stenosis (AS)
> 65 years: 1-2%
> 75 years: 12%
The rate of progression from aortic sclerosis to stenosis is _____% per year.
1.8-1.9%
Valvular AS has three principal causes:
(1) Congenital bicuspid valve with superimposed calcification
(2) Calcification of a normal trileaflet valve
(3) Rheumatic disease
Rarely, AS is caused by severe atherosclerosis of the aorta and aortic valve; this form of AS occurs most frequently in patients with severe hypercholesterolemia and is observed in children with _____.
Homozygous type II hyperlipoproteinemia
Rheumatoid involvement of the valve is a rare cause of AS and results in _____ of the valve leaflets and involvement of the _____.
Nodula thickening
Proximal portion of the aorta
_____ affecting a congenital bicuspid or normal trileaflet valve is now the most common cause of AS in adults
Calcific (formerly “senile” or “degenerative”) aortic valve disease
Aortic sclerosis, identified by either echocardiography or computed tomography (CT), is the initial stage of calcific valve disease and, even in the absence of valve obstruction or known cardiovascular disease, is associated with an increased risk of _____.
Myocardial infarction (MI)
Cardiovascular and all-cause mortality
_____ valves typically produce severe obstruction in infancy and are the most common malformations found in fatal valvular AS in children younger than 1 year but also may be seen in young adults with an anatomy that mimics bicuspid valve disease.
Unicuspid
A congenital bicuspid aortic valve (BAV) is present in approximately 1% to 2% of the population, with a male predominance of approximately _____.
3:1
A BAV may be an isolated abnormality (approximately 50% of the time) or occur in the context of a genetic syndrome (e.g.,Turner syndrome), alongside other congenital heart defects (e.g., hypoplastic left heart, coarctation of the aorta), or with a _____ (most common nonvalvular manifestation).
Thoracic aortic aneurysm
The most prevalent anatomy for a bicuspid valve is two cusps with a right-left systolic opening, consistent with congenital fusion of the _____, seen in 70% to 80% of patients
Right and left coronary cusps
An anterior-posterior orientation, with fusion of the right and noncoronary cusps, is less common, seen in approximately 20% to 30% of patients. Fusion of the left and noncoronary cusps is rarely seen.
A prominent ridge of tissue or raphe may be present in the larger of the two cusps so that the closed valve in diastole may mimic a trileaflet valve.
Unicuspid valves are distinguished from a bicuspid valve by having only ___ aortic commissure.
One
The risk of aortic dissection in patients with BAV is _____ times higher than in the general population
Patients with BAV also are at increased risk for endocarditis (0.4 per 100,000) accounting for approximately 1200 deaths per year, however, the most common cardiac event is need for ______, and most patients with BAV develop calcific valve stenosis later in life, typically presenting with severe AS _______
5-9x
AVR
After the age of 50 years
Although the histopathologic features of calcific stenosis of a BAV are no different from those of a trileaflet valve, the turbulent flow and increased leaflet stress caused by the abnormal architecture are postulated to result in accelerated valve changes,
Rheumatic AS results from _____, leading to retraction and stiffening of the free borders of the cusps
(1) Adhesions and fusions of the commissures and cusps
(2) Vascularization of the leaflets of the valve ring
Normal valve leaflets comprise the fibrosa (facing the aorta), ventricu- laris (facing the ventricle), and spongiosa (located between the fibrosa and ventricularis). _____ are the most predominant cell type; endothelial and smooth muscle cells are also present.
Valve interstitial cells (VICs)
The most consistently observed genetic association is for _____.
Heritable forms of calcific aortic valve disease have been linked to ________
Lipoprotein(a) (Lp(a))
NOTCH1 mutation
Progressive valve obstruction imposes a _____overload state that leads to numerous changes in the structure and function of the left ventricle and accompanying changes in the pulmonary and systemic vasculature.
Chronic pressure overload
LV responses to AS
Hypertrophic myocardial remodeling
Myocardial fibrosis
Myocardial ischemia
Left ventricular diastolic dysfunction
left ventricular systolic dysfunction
The hypertrophied and pressure-overloaded left ventricle transmits increased pressure to the pulmonary vasculature, which leads to pulmonary hypertension in many patients with AS, becoming severe in _____%
15-20%
Maintenance of cardiac output in the face of an obstructed aortic valve imposes a chronic increase in LV pressure. In response, the ventricle typically undergoes hypertrophic remodeling characterized by _______ and ________
Myocyte hypertrophy and increased wall thickness
LV remodeling may manifest as concentric remodeling, ________ or ________
Concentric hypertrophy, or eccentric hypertrophy
LV remodeling reduces wall stress (afterload) and is considered one of the important compensatory mechanisms to maintain LV ejection performance,
In patients with AS, several studies have now documented that increased LV hypertrophic remodeling is associated with more _________ and ________, as well as higher mortality.
Severe ventricular dysfunction and heart failure (HF) symptoms
As a part of the hypertrophic remodeling process, _____ and _______ (not fibrosis from prior MI) may develop, although the incidence and extent of fibrosis are variable and unpredictable and the underlying biologic mechanisms not yet clarified
Diffuse and replacement myocardial fibrosis
What type of fibrosis tend to regress after AVR?
Diffuse fibrosis tends to regress after AVR, whereas replacement fibrosis does not.
In patients with AS, the _____, ______ and _____ all elevate myocardial oxygen (O2) consumption.
Hypertrophied left ventricle, increased systolic pressure, and prolongation of ejection
At the same time, even in the absence of epicardial coronary artery disease (CAD), _______ in the hypertrophied ventricle, ______, _______, ________ all serve to decrease the coronary perfusion pressure gradient and myocardial blood flow
Decreased myocardial capillary density
Endothelial cell loss
Increased LV end-diastolic pressure (LVEDP)
Shortened diastole
_____ underlies symptoms of angina in patients with AS that is often indistinguishable from that caused by epicardial coronary obstruction
Impaired myocardial flow reserve
Myocardial flow reserve is independently associated with aerobic exercise capacity and HF functional class in severe AS and appears to be influenced by the extent of LV hypertrophic remodeling and fibrosis, endothelial cell loss, and severity of valve obstruction.
_________ or ________ may exacerbate this ischemic imbalance and provoke angina that may not be experienced at rest.
Exercise or other states of increased O2 demand
______ each contribute to increased chamber stiffness and higher end diastolic pressures.
Higher cardiomyocyte stiffness, increased myocardial fibrosis, advanced-glycation end products, and metabolic abnormalities