-
The normal aortic valve orifice area (AVA) is 3 to 4 cm2; clinically significant gradients occur when AVA is reduced by one half, and symptoms usually arise when AVA is one fourth of normal size.
-
Gradients are less predictive (a mean gradient > 50 mm Hg has >90% positive predictive value for severe AS, but there is no clear cutoff for a good negative predictive value3).
-
Most common etiologies: Congenital, rheumatic, and calcific (degenerative) (See Table 12-2.)
-
Under 70 years: >50% congenital; over 70 years: ˜ 50% degenerative4
-
Pressure gradient between the left ventricle (LV) and aorta (increased afterload)
-
Initially, cardiac output is maintained through compensatory mechanisms of left ventricular hypertrophy (LVH), increased preload, and increased myocardial contractility.
-
If preload reserve is exceeded or if LV function declines, cardiac output fails to increase (fixed cardiac output).
-
Cardinal manifestations: Classic triad of angina, exertional syncope, and congestive heart failure (CHF).
-
Angina is due to increased myocardial demand/decreased coronary flow reserve.6
-
CHF results from diastolic dysfunction, systolic dysfunction, or both.
TABLE 12-1 Grading of severity of AS | ||||||||||||
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TABLE 12-2 Etiology of AS | ||||||||||||||||||||||
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Progression of AS is poorly understood; the latent phase is prolonged.
-
Rate of progression
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The onset of symptoms marks an important transition with a marked decline in survival (50% survival over 2, 3, and 5 years for patients with CHF, syncope, and exertional angina, respectively).16
-
Presence of symptoms may be difficult to gauge, especially in sedentary/elderly individuals.
-
Systolic ejection murmur is heard best in the aortic area/apex radiating to neck and right clavicle.
-
Gallavardin phenomenon (disappearance of the murmur over the sternum and reappearance over the apex, mimicking mitral regurgitation (MR))
-
Intensity of murmur does not accurately reflect severity of stenosis.
-
Later peaking murmur is associated with worsening severity of stenosis.
-
S2 is absent, single, paradoxically split in severe AS.
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Pulsus parvus et tardus (slow rising arterial pulse with reduced peak) in severe AS
-
Chest x-ray can show dilated proximal ascending aorta (poststenotic dilatation) and calcification of cusps on lateral films.
-
Electrocardiogram
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– Usually normal sinus rhythms (NSR), but AF is common in elderly AS patients
-
– Complete heart block may occur in calcific AS
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– Left atrial enlargement present in 80% of patients
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– LVH with secondary ST-T changes
-
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Echo
-
– Useful for diagnosis, determining severity (AVA, velocity, gradient; see Table 12-1)
-
– AVA is determined using the continuity equation (conservation of mass).
-
– Peak pressure gradient is determined using Continuous Wave (CW) Doppler.
-
-
Recommendations for serial studies (in the absence of symptoms)1
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Mild: Every 5 years
-
Moderate: Every 2 years
-
Severe: Every 6 months to 1 year
-
Contraindicated in symptomatic patients
-
Should be considered in patients severe AS, with unclear symptom status
-
Guidelines recommend consideration for surgery in asymptomatic patients with abnormal response to exercise (symptoms, <20 mm Hg increase in BP, ST depression, and/or complex ventricular arrhythmias).21
-
Employed in patients with AS, depressed LVEF with two primary goals
-
DSE can help distinguish severe stenosis from pseudo (flow dependent) AS.22
-
DSE can help to identify patients with pre-operative cardiac reserve (increase in stroke volume by >20%, or in mean transvalvular gradient of 10 mm Hg) as this subset of patients with low EF tends to have better outcomes (surgical mortality of 6% vs. 33%).23
-
Catheterization is used to assess coronary anatomy (prior to surgery).
-
Catheterization used to confirm/clarify diagnosis, severity by determining transvalvular gradient (simultaneous aortic, LV pressures are most accurate) and calculation of AVA by Gorlin formula or Hakki formula.
-
The gradient is dependent on transvalvular flow, so errors occur in patients with low cardiac output.
-
Dobutamine can be used to distinguish pseudostenosis from true anatomically severe AS.
-
Identify patients that warrant surgery with close monitoring for onset of symptoms.
-
Medical therapy has a limited role in providing a survival benefit or slowing progression.
-
Identify subset of asymptomatic severe AS patients at risk for SCD and/or onset symptoms that would require surgery in the near future.
-
No randomized controlled data support the strategy of referring “high-risk” patients with asymptomatic severe AS for AVR, but this is a Class II recommendation (see Table 12-3).
-
Antibiotic prophylaxis is indicated if high risk for endocarditis (see Chapter 13).26
-
Afterload agents are considered to be contraindicated because of concern over hemodynamic collapse (supporting data is lacking).
-
Considered to be contraindicated because of concern over hemodynamic collapse (supporting data is lacking)
-
ACE inhibitors are well tolerated.29
-
Data on the role of statins in slowing progression of AS is conflicting.
-
A single randomized controlled trial showed no effect of statins on progression of AS.36
-
Several randomized controlled trials of statins in AS are pending.
TABLE 12-3 Indications for AVR in AS | |||||||||||||||||||||||||||||||||
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AVR is the only effective treatment for symptomatic AS.
-
Symptoms/high risk features are the chief indications for AVR.
-
Operative mortality for AVR ˜5% to 30% depending on the patient population
-
Predictors of higher operative mortality and lower late survival: CHF, low LVEF, chronic kidney disease, urgent procedures, and need for concomitant CABG or MVR39
-
Outcomes similar in patients with preserved LV function and with moderate LV dysfunction
-
Provocative testing (DSE) can identify patients with contractile reserve; this subgroup may have better surgical outcomes.23
-
Surgical mortality is very high (30%-50%) in patients with severe AS and decompensated heart failure who are taken directly to surgery42 (balloon valvuloplasty and medical optimization are important bridge therapies).
-
In patients with severe AS who need surgical intervention, but are poor candidates, percutaneous AVR may represent a safe, viable alternative.43
-
Aortic regurgitation (AR) is due to ineffective coaptation of aortic cusps.
-
The prevalence of chronic AR increases with age; the majority of patients with AR have trace or mild AR.44
-
Grading of severity is based on several qualitative and/or quantitative measures. (See Table 12-4.)
-
AR can be due to primary valvular disease and/or aortic pathology (see Table 12-5).
-
AR can be acute or chronic, and the clinical presentation of each entity is distinct.
-
Chronic AR is more common than acute AR.
-
Acute AR is commonly caused by endocarditis, aortic dissection, and trauma.
-
Chronic AR is usually due to degenerative, aortic root, congenital abnormalities.
-
Large regurgitant volume into a nondilated LV leads to an abrupt increase in LV end diastolic pressure (LVEDP).
-
Compensatory tachycardia usually insufficient to maintain cardiac output
-
Poor hemodynamic tolerance: LVEDP equalizes with diastolic aortic pressure with subsequent pulmonary edema and cardiogenic shock.
TABLE 12-4 Grading of severity of AR | ||||||||||||||||||||||||||||||||||
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TABLE 12-5 Etiology of AR | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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-
Combined volume and pressure overload on the LV
-
Volume overload due to regurgitant volume
-
Pressure overload due to increased afterload (hypertension [HTN] from increased aortic stroke volume)
-
Three compensatory mechanisms initially preserve cardiac output: Increased LV end diastolic volume; increased chamber compliance; LVH (eccentric/concentric).
-
Compensated phase can last for years/decades.
-
Eventually, progressive LV dilation and LV systolic dysfunction lead to CHF.
-
Patients with acute AR present with marked dyspnea and pulmonary edema.
-
Patients with chronic AR can be asymptomatic for many years.
-
Angina without structural coronary artery disease is due to decreased coronary perfusion (due to high LVEDP).
-
Exertional dyspnea is the most common presenting symptom in chronic AR (late stage).
-
Syncope and sudden cardiac death are rare in absence of other symptoms.
-
Progression of AR results from complex interplay of multiple variables.
-
Mild AR: Minimal data on natural history; Most patients with mild AR probably do not progress to severe AR.
-
Moderate to severe AR
-
Asymptomatic patients with normal systolic function
-
– Unlike AS, onset of symptoms is not the only important factor
-
Asymptomatic patients with systolic dysfunction
-
– Majority will need AVR in 2 to 3 years
-
Symptomatic patients
-
– No contemporary studies, but outcomes are poor with medical therapy
-
-
-
The high-frequency decrescendo blowing diastolic murmur is heard best over the left lower sternal border (LLSB) through stethoscope’s diaphragm with patient sitting upright during forced expiration.
-
Murmurs that are louder over right lower scapular border (RLSB) are more likely due to aortic root/ascending aorta pathology, rather than primary valve abnormalities.
-
Duration of murmur correlates with severity (mild AR – short murmur; severe AR – typically holodiastolic).
-
In acute AR, the diastolic murmur and peripheral signs (see Table 12-6) may be absent (the only clue may be absent S2 with hypotension/pulmonary edema).
-
Austin Flint murmur (mid-late diastolic rumble that resembles MS – due to vibration from AR jet striking the mitral valve)
-
Pulse: High-amplitude, rapidly collapsing pulse (waterhammer pulse)
-
Chest x-ray can be normal or demonstrate pulmonary edema, cardiomegaly, or dilated aorta.
-
ECG shows LAD, LVH and signs of LV diastolic volume overload (high QRS amplitude and tall T waves with ST depression), and conduction abnormalities.
-
Assessment of anatomy of aortic leaflets, aortic root, LV size/function, and severity of AR
-
Estimation of severity is based on color flow and Doppler parameters (Table 12-4)
-
Supportive findings:
-
– Early mitral valve closure by M-Mode (can be masked by tachycardia)
-
– AR pressure half time: Mild >500 milliseconds and severe <200 milliseconds (confounded by filling volumes and diastolic function)
-
– Holodiastolic flow reversal in descending aorta reflective of at least moderately severe AR
-
-
Recommendations for serial studies in asymptomatic patients
-
– Mild AR and normal LV size and function: Every 2 to 3 years
-
– Patients with LV dilation: Every 6 to 12 months
-
– Patients with advanced LV dilation (LVIDs >50 mm, LVIDd >70 mm): Risk of progression 10%-20%/year;46 studies every 4-6 mos.
-
– Associated aortic root disease: Monitoring of aortic root size
-
TABLE 12-6 Auscultatory and peripheral findings in severe AR: A glossary of eponyms | ||||||||||||||||||||||
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