A. Principles: irrespective of how acute or severe its presentation, severe aortic stenosis (AS) should always be considered a surgical disease.

1. Etiology: principally degenerative, with progressive, age-related calcification of normal trileaflet valve. Calcification of congenitally bicuspid valve may lead to presentation earlier in life. Rheumatic disease is increasingly less common.

2. Progression: on average, decrease of 0.1 cm²/year in valve area and increase of 7 mm Hg/year in mean transvalvular gradient, but rate of progression is highly variable and difficult to predict for individual patients. Older age, renal failure, hypertension, smoking, and hyperlipidemia associated with more rapid progression.

3. Clinical natural history: serious without symptoms but poor once even mild symptoms occur.

Progressive obstruction to left ventricular (LV) outflow, characterized by increased transvalvular velocity and pressure gradient and reduced effective aortic orifice. High afterload leads to compensatory, concentric LV hypertrophy, diastolic dysfunction, enhanced wall stress, and ultimate failure due to “afterload mismatch.” Timely intervention to relieve the mechanical obstruction often reverses ventricular dysfunction. Gradient is determined by valve area but also flow and aortic compliance, so that discordance among gradient-valve area is frequent.

1. Acute presentation: chest discomfort (angina), syncope, or heart failure.

2. Prognosis: average survival 1 to 3 years from symptom onset without surgical intervention.

3. Clinical examination: slow rising, late-peaking, low-amplitude carotid pulse (parvus et tardus). Harsh, late-peaking basal systolic ejection murmur and decreased (or absent) aortic component of S2; radiation of murmur to apex may mimic mitral regurgitation (MR) (Gallavardin phenomenon). Murmur may be diminished or absent in patients with reduced ejection fraction (EF) and progressive LV failure.

1. Electrocardiogram (ECG) and chest radiograph: LV hypertrophy nonspecific and not always present.

2. Echocardiography.

a. Two-dimensional echocardiography defines valve anatomy and calcification, LV hypertrophy, and systolic function.

b. Doppler echocardiography measures transaortic jet velocity, pressure gradient, and effective aortic orifice area (severe if 4 m/s or greater, 40 mm Hg [mean] or greater, and <1.0 cm², respectively). Gradient is often low despite tight valve area, even with normal LV function, requiring additional testing.

c. Patients with suspected AS, severe LV dysfunction, and low cardiac output (and hence low transvalvular pressure gradient) may benefit from dobutamine stress to clarify severity. With dobutamine, “true” severe AS gradient increases with unchanged valve area. Contractile reserve (>20% increase in stroke volume with dobutamine) predicts better outcome following aortic valve replacement (AVR), but AVR should not be denied to severe AS even without contractile reserve.

3. Computed tomography measures the large amount of aortic valve calcium in severe AS and permits evaluation of aortic root dimensions.

4. Cardiac catheterization verifies severity of AS in difficult cases and provides preoperative coronary angiography.

1. Intensive care unit management: cautious use of diuretics for heart failure to avoid excessive hypovolemia. Support blood pressure by all means in hypotensive patients. Caution with use of vasodilators, given propensity for hypotension (limited ability to augment cardiac output).

2. AVR, typically with surgery, is the lifesaving intervention. For patients with bicuspid aortic valve and ascending aortic dilation, concomitant ascending aortic replacement may be necessary.

3. Transcatheter aortic valve replacement (TAVR) is a reasonable alternative to surgical valve replacement for symptomatic patients with severe AS deemed inoperable or high risk for surgery.

4. Percutaneous intervention with balloon valvuloplasty is rarely useful, except as a palliative measure (risky and only transiently effective) or in patients with associated severe obstructive pulmonary disease to triage the AS component of dyspnea.

A. Etiology: primary valvular aortic regurgitation (AR) may be a sequela of endocarditis, bicuspid aortic valve, rheumatic heart disease, or valvular prolapse. It may also present as secondary complication of aortic root disease, aortic dissection, or aortic trauma. Chronic AR of any cause may present acutely with heart failure.

B. Pathophysiology: over time, chronic AR leads to both increased preload (increased end-diastolic volume) and increased afterload (increased systolic pressure and wall stress) with associated eccentric ventricular hypertrophy and LV cavity dilation. Progressive rise in end-systolic wall stress ultimately results in afterload mismatch, decline in systolic function, and heart failure.
Acute, severe AR abruptly reduces ventricular compliance, generating high filling pressures and heart failure despite low-intensity murmur.

C. Clinical presentation.

1. Symptoms: exertional dyspnea and heart failure; angina prominent late in course.

2. Physical examination: classically, wide pulse pressure reflecting large stroke volume, with associated diastolic decrescendo murmur at the base. Severity of AR correlates better with duration than intensity of murmur. Chronic, severe AR may be associated with a number of characteristic signs or arterial hyperpulsatility on physical examination including a “water hammer” (Corrigan) pulse, capillary pulsations (Quincke sign), and a variety of other auscultatory findings of wide pulse pressure. Functional mitral stenosis (MS) may be audible as an apical diastolic rumble (Austin-Flint murmur). Acutely, these signs may be absent, and the diastolic murmur is often unimpressive or short due to rapid equalization of aortic and LV end-diastolic pressures.

1. ECG and chest radiograph: Acutely, pulmonary edema may contrast with normal heart size and lack of ventricular hypertrophy. Chronic AR is associated with prominent ventricular enlargement (cor bovinum). Severe aneurysmal dilation of the aorta may suggest primary disease of the aortic root as a mechanism for AR.

2. Echocardiography.

a. May be helpful in evaluation of leaflet anatomy and motion as well as size and shape of the aortic root, to identify the cause of AR. Ventricular chamber dimensions, volumes, EF, and mass can also be assessed. Transesophageal echocardiography (TEE) may provide more detailed assessment where transthoracic imaging is inadequate.

b. Doppler and color-flow imaging show the regurgitant jet. AR may be quantified by calculating the effective regurgitant orifice area and regurgitant volume (severe if ≥0.30 cm² and ≥60 mL/beat, respectively).

3. Cardiac catheterization: may permit assessment of AR severity by aortography and coronary angiography may be performed in older patients (if no large vegetations) as a prelude to surgical intervention.

1. Afterload reduction with intravenous or oral vasodilators is central to the acute medical treatment of severe AR. Intra-aortic balloon counterpulsation and β-blockade are contraindicated.

2. Surgical valve replacement is indicated in chronic AR for symptomatic patients and those with evidence of LV dysfunction (EF ≤ 55%) or severe LV cavity dilation (end-diastolic dimension ≥75 mm Hg, endsystolic dimension ≥55 mm or ≥25 mm/m²). Valve replacement may be urgently required in patients with acute, severe AR, and heart failure. Aortic valve repair is sometimes possible. Periannular repair is necessary for perivalvular abscesses in patients with endocarditis.

3. For patients with AR secondary to aortic root disease, progressive aortic enlargement (beyond 50 mm in those with a bicuspid valve and beyond 55 mm in those with a tricuspid valve) may be an independent indication for surgical intervention to prevent rupture. In some patients, a structurally normal aortic valve may be preserved during surgical repair or replacement of the enlarged aortic root.

1. Primary mitral valve (MV) disease: due most commonly to myxomatous degeneration (e.g., MV prolapse), rheumatic heart disease, infective endocarditis, or annular calcification.

2. Ischemic or functional MR: most commonly due to valve tenting, secondary to chordal traction following progressive ventricular remodeling in patients with cardiomyopathy or previous myocardial infarction. Rarely a consequence of acute papillary muscle rupture, for example, following acute myocardial infarction.

1. Chronic, severe MR increases LV end-diastolic volume and promotes progressive eccentric hypertrophy, further distortion of the papillary muscle architecture, and additional MR. Progressive volume loading, with attendant rises in wall stress, overwhelms compensatory mechanisms and leads to myocardial failure.

2.

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