Aortic stenosis (AS) refers to a narrowing of the valvular orifice, restricting flow from the left ventricle into the ascending aorta during systole. Etiologies of AS include senile degeneration (calcific), congenital bicuspid or unicuspid valves, and, rarely in North America, rheumatic disease.

1. Pathophysiology
1. A narrowing of the aortic valve orifice leads to restriction of flow from the left ventricle into the ascending aorta. This causes increased left ventricular (LV) chamber pressures, resulting in increased LV wall tension, myocardial oxygen demand, and compensatory LV concentric hypertrophy with increased susceptibility to ischemia and arrhythmias.
2. Adequate coronary perfusion pressure is vital and dependent on maintenance of diastolic pressure through preservation of systemic vascular resistance.
3. Increasing LV wall thickness subsequently leads to diastolic dysfunction with impairment of active relaxation and passive ventricular filling during diastole.
2. Diagnosis
1. Physical exam: Auscultation reveals a loud, late-peaking systolic murmur best heard at the right upper sternal border, radiating to the carotids, with delayed carotid upstroke.
2. Symptoms: Patients present with dyspnea on exertion, angina, or presyncope/syncope. The onset of symptoms strongly correlates with disease progression and dramatic increase in risk of sudden cardiac death.
3. Diagnosis: Echocardiography is used to diagnose AS but cardiac catheterization may also be used. Pressure gradients from simultaneous measurement obtained via catheterization are typically lower than peak-to-peak echocardiography-derived gradients.
3. Severe AS: Aortic valve area (AVA) less than 1.0 cm², or 0.6 cm/m² when normalized to body surface area (BSA) for extremes in body size. Mean gradients greater than 40 mm Hg, or peak flow velocity greater than 4 m/s. Pressure gradients are flow dependent and the severity may be underestimated in patients with low cardiac output or decreased LV systolic or diastolic function.
4. Hemodynamic Management
1. Heart rate: Reduction is essential in patients with severe AS. Tachycardia leads to significantly increased myocardial oxygen demand and decreased diastolic filling and perfusion time. Extremes of bradycardia can be deleterious because of fixed stroke volume of the thickened ventricle or when it leads to decreased coronary perfusion.
2. Rhythm: Sinus rhythm becomes imperative as the hypertrophied left ventricle becomes dependent on atrial contraction to maintain LV diastolic filling. In the setting of impaired LV relaxation, up to 40% of LV end-diastolic volume is contributed by atrial contraction.
3. Afterload: Hypotension is poorly tolerated and should be treated immediately because of the high susceptibility of the hypertrophied myocardium to ischemia. First-line treatment is a pure vasoconstrictor such as phenylephrine to avoid tachycardia while improving coronary perfusion. In patients with decompensated heart failure and severe AS, afterload reduction can be very carefully titrated with intensive hemodynamic monitoring to improve forward flow. In moderate or asymptomatic AS, hypertension can be treated following standard medical guidelines.
4. Preload: Diastolic dysfunction from concentric hypertrophy may require elevated filling pressure for adequate stroke volume. However, in decompensated AS, aggressive fluid administration may lead to pulmonary edema.
5. Contractility: Inotropic support may be needed in decompensated severe AS. However, inodilators such as dobutamine and milrinone can lead to marked reduction in systemic blood pressure and tachyarrhythmias.
5. Treatment
1. For mild to moderate asymptomatic AS, medical therapy aimed at blood pressure and heart rate control following established guidelines is generally sufficient.
2. The definitive treatment for severe AS is aortic valve replacement (AVR). Indications for surgical AVR (SAVR) or transcatheter AVR (TAVR) include symptomatic severe AS or severe AS with heart failure. SAVR is recommended for patients who are younger than age 65 and in those with asymptomatic severe AS with rapid progression. Currently, TAVR is recommended in patients who meet indications for AVR but are age 80 or older or at high-to-prohibitive surgical risk but with an expected survival of greater than 12 months. The choice between SAVR and TAVR in all other patients should be made as part of shared decision-making with a multispecialty team.
3. Percutaneous balloon dilation: results in a modest reduction in the severity of AS but is often complicated by severe aortic regurgitation (AR), restenosis, and clinical deterioration. Percutaneous aortic balloon dilation as a bridge to AVR is controversial. Palliative balloon dilation is not recommended because of the associated morbidity and lack of improved mortality.
6. Postoperative AS Treatment Care: Although LV outflow resistance and LV cavity pressures should improve following AVR, LV hypertrophic remodeling may not resolve for months. Persistent LV hypertrophy requires higher filling pressures to maintain cardiac output and the thickened myocardium remains susceptible to ischemia at low coronary perfusion pressures.
7. Hypertrophic Obstructive Cardiomyopathy (HOCM): HOCM is subvalvular dynamic obstruction of the left ventricular outflow tract (LVOT) caused by regional hypertrophy of the myocardium. Patients with HOCM are prone to lethal ventricular arrhythmias. Dynamic LVOT obstruction can lead to refractory hypotension and is exacerbated by ventricular underfilling, increased inotropy, decreased afterload, and tachycardia. Acute management includes increasing preload, increasing afterload with pure α-agonists such as phenylephrine, and administration of β-blockers, such as esmolol, to decrease inotropy and chronotropy.