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Noncardiac surgery in patients with aortic stenosis

Prashant Vaishnava, MD
Kim A Eagle, MD, MACC
Section Editor
Catherine M Otto, MD
Deputy Editor
Susan B Yeon, MD, JD, FACC


Risk models have identified severe aortic stenosis (AS) as a major clinical predictor of adverse outcomes [1]. Population studies from the United States and Europe have reported AS in approximately 1 to 2 percent of individuals 65 to 75 years old with prevalence increasing to 3 to 8 percent in individuals ≥75 years old [2-6]. In the Helsinki Aging study, nearly 3 percent of the individuals between 75 and 86 years of age had critical AS [3]. Patients with AS frequently have concurrent cardiovascular disease with approximately half of patients with AS aged 50 years and older having concomitant coronary heart disease [7,8]. (See "Clinical manifestations and diagnosis of aortic stenosis in adults" and "Evaluation of cardiac risk prior to noncardiac surgery" and "Valvular heart disease in elderly adults", section on 'Underlying atherosclerosis'.)

The presence of valvular disease has potentially important implications for perioperative management as well as perioperative risk. The perioperative considerations in patients with native aortic valve stenosis who are undergoing noncardiac surgery will be reviewed here. The perioperative management of patients with aortic regurgitation, mitral valve disease, and prosthetic heart valves is discussed elsewhere. (See "Noncardiac surgery in patients with mitral or aortic regurgitation" and "Medical management and indications for intervention for mitral stenosis" and "Overview of the management of patients with prosthetic heart valves" and "Antithrombotic therapy for prosthetic heart valves: Indications".)


Aortic stenosis (AS) results in fixed obstruction to left ventricular (LV) emptying. The stenotic process is usually gradual in onset and progression, giving the heart ample opportunity to adapt. The LV myocardium hypertrophies over time, resulting in the generation of greater pressure during systole, which forces blood past the fixed mechanical obstruction. As a result, the cardiac output and LV end-diastolic volume are maintained and patients can remain asymptomatic for a prolonged period of time, even with severe AS. (See "Clinical manifestations and diagnosis of aortic stenosis in adults" and "Natural history, epidemiology, and prognosis of aortic stenosis".)

However, the chronic pressure overload state that results in the compensatory concentric LV hypertrophy also reduces the compliance of the left ventricle. As a result, diastolic dysfunction develops over time, the end diastolic pressure of the LV increases, and patients eventually develop symptoms of chest pain or dyspnea. The concentric hypertrophy also reduces coronary flow reserve, rendering the patient more susceptible to ischemia in situations of increased myocardial oxygen demand, even in the absence of obstructive coronary artery disease [9]. In addition, due to fixed obstruction of the LV outflow tract, decreases in systemic vascular resistance can result in relative systemic hypotension and subsequent ischemia from reduced coronary perfusion. An additional potential cause of hypotension in patients with AS is elevated LV pressures causing mechanoreceptor stimulation and reflex bradycardia and/or systemic vasodilation. (See "Clinical manifestations and diagnosis of aortic stenosis in adults".)

Therefore, clinical deterioration can occur in patients with asymptomatic AS during the hemodynamic stress associated with noncardiac surgery (as well as other states that require augmentation of cardiac output such as infection, anemia, or pregnancy). The hemodynamic stress of noncardiac surgery is a combination of anesthetic and surgical stress.


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Literature review current through: Sep 2016. | This topic last updated: Jun 27, 2016.
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