Aortic stenosis pathophysiology

Aortic Stenosis Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Aortic Stenosis from other Diseases
Epidemiology and Demographics
Risk Factors
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Cardiac Stress Test
Electrocardiogram
Chest X Ray
CT
MRI
Echocardiography
Cardiac Catheterization
Aortic Valve Area
Aortic Valve Area Calculation
Treatment
General Approach
Medical Therapy
Surgery
Percutaneous Aortic Balloon Valvotomy (PABV) or Aortic Valvuloplasty
Transcatheter Aortic Valve Replacement (TAVR) TAVR vs SAVR Critical Pathway Patient Selection Imaging Evaluation Valve Types TAVR Procedure Post TAVR management AHA/ACC Guideline Recommendations
Follow Up
Prevention
Precautions and Prophylaxis
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Aortic stenosis pathophysiology On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Aortic stenosis pathophysiology All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Aortic stenosis pathophysiology
CDC on Aortic stenosis pathophysiology
Aortic stenosis pathophysiology in the news
Blogs on Aortic stenosis pathophysiology
Directions to Hospitals Treating Aortic stenosis pathophysiology
Risk calculators and risk factors for Aortic stenosis pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editors-In-Chief: Claudia P. Hochberg, M.D. [2], Abdul-Rahman Arabi, M.D. [3], Keri Shafer, M.D. [4], Priyamvada Singh, MBBS [5], Mohammed A. Sbeih, M.D. [6]; Assistant Editor-In-Chief: Kristin Feeney, B.S. [7]

Overview

Aortic stenosis results in the onset of a chronic pressure overload of the left ventricle. As the disease progresses, an aortic stenosis can result in compromised functional integrity of the surrounding mitral valve. The most common complication of aortic stenosis is left ventricular hypertrophy. Aortic stenosis could be subvalvular, supravalvular or at the level of the aortic valve.

Pathophysiology

When the aortic valve becomes stenosed, it can result in the formation of a pressure gradient between the left ventricle (LV) and the aorta . The more constricted the valve, the higher the gradient between the LV and the aorta. For instance, with a mild AS, the gradient may be 20 mmHg. This means that, at peak systole, while the LV may generate a pressure of 140 mmHg, the pressure that is transmitted to the aorta will only be 120 mmHg. So, while a blood pressure cuff may measure a normal systolic blood pressure, the actual pressure generated by the LV would be considerably higher.

In individuals with AS, the left ventricle (LV) has to generate an increased pressure in order to overcome the increased afterload caused by the stenotic aortic valve and eject blood out of the LV. The more severe the aortic stenosis, the higher the gradient is between the left ventricular systolic pressures and the aortic systolic pressures. Due to the increased pressures generated by the left ventricle, the myocardium (muscle) of the LV undergoes hypertrophy (increase in muscle mass). This is seen as thickening of the walls of the LV. The type of hypertrophy most commonly seen in AS is concentric hypertrophy, meaning that all the walls of the LV are (approximately) equally thickened.

In adults with AS, the obstruction develops gradually—usually over decades. During this time, the left ventricle adapts to the systolic pressure overload through a hypertrophic process. However, if the hypertrophic process is inadequate and relative wall thickness does not increase in proportion to pressure, wall stress increases and the high afterload causes a decrease in ejection fraction.