Aortic regurgitation symptoms

Aortic Regurgitation Microchapters
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Varun Kumar, M.B.B.S.; Lakshmi Gopalakrishnan, M.B.B.S.

Overview

Aortic insufficiency can cause many symptoms such as dyspnea, weakness, and symptoms of congestive heart failure. Chronic aortic insufficiency maybe without symptoms for several years until decrease in the stroke volume and cardiac output due to heart failure progression.

History and Symptoms

Acute Aortic Insufficiency

In acute severe aortic regurgitation (AR), there is a sudden decrease in stroke volume and increase in left ventricular end diastolic volume and left ventricular end diastolic pressure which manifests as either sudden and severe dyspnea and/or chest pain, if there is an aortic dissection. Based on the history and symptoms, the cause of the acute symptoms can be suspected.

Type A aortic dissection:

• Chest pain of the following characteristics:
  • Sudden onset
  • Intense
  • Tearing and sharp
  • Worsened by deep breathing or cough
  • Relieved by sitting upright
• Unexplained syncope
• Previous history of:
  • Hypertension
  • Marfan syndrome
  • Connective tissue disorder

Infective endocarditis:

• Persistent fever
• New valvular regurgitation murmur
• Positive previous blood culture
• High risk factors:
  • Pre-existing cardiac abnormality
  • Prosthetic valve
  • Recent surgical or medical procedures
  • Intravenous drug use
  • Recent bacterial infection
• History of previous endocarditis

Symptomatic severe chronic AR:

• Previous history of aortic valve disease

Chronic Aortic Insufficiency

In chronic aortic regurgitation (AR), patients are usually asymptomatic for many years as the stroke volume is maintained by increased force of left ventricular contraction secondary to increased left ventricular preload as explained by Frank-Starling mechanism.

With progression of AR, the compensatory mechanisms begin to fail causing gradual enlargement of the left ventricle, thereby progressively increasing left ventricular end diastolic pressure, decreasing stroke volume and cardiac output leading to left ventricular failure manifesting as:

• Dyspnea on exertion
• Orthopnea
• Paroxysmal nocturnal dyspnea
• Palpitations (due to compensatory tachycardia)
• Chest pain (if left ventricular end diastolic pressure compromises coronary perfusion)

Once symptoms arise, cardiac function usually worsens more rapidly and mortality may exceed 10% per year.