Aortic Stenosis

The triad of angina, syncope, and congestive heart failure represents the progression of symptoms associated with AS. These symptoms correlate directly with mortality; the 50% survival data for these symptoms are 5, 3, and 2 years from the onset of each symptom, respectively. Angina results from both increased demand and decreased supply of coronary blood flow. Increased muscle mass from LVH and the high-energy requirements to generate increased (high) systolic pressure combine to increase demand for coronary blood flow. In addition, insufficient supply secondary to decreased perfusion gradients and a decrease in coronary vasculature relative to the increased myocardial mass result in diminished relative myocardial blood supply. Therefore, up to one-third of patients with AS can have angina in the absence of significant coronary artery disease.

Aortic Insufficiency

Patients with AI have variable clinical presentations based primarily on the rapidity with which the left ventricular volume overload develops. When the volume increase occurs gradually, as in chronic AI, there is usually a long asymptomatic period. The onset of fatigue and dyspnea signals either reduced cardiac output or increased LVEDP, indicative of impairment of left ventricular contractile function. When AI occurs acutely, the ventricular compliance is unchanged; therefore, increased left ventricular diastolic volumes from regurgitant flow lead to rapid rises in LVEDP and the clinical picture of congestive failure.

Mitral Stenosis

In MS, the slow and progressive obstruction to flow across the MV leads to gradual increase in left atrial pressure and volume. Symptoms of pulmonary congestion result from elevations in left atrial pressures and not from poor left ventricular systolic function. Atrial fibrillation develops secondary to atrial dilation.

Mitral Regurgitation

The time course for the development of MR determines the severity of the symptoms. When the volume of regurgitant flow from the LV to the LA increases gradually, the LA compensates by gradual dilation. In contrast, the onset of acute MR can lead to rapid increases in left atrial pressures, severe pulmonary congestion, and congestive heart failure.

References

• Lilly LS. Valvular heart disease. In: Lilly LS, ed. Pathophysiology of Heart Disease: An Introduction to Cardiovascular Medicine. 7th ed. Wolters Kluwer; 2021:202-231.
• Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA guideline for the management of patients with valvular heart disease: executive summary: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2021;143:e35-e71.