A 65-year-old man presents to his primary care physician complaining of dyspnea, chest pain, and several syncopal episodes. His symptoms have worsened over the past few months and his third syncopal episode prompted this visit. On examination, a systolic ejection murmur is auscultated with an ejection click in the right second intercostal space. Rales are present at the lung bases. He has a history of rheumatic fever in his twenties. Which of the following might explain the angina pectoris in this patient?
The angina pectoris seen in aoic stenosis is caused by left ventricular hyperophy. The ventricle must generate greater pressures to overcome the occluded outflow tract, and hyperophy occurs. This contributes to cardiac ischemia in several ways. An increased myocardial mass increases myocardial oxygen demand, while the increased wall tension decreases perfusion. The myocardium is perfused during diastole, and coronary perfusion relies on this relaxation. When mural diastolic pressures remain elevated in hyperophy, perfusion is limited and ischemia results. Hyperophy does not accelerate atherosclerosis. Pulmonary hypeension seen in aoic stenosis, results in pulmonary edema and a thus a mild hindrance to alveolar gas exchange. One would not expect the PO2 to decrease enough to cause angina. Stenotic valves do not occlude the coronary aeries. Ref: Clark M.B., Friedewald W.T. (2011). Chapter 113. Insurance Issues for Patients with Hea Disease. In V. Fuster, R.A. Walsh, R.A. Harrington (Eds), Hurst's The Hea, 13e.
Increased ventricular wall tension limits perfusion
Left ventricular hyperophy accelerates atherosclerotic disease
Pulmonary hypeension decreases the PO2 of aerial blood
Stenotic valves occlude the coronary aeries