A 52-year-old woman comes to the office due to several years of shortness of breath with exertion. She describes her symptoms as progressive. Recently, the patient has barely been able to walk a block without becoming out of breath. Occasionally, she becomes dyspneic even at rest. She has noticed puffiness of both ankles at the end of the day. The patient denies any palpitations, chest pain, weight loss, lightheadedness, or syncope. She emigrated from Mexico at age 25. Medical history is unremarkable. On physical examination, the patient appears comfortable. Blood pressure is 131/78 mm Hg and pulse is 86/min and regular. With the patient on her left side, an early diastolic heart sound is heard followed by a diastolic rumble. Which of the following are the most likely hemodynamic findings in this patient?

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Explanation: 11ec25c8_d872_ecc8_bc81_435c5e6f1b53_MD0003_00 This patient's progressive exertional dyspnea and early diastolic sound (ie, opening snap) followed by a rumbling diastolic murmur are consistent with mitral stenosis (MS). MS usually occurs in the setting of underlying rheumatic heart disease; in the United States it is most frequently seen in patients who emigrated from Latin America, Africa, or Asia. Progressive dyspnea on exertion is the most common presenting symptom. The hemodynamic alterations that occur with MS result from restricted diastolic filling of the left ventricle. As the severity of the stenosis worsens, there is increased left atrial pressure that leads to left atrial dilation. Consequent increased pulmonary artery (PA) pressures (systolic and diastolic) then occur via 2 mechanisms: The passive (or postcapillary) component of pulmonary hypertension is most prominent and results from transmission of elevated pressure backward from the left atrium to the pulmonary veins, pulmonary capillaries, and pulmonary arteries. Clinically, this process is typically evidenced by pulmonary edema and its associated symptoms (eg, orthopnea, paroxysmal nocturnal dyspnea, hemoptysis), as well as peripheral edema. The reactive (or precapillary) component of pulmonary hypertension is only sometimes present and occurs independent of left atrial pressure. In this process, MS triggers endothelin-mediated pulmonary arteriolar vasoconstriction and pathologic vascular remodeling through a poorly understood mechanism. Left ventricular (LV) diastolic pressure is generally unaffected in MS as the left ventricle is downstream of the pathologic stenosis. In severe MS, LV diastolic pressure may be lower than normal. (Choice A) Increased LV diastolic and PA systolic and diastolic pressures occur in pulmonary hypertension that is secondary to LV failure (Group 2 pulmonary hypertension). MS is a unique cause of Group 2 pulmonary hypertension in that LV diastolic pressure remains normal. Group 2 (Choice C) Reduced pulmonary arterial compliance, as occurs with age, increases PA systolic pressure and has little effect on PA and LV diastolic pressures. (Choice D) Increased LV diastolic pressure with normal PA pressures occurs in early LV failure, before the elevated pressures are transmitted back to the pulmonary circulation and clinical decompensation occurs. (Choice E) Normal PA pressures are not expected in this patient with symptomatic evidence of advanced MS (eg, severe dyspnea on exertion, peripheral edema). Educational objective: The expected hemodynamic alterations of mitral stenosis are elevated pulmonary artery pressures with normal left ventricular pressures. The pulmonary hypertension is primarily passive, resulting from transmission of elevated left atrial pressure backward to the pulmonary circulation. There may also be a reactive component involving endothelin-mediated pulmonary arteriolar vasoconstriction and remodeling. References: Mitral stenosis. (http://www.ncbi.nlm.nih.gov/pubmed/28613493)

A 52-Year-Old Woman Comes to the Office Due to Several