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A 71-year-old woman with a history of longstanding hypertension, diabetes mellitus, and obesity presents for evaluation of dyspnea on exertion. Her symptoms started about 3 years ago and gradually worsened over the past 2 years. She reports shortness of breath with mild physical activities, such as climbing less than 1 flight of stairs, and even with walking only few steps carrying her laundry basket. She sleeps on 2 pillows and reports occasional bilateral ankle edema. She denies resting or exertional chest pain. A 12-lead electrocardiogram demonstrated normal sinus rhythm, mild left ventricular hypertrophy, and nonspecific ST changes. A transthoracic echocardiogram showed mild left ventricular concentric hypotrophy with preserved ejection fraction (65%). Mitral inflow Doppler parameters were normal, with septal annual E′ velocity of 8 cm/s. Her right ventricular function was normal, with a resting right ventricular systolic pressure of 37 mm Hg. Pulmonary function test demonstrated mild restrictive pattern.
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She was referred by her internist for an exercise stress echocardiogram. She exercised 3 minutes on the Bruce protocol and stopped due to severe dyspnea. She demonstrated a hypertensive response to exercise and did not reach her target heart rate. At rest, her blood pressure was 141/85 mm Hg and her heart rate was 70 bpm. At peak exercise, her blood pressure was 188/110 mm Hg and her heart rate was 96 bpm. Peak stress echocardiographic images demonstrated normal wall motion augmentation in all segments. Due to persistent symptoms, coronary angiography was performed and showed mild nonobstructive coronary artery disease and an left ventricular end-diastolic pressure of 14 mm Hg.
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Her medications included hydrochlorothiazide 25 mg/d orally and amlodipine besylate (Norvasc) 10 mg/d orally. Her cardiovascular exam was unremarkable with the exception of mild ankle edema bilaterally. Laboratories values demonstrated that complete blood count, serum electrolytes, and kidney function were within normal limits, and notably, her brain natriuretic peptide (BNP) was 87 pg/mL (normal range, <100 pg/mL).
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She underwent a right heart catheterization that showed the following: right atrium: 8 mm Hg; pulmonary artery (PA): 34/13 mm Hg; and pulmonary capillary wedge pressure (PCWP): 15 mm Hg. She was subsequently referred to a heart failure program at a tertiary care center where an exercise hemodynamic study was performed and demonstrated significant exercise-induced elevation in pulmonary and wedge pressures (peak exercise PA: 47/27 mm Hg; PCWP: 28 mm Hg). She was diagnosed with heart failure with preserved ejection fraction (HFpEF) and enrolled in an investigational trial evaluating the safety and clinical benefits of an interatrial shunt device (IASD) aimed at relieving excessive left atrial pressure, which is a common physiopathologic pathway in HFpEF symptomatology. Pre- and post-IASD® hemodynamics are summarized in Figures 6-1 and 6-2.
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