What Doppler echocardiography and the E/A ratio reveal
Doppler echocardiography is used to further evaluate the characteristics of blood flow, showing the relationship among left ventricular (LV) relaxation, atrial pressure, atrial contraction, and blood flow velocity across the mitral valve during diastole. The peak velocity of blood flow during early diastole (called the “E wave”) and late diastole (the atrial contraction, or “A wave”) is measured and the E/A ratio (reflecting the transmitral blood flow pattern) is calculated (FIGURE).3
FIGURE
The E/A ratio* and what it reveals
A, atrial contraction; E, early passive filling; MVC, mitral valve closes; MVO, mitral valve opens.
*E/A ratio represents the relationship between the peak velocity of blood flow during early diastole (E wave) and late diastole (A wave).
Adapted from: Aurigemma GP, Gaasch WH. N Engl J Med. 2004.3
Normally, transmitral flow velocity is greater during early diastole than during atrial contraction, and the E/A ratio is approximately 1.5 (E>A). With early diastolic dysfunction, impaired relaxation prevents blood from flowing passively into the LV during early diastole. This causes reversal of the E/A ratio, which drops to <1 (E<A). As diastolic function worsens, atrial contraction is impaired, and left atrial pressure rises. The result: A reduction in the A wave amplitude and proportionally more blood flow during early diastole and a “pseudonormal” (E>A) ratio, with a greater difference between the E and A than is normally observed. This finding is an independent predictor of all-cause mortality in patients with asymptomatic HF.16
Cardiac catheterization. Invasive measurement of LV filling pressures is the gold standard for diagnosing HFPEF. If echocardiography does not lead to a clear diagnosis, cardiac catheterization can provide information about concomitant pulmonary hypertension and mechanical asynchrony that may contribute to symptomatic HF.1 When the diagnosis is uncertain, additional testing—eg, plasma brain natriuretic peptide (BNP), chest x-ray, or exercise testing—may be necessary to establish a diagnosis of symptomatic HF.
The diagnostic criteria developed by HFSA include clinical evidence of HF and:
- echocardiographic evidence of LV hypertrophy or left atrial enlargement (without atrial fibrillation) or
- evidence of diastolic dysfunction on Doppler echocardiography or cardiac catheterization.14
It is important to note that the diagnostic criteria have not been validated, and the sensitivity and specificity of the various clinical findings are not known.
CASE Carrie W, a 76-year-old woman referred to you by a colleague, presents for follow-up after being hospitalized for HF. She recalls feeling fatigue, chest pain, and out of breath with even minimal exertion before being admitted to the hospital.
You obtain her hospital records, which show that echocardiography found impaired LV relaxation based on a reversed E/A ratio and an EF of 65%. In addition, BNP was elevated, and a chest x-ray showed pulmonary vascular congestion. You note that her blood pressure was 175/103 mm Hg on admission and an EKG showed LV hypertrophy and sinus tachycardia, but no ischemia.
Before being hospitalized, Ms. W was taking extended-release metoprolol, aspirin, and lisinopril. The hospitalist added lovastatin and increased the daily dose of extended-release metoprolol from 25 to 100 mg.
What changes, if any, would you make in her medication regimen?
Diastolic dysfunction as chronic disease
Often asymptomatic, diastolic dysfunction should be thought of as a chronic progressive disease characterized by complex physiologic adaptations that vary over time (See “Staging heart failure: The clinical course of HFPEF”.13) Patients with HFPEF have a difficult time tolerating hemodynamic stress and any perturbation of afterload, heart rate, or ventricular function can precipitate an acute exacerbation.2 Clinical factors that precipitate acute decompensation of HFPEF—which we’ll discuss a bit later—include uncontrolled hypertension; atrial fibrillation; and noncardiovascular comorbidities such as lung disease, renal impairment, or sepsis.2
Staging heart failure: The clinical course of HFPEF13
The ACC/AHA staging system for HF can be applied to patients with HFPEF, both to classify disease severity and to track the progression of the disease. Patients at Stage A are at high risk of developing HF, but early and aggressive treatment of hypertension and other cardiovascular risk factors may delay or potentially prevent the onset of overt disease. Stage B refers to patients with known structural disease, such as a history of myocardial infarction or systolic or diastolic dysfunction, but no symptoms of HF.
Patients at Stage C have evidence of structural disease and symptoms of HF, such as fatigue, shortness of breath, or reduced exercise tolerance. This stage represents the spectrum of patients falling into New York Heart Association (NYHA) Class 1 through 3 categories. Finally, patients at Stage D—analogous to NYHA Class 4—have refractory HF, with marked symptoms even at rest despite maximal medical therapy.