Introduction Exercise Testing in Patients with Valvular Heart Disease

The Big Heart Disease Lie

Treatment for Cardiovascular Disease

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Exercise testing (ET) has been the cornerstone in the diagnosis and prognostic evaluation of coronary artery disease (see Chapter 14).12 Even in apparently healthy men exercise testing provides important prognostic informations.3 Although ET was recently recommended in the management of asymptomatic patients with valvular heart disease (VHD),4,5 this recommendation is based on a small database. In the Euro Heart Survey on Valvular Heart Disease of the European Society of Cardiology, exercise testing was used in less than 8% of 5001 patients, evaluated in hospital or as an outpatient in 27 European countries.6 The reasons for performing exercise testing in these patients are listed in Table 16-1.

There are several explanations for the infrequent use of exercise testing in patients with VHD. Previously exercise testing was used to diagnose coronary artery disease also in adult patients with VHD, particularly in patients with aortic stenosis. But because of the occurrence of false-positive tests among adult patients with VHD this is considered a class III indication in the ACC/AHA Recommendations for exercise testing for the diagnosis of coronary artery disease (CAD) in patients with VHD.1,7 Nonetheless ET is still used for this purpose as shown in Table 16-1. The incidence of false-positive tests in these patients is attributed to left ventricular hypertrophy (LVH) and/or repolarization disturbances at rest. Yet many patients with moderate-severe valve lesions may have a normal

ECG and no severe LVH. In these patients the production of severe ST-segment depression (>2 mm) most likely indicates a pathological reaction which requires further diagnosis, even if it may not indicate associated CAD.

A further reason for the infrequent use of ET in patients with VHD is the fact that until recently patients with valvular heart disease were operated on only after severe symptoms had occurred, typically NYHA class III or IV; thus in this stage of the disease there is no need for further exercise testing to induce symptoms or hemodynamic alterations. The treatment in these patients is unanimously agreed upon and consists of valve surgery.

In the 2002 update of the AHA guidelines, assessment of functional capacity and symptomatic responses was considered a class I recommendation only in patients with aortic insufficiency and a history of equivocal symptoms.1

Yet exercise testing can also be of value in patients with atypical symptoms in other types of valve disease, particularly in the elderly in whom the symptomatic status is difficult to assess because of inactivity.

With the widespread availability of Doppler echocardiography, increasingly asymptomatic or mildly symptomatic patients are being diagnosed for whom exercise testing has become important to assess functional capacity objectively, and to determine if symptoms occur during exercise and if pathological hemodynamic responses (e.g. inadequate blood pressure increase) appear during exercise. This information is of importance

Table 16-1. Reasons for performing exercise testing (in 70% bicycle exercise tests) in 8% of all patients with VHD


Detection of coronary artery disease


Assessment of functional capacity in patients with no or


equivocal symptoms

Prior to allowing strenuous exercise


Prognostic evaluation in the presence of left ventricular



Routine basis


Source: Lung, 2003.6 With permission from Oxford University Press and European Society of Cardiology.

Source: Lung, 2003.6 With permission from Oxford University Press and European Society of Cardiology.

in the decision on medical or surgical therapy and for advice concerning exercise and leisure time activities (Table 16-2).

The occurrence of hypotension during exercise testing in asymptomatic patients with VHD is also an important indicator of hemodynamic impairment. It is not specific for patients with valvular heart disease, since it has been described in patients with CAD8,9 and in hypertrophic obstructive cardiomyopathy.1012

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