Stress Testing

For many years, it has been known that the symptoms of CAD depend on the balance of myocardial oxygen supply and oxygen demand. Most patients with CAD have normal resting blood flow, even in the presence of epicardial coronary artery stenosis. Myocardial perfusion pressure and blood flow are maintained by compensatory dilation of the coronary arterioles. During stress, myocardial oxygen demand increases, but myocardial blood flow cannot increase any further, leading to the development of ischemia. Myocardial ischemia results in progressive metabolic and functional alterations, including reduced relative perfusion, abnormal regional dia-stolic and systolic myocardial function, and electrical repolarization abnormalities. On these principles, various stress testing modalities attempt to indirectly establish the diagnosis of obstructive CAD by identifying one or several of these sequelae.

Stress may be accomplished by a number of methods, including exercise, pharmacologic maneuvers, and even mental tests. The choice depends on the specific patient. Whenever possible, exercise is the preferred modality, because the information obtained may be more easily related to functional limitations. The choice of electrocardiography (ECG), echocardiography, nuclear perfusion imaging, or magnetic resonance imaging (MRI) also depends on specific circumstances and local expertise. There is no clear superiority of any of these modalities. However, specificity appears to be higher with stress echocar-diography and sensitivity higher with nuclear perfusion imaging. Accordingly, many clinicians prefer stress echocardiography for individuals with lower pretest probability of having disease, and nuclear perfusion imaging for those with higher risk. Even though exercise ECG is less costly, this modality is less commonly used than imaging stress modalities because of its lower sensitivity and specificity. In addition, exercise ECG cannot localize the ischemic region, rendering it less useful as a guide for targeting revascularization.

Over the last decade, the prognostic utility of stress testing has been increasingly recognized. Exercise capacity, heart rate (HR) response, and the extent of ST depression, wall motion, and perfusion abnormalities are powerful predictors of outcome. Patients with decreased exercise tolerance and chronotropic incompetence during exercise stress testing have been shown to have increased adverse events, independently of other factors.

Chronotropic incompetence may be a marker of impaired autonomic dysfunction, which has been associated with cardiac events. Chronotropic response may be defined as the proportion of age-predicted maximal HR achieved, or the proportion of HR reserve used. The latter is defined as follows:

Proportion of HR Reserve Used =

It is the preferred method, because it has been shown to be largely independent of age, functional capacity, or exercise protocol. Chronotropic incompetence is defined as failure to use at least 80% of the HR reserve. Chronotropic incompetence has been shown to be associated with angiographic severity of CAD and increased mortality.

HR recovery is another index that appears to be related to autonomic tone. Most evidence suggests that a rapid reactivation of vagal tone is the major determinant of HR fall during the first 30 seconds to 1 minute after exercise. Unlike chronotropic incompetence, HR recovery is not significantly affected by the administration of P-blockers. HR recovery is calculated as the difference in HR at peak versus HR at 1 minute after exercise. A value of less than 12 beats/ min is considered abnormal. Patients evaluated for suspected or known CAD who have an abnormal HR recovery have a markedly increased mortality rate, independent of other risk factors.1

Although both impaired chronotropic response and HR recovery are powerful predictors of outcomes, it is unknown whether these factors are modifiable. Moreover, their association with mortality may be independent of the presence or severity of CAD. Therefore, they may have limited value in guiding diagnostic and therapeutic strategies.

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