A cardiac stress test is performed to evaluate the ability of arterial blood flow to the left ventricular heart muscle, to increase with exercise, as compared to resting blood flow rates, and some indication of overall physical fitness. The test is not capable of detecting the presence/absence of the atheroma lesions of atherosclerosis, thus usually misses disease which most commonly produces future angina or heart attack events. Also, it is not designed to evaluate the presence or influences of emotional stresses, even though these probably play a role in heart attacks.
The patient either walks on a treadmill or is given IV medications to "simulate exercise" while connected to an EKG machine, usually the standard 10 connections used to record a 12 lead EKG, and blood pressure response is repeatedly checked. Using EKG and blood pressure monitoring alone, the test is variously called a cardiac stress test, exercise stress test, exercise treadmill test or exercise EKG test. If radioactive isotopes are also used, then it is usually called a nuclear Thalium or Cardiolite (Technetium Tc99m Sestamibi) stress test (see gamma camera) or a Rubidium (Rubidium, RB-82) PET stress test.
The stress test is used to check both overall physical exercise capacity and is generally able to detect high grade, 75% or greater stenosis of the coronary arteries supplying the cardiac muscle. Stress tests are based on research, first done in the 1960s, which demonstrated that coronary artery blood flow rate must increase several fold and in proportion to heart muscle wall tension, reflected by systolic blood pressure and heart rate. Heart rate is the most important variable for stress testing because heart muscle contraction blocks heart muscle capillary blood flow during each heart beat and the time for blood flow between heart contractions progressively shortens as heart rate increases; e.g. about 40 seconds per minute, at heart rates of about 60 BPM, down to less than 10 seconds per minute, at heart rates in the 180 BPM range.
Generally, if one or more of the major epicardial heart arteries has a stenosis of 75% or greater, then abnormalities in the EKG waveforms, nuclear scan or echocardiographic images can usually be detected while the individual is at an elevated heart rate and exercise workload. Such high grade narrowing are typically responsible for angina episodes which reproducibly occur at a given level of exercise. However, most heart attacks result from rupture of atheroma lesions associated with only mild narrowing, 20-30% on average by IVUS clinical studies, thus the tests do not work well for detecting likelihood of impending heart attack.
Sometimes radioactive isotopes are injected intravenously at approximately one minute prior to the end of exercise. This protocol would be called a nuclear cardiac stress test. Either a gamma camera or PET imaging machine is used to create several 2 dimensional pictures, from different angles, of the radioactive particle decay emissions emanating from the radioactive isotopes which have been absorbed by the heart muscle cells from the blood after the intravenous injection. These images are compared with resting radioactive isotope emission distribution images for differences. Variations of nuclear cardiac stress tests include a thallium, technetium or rubidium (only used for PET machines) stress test, depending on the radioactive atomic element used.
Sometimes heart muscle size, contraction and wall motion is physically evaluated before and immediately after the exercise phase using an echocardiography machine. This protocol would be called a echocardiographic cardiac stress test.
Sometimes, if an individual is unable to perform enough physical exercise walking up an incline, then exercise is simulated using medications to stimulate faster heart rate, more intense contraction and/or peripheral arteriole vasodilatation.
Unfortunately, the value of such a test is limited, especially for asymptomatic individuals. According to United States data, 2004, for about 65% of men and 47% of women, the first symptom of cardiovascular disease is heart attack or sudden death (death within one hour of symptom onset.)
Stess testing, even if done in time, will detect only some of these people before symptoms, bebility or death. Stress testing methods, though more effective than a resting EKG, only detect high grade flow limitations; this assuming the testing is fully and aggressively perfomed. However, most artery flow disrupting events occur at locations with less than 50% lumen narrowing, a degree of stenosis too small for stress testing methods to detect.
Historically, through the mid-1980s, it was believed that detecting these high grade stenoses was the key to recognizing people who would have heart attacks in the future. However, there was also long-standing experience that some people could exercise all the way to maximum predicted heart rate, have no abnormal symptoms and completely normal stress test results, only to die of a massive heart attack within a few days to weeks. From the 1960s to 1990s, despite the success of stress testing indentifying many who were at high risk for heart attack, its failure to correctly identify many others was a conundrum, discussed in medical circles but unexplained.
The high grade stenoses which are detected by stress test methods are often, though not always, responsible for recurring symptoms of angina. Cardiac stress tests do detect some individuals who already have with very advanced coronary arterial disease and stenosis, some of whom did not recognize that they had advanced disease. However, stress test results are also sometimes abnormal in some people who do not have high grade narrowings of their coronary arteries as visualized by coronary angiography, which provides more accurate information and partial visualization of the coronary artery lumens. This was long viewed as a false positive result, with some of these individuals diagnosed as having Syndrome X, i.e meaning clear recurring signs of angina, though with smooth open coronary artery lumens on coronary angiography. The actual underlying issues responsible for this apparent conundrum are now better understood, see atheroma.
In the 1950s, heart attacks were commonly attributed to coronary thrombosis, a clot closure of a coronary artery, based on post mortem examination findings. In the late 1950s to early 1960s, this concept became replaced by the concept of stenosis based on the angiographic view of the lumens of the coronary arteries. In turn the angiographic view led to promotion of cardiac stress testing to detect stenoses, i.e. the severe ones more commonly present in people experiencing recurrent angina with physical exertion.
By the early to mid-1990s, it became more widely recognized that rupture of more rapidly evolving and unstable atheroma, hidden within the walls of the coronary arteries, even though they often produce little or no stenosis of the coronary lumen, is the primary event which produces most heart attacks, thus somewhat back to the coronary thrombosis view, though with more sophistication of understanding some of the complexities.
Unfortunately, cardiac stress tests are only capable of detecting high grade limitations of blood flow to the left ventricular heart muscle (provided the limitations are not matched by similar limitations to the opposite portion of the left ventricular muscle), such as may produce recurring angina, not the atheroma which produce heart attacks. Stess test methods do not evaluate blood flow to non-left-ventricle heart muscle. Thus stress test results are often falsely negative for far too many people, in terms of predicting who is at high risk for myocardial infarction, missing the majority destined to have a heart attack.
It has become clear that stress testing recognizes most people who will have heart attacks too late, unfortunately, after the disease and symptoms of the disease are very advanced. By the time the disease is this advanced, a majority of people have already had heart attacks or died.