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Cardiac stress test
Cardiac stress test
Cardiac stress test
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Cardiac stress test
A male patient walks on a stress test treadmill to have his heart's function checked.
Other namesCardiopulmonary exercise test
ICD-9-CM89.4
MeSHD025401
MedlinePlus003878

A cardiac stress test is a cardiological examination that evaluates the cardiovascular system's response to external stress within a controlled clinical setting. This stress response can be induced through physical exercise (usually a treadmill) or intravenous pharmacological stimulation of heart rate.[1]

As the heart works progressively harder (stressed) it is monitored using an electrocardiogram (ECG) monitor. This measures the heart's electrical rhythms and broader electrophysiology. Pulse rate, blood pressure and symptoms such as chest discomfort or fatigue are simultaneously monitored by attending clinical staff. Clinical staff will question the patient throughout the procedure asking questions that relate to pain and perceived discomfort. Abnormalities in blood pressure, heart rate, ECG or worsening physical symptoms could be indicative of coronary artery disease.[2]

Stress testing does not accurately diagnose all cases of coronary artery disease, and can often indicate that it exists in people who do not have the condition. The test can also detect heart abnormalities such as arrhythmias, and conditions affecting electrical conduction within the heart such as various types of fascicular blocks.[3]

A "normal" stress test does not offer any substantial reassurance that a future unstable coronary plaque will not rupture and block an artery, inducing a heart attack. As with all medical diagnostic procedures, data is only from a moment in time. A primary reason stress testing is not perceived as a robust method of CAD detection — is that stress testing generally only detects arteries that are severely narrowed (~70% or more).[4][5][6]

Stress testing and echocardiography

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A stress test may be accompanied by echocardiography.[7] The echocardiography is performed both before and after the exercise so that structural differences can be compared.

A resting echocardiogram is obtained prior to stress. The ultrasound images obtained are similar to the ones obtained during a full surface echocardiogram, commonly referred to as transthoracic echocardiogram. The patient is subjected to stress in the form of exercise or chemically (often dobutamine). After the target heart rate is achieved, 'stress' echocardiogram images are obtained. The two echocardiogram images are then compared to assess for any abnormalities in wall motion of the heart. This is used to detect obstructive coronary artery disease.[8]

Cardiopulmonary exercise stress testing

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Cardiopulmonary exercise test using a treadmill.

While also measuring breathing gases (e.g., oxygen saturation, maximal oxygen consumption), the test is often referred to as a cardiopulmonary exercise test. Common indications for a cardiopulmonary exercise test include evaluation of shortness of breath, workup before heart transplantation, and prognosis and risk assessment of heart failure patients.

The test is also common in sport science for measuring athletes' maximal oxygen consumption, V̇O2 max.[9] In 2016, the American Heart Association published an official scientific statement advocating that cardiorespiratory fitness, quantifiable as V̇O2 max and measured during a cardiopulmonary exercise test, be categorized as a clinical vital sign and should be routinely assessed as part of clinical practice.[10]

The CPX test can be done on a treadmill or cycle ergometer. In untrained subjects, V̇O2 max is 10% to 20% lower when using a cycle ergometer compared with a treadmill.[11]

Stress testing using injected nuclear markers

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A nuclear stress test uses a gamma camera to image radioisotopes injected into the bloodstream. The best known example is myocardial perfusion imaging. Typically, a radiotracer (Tc-99 sestamibi, Myoview or thallous chloride 201) may be injected during the test. After a suitable waiting period to ensure proper distribution of the radiotracer, scans are acquired with a gamma camera to capture images of the blood flow. Scans acquired before and after exercise are examined to assess the state of the coronary arteries of the patient. By showing the relative amounts of radioisotope within the heart muscle, the nuclear stress tests more accurately identify regional areas of reduced blood flow.[12]

Stress and potential cardiac damage from exercise during the test is a problem in patients with ECG abnormalities at rest or in patients with severe motor disability. Pharmacological stimulation from vasodilators such as dipyridamole or adenosine, or positive chronotropic agents such as dobutamine can be used. Testing personnel can include a cardiac radiologist, a nuclear medicine physician, a nuclear medicine technologist, a cardiology technologist, a cardiologist, and/or a nurse. The typical dose of radiation received during this procedure can range from 9.4 to 40.7 millisieverts.[13]

[edit]
Stress-ECG of a patient with coronary heart disease: ST-segment depression (arrow) at 100 watts of exercise. A: at rest, B: at 75 watts, C: at 100 watts, D: at 125 watts.

The American Heart Association recommends ECG treadmill testing as the first choice for patients with medium risk of coronary heart disease according to risk factors of smoking, family history of coronary artery stenosis, hypertension, diabetes and high cholesterol. In 2013, in its "Exercise Standards for Testing and Training", the AHA indicated that high frequency QRS analysis during ECG treadmill test have useful test performance for detection of coronary heart disease.[14]

  • Perfusion stress test (with 99mTc labelled sestamibi[15]) is appropriate for select patients, especially those with an abnormal resting electrocardiogram.
  • Intracoronary ultrasound or angiogram can provide more information but is invasive and carries the risk of complications associated with cardiac catheterization procedures.[16]

Diagnostic value

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The common approach for stress testing recommended by the American College of Cardiology[17][18] and the American Heart Association[19] involves several methods to assess cardiac health. These methods provide information for diagnosing and managing heart-related conditions. Two primary stress tests utilized are a treadmill test using ECG/electrophysiology metrics and nuclear testing, each have unique sensitivity and specificity values.

The treadmill test, employing the modified Bruce protocol,[20] demonstrates a sensitivity range of around 73-90% and a specificity range of around 50-74%. Sensitivity refers to the percentage of individuals with the condition correctly identified by the test, while specificity denotes the percentage of individuals without the condition correctly identified as not having it.[21] The nuclear stress test exhibits a sensitivity of 81% and a specificity ranging from 85 to 95%.[22]

To arrive at the patient's post test likelihood of disease, the interpretation of the stress test result necessitates the integration of the patient's pretest likelihood with the test's sensitivity and specificity. This method, initially introduced by Diamond and Forrester in the 1970s, provides an estimate of the patient's post-test likelihood of disease.[23][24] Stress tests have limitations in assessing the significance and nature of cardiac problems, they should be seen in context - as an initial assessment that can lead to a number of other diagnostic approaches in the broader management of cardiac diseases.[25]

According to data from the US Centers for Disease Control and Prevention (CDC) common first systems of coronary artery disease is a heart attack. According to the American Heart Association, a significant percentage of individuals, approximately 65% of men and 47% of women, present with a heart attack or sudden cardiac arrest as their first symptom of cardiovascular disease. Consequently, stress tests performed shortly before these events may not be highly relevant for predicting infarction in the majority of individuals tested.[26][27]

Contraindications and termination conditions

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Stress cardiac imaging is not recommended for asymptomatic, low-risk patients as part of their routine care.[28] Some estimates show that such screening accounts for 45% of cardiac stress imaging, and evidence does not show that this results in better outcomes for patients.[28] Unless high-risk markers are present, such as diabetes in patients aged over 40, peripheral arterial disease, or a risk of coronary heart disease greater than 2 percent yearly, most health societies do not recommend the test as a routine procedure.[28][29][30][31]

Absolute contraindications to cardiac stress test include:

Indications for termination: A cardiac stress test should be terminated before completion under the following circumstances:[33][34]

Absolute indications for termination include:

  • Systolic blood pressure decreases by more than 10 mmHg with increase in work rate, or drops below baseline in the same position, with other evidence of ischemia.
  • Increase in nervous system symptoms: Dizziness, ataxia or near syncope
  • Moderate to severe anginal pain (above 3 on standard 4-point scale[34])
  • Signs of poor perfusion,[33] e.g. cyanosis or pallor[34]
  • Request of the test subject
  • Technical difficulties (e.g. difficulties in measuring blood pressure or EGC[34])
  • ST Segment elevation of more than 1 mm in aVR, V1 or non-Q wave leads
  • Sustained ventricular tachycardia

Relative indications for termination include:

  • Systolic blood pressure decreases by more than 10 mmHg with increase in work rate, or drops below baseline in the same position, without other evidence of ischemia.
  • ST or QRS segment changes,[34] e.g. more than 2 mm[33] horizontal or downsloping[34] ST segment depression in non-Q wave leads, or marked axis shift
  • Arrhythmias other than sustained ventricular tachycardia e.g. Premature ventricular contractions, both multifocal or triplet; heart block; supraventricular tachycardia or bradyarrhythmias[34]
  • Intraventricular conduction delay or bundle branch block or that cannot be distinguished from ventricular tachycardia
  • Increasing chest pain
  • Fatigue, shortness of breath, wheezing, claudication or leg cramps
  • Hypertensive response (systolic blood pressure > 250 mmHg or diastolic blood pressure > 115 mmHg)

Adverse effects

[edit]

Side effects from cardiac stress testing may include[citation needed]

  • Palpitations, chest pain, myocardial infarction, shortness of breath, headache, nausea or fatigue.
  • Adenosine and dipyridamole can cause mild hypotension.
  • As the radioactive tracers used for this test are chemically carcinogenic, frequent use of these tests carries a small risk of cancer.[35]

Use of pharmacological agents to stress the heart

[edit]

Pharmacologic stress testing relies on coronary steal. Vasodilators are used to dilate coronary vessels, which causes increased blood velocity and flow rate in normal vessels and less of a response in stenotic vessels. This difference in response leads to a steal of flow and perfusion defects appear in cardiac nuclear scans or as ST-segment changes.[36]

The choice of pharmacologic stress agents used in the test depends on factors such as potential drug interactions with other treatments and concomitant diseases.

Pharmacologic agents such as adenosine, regadenoson (Lexiscan), or dipyridamole is generally used when a patient cannot achieve adequate work level with treadmill exercise, or has poorly controlled hypertension or left bundle branch block. However, an exercise stress test may provide more information about exercise tolerance than a pharmacologic stress test.[37]

Commonly used agents include:

Regadenoson or dobutamine is often used in patients with severe reactive airway disease (asthma or COPD) as adenosine and dipyridamole can cause acute exacerbation of these conditions. If the patient's asthma is treated with an inhaler then it should be used as a pre-treatment prior to the injection of the pharmacologic stress agent. In addition, if the patient is actively wheezing then the physician should determine the benefits versus the risk to the patient of performing a stress test especially outside of a hospital setting. Caffeine is usually held 24 hours prior to an adenosine stress test, as it is a competitive antagonist of the A2A adenosine receptor and can attenuate the vasodilatory effects adenosine.[citation needed]

Aminophylline may be used to attenuate severe and/or persistent adverse reactions to adenosine and regadenoson.[39]

History

[edit]

Cardiac stress testing, used since the 1960s, has a history rooted in the diagnostic and prognostic assessment of patients with suspected coronary artery disease. It has evolved to evaluate inducible myocardial ischemia as an indicator of adverse outcomes. The factors influencing mortality risk have changed over time due to decreasing angina symptoms, increasing prevalence of conditions like diabetes and obesity, and the rise in pharmacologic testing for patients unable to exercise during stress tests.[40]

See also

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References

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Revisions and contributorsEdit on WikipediaRead on Wikipedia

Cardiac stress test

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from Grokipedia
A cardiac stress test is a noninvasive diagnostic procedure that evaluates the heart's response to physical or pharmacological simulation of exercise, primarily to detect (CAD) by monitoring , , electrocardiogram (ECG) changes, and symptoms. It assesses how well the heart handles increased workload, identifying reduced blood flow to the heart muscle (myocardial ischemia) or arrhythmias that may not appear at rest. The primary purposes of a cardiac stress test include diagnosing CAD in patients with symptoms like or , evaluating the effectiveness of treatments such as medications or procedures for known heart conditions, determining the severity of heart disease, and assessing exercise tolerance to guide safe levels or preoperative risks. It is indicated for individuals with suspected myocardial ischemia, recent without prior , or worsening symptoms in those with established CAD. Recent advancements as of 2025, such as stress cardiac (MRI) for enhanced diagnosis and applications in ECG analysis, continue to improve the utility of these tests. There are several types of cardiac stress tests, tailored to patient needs and capabilities, including exercise-based, pharmacological, and imaging-enhanced variants. The procedure is conducted in a controlled medical setting with continuous monitoring to ensure safety. While generally safe, absolute contraindications include acute , , or severe .

Overview and Purpose

Definition and Principles

A cardiac stress test is a non-invasive or minimally invasive diagnostic procedure designed to evaluate the heart's function and blood flow by simulating physical or physiological stress, thereby increasing myocardial oxygen demand to uncover abnormalities such as ischemia, arrhythmias, or other dysfunctions that may not be apparent during rest. This approach allows clinicians to assess how the cardiovascular system responds under conditions of elevated workload, revealing potential limitations in coronary or electrical stability. The underlying physiological principles of the cardiac stress test revolve around the heart's response to increased , which elevates , , and myocardial oxygen consumption through activation and enhanced preload. In healthy individuals, rises via the Frank-Starling mechanism, where greater venous return stretches myocardial fibers to augment , combined with effects on . However, in (CAD), this heightened often exceeds the available oxygen supply due to stenotic vessels, resulting in supply- mismatch that manifests as myocardial ischemia; this can be detected through electrocardiographic (ECG) changes like ST-segment depression, regional wall motion abnormalities, or perfusion defects. These principles, rooted in the early 20th-century observations of the Frank-Starling law and the of CAD, underscore the test's ability to provoke and identify latent cardiac vulnerabilities. Key components of a cardiac stress test include an initial baseline assessment of resting , ECG, and symptoms; induction of stress, commonly via exercise such as walking to replicate natural exertion; continuous monitoring of ECG, , , and oxygenation throughout the procedure; and a recovery phase to observe return to baseline and any delayed abnormalities. This structured framework ensures safe provocation of stress while capturing dynamic responses, with exercise serving as the preferred method when feasible due to its physiological fidelity.

Clinical Indications and Utility

Cardiac stress testing is primarily indicated for the evaluation of patients presenting with suggestive of stable angina, particularly those with an intermediate pretest probability of obstructive (CAD), where it aids in confirming or excluding ischemia as the cause. According to the 2021 AHA/ACC Chest Pain Guideline, is recommended (Class 1, Level of Evidence B-NR) for intermediate- to high-risk patients with stable chest pain and no known CAD to diagnose myocardial ischemia and guide management. This approach integrates Bayesian principles, using pretest probability models such as the Diamond-Forrester or CAD Consortium scores—based on age, sex, and chest pain characteristics—to select appropriate candidates, as low-probability patients may defer testing while high-probability cases warrant direct angiography. Additional key indications include risk stratification following acute (MI) and preoperative assessment for noncardiac in elevated-risk patients. In stable patients post-non-ST-elevation (NSTEACS), predischarge is useful for identifying residual ischemia and stratifying long-term risk, provided symptoms have resolved and the patient is clinically stable, typically at least 12-24 hours for and 2-5 days after for NSTEMI; the 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With recommends noninvasive prior to hospital discharge in select low- to intermediate-risk patients without prior invasive . For perioperative , the 2024 AHA/ACC Guideline recommends (Class 1) in high-risk patients (e.g., ≥1 with poor functional capacity <4 metabolic equivalents) undergoing intermediate- or high-risk to detect significant ischemia that may alter management. The test holds utility in specific populations, such as asymptomatic individuals with multiple CAD risk factors like diabetes or hypertension, where it may support risk assessment in select cases per appropriate use criteria, though routine screening is not endorsed without symptoms or functional changes. It also facilitates monitoring the efficacy of revascularization or medical therapy in patients with chronic coronary disease (CCD) who experience persistent symptoms despite guideline-directed medical therapy (GDMT), as outlined in the 2023 AHA/ACC CCD Guideline (Class 1, Level of Evidence B-NR). Guideline frameworks from the ACC/AHA emphasize evidence-based selection, with Class 1 recommendations for intermediate-risk patients to optimize diagnostic yield. Prognostically, a normal stress test result indicates a low annual event rate of less than 1% for cardiac death or MI, enabling reassurance and conservative management, while abnormal findings prompt further interventions such as coronary angiography. This utility spans exercise, pharmacological, or imaging-enhanced modalities, depending on patient factors.

Types of Cardiac Stress Tests

Exercise-Based Tests

Exercise-based cardiac stress tests, also known as exercise electrocardiography (ECG) tests, involve physical exertion to evaluate cardiac function under stress, primarily using treadmill or bicycle protocols. These tests are suitable for patients capable of ambulating or pedaling, allowing direct assessment of the heart's response to increased demand. The standard approach uses incremental workloads to gradually elevate heart rate and myocardial oxygen consumption, monitoring for ischemic changes via ECG. The most common protocol is the , introduced in 1963 and widely adopted as the gold standard for treadmill testing in adults. It consists of three-minute stages with progressive increases in speed and incline: stage 1 begins at 1.7 mph and 10% grade (approximately 5 metabolic equivalents, or METs), stage 2 at 2.5 mph and 12% grade, and subsequent stages further escalate until the patient reaches exhaustion or an endpoint. For patients with lower functional capacity, such as those recovering from , the Naughton protocol employs a constant speed of 2.0 mph with gradual incline increases over two-minute stages (e.g., 0% to 3.5% in early stages), while the Balke protocol maintains a fixed speed of 3.3 mph and increments the grade every one to two minutes. These protocols aim to achieve at least 85% of the maximum predicted heart rate, calculated as 220 minus the patient's age, though tests may be symptom-limited if fatigue, angina, or significant ECG changes occur first. Equipment typically includes a motorized treadmill for walking or running, or an upright/recumbent cycle ergometer for pedaling, selected based on patient mobility and preference. Continuous 12-lead ECG monitoring tracks ST-segment changes, arrhythmias, and heart rate, while automated blood pressure cuffs measure systolic and diastolic pressures at rest, during each stage, and in recovery. Safety features, such as emergency stop buttons and resuscitation equipment, are standard in the testing environment. Key physiological responses evaluated include heart rate progression, which normally increases by about 10 beats per minute per MET achieved; exercise capacity, quantified in METs (e.g., >10 METs indicates good ); and heart rate recovery, defined as a drop of at least 12 beats per minute in the first minute post-exercise, reflecting vagal reactivation. Endpoints are either target heart rate attainment for diagnostic adequacy or symptom-limited cessation to avoid undue risk, providing insights into chronotropic competence and overall cardiovascular reserve. Advantages of exercise-based tests include direct evaluation of functional capacity through METs achieved, reproduction of patient-specific exertional symptoms like dyspnea or , and cost-effectiveness without exposure to or pharmacological agents. These tests offer prognostic value, with higher exercise tolerance correlating to lower mortality risk, and can integrate briefly with modalities for enhanced detection if needed.

Pharmacological Stress Tests

Pharmacological stress tests are employed to simulate the cardiovascular effects of exercise in patients who are unable to perform due to conditions such as orthopedic limitations, physical deconditioning, or (COPD). These tests induce stress through medications that either increase myocardial oxygen demand or enhance coronary blood flow, allowing assessment of cardiac function under simulated exertion. Approximately 52% of cardiac stress tests utilize pharmacological agents, reflecting their widespread application in clinical practice. The primary pharmacological agents fall into two categories: vasodilators, which promote coronary hyperemia by dilating , and inotropic agents, which elevate and contractility to mimic exercise-induced demand. Common vasodilators include , administered as an intravenous infusion at 140 mcg/kg/min for 4 to 6 minutes to achieve maximal coronary . Another vasodilator is dipyridamole, given intravenously at 0.56 mg/kg over 4 minutes, which inhibits uptake and thereby induces similar hyperemic effects. , a selective agonist, is also frequently used at a fixed dose of 0.4 mg as a rapid intravenous bolus followed by a , offering ease of administration and comparable coronary flow augmentation. In contrast, serves as an inotropic and beta-adrenergic stimulant, starting at 5 mcg/kg/min and titrated upward in 3-minute stages to a maximum of 40 mcg/kg/min, thereby increasing myocardial oxygen consumption akin to physical exertion. Hemodynamically, vasodilators like produce a 3- to 5-fold increase in coronary blood flow but may cause transient and carry a risk of due to non-selective activation. Dipyridamole similarly elevates coronary perfusion 3.8- to 7-fold, with effects peaking around 6.5 minutes post-infusion. Dobutamine, by contrast, raises and contractility without direct , targeting 85% of the age-predicted maximum to replicate . Protocols for pharmacological stress tests involve continuous electrocardiographic monitoring and vital sign assessment throughout the procedure to detect ischemic changes or hemodynamic . The infusion is typically paired with radiotracer administration for imaging, though the core stress induction remains drug-driven. Reversal agents, such as (50-250 mg intravenously) for vasodilator-induced effects or beta-blockers like metoprolol for , are available to terminate symptoms if needed, administered at least 1 minute after tracer injection to avoid interference.

Imaging-Enhanced Tests

Imaging-enhanced cardiac stress tests integrate functional imaging modalities with physiological stress to detect (CAD) by visualizing myocardial ischemia or defects, offering greater diagnostic accuracy than alone. These tests typically combine exercise or pharmacological stress induction with either or nuclear imaging to assess regional wall motion abnormalities or blood flow distribution, respectively. Such enhancements allow for the identification of inducible ischemia in patients unable to achieve adequate exercise or those with baseline ECG abnormalities. Stress echocardiography employs imaging to evaluate left ventricular wall motion and thickening before and immediately after stress, detecting ischemia-induced abnormalities such as hypokinesis or akinesis. Protocols include exercise echocardiography, where images are acquired at baseline, peak exercise, and recovery, or pharmacological variants using infusion (up to 40 mcg/kg/min) with atropine if needed to simulate stress in non-exercising patients. This modality demonstrates a sensitivity of 80-85% and specificity of 80-88% for detecting significant CAD, comparable to nuclear methods but with advantages in portability and absence of . Nuclear myocardial perfusion imaging (MPI) uses single-photon emission computed tomography (SPECT) or positron emission tomography (PET) with radiotracers to map myocardial blood flow at rest and during stress, identifying reversible perfusion defects indicative of ischemia. Common SPECT tracers include technetium-99m sestamibi or tetrofosmin, administered in a rest-stress or stress-rest sequence, while PET employs rubidium-82 or ammonia-13 for higher resolution; SPECT MPI achieves sensitivity of 85-90% and specificity of 70-75% for CAD, with PET offering superior accuracy (sensitivity up to 90%, specificity 80-85%) particularly in obese patients or multivessel disease. The effective radiation dose for a typical SPECT rest-stress protocol is approximately 10-15 mSv, depending on tracer and dosing. Gated imaging during acquisition enables simultaneous assessment of left ventricular ejection fraction and volumes, enhancing prognostic value. Compared to nuclear MPI, stress echocardiography is preferred for its lower cost, lack of , and bedside applicability, making it ideal for initial evaluation in low-to-intermediate risk patients; however, nuclear imaging excels in detecting three-vessel or left main CAD due to its quantitative assessment and correction capabilities. Both modalities follow similar stress induction methods, such as exercise or vasodilators like , but imaging-specific protocols optimize detection of subtle defects. Acquisition typically sequences rest imaging first followed by stress to minimize artifacts, though stress-first approaches reduce in low-risk cases.

Specialized Variants

Cardiopulmonary exercise testing (CPET) represents a specialized variant of cardiac that integrates respiratory with incremental exercise to evaluate integrated cardiopulmonary function. During CPET, key parameters such as peak oxygen uptake (VO₂ max), anaerobic threshold, and ventilatory efficiency (measured as the VE/VCO₂ slope) are quantified using breath-by-breath to assess aerobic capacity and dynamics. Protocols typically involve a ramped or cycle ergometer protocol progressing to symptom-limited exhaustion, allowing for the detection of exercise-limiting factors beyond standard electrocardiographic changes. CPET is particularly indicated for differentiating cardiac from pulmonary contributions to exercise intolerance, such as in unexplained dyspnea, where patterns like elevated VE/VCO₂ slopes (>34) suggest cardiac limitation due to impaired or ventilation-perfusion mismatch. In patients, it provides prognostic insights; for instance, a peak VO₂ <14 mL/kg/min is associated with increased mortality risk and serves as a criterion for advanced therapies like transplantation, especially in those on beta-blocker therapy. These metrics help stratify disease severity and guide therapeutic decisions, outperforming resting assessments in predictive accuracy. The procedure requires specialized equipment, including a metabolic cart equipped with rapid-response gas analyzers for continuous measurement of oxygen consumption (VO₂) and carbon dioxide production (VCO₂), connected via a face mask or mouthpiece to capture expired air. Ventilatory volumes are monitored through flow sensors, enabling derivation of parameters like the anaerobic threshold via the V-slope method. In heart failure evaluation, the Weber classification system utilizes peak VO₂ thresholds to categorize patients into classes A-D (e.g., class C: 10-14 mL/kg/min; class D: <10 mL/kg/min), correlating with functional capacity and survival prognosis. Beyond CPET, pharmacological myocardial perfusion imaging (MPI) with positron emission tomography (PET) serves as a specialized option for high-risk patients unable to exercise, employing vasodilators like to induce stress while quantifying absolute myocardial blood flow and detecting multivessel disease with higher sensitivity than SPECT. Emerging stress cardiac magnetic resonance (CMR) imaging, often using for inotropic stress, excels in viability assessment by combining perfusion, wall motion, and late gadolinium enhancement to identify hibernating myocardium without ionizing radiation, aiding revascularization decisions in ischemic cardiomyopathy.

Procedure and Protocols

Patient Preparation

Patient preparation for a cardiac stress test is essential to ensure both safety and diagnostic accuracy, involving adjustments to medications and diet, comprehensive baseline evaluations, and logistical arrangements at the testing facility. Guidelines recommend reviewing the patient's medical history to identify any absolute or relative contraindications, such as unstable angina or severe aortic stenosis, prior to proceeding. Specific instructions on medications aim to optimize heart rate response and minimize interference with stress induction. For exercise-based tests, beta-blockers and calcium channel blockers are typically withheld for 24 to 48 hours beforehand to allow achievement of adequate heart rate increases, though this is not always routine and depends on the clinical context; timing and dosage should be documented if continued. In pharmacological stress tests using dobutamine, beta-blockers should be withheld for at least 24 hours, while for vasodilator agents like adenosine or regadenoson, xanthine derivatives (e.g., theophylline) are discontinued 12 to 24 hours prior to avoid blunting the response. Other antianginal medications, such as nitrates or digoxin, may also require withholding, particularly if ST-segment changes could be obscured, with digoxin effects persisting up to two weeks after discontinuation. Patients are advised to bring a list of all current medications for review. Dietary and lifestyle preparations focus on avoiding substances that could alter physiological responses. Caffeine-containing products, including coffee, tea, chocolate, and certain medications, must be avoided for 12 to 24 hours prior, as they can block adenosine receptors in pharmacological tests or provoke arrhythmias in exercise protocols. Fasting is not strictly required, but patients should abstain from food for at least three hours before the test to enhance exercise tolerance; a light meal earlier in the day is permissible, and routine medications can be taken with small sips of water. Smoking and alcohol should be avoided for at least 24 hours to prevent impacts on heart rate and blood pressure. Baseline assessments begin with a thorough review of the patient's history, including symptoms, cardiovascular risk factors, allergies, and recent illnesses, followed by a physical examination to evaluate vital signs, cardiac auscultation, and overall fitness. A resting 12-lead electrocardiogram (ECG) is performed supine and standing to identify baseline abnormalities, such as ST-segment depression greater than 1 mm or left bundle branch block, which may affect test interpretation; the test is postponed if resting systolic blood pressure exceeds 200 mm Hg or diastolic exceeds 110 mm Hg. Informed consent is obtained after explaining the procedure, potential benefits for diagnosing coronary artery disease, and risks such as arrhythmias or chest pain, ensuring the patient understands termination criteria. Laboratory tests are selectively ordered based on the test modality. For tests involving contrast agents or pharmacological drugs, electrolytes, renal function (e.g., creatinine), and complete blood count may be checked to assess eligibility and mitigate risks like nephrotoxicity. Women of childbearing potential undergo a pregnancy test prior to nuclear imaging or radiation-involving procedures to avoid fetal exposure. The testing facility must be equipped for immediate intervention, with intravenous access established (e.g., a 20- to 24-gauge cannula) for potential medication administration or hydration. Emergency equipment, including a defibrillator, crash cart with resuscitation drugs, and oxygen, must be readily available, and the procedure is supervised by qualified personnel trained in advanced cardiac life support.

Test Execution and Monitoring

The execution of a cardiac stress test begins with a baseline recording phase lasting 2 to 3 minutes, during which the patient is positioned supine and then standing to obtain initial electrocardiographic (ECG) tracings and vital signs, establishing a reference for subsequent changes. For exercise-based tests, patients walk on a treadmill or pedal a stationary bike while connected to monitoring equipment, with intensity gradually increasing via faster speed or incline; the procedure tracks heart rate, blood pressure, ECG, and symptoms, and takes 30–60 minutes with close monitoring. This is followed by the stress induction phase, where exercise or pharmacological agents progressively increase myocardial demand; for exercise-based tests, this typically involves a treadmill or cycle ergometer using standardized protocols such as the , with stages escalating in workload every 2 to 3 minutes until an endpoint is reached, aiming for a total duration of 6 to 12 minutes. The recovery phase then ensues, involving a cool-down period of 5 to 10 minutes of monitoring while the patient rests or walks slowly, allowing observation of heart rate deceleration and resolution of any abnormalities. Continuous monitoring occurs throughout the test to detect physiological responses in real time. A 12-lead ECG is recorded continuously via hardwired or telemetry systems, with ST-segment analysis performed at 60 to 80 milliseconds after the J-point to identify ischemic changes, and tracings printed at least every minute or stage. Blood pressure is measured every 1 to 2 minutes using an automated cuff, tracking systolic increases (typically 30 to 50 mm Hg) and any drops exceeding 10 mm Hg. Symptoms such as chest pain, dyspnea, or fatigue are assessed subjectively using the Borg scale (ratings 6 to 20) at regular intervals, while heart rate is monitored to reach a target of 85% of the age-predicted maximum, calculated as (220 minus age) multiplied by 0.85. The test is overseen by a qualified physician or advanced practice clinician with Advanced Cardiac Life Support certification, who interprets ECG changes and symptoms in real time, while a trained technician manages equipment setup, electrode placement, and data acquisition. For submaximal tests in elderly or deconditioned patients, protocols adjust workloads to avoid excessive strain, prioritizing safety over peak achievement. Endpoints for terminating the stress phase include attainment of the target heart rate, patient fatigue or volitional exhaustion, evidence of ischemia such as horizontal or downsloping ST-segment depression greater than 1 mm in two contiguous leads, significant hypotension (systolic drop >10 mm Hg despite increased workload), or development of arrhythmias like frequent ventricular ectopy. In pharmacological variants, endpoints align similarly but are triggered by peak drug infusion or comparable physiological thresholds.

Post-Test Evaluation

Following the completion of a cardiac stress test, patients undergo a supervised recovery phase to ensure hemodynamic stability and monitor for potential delayed complications. In exercise-based tests, individuals typically engage in a cool-down period of slow walking to prevent venous pooling and abrupt drops in , with continuous monitoring of (HR), (BP), and electrocardiogram (ECG) for 6 to 8 minutes or until these parameters return to near-baseline levels. are checked every 5 minutes, and observation continues for arrhythmias, ischemic changes, or symptoms such as or dyspnea, which may occur post-exercise due to vagal reactivation or residual effects. For pharmacological stress tests, recovery involves continuous ECG monitoring for at least 4 minutes and assessments every minute for 3 to 5 minutes or until stable, with readiness to administer reversal agents like for vasodilator-induced complications such as severe (systolic <80 mm Hg) or bronchospasm. Supervised rest persists until HR falls below 100 beats per minute, prioritizing patient safety during this transition. Documentation during post-test evaluation captures essential metrics to support preliminary analysis and future comparisons. Key elements recorded include peak HR achieved, metabolic equivalents (METs) attained, exercise duration or pharmacological infusion details, symptoms experienced, ECG tracings (including ST-segment changes), and the reason for test termination (e.g., fatigue, angina, or target HR reached). A preliminary report is generated promptly, summarizing these findings and baseline comparisons, which is shared with the patient and referring physician to guide immediate management decisions. In imaging-enhanced tests, such as stress echocardiography or myocardial perfusion imaging, post-stress images are documented alongside rest images to note any wall motion abnormalities or perfusion defects. Patients receive clear discharge instructions to facilitate safe recovery and ongoing vigilance. They are advised to resume normal activities gradually unless contraindicated by test results, such as avoiding vigorous exertion if ischemia was detected, and to report any new or persistent symptoms like chest pain, shortness of breath, or palpitations immediately to their healthcare provider. Medications withheld prior to the test, such as beta-blockers, should be resumed as prescribed, and hydration is encouraged to aid clearance of pharmacological agents if used. For those with implantable devices like pacemakers, activity levels are tailored based on documented HR responses to prevent inappropriate device activation. Quality control measures ensure the reliability and usability of test data for clinical and longitudinal purposes. If imaging modalities were employed, technicians verify the quality of acquired images—checking for artifacts, adequate resolution, and proper protocol adherence (e.g., gated imaging post-stress in SPECT studies)—to confirm diagnostic validity. All raw data, including ECG strips, vital sign logs, and imaging files, are archived securely in electronic health records for serial testing comparisons, adhering to standards that minimize radiation exposure (e.g., <9 mSv effective dose in optimized protocols) while maintaining traceability. This process supports reproducibility and integration with broader patient care pathways.

Interpretation and Diagnostic Value

Analyzing Results

Interpreting the results of a cardiac stress test involves a systematic evaluation of electrocardiographic (ECG) changes, imaging findings if applicable, and patient symptoms to identify evidence of myocardial ischemia or other abnormalities. The primary focus is on detecting inducible ischemia, which manifests as reversible perfusion defects or wall motion abnormalities under stress compared to baseline. Analysis typically occurs post-test, with clinicians correlating multiple modalities for diagnostic accuracy. In ECG-based stress testing, key indicators of ischemia include ST-segment depression, measured 80 ms after the J-point. A horizontal or downsloping ST depression of ≥1 mm is considered a standard marker for ischemia, as it reflects subendocardial oxygen supply-demand mismatch during stress. Upsloping ST depression is less specific and often not diagnostic on its own, potentially arising from non-ischemic causes like rate-related changes. Additional ECG findings, such as T-wave inversions or stress-induced arrhythmias (e.g., ventricular ectopy), may support ischemia but require correlation with other data for confirmation. For imaging-enhanced tests, echocardiography assesses regional wall motion using a standardized 16-segment model of the left ventricle, scoring each segment from 1 (normal) to 4 (dyskinetic). Inducible ischemia is indicated by new or worsening wall motion abnormalities in ≥2 contiguous segments during stress, reflecting reduced to affected myocardial territories. In nuclear perfusion imaging, the summed stress score (SSS) quantifies defect extent and severity across 17 segments, with scores of 0-4 typically normal, 4-8 mildly abnormal, and >8 suggesting high-risk ischemia based on perfusion defect size. Symptom integration enhances result interpretation, particularly when angina coincides with ECG or imaging changes, as this combination strengthens the likelihood of true ischemia. The Duke Treadmill Score provides a composite metric for exercise ECG tests, calculated as exercise duration in minutes minus 5 times the maximum ST-segment deviation in mm minus 4 times the angina index (0 for no angina, 1 for non-limiting, 2 for exercise-limiting). Higher scores indicate lower risk, aiding in risk stratification alongside clinical context. False-positive results, which can mimic ischemia, must be scrutinized to avoid misdiagnosis. (LVH) often causes baseline repolarization abnormalities that exaggerate ST changes during stress. therapy induces secondary ST depression, reducing test specificity in treated patients. Motion artifacts in imaging modalities, such as patient movement during nuclear scans, can create apparent perfusion defects unrelated to coronary disease.

Sensitivity, Specificity, and Prognostic Insights

The diagnostic accuracy of cardiac stress tests varies by modality and is typically evaluated against (CAD) as confirmed by invasive . For exercise (ECG), a of over 24,000 patients across 147 studies reported a sensitivity of 68% and specificity of 77% in detecting CAD. Stress demonstrates improved performance, with meta-analyses indicating sensitivities ranging from 80% to 88% and specificities from 77% to 86% for identifying significant CAD, particularly when assessing wall motion abnormalities under stress. Nuclear myocardial perfusion imaging (MPI), such as single-photon emission computed tomography (SPECT), achieves sensitivities of 85% to 90%, though specificities are generally lower at around 70% to 80%, due to potential artifacts from attenuation. Beyond diagnosis, cardiac stress tests provide substantial prognostic value for future cardiac events, including and death. A normal stress test result is associated with a low annual event rate of 0.5% to 1%, reflecting excellent negative predictive value for adverse outcomes over 1 to 5 years of follow-up in patients with suspected CAD. In contrast, high-risk features—such as early-onset ischemia, extensive defects, or low exercise capacity—correlate with elevated annual risks of 5% to 10%, enabling effective risk stratification to guide intensity. Evidence from landmark trials underscores these metrics in clinical management. The COURAGE trial, involving over 2,200 patients with stable CAD, demonstrated that effectively identifies candidates for optimal medical therapy versus , with no significant difference in hard outcomes between plus medical therapy and medical therapy alone, highlighting the test's role in safe deferral of invasive procedures. Recent updates in the 2023 AHA/ACC guideline for chronic coronary disease emphasize for stratification, recommending its use to categorize patients into low-, intermediate-, or high-risk groups based on ischemia extent and functional capacity, thereby informing personalized treatment plans. Despite these strengths, accuracy can be reduced in certain populations, necessitating cautious interpretation. In women, exercise ECG sensitivity and specificity are lower (often 50% to 60% for both) due to higher rates of false positives from baseline ST-segment changes and lower pretest CAD probability. Obese patients face challenges with image quality in and attenuation artifacts in nuclear MPI, potentially decreasing specificity by 10% to 20% and increasing nondiagnostic rates up to 30%. In such cases, complementary tests like coronary (CCTA) are often recommended to enhance diagnostic confidence.

Limitations and Complementary Tests

Cardiac stress testing, while valuable for detecting ischemia, has inherent limitations in accurately localizing coronary lesions, particularly in distinguishing between single-vessel and multivessel disease. In cases of multivessel coronary artery disease, the test may fail to pinpoint specific stenoses due to diffuse perfusion abnormalities that obscure territorial defects. This challenge is exacerbated in scenarios of balanced ischemia, where uniform reductions in myocardial blood flow across multiple territories lead to reduced sensitivity, often resulting in false-negative results on myocardial perfusion imaging. Additionally, stress echocardiography exhibits significant operator dependency, as image acquisition and interpretation rely heavily on the technician's skill in obtaining clear views and assessing wall motion abnormalities, which can introduce variability and reduce reproducibility. Patient-specific factors further compromise the reliability of cardiac stress tests. In individuals with , acoustic windows are often obscured by excess , limiting the feasibility of and potentially necessitating contrast agents or alternative modalities to achieve diagnostic-quality images. Patients with (LBBB) face a high of false-positive septal defects during nuclear , particularly with exercise or vasodilator protocols, which can mimic ischemia and lead to unnecessary downstream testing. Moreover, is contraindicated in , as it may provoke further myocardial injury in unstable patients. To address these gaps, complementary tests are often employed to refine diagnosis and guide management. Coronary computed tomography angiography (CCTA) serves as a useful adjunct for low-risk patients with suspected , providing detailed anatomic visualization of stenoses without the functional limitations of . For individuals with high-risk stress test results indicating severe ischemia, invasive coronary angiography is recommended to confirm lesion severity and facilitate revascularization decisions. In cases where other modalities are contraindicated—such as in patients unable to exercise, with poor echocardiographic windows, or contraindications to nuclear agents—stress cardiac (MRI) offers a robust alternative, enabling assessment of and viability with high . Emerging technologies, including AI-assisted interpretation, are addressing interpretive variability in stress testing. Machine learning algorithms applied to myocardial perfusion imaging have demonstrated improved detection of perfusion defects, with 2024 studies showing enhanced sensitivity and reduced inter-observer discordance in identifying coronary artery disease.

Safety and Risks

Contraindications

Cardiac stress testing, whether exercise-based or pharmacological, carries risks that necessitate careful patient selection. Contraindications are categorized as absolute, where the procedure should not be performed due to high risk of adverse events, and relative, where the test may be considered only after weighing risks and benefits or opting for alternatives. These recommendations are based on class III indications (no benefit or potential harm) from the American College of Cardiology (ACC) and American Heart Association (AHA) guidelines. Absolute contraindications include conditions posing immediate life-threatening risks during stress induction: Relative contraindications involve elevated but potentially manageable risks, often requiring modification or deferral: Special considerations apply in certain populations. Pregnancy represents a relative for nuclear due to fetal from agents, though exercise-based testing without may be performed if clinically justified. Patients with mobility limitations or inability to exercise adequately due to orthopedic, pulmonary, or neurological issues should undergo pharmacological instead, using agents like or to simulate physiological stress. Pharmacological agents have additional specific contraindications: and dipyridamole are contraindicated in patients with second- or third-degree atrioventricular (AV) block (without pacemaker) or severe bronchospastic airway disease (e.g., , ); is contraindicated in recent , , significant outflow tract obstruction, or tachyarrhythmias. In all cases, a thorough risk-benefit assessment is mandatory prior to proceeding, aligning with (ESC) and ACC/AHA class III recommendations.

Adverse Effects

Cardiac stress tests, whether exercise-based or pharmacologic, are associated with a range of adverse effects, most of which are mild and transient. Common effects in exercise stress testing include and muscle soreness, which typically resolve shortly after the procedure. In pharmacologic stress testing using vasodilators such as or dipyridamole, patients may experience flushing and , occurring in approximately 5-10% of cases. Transient myocardial ischemia can also occur during the test, manifesting as or ECG changes, but it is generally self-limiting. Serious complications, though rare, include arrhythmias such as (occurring in about 1 in 5,000 tests), (1 in 2,500 tests), and death (1 in 10,000 tests). These rates apply primarily to exercise , with pharmacologic variants carrying similar or slightly higher risks depending on the agent. For stress testing, the incidence of is around 10%, which can be more pronounced than with vasodilators. Overall mortality risk across all modalities remains low at less than 0.01%. Specific to pharmacologic agents, can induce in about 1% of patients and atrioventricular (AV) block in roughly 1%, particularly in those with underlying or conduction issues. Management of these effects involves immediate administration of to reverse adenosine's actions or atropine for and AV block, with symptoms typically resolving within minutes. prior to testing highlights these potential adverse effects, and continuous post-test monitoring helps mitigate risks by allowing prompt intervention if needed.

Termination Criteria

The termination criteria for a cardiac stress test are predefined conditions that prompt immediate cessation of the procedure to safeguard patient safety, based on monitoring of symptoms, electrocardiographic (ECG) changes, and hemodynamic parameters during exercise or pharmacological stress. These criteria are outlined in guidelines from the American College of Cardiology (ACC) and American Heart Association (AHA) to prevent complications such as myocardial ischemia or arrhythmias.

Symptomatic Criteria

Severe or moderate-to-severe that worsens with exertion indicates termination, as it signals potential ischemia requiring prompt intervention. , , near-syncope, , or other neurologic symptoms also warrant stopping the test to avoid syncope or . Additionally, the patient's explicit request to stop due to fatigue, leg cramps, wheezing, , or excessive serves as an absolute indication, prioritizing individual tolerance.

ECG and Hemodynamic Criteria

ECG changes such as ST-segment elevation greater than 1 mm in leads without diagnostic Q waves (excluding aVR or V1), or sustained , necessitate immediate termination due to high risk of acute coronary events. Hemodynamically, a drop in systolic exceeding 10 mm Hg from baseline despite increasing workload, particularly with signs of ischemia, is an absolute stop signal, as it may reflect ventricular dysfunction. Relative indications include greater than 2 mm (horizontal or downsloping), marked axis shifts, multifocal premature ventricular contractions, , , or bradyarrhythmias, especially if accompanied by a exceeding the age-predicted target (85% of maximum) with ischemic features. Hypertensive responses, defined as systolic above 250 mm Hg or diastolic above 115 mm Hg, also prompt cessation to mitigate cardiovascular strain.

Other Criteria

Development of a new left bundle branch block (LBBB) or exercise-induced bundle branch block during the test requires termination, as it can obscure ischemia detection and mimic ventricular tachycardia, complicating interpretation. Signs of poor perfusion, such as or , or technical issues preventing adequate ECG or monitoring, are absolute indications to halt the procedure. For pharmacological stress testing, termination occurs upon reaching peak vasodilator or inotropic effects (e.g., target with or maximal infusion with /dipyridamole) or if side effects emerge, including severe with vasodilators, significant arrhythmias, or new wall motion abnormalities on imaging. (systolic below 90 mm Hg) or severe (systolic above 240 mm Hg or diastolic above 120 mm Hg) during infusion similarly dictates stopping.

Protocol for Termination

Upon meeting any criterion, the test protocol involves gradual deceleration of to allow recovery and prevent , with continuous monitoring of and ECG. Facilities conducting stress tests must maintain (ACLS) readiness, including defibrillator access and trained personnel, to manage any emergent arrhythmias or hemodynamic instability. The reason for early termination—whether symptomatic, ECG-related, or otherwise—is documented in the patient's record, along with pre- and post-termination , to inform clinical follow-up.

Historical Development

Early Innovations

The foundation of cardiac stress testing rests on the electrocardiogram (ECG), pioneered by , who developed the string galvanometer in 1903, enabling the recording of the heart's electrical activity and earning him the 1924 Nobel Prize in Physiology or Medicine. This innovation provided the essential tool for detecting exercise-induced ECG changes, laying the groundwork for despite initial limitations in portability and sensitivity. In the late 1920s, Arthur M. Master introduced the two-step test, a standardized exercise protocol involving ascending and descending two steps for 1.5 minutes to provoke ECG alterations indicative of (CAD). First described in 1929, this simple, non-invasive method assessed cardiac tolerance post-exercise by measuring , , and ECG changes, marking the earliest systematic approach to unmasking silent ischemia in patients without resting abnormalities. By the 1930s, it gained traction for evaluating , particularly in high-risk groups such as aviation pilots, where detecting occult ischemia was critical for flight safety amid the era's expanding military and demands. Advancements in the shifted toward more controlled and progressive protocols, with ergometry emerging as an alternative to stepping tests, allowing ECG monitoring during upright or reclined pedaling to simulate physiological stress while minimizing orthostatic effects. This paved the way for A. Bruce's multistage protocol in 1963, which incrementally increased speed and incline to achieve maximal exertion, improving diagnostic accuracy for CAD over the fixed-intensity Master test by better quantifying exercise capacity and ischemic thresholds. The , developed through studies on healthy and cardiac patients, became a cornerstone for standardized stress ECG testing due to its reproducibility and ability to elicit symptoms in a graded manner. The introduced imaging modalities to enhance beyond ECG alone, with thallium-201 enabling myocardial assessment during exercise, first applied clinically around 1974 to visualize ischemia-induced defects. This radiotracer, injected at peak stress, highlighted underperfused areas via imaging, revolutionizing detection of multivessel disease. Concurrently, stress echocardiography concepts emerged in the late , using M-mode and early two-dimensional to detect exercise-induced wall motion abnormalities, with initial reports in demonstrating its feasibility for ischemia evaluation. These innovations by pioneers like and early nuclear cardiologists expanded 's diagnostic scope, focusing on functional rather than solely electrical responses.

Modern Advancements

In the 1990s, (SPECT) imaging for cardiac stress testing underwent standardization through the development of consensus protocols by the American Society of Nuclear Cardiology (ASNC), which established uniform guidelines for tracer use, acquisition parameters, and interpretation to enhance reproducibility and diagnostic accuracy across institutions. Advancements in the 2000s shifted toward (PET) for quantitative myocardial assessment, enabling precise measurement of myocardial blood flow (MBF) and flow reserve using tracers like and ammonia, which demonstrated superior sensitivity (91%) and specificity (86%) compared to SPECT in detecting . By the , stress cardiovascular magnetic resonance (CMR) gained widespread adoption as a non-ionizing alternative, with studies like CE-MARC (2012) showing higher diagnostic accuracy (AUC 0.89) than SPECT for ischemia detection, supported by technical improvements in 3D and artifact reduction techniques. Pharmacological stress agents evolved with the 2008 FDA approval of , a selective A2A agonist administered as a single intravenous bolus, offering a safer and more convenient alternative to continuous infusion by reducing side effects like while maintaining comparable vasodilatory efficacy. In the 2020s, digital innovations include pilot studies exploring wearable ECG devices for remote home-based stress monitoring, allowing continuous assessment of and ischemia signals in patients unable to visit clinics, though validation against traditional methods remains ongoing. algorithms for automated interpretation of stress test results, particularly ECG and , have shown promise in recent studies, with models achieving specificity improvements of up to 10-20% over manual reading by identifying subtle defects and reducing false positives. Guideline updates reflect these innovations; the 2021 ACC/AHA chest pain evaluation guideline emphasized shared decision-making to incorporate patient preferences in selecting stress testing modalities, balancing benefits against risks like radiation exposure. The 2024 ACC/AHA Appropriate Use Criteria for multimodality imaging in cardiovascular evaluation of patients undergoing nonemergent, noncardiac surgery prioritize the appropriate use of low-radiation protocols, such as PET/CMR hybrids and dose-optimized SPECT, amid growing concerns over test overuse in low-risk populations, which can lead to unnecessary downstream procedures without improving outcomes. In November 2025, results from the CorCMR trial demonstrated that stress cardiovascular magnetic resonance (CMR) imaging, by quantifying myocardial blood flow, reclassified the cause of in 53% of patients with with no obstructive coronary arteries (ANOCA), leading to improved , , and .

References

  1. https://www.mayoclinic.org/tests-procedures/stress-test/about/pac-20385234
  2. https://www.ncbi.nlm.nih.gov/books/NBK499903/
  3. https://www.heart.org/en/health-topics/heart-attack/diagnosing-a-heart-attack/exercise-stress-test
  4. https://www.mayoclinic.org/tests-procedures/nuclear-stress-test/about/pac-20385231
  5. https://newsroom.heart.org/news/stress-cardiac-mri-tests-may-help-improve-angina-diagnosis-and-treatment
  6. https://www.jacc.org/doi/10.1016/j.jacadv.2025.102141
  7. https://my.clevelandclinic.org/health/diagnostics/16984-exercise-stress-test
  8. https://www.merckmanuals.com/professional/cardiovascular-disorders/cardiovascular-tests-and-procedures/stress-testing
  9. https://www.ahajournals.org/doi/10.1161/cir.0b013e31829b5b44
  10. https://www.jacc.org/doi/10.1016/j.jacc.2021.07.053
  11. https://www.ahajournals.org/doi/10.1161/01.CIR.96.1.345
  12. https://www.uptodate.com/contents/stress-testing-in-predischarge-risk-stratification-of-patients-with-non-st-elevation-acute-coronary-syndrome
  13. https://www.ahajournals.org/doi/10.1161/CIR.0000000000001309
  14. https://www.ahajournals.org/doi/10.1161/CIR.0000000000001285
  15. https://www.jacc.org/doi/10.1016/j.jacc.2023.03.410
  16. https://professional.heart.org/-/media/PHD-Files-2/Science-News/2/2023/2023_chronic_coronary_disease_guideline_slide_set.pdf
  17. https://www.ahajournals.org/doi/10.1161/CIR.0000000000001168
  18. https://www.ecrjournal.com/articles/prognostic-value-stress-myocardial-single-photon-emission-computed-tomography-elderly?language_content_entity=en
  19. https://pmc.ncbi.nlm.nih.gov/articles/PMC3443465/
  20. https://ecgwaves.com/topic/exercise-stress-test-exercise-ecg-protocols-evaluation-parameters/
  21. https://pmc.ncbi.nlm.nih.gov/articles/PMC6078558/
  22. https://www.nejm.org/doi/full/10.1056/NEJM199910283411804
  23. https://www.racgp.org.au/afp/2012/march/cardiac-stress-testing
  24. https://www.sciencedirect.com/science/article/abs/pii/S1071358123064899
  25. https://www.ncbi.nlm.nih.gov/books/NBK555963/
  26. https://www.ncbi.nlm.nih.gov/books/NBK544321/
  27. https://www.ncbi.nlm.nih.gov/books/NBK557682/
  28. https://www.ncbi.nlm.nih.gov/books/NBK448062/
  29. https://www.ahajournals.org/doi/10.1161/01.cir.95.6.1686
  30. https://www.ahajournals.org/doi/10.1161/CIRCIMAGING.119.009318
  31. https://www.jacc.org/doi/10.1016/j.jacadv.2025.102145
  32. https://www.ahajournals.org/doi/10.1161/01.cir.0000080946.42225.4d
  33. https://www.ahajournals.org/doi/10.1161/circimaging.112.978270
  34. https://www.ahajournals.org/doi/10.1161/CIRCIMAGING.109.854893
  35. https://www.ahajournals.org/doi/10.1161/circulationaha.107.688101
  36. https://www.acc.org/Latest-in-Cardiology/Articles/2020/11/19/14/33/The-Latest-ASE-Guidelines-for-Stress-Echocardiography-in-IHD
  37. https://pmc.ncbi.nlm.nih.gov/articles/PMC2000933/
  38. https://www.ncbi.nlm.nih.gov/books/NBK557886/
  39. https://pmc.ncbi.nlm.nih.gov/articles/PMC7807922/
  40. https://pmc.ncbi.nlm.nih.gov/articles/PMC3177547/
  41. https://pmc.ncbi.nlm.nih.gov/articles/PMC12566257/
  42. https://pmc.ncbi.nlm.nih.gov/articles/PMC10452308/
  43. https://www.ncbi.nlm.nih.gov/books/NBK560729/
  44. https://www.ahajournals.org/doi/10.1161/JAHA.120.018822
  45. https://pmc.ncbi.nlm.nih.gov/articles/PMC3650901/
  46. https://pmc.ncbi.nlm.nih.gov/articles/PMC4176813/
  47. https://pmc.ncbi.nlm.nih.gov/articles/PMC7546497/
  48. https://www.ahajournals.org/doi/10.1161/CIR.0b013e31829b5b44
  49. https://www.asnc.org/wp-content/uploads/2024/06/ASNC-SPECT-ProtocolsTracers-Guidelines2016.pdf
  50. https://stanfordhealthcare.org/medical-tests/s/stress-test.html
  51. https://www.asnc.org/wp-content/uploads/2024/05/ASNC-Practice-Point-Exercise-Stress-Testing.pdf
  52. https://www.ahajournals.org/doi/pdf/10.1161/circulationaha.109.192520
  53. https://www.ahajournals.org/doi/10.1161/01.cir.0000034670.06526.15
  54. https://www.asecho.org/wp-content/uploads/2019/11/Stress2019.pdf
  55. https://www.jacc.org/doi/10.1016/j.jacc.2021.08.022
  56. https://pmc.ncbi.nlm.nih.gov/articles/PMC1768798/
  57. https://www.acc.org/Latest-in-Cardiology/ten-points-to-remember/2023/01/31/16/55/challenges-in-cv-evaluation
  58. https://pubmed.ncbi.nlm.nih.gov/7989982/
  59. https://pmc.ncbi.nlm.nih.gov/articles/PMC4613789/
  60. https://www.ahajournals.org/doi/10.1161/01.cir.99.17.2345
  61. https://www.sciencedirect.com/science/article/pii/S2211568421000395
  62. https://www.nature.com/articles/s41598-024-64445-2
  63. https://www.aafp.org/pubs/afp/issues/2017/0901/p293.html
  64. https://www.escardio.org/static-file/Escardio/Subspecialty/EACVI/position-papers/eae-sicari-stress-echo.pdf
  65. https://emedicine.medscape.com/article/1827089-technique
  66. https://www.asecho.org/wp-content/uploads/2020/01/Stress-Echo-2020.pdf
  67. https://pmc.ncbi.nlm.nih.gov/articles/PMC2435435/
  68. https://www.ahajournals.org/doi/10.1161/01.cir.0000036741.27574.ce
  69. https://pmc.ncbi.nlm.nih.gov/articles/PMC6932281/
  70. https://academic.oup.com/book/24348/chapter/187192898
  71. https://bcmj.org/articles/stress-testing-contribution-dr-robert-bruce-father-exercise-cardiology
  72. https://pmc.ncbi.nlm.nih.gov/articles/PMC6932031/
  73. https://jnm.snmjournals.org/content/49/3/399
  74. https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/thallium-201
  75. https://www.uscjournal.com/articles/past-present-and-future-stress-echocardiography-how-far-have-we-come-and-how-far-can-we-1?language_content_entity=en
  76. https://pubmed.ncbi.nlm.nih.gov/18165125/
  77. https://pmc.ncbi.nlm.nih.gov/articles/PMC4816914/
  78. https://www.ahajournals.org/doi/10.1161/CIRCIMAGING.116.003951
  79. https://www.accessdata.fda.gov/drugsatfda_docs/nda/2008/022161s000_LEXISCAN_APPROV.pdf
  80. https://pmc.ncbi.nlm.nih.gov/articles/PMC9695982/
  81. https://pubmed.ncbi.nlm.nih.gov/39081945/
  82. https://www.ahajournals.org/doi/10.1161/CIR.0000000000001029
  83. https://www.jacc.org/doi/10.1016/j.jacc.2024.07.022
  84. https://www.nature.com/articles/s41591-025-04044-4
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