Echocardiography was performed using contrast for all studies. The contrast agent used was a commercially available sulfur hexafluoride microbubble preparation, SonoVue (Bracco Imaging SpA). This agent was administered in 0.3-mL bolus doses intravenously for each image acquisition followed by 1 to 2 mL of saline flush. After acquisition of resting images to exclude significant valvular disease, intravenous dobutamine was infused at a starting dose of 10 µg·kg–1·min–1 followed by increasing doses of 20 µg·kg–1·min–1, 30 µg·kg–1·min–1, up to a maximum of 40 µg·kg–1·min–1 in 3-minute stages. Intravenous atropine was administered in 300-μg boluses up to a maximum of 1200 μg for those patients not achieving 85% of the predicted maximal heart rate. Images were taken in the apical 2-chamber, 3-chamber, 4-chamber, and parasternal short-axis views at baseline, low-dose stress, high-dose stress, and recovery
Stress echocardiography involves using cardiac ultrasound imaging along with exercise or pharmacological stressors like dobutamine to detect changes in heart wall motion that indicate reduced pumping function during stress. This can help identify blockages in the arteries to the heart. Dobutamine stress echocardiography involves gradually increasing doses of dobutamine, a drug that increases heart rate and contraction. Images are taken at each dose to detect any new wall motion abnormalities that would suggest ischemia. While it is effective for evaluating coronary artery disease, it also carries risks of side effects like arrhythmias that require emergency drugs like esmolol to reverse. Interpreting any new wall motion abnormalities seen under stress is important for diagnosis.
Stress echocardiography combines echocardiography with physical, pharmacological, or electrical stress to effectively evaluate for myocardial ischemia. It is used to screen for coronary artery disease and identify affected coronary territories. Stress echocardiography can also differentiate viable myocardium from scarred tissue and provides important prognostic information after myocardial infarction and before noncardiac surgery. Dobutamine stress echocardiography is widely used to assess viable myocardium while exercise stress echocardiography is preferred when possible due to its safety. Stress echocardiography techniques are safe and relatively inexpensive options for evaluating myocardial ischemia and viability.
Stress echocardiography uses ultrasound imaging during exercise or pharmacologic stress testing to detect ischemia-induced changes in heart wall motion. It has several advantages over nuclear stress testing including better visualization of cardiac structures and no radiation exposure. Various stress agents can be used including exercise, dobutamine, dipyridamole, and adenosine. Detection of new or worsening wall motion abnormalities or improvement after revascularization indicates viable myocardium. Factors like image quality, timing of acquisition, and operator experience can impact test sensitivity. Stress echo is an established technique for diagnosing coronary artery disease and assessing myocardial viability.
This document summarizes dobutamine stress echocardiography (DSE). Key points include:
- DSE uses the drug dobutamine to simulate exercise and increase heart rate, contractility, and myocardial oxygen demand to detect ischemia.
- It is useful for evaluating ischemia, viability, and valvular dysfunction in patients unable to exercise.
- The document reviews the DSE protocol, interpretation of wall motion abnormalities, indications, side effects, and applications for assessing ischemic heart disease, viability, valvular stenosis like mitral and aortic stenosis, and pulmonary hypertension.
The document discusses myocardial perfusion imaging (MPI), including:
1) MPI involves injecting a radiotracer at rest and stress to compare perfusion and detect decreased perfusion indicating myocardial ischemia or infarction.
2) Pharmacological agents like adenosine and dipyridamole are used for stress in patients who cannot exercise.
3) Stress imaging typically begins 15-45 minutes after radiotracer injection to allow for myocardial uptake.
This document discusses the physiological basis, methodology, safety, protocol, interpretation, and applications of stress echocardiography. Some key points:
- Stress echocardiography assesses the relationship between induced myocardial ischemia and regional wall motion abnormalities seen on ultrasound. Various stressors can be used including exercise, dobutamine, and dipyridamole.
- The technique is reasonably safe but pharmacological stress carries a higher risk than physical exercise. Side effects include arrhythmias, hypotension, and angina.
- Abnormalities are classified as hypokinesis, akinesis, dyskinesis, or scar. Inducible wall motion abnormalities indicate ischemia and have diagnostic and prognostic value for coronary artery
Stress echocardiography involves performing echocardiography at rest and during periods of stress, either through exercise or pharmacologically. It can evaluate cardiac function and detect regional wall motion abnormalities indicative of ischemia. Exercise stress echocardiography is commonly done with treadmill or bicycle exercise to detect coronary artery disease. Pharmacological stress with dobutamine or vasodilators like dipyridamole can be used for patients unable to exercise. The test aims to stimulate the heart and reveal any impairments in cardiac function during higher demand.
Exercise stress echocardiography in patients with aortic stenosis: impact of baseline diastolic dysfunction and functional capacity on mortality and aortic valve replacement
Authors: Andrew N. Rassi, Wael AlJaroudi, Sahar Naderi, M Chadi Alraies, Venu Menon, Leonardo Rodriguez, Richard Grimm, Brian Griffin, Wael A. Jaber
http://www.thecdt.org/article/view/2855
Stress echocardiography involves using cardiac ultrasound imaging along with exercise or pharmacological stressors like dobutamine to detect changes in heart wall motion that indicate reduced pumping function during stress. This can help identify blockages in the arteries to the heart. Dobutamine stress echocardiography involves gradually increasing doses of dobutamine, a drug that increases heart rate and contraction. Images are taken at each dose to detect any new wall motion abnormalities that would suggest ischemia. While it is effective for evaluating coronary artery disease, it also carries risks of side effects like arrhythmias that require emergency drugs like esmolol to reverse. Interpreting any new wall motion abnormalities seen under stress is important for diagnosis.
Stress echocardiography combines echocardiography with physical, pharmacological, or electrical stress to effectively evaluate for myocardial ischemia. It is used to screen for coronary artery disease and identify affected coronary territories. Stress echocardiography can also differentiate viable myocardium from scarred tissue and provides important prognostic information after myocardial infarction and before noncardiac surgery. Dobutamine stress echocardiography is widely used to assess viable myocardium while exercise stress echocardiography is preferred when possible due to its safety. Stress echocardiography techniques are safe and relatively inexpensive options for evaluating myocardial ischemia and viability.
Stress echocardiography uses ultrasound imaging during exercise or pharmacologic stress testing to detect ischemia-induced changes in heart wall motion. It has several advantages over nuclear stress testing including better visualization of cardiac structures and no radiation exposure. Various stress agents can be used including exercise, dobutamine, dipyridamole, and adenosine. Detection of new or worsening wall motion abnormalities or improvement after revascularization indicates viable myocardium. Factors like image quality, timing of acquisition, and operator experience can impact test sensitivity. Stress echo is an established technique for diagnosing coronary artery disease and assessing myocardial viability.
This document summarizes dobutamine stress echocardiography (DSE). Key points include:
- DSE uses the drug dobutamine to simulate exercise and increase heart rate, contractility, and myocardial oxygen demand to detect ischemia.
- It is useful for evaluating ischemia, viability, and valvular dysfunction in patients unable to exercise.
- The document reviews the DSE protocol, interpretation of wall motion abnormalities, indications, side effects, and applications for assessing ischemic heart disease, viability, valvular stenosis like mitral and aortic stenosis, and pulmonary hypertension.
The document discusses myocardial perfusion imaging (MPI), including:
1) MPI involves injecting a radiotracer at rest and stress to compare perfusion and detect decreased perfusion indicating myocardial ischemia or infarction.
2) Pharmacological agents like adenosine and dipyridamole are used for stress in patients who cannot exercise.
3) Stress imaging typically begins 15-45 minutes after radiotracer injection to allow for myocardial uptake.
This document discusses the physiological basis, methodology, safety, protocol, interpretation, and applications of stress echocardiography. Some key points:
- Stress echocardiography assesses the relationship between induced myocardial ischemia and regional wall motion abnormalities seen on ultrasound. Various stressors can be used including exercise, dobutamine, and dipyridamole.
- The technique is reasonably safe but pharmacological stress carries a higher risk than physical exercise. Side effects include arrhythmias, hypotension, and angina.
- Abnormalities are classified as hypokinesis, akinesis, dyskinesis, or scar. Inducible wall motion abnormalities indicate ischemia and have diagnostic and prognostic value for coronary artery
Stress echocardiography involves performing echocardiography at rest and during periods of stress, either through exercise or pharmacologically. It can evaluate cardiac function and detect regional wall motion abnormalities indicative of ischemia. Exercise stress echocardiography is commonly done with treadmill or bicycle exercise to detect coronary artery disease. Pharmacological stress with dobutamine or vasodilators like dipyridamole can be used for patients unable to exercise. The test aims to stimulate the heart and reveal any impairments in cardiac function during higher demand.
Exercise stress echocardiography in patients with aortic stenosis: impact of baseline diastolic dysfunction and functional capacity on mortality and aortic valve replacement
Authors: Andrew N. Rassi, Wael AlJaroudi, Sahar Naderi, M Chadi Alraies, Venu Menon, Leonardo Rodriguez, Richard Grimm, Brian Griffin, Wael A. Jaber
http://www.thecdt.org/article/view/2855
Cardiac stress tests are used to diagnose coronary artery disease by assessing how the heart responds to induced stress. Stress can be induced through exercise on a treadmill or stationary bike or through pharmacological agents. The test measures for changes in electrocardiography, echocardiography, or nuclear imaging before and after stress is applied to detect any signs of ischemia. Stress tests are indicated for diagnosing chest pain, prior heart attacks, or post-revascularization and help evaluate the heart's response to physical or drug stimulation.
The document discusses different types of exercise tests used to evaluate cardiovascular function, including isometric, dynamic, and mixed exercises. It describes the Bruce protocol treadmill exercise test in detail as the gold standard. The document lists various indications for exercise tolerance testing according to guidelines including diagnosing coronary artery disease, risk assessment after acute myocardial infarction, and evaluating persons with valvular heart disease or congenital heart conditions. Contraindications and subject preparations are also outlined.
This document discusses dobutamine stress echo, including:
1. Dobutamine stress echo is used to detect myocardial ischemia by inducing wall motion abnormalities, ECG changes, and symptoms through increasing myocardial oxygen demand.
2. Echo is used to visualize any wall motion abnormalities induced during stress. Dobutamine is preferable to other stressors as it more effectively precipitates myocardial dysfunction and is well-suited for imaging.
3. The test involves gradually increasing doses of dobutamine infusion while monitoring for changes on ECG and echo. It has various clinical applications including diagnosing CAD, assessing viability, and perioperative risk assessment. Serious complications are very rare.
This document provides information about exercise electrocardiography (ECG or EKG). It discusses how exercise ECG is a non-invasive tool to evaluate the cardiovascular system's response to exercise. During exercise, the body's metabolic rate and cardiac output increase significantly. The document outlines safety precautions for exercise ECG and describes physiological responses like changes in heart rate and oxygen uptake during exercise and recovery. Contraindications for the test and criteria for terminating the test early are also summarized. Finally, the document discusses benefits of exercise testing after a heart attack and some prognostic scoring systems used with exercise ECG.
1. Exercise testing involves monitoring a patient's physiological responses like ECG, heart rate, and blood pressure as the level of physical activity is gradually increased in a controlled setting.
2. It is used to evaluate cardiac function and exercise capacity in patients with conditions like heart disease or claudication.
3. Contraindications include recent heart attacks or procedures, unstable angina, and certain arrhythmias or heart failure. Precautions like rest and informed consent are required.
Stress echocardiography enables evaluation of cardiac function at rest and during exercise or pharmacologic stress. It can detect wall motion abnormalities indicative of ischemia and assess valvular function, left ventricular outflow tract gradients, and pulmonary pressures. Exercise or pharmacologic agents like dobutamine are used to induce stress. Indications include evaluating known or suspected coronary artery disease, viability, and valvular diseases. The test is contraindicated in acute coronary syndromes or hemodynamically significant valvular stenosis. Imaging is performed at rest and peak stress to detect new or worsening wall motion abnormalities. Doppler can also evaluate hemodynamic changes with stress.
Stress testing involves using exercise or medications to increase the heart rate and evaluate how the cardiovascular system responds to stress. There are several types of stress tests, with exercise stress tests being the most common. Exercise stress tests use treadmills or bicycles to gradually increase workload and monitor the patient's heart rate, blood pressure, ECG and symptoms. Stress tests can help detect ischemia, evaluate functional capacity and prognosis, and assess the effects of treatment in patients with suspected or known heart disease.
1. Treadmill testing (TMT) is used to detect myocardial ischemia by stressing the cardiovascular system during exercise and observing the physiological responses.
2. During TMT, increases in heart rate, blood pressure, cardiac output and oxygen consumption are measured along with ECG changes to detect ischemia.
3. Abnormal responses that may indicate ischemia include ST segment depression, elevated systolic blood pressure, chest pain, and failure to reach target heart rate.
Dobutamine stress echocardiography (DSE) is useful for diagnosing coronary artery disease and assessing myocardial viability. DSE can detect ischemia through worsening or new wall motion abnormalities and has high diagnostic accuracy compared to other stress tests. It is preferred over exercise stress in patients with arrhythmias, conduction disturbances, or respiratory issues. DSE also helps identify hibernating myocardium and predicts improved survival in ischemic cardiomyopathy patients after revascularization. While generally safe, pharmacological stress does carry higher risks than exercise stress.
The key points of exercise testing include manually measuring systolic blood pressure for safety, adjusting the protocol based on patient history, using the BORG scale to assess exertion rather than age-predicted heart rates, focusing on METs rather than exercise duration, using a ramp protocol when possible, avoiding hyperventilation and a cool down walk, using standard ECG analysis and a 3 minute recovery period, and considering heart rate recovery. The most important prognostic measurement is exercise capacity in METs. The most appropriate indicator of a maximal effort is the BORG scale.
The document summarizes the treadmill exercise stress test, which evaluates blood flow to the heart muscle during physical exercise compared to at rest. It discusses the purpose of stress tests to detect abnormalities, describes how a regular treadmill stress test is performed involving gradually increasing the treadmill speed and monitoring the EKG and blood pressure. The nursing role is to prepare the patient, monitor them during the test, and provide instructions afterwards depending on the results.
This document discusses questions related to cardiac stress testing, including treadmill tests. It addresses indications for stress testing, how medications like beta-blockers may affect results, fasting requirements, contraindications, and the importance of Bayesian statistics in test ordering. Key points covered include overnight fasting or 2 hours post-prandial for exercise treadmill tests, >4 hours fasting for myocardial perfusion imaging tests, using stress tests to diagnose coronary artery disease or assess prognosis, and common reasons for exercise test termination.
Stress tests use physical or pharmacological stress to detect coronary artery disease. Exercise treadmill testing is commonly used but has limitations. Myocardial perfusion imaging and stress echocardiography can detect ischemia through abnormal perfusion or wall motion changes during stress. The choice of stress test depends on the patient's clinical characteristics and contraindications to certain stress modalities.
This document provides an overview of stress echocardiography including objectives, indications, protocols, interpretation, and complications. Key points include: stress echo can evaluate CAD using exercise or pharmacologic stress with dobutamine; it has good sensitivity and specificity for CAD compared to nuclear imaging; and provides prognostic information on cardiac events. Interpretation focuses on changes in wall motion, ejection fraction, and detection of ischemia. Stress echo helps evaluate multiple conditions including viability, valvular disease, and cardiomyopathies.
Investigating stable IHD- Treadmill, Dobutamine stress echo or Stress thalliumcardiositeindia
This document discusses options for stress testing in patients with stable ischemic heart disease, including treadmill exercise testing (ETT), dobutamine stress echocardiography (DST), and myocardial perfusion imaging (MPI) with thallium or SPECT. ETT is preferred for most patients who can exercise and have a normal baseline ECG. DST and MPI are alternatives for those with intermediate pretest probability or non-diagnostic ETT. Each test has advantages and limitations regarding sensitivity, specificity, cost, radiation exposure, and ability to evaluate ventricular function, ischemia, and viability. Information from stress tests provides important prognostic indicators to guide clinical decisions.
The document discusses the treadmill test, which involves walking on a treadmill at increasing difficulty levels while monitoring electrocardiogram, heart rate, and blood pressure. It is used to evaluate how the heart responds to exertion and determine things like blood flow adequacy and likelihood of heart disease. Contraindications and techniques for administering the test are provided, along with details on the Bruce protocol and MET and Karvonen methods for calculating exercise intensity.
The document provides details about treadmill exercise testing, including:
1) It is used to assess cardiovascular disease by estimating functional capacity and the likelihood of coronary artery disease.
2) Safety precautions and equipment are required, and protocols like the Bruce protocol are commonly used to gradually increase workload over stages.
3) Measurements of oxygen uptake, ventilation, and other cardiorespiratory parameters are obtained to evaluate functional capacity and diagnose cardiovascular impairment.
This document discusses exercise tolerance tests (ETT) and stress testing to evaluate cardiac efficiency. It provides details on how cardiac efficiency can be determined through various clinical exams, tests like electrocardiography and echocardiography, and by performing cardiac efficiency tests. These tests measure the body's cardiovascular and respiratory response to standardized exercises and how quickly the body returns to baseline after exertion, providing insight into cardiac reserve and physical fitness. The document outlines protocols for ETTs and indexes used to evaluate physical fitness and cardiac efficiency. Factors influencing the body's response to exercise and components of physical fitness are also discussed.
The document describes a study comparing instantaneous wave-free ratio (iFR) to fractional flow reserve (FFR) for assessing coronary stenosis.
The study involved 2492 patients with intermediate coronary lesions randomized 1:1 to iFR-guided or FFR-guided percutaneous coronary intervention (PCI). The primary endpoint was a composite of death, myocardial infarction, or urgent revascularization at 30 days, 1 year, and 5 years.
Results showed non-inferiority of iFR-guided PCI compared to FFR-guided PCI for the primary endpoint. An iFR cutoff of 0.89 provided comparable classification of lesions to an FFR cutoff of 0.80. iFR assessment does not require induction
This study aimed to identify biomarkers associated with obstructive sleep apnea (OSA) severity and treatment effectiveness. The researchers measured biomarkers related to glucose regulation in patients before and after continuous positive airway pressure (CPAP) therapy. They found that levels of DHEA, cortisol and 17-OH progesterone were lower in OSA patients compared to normal ranges and did not change with CPAP. Serum glucose, HDL and triglycerides were not reliable markers of treatment response. The study was conducted at a comprehensive neurology and sleep center using patient medical records and biochemical analysis to obtain biomarker measurements.
Cardiac stress tests are used to diagnose coronary artery disease by assessing how the heart responds to induced stress. Stress can be induced through exercise on a treadmill or stationary bike or through pharmacological agents. The test measures for changes in electrocardiography, echocardiography, or nuclear imaging before and after stress is applied to detect any signs of ischemia. Stress tests are indicated for diagnosing chest pain, prior heart attacks, or post-revascularization and help evaluate the heart's response to physical or drug stimulation.
The document discusses different types of exercise tests used to evaluate cardiovascular function, including isometric, dynamic, and mixed exercises. It describes the Bruce protocol treadmill exercise test in detail as the gold standard. The document lists various indications for exercise tolerance testing according to guidelines including diagnosing coronary artery disease, risk assessment after acute myocardial infarction, and evaluating persons with valvular heart disease or congenital heart conditions. Contraindications and subject preparations are also outlined.
This document discusses dobutamine stress echo, including:
1. Dobutamine stress echo is used to detect myocardial ischemia by inducing wall motion abnormalities, ECG changes, and symptoms through increasing myocardial oxygen demand.
2. Echo is used to visualize any wall motion abnormalities induced during stress. Dobutamine is preferable to other stressors as it more effectively precipitates myocardial dysfunction and is well-suited for imaging.
3. The test involves gradually increasing doses of dobutamine infusion while monitoring for changes on ECG and echo. It has various clinical applications including diagnosing CAD, assessing viability, and perioperative risk assessment. Serious complications are very rare.
This document provides information about exercise electrocardiography (ECG or EKG). It discusses how exercise ECG is a non-invasive tool to evaluate the cardiovascular system's response to exercise. During exercise, the body's metabolic rate and cardiac output increase significantly. The document outlines safety precautions for exercise ECG and describes physiological responses like changes in heart rate and oxygen uptake during exercise and recovery. Contraindications for the test and criteria for terminating the test early are also summarized. Finally, the document discusses benefits of exercise testing after a heart attack and some prognostic scoring systems used with exercise ECG.
1. Exercise testing involves monitoring a patient's physiological responses like ECG, heart rate, and blood pressure as the level of physical activity is gradually increased in a controlled setting.
2. It is used to evaluate cardiac function and exercise capacity in patients with conditions like heart disease or claudication.
3. Contraindications include recent heart attacks or procedures, unstable angina, and certain arrhythmias or heart failure. Precautions like rest and informed consent are required.
Stress echocardiography enables evaluation of cardiac function at rest and during exercise or pharmacologic stress. It can detect wall motion abnormalities indicative of ischemia and assess valvular function, left ventricular outflow tract gradients, and pulmonary pressures. Exercise or pharmacologic agents like dobutamine are used to induce stress. Indications include evaluating known or suspected coronary artery disease, viability, and valvular diseases. The test is contraindicated in acute coronary syndromes or hemodynamically significant valvular stenosis. Imaging is performed at rest and peak stress to detect new or worsening wall motion abnormalities. Doppler can also evaluate hemodynamic changes with stress.
Stress testing involves using exercise or medications to increase the heart rate and evaluate how the cardiovascular system responds to stress. There are several types of stress tests, with exercise stress tests being the most common. Exercise stress tests use treadmills or bicycles to gradually increase workload and monitor the patient's heart rate, blood pressure, ECG and symptoms. Stress tests can help detect ischemia, evaluate functional capacity and prognosis, and assess the effects of treatment in patients with suspected or known heart disease.
1. Treadmill testing (TMT) is used to detect myocardial ischemia by stressing the cardiovascular system during exercise and observing the physiological responses.
2. During TMT, increases in heart rate, blood pressure, cardiac output and oxygen consumption are measured along with ECG changes to detect ischemia.
3. Abnormal responses that may indicate ischemia include ST segment depression, elevated systolic blood pressure, chest pain, and failure to reach target heart rate.
Dobutamine stress echocardiography (DSE) is useful for diagnosing coronary artery disease and assessing myocardial viability. DSE can detect ischemia through worsening or new wall motion abnormalities and has high diagnostic accuracy compared to other stress tests. It is preferred over exercise stress in patients with arrhythmias, conduction disturbances, or respiratory issues. DSE also helps identify hibernating myocardium and predicts improved survival in ischemic cardiomyopathy patients after revascularization. While generally safe, pharmacological stress does carry higher risks than exercise stress.
The key points of exercise testing include manually measuring systolic blood pressure for safety, adjusting the protocol based on patient history, using the BORG scale to assess exertion rather than age-predicted heart rates, focusing on METs rather than exercise duration, using a ramp protocol when possible, avoiding hyperventilation and a cool down walk, using standard ECG analysis and a 3 minute recovery period, and considering heart rate recovery. The most important prognostic measurement is exercise capacity in METs. The most appropriate indicator of a maximal effort is the BORG scale.
The document summarizes the treadmill exercise stress test, which evaluates blood flow to the heart muscle during physical exercise compared to at rest. It discusses the purpose of stress tests to detect abnormalities, describes how a regular treadmill stress test is performed involving gradually increasing the treadmill speed and monitoring the EKG and blood pressure. The nursing role is to prepare the patient, monitor them during the test, and provide instructions afterwards depending on the results.
This document discusses questions related to cardiac stress testing, including treadmill tests. It addresses indications for stress testing, how medications like beta-blockers may affect results, fasting requirements, contraindications, and the importance of Bayesian statistics in test ordering. Key points covered include overnight fasting or 2 hours post-prandial for exercise treadmill tests, >4 hours fasting for myocardial perfusion imaging tests, using stress tests to diagnose coronary artery disease or assess prognosis, and common reasons for exercise test termination.
Stress tests use physical or pharmacological stress to detect coronary artery disease. Exercise treadmill testing is commonly used but has limitations. Myocardial perfusion imaging and stress echocardiography can detect ischemia through abnormal perfusion or wall motion changes during stress. The choice of stress test depends on the patient's clinical characteristics and contraindications to certain stress modalities.
This document provides an overview of stress echocardiography including objectives, indications, protocols, interpretation, and complications. Key points include: stress echo can evaluate CAD using exercise or pharmacologic stress with dobutamine; it has good sensitivity and specificity for CAD compared to nuclear imaging; and provides prognostic information on cardiac events. Interpretation focuses on changes in wall motion, ejection fraction, and detection of ischemia. Stress echo helps evaluate multiple conditions including viability, valvular disease, and cardiomyopathies.
Investigating stable IHD- Treadmill, Dobutamine stress echo or Stress thalliumcardiositeindia
This document discusses options for stress testing in patients with stable ischemic heart disease, including treadmill exercise testing (ETT), dobutamine stress echocardiography (DST), and myocardial perfusion imaging (MPI) with thallium or SPECT. ETT is preferred for most patients who can exercise and have a normal baseline ECG. DST and MPI are alternatives for those with intermediate pretest probability or non-diagnostic ETT. Each test has advantages and limitations regarding sensitivity, specificity, cost, radiation exposure, and ability to evaluate ventricular function, ischemia, and viability. Information from stress tests provides important prognostic indicators to guide clinical decisions.
The document discusses the treadmill test, which involves walking on a treadmill at increasing difficulty levels while monitoring electrocardiogram, heart rate, and blood pressure. It is used to evaluate how the heart responds to exertion and determine things like blood flow adequacy and likelihood of heart disease. Contraindications and techniques for administering the test are provided, along with details on the Bruce protocol and MET and Karvonen methods for calculating exercise intensity.
The document provides details about treadmill exercise testing, including:
1) It is used to assess cardiovascular disease by estimating functional capacity and the likelihood of coronary artery disease.
2) Safety precautions and equipment are required, and protocols like the Bruce protocol are commonly used to gradually increase workload over stages.
3) Measurements of oxygen uptake, ventilation, and other cardiorespiratory parameters are obtained to evaluate functional capacity and diagnose cardiovascular impairment.
This document discusses exercise tolerance tests (ETT) and stress testing to evaluate cardiac efficiency. It provides details on how cardiac efficiency can be determined through various clinical exams, tests like electrocardiography and echocardiography, and by performing cardiac efficiency tests. These tests measure the body's cardiovascular and respiratory response to standardized exercises and how quickly the body returns to baseline after exertion, providing insight into cardiac reserve and physical fitness. The document outlines protocols for ETTs and indexes used to evaluate physical fitness and cardiac efficiency. Factors influencing the body's response to exercise and components of physical fitness are also discussed.
The document describes a study comparing instantaneous wave-free ratio (iFR) to fractional flow reserve (FFR) for assessing coronary stenosis.
The study involved 2492 patients with intermediate coronary lesions randomized 1:1 to iFR-guided or FFR-guided percutaneous coronary intervention (PCI). The primary endpoint was a composite of death, myocardial infarction, or urgent revascularization at 30 days, 1 year, and 5 years.
Results showed non-inferiority of iFR-guided PCI compared to FFR-guided PCI for the primary endpoint. An iFR cutoff of 0.89 provided comparable classification of lesions to an FFR cutoff of 0.80. iFR assessment does not require induction
This study aimed to identify biomarkers associated with obstructive sleep apnea (OSA) severity and treatment effectiveness. The researchers measured biomarkers related to glucose regulation in patients before and after continuous positive airway pressure (CPAP) therapy. They found that levels of DHEA, cortisol and 17-OH progesterone were lower in OSA patients compared to normal ranges and did not change with CPAP. Serum glucose, HDL and triglycerides were not reliable markers of treatment response. The study was conducted at a comprehensive neurology and sleep center using patient medical records and biochemical analysis to obtain biomarker measurements.
This document provides an overview of vascular laboratory assessments for peripheral arterial disease (PAD). It discusses the importance of noninvasive tests like ankle-brachial pressure index (ABPI) in evaluating PAD and outlines the history, indications, modalities, and clinical applications of various physiologic tests. These include segmental limb pressure monitoring, exercise testing, reactive hyperemia testing, toe-brachial indexing, and plethysmography for evaluating the severity and location of PAD.
Prospective, randomized comparison of two biphasicalatawi2
This study compared the effectiveness and safety of two biphasic waveforms - biphasic truncated exponential (BTE) and biphasic rectilinear (BR) - for external cardioversion of atrial fibrillation. 141 patients were randomized to receive transthoracic shocks using either the BTE or BR waveform. The success rate was similar between the two waveforms (93% for BR vs 97% for BTE), though cumulative energy delivered was lower in the BTE group. Only duration of atrial fibrillation was significantly associated with cardioversion success. No significant complications occurred with either waveform. The study found no significant difference in efficacy between the BR and BTE waveforms for transthoracic cardio
This study evaluated the outcomes of 23 patients presenting with pulseless electrical activity (PEA) due to confirmed pulmonary embolism (PE) who were treated with thrombolysis. All patients received 50 mg of tissue plasminogen activator (tPA) intravenously during ongoing cardiopulmonary resuscitation (CPR). Return of spontaneous circulation occurred in most patients within 15 minutes of tPA administration. At a mean follow up of 22 months, 20 of the 23 patients (87%) were still alive with significant reductions in pulmonary artery pressures and right ventricular enlargement. The study demonstrated that rapid administration of low-dose tPA during CPR for PEA due to PE is safe and effective for restoring circulation and
1) A study examined 103 heart attack patients treated with high-dose statins and found plaque volume decreased slightly (0.9%) in the arteries not responsible for the heart attack.
2) A randomized study of 296 heart attack patients found that performing revascularization of additional blocked arteries beyond the heart attack artery led to fewer total cardiac events (10% vs 21%) over 12 months compared to only treating the heart attack artery.
3) A study of 738 patients with chronic total blockages and good collateral blood flow found that revascularizing the blockages reduced cardiac death and total cardiac events compared to medical treatment alone, showing benefit of revascularization even in patients with established collateral circulation.
This document summarizes a talk on nuclear cardiac imaging (myocardial perfusion imaging). It begins with an introduction to MPI, describing what it is, how images look, and its clinical value. Examples of MPI images showing normal perfusion, ischemia, and infarction are provided. The document then discusses the diagnostic approach and different populations that benefit from MPI, highlighting its use in diagnosing and prognosing coronary artery disease. Throughout, it emphasizes the importance and advantages of MPI, especially for evaluating women's cardiac risk.
REVIEW ARTICLE SEPTEMBER 2021 medical.pptxArunDeva8
This document summarizes the evolving use of biomarkers in the management of heart failure. It discusses how biomarkers such as BNP, NT-proBNP, cTn, ST2, and galectin-3 can be used to diagnose heart failure, establish disease prognosis and severity, and predict patient outcomes. Elevated levels of these biomarkers are associated with worse symptoms and higher mortality in heart failure patients. The document also presents a case study of an elderly male patient presenting with heart failure symptoms and discusses the clinical implications of his elevated BNP and cTnT biomarker levels.
Highlights from American College of Cardiology 2019ArunSharma10
The document summarizes highlights from the 2019 American College of Cardiology Annual Scientific Session. Key findings presented included:
1) Results from two major studies showed transcatheter aortic valve replacement (TAVR) may be preferred over surgical replacement for patients with severe aortic stenosis even at low surgical risk.
2) Data from the Apple Heart Study suggested the Apple Watch can help detect atrial fibrillation in some patients.
3) The new 2019 ACC/AHA guidelines on primary prevention of cardiovascular disease recommend against broad use of aspirin, based on results from three recent trials.
Low dose dopamine increases GFR and RBF. The DAD-HF trial investigated 60 patients randomized to low dose furosemide (continuous infusion 0.5 mg/kg/day) with or without low dose dopamine (2 μg/kg/min). Dopamine preserved renal function compared to furosemide alone in patients with acute decompensated heart failure. There were no significant differences found in a trial comparing high vs low dose furosemide or bolus vs continuous infusion on renal function or symptoms. Novel agents targeting fluid overload, renal function, contractility, and vasomotion may provide new therapeutic options for acute heart failure.
Prof. U. C. SAMAL provides an overview of acute decompensated heart failure and what is new in the field. He discusses similarities and differences between acute myocardial infarction and acute heart failure syndromes. Mortality rates are high for both conditions, though clinical benefits of interventions are greater for acute MI based on published clinical trials. The document then discusses definitions and classifications of acute heart failure syndromes, as well as guidelines for diagnosis and treatment from ESC and ACC/AHA. Biomarkers that can help with diagnosis, prognosis, and guiding therapy are also summarized.
Although right ventricular (RV) apical pacing is an established practice since the first pacemaker implant in early sixties, recent studies have highlighted its deleterious effects. This has led to a concept of ‘minimizing RV pacing’ to prevent long term negative effects of RV pacing. New features have been added to pacemaker models to achieve this aim. This article looks at negative effects of RV pacing and how to minimize it.
The document summarizes a study comparing outcomes of patients who underwent aortic arch surgery using antegrade cerebral perfusion (ACP) versus without ACP. The study found significantly lower rates of postoperative stroke (2% vs 13%) and better 3-year survival (93% vs 78%) in the ACP group. Multivariate analysis confirmed ACP was associated with reduced stroke risk and improved long-term survival. The results suggest ACP provides neuroprotective and survival advantages over surgery without ACP for aortic arch pathology requiring prolonged repair periods.
The effects of_rosuvastatin_on_plaque_regression_i19844
This study evaluated the effects of rosuvastatin versus atorvastatin on plaque regression in patients with mild to moderate coronary stenosis and vulnerable plaque. 30 patients received either rosuvastatin 20 mg or atorvastatin 40 mg daily for 12 months. Intravascular ultrasound was performed at baseline and follow-up to measure atheroma volume, lipid pool size, and other metrics. Both statins significantly reduced LDL cholesterol by over 40% from baseline to follow-up. Both treatments also significantly reduced total atheroma volume while increasing lumen volume, with no significant differences between the groups. Follow-up LDL levels correlated with reductions in atheroma, lipid pools, and increases in lumen size.
Invasive coronary physiology to select patients for coronary revascularisation has become established in contemporary guidelines for the management of stable coronary artery disease. Compared to revascularisation based on angiography alone, the use of coronary physiology has been shown to improve clinical outcomes and cost efficiency. However, recent data from randomised controlled trials have cast doubt upon
the value of ischaemia testing to select patients for revascularisation. Importantly, 20-40% of patients have
persistence or recurrence of angina after angiographically successful percutaneous coronary intervention
(PCI). This state-of-the-art review is focused on the transitioning role of invasive coronary physiology from
its use as a dichotomous test for ischaemia with fixed cut-points, towards its utility for real-time guidance of PCI to optimise physiological results. We summarise the contemporary evidence base for ischaemia testing
in stable coronary artery disease, examine emerging indices which allow advanced physiological guidance
of PCI, and discuss the rationale and evidence base for post-PCI physiological assessments to assess the success of revascularisation.
The document summarizes research on sleep apnea in heart failure patients. It finds:
- Sleep apnea is highly prevalent in heart failure patients, with studies finding 47-49% have an apnea-hypopnea index over 15 events per hour. Central sleep apnea makes up 15-46% of cases.
- Central sleep apnea independently predicts mortality in heart failure patients and is associated with reduced left and right ventricular function.
- Treatments for central sleep apnea like supplemental nocturnal oxygen, theophylline, acetazolamide, and CPAP can improve sleep quality and reduce apnea episodes and symptoms. However, a large clinical trial found CPAP did not significantly impact heart transplantation-free
The document discusses the use of clinical examination to measure congestion in heart failure patients. It finds that the clinical examination is a cheap, low-risk way to assess hemodynamic status and risk stratify patients by measuring parameters like jugular venous pressure and using dynamic maneuvers. The presence of clinical congestion on examination or at discharge is associated with worse outcomes like rehospitalization and death. Maintaining decongestion after discharge is also linked to lower mortality. Overall, the clinical exam provides useful information and remains a foundation for congestion assessment.
1. A Cochrane review found that for untrained bystanders, continuous chest compressions without rescue breathing improved survival to hospital discharge compared to interrupted CPR. For trained professionals, interrupted CPR had slightly better outcomes.
2. The AHA recommends that untrained lay rescuers provide continuous chest compressions with or without dispatcher assistance for adults in cardiac arrest. For trained lay rescuers, compression-only CPR is recommended.
3. A study found no difference in outcomes between continuous compressions with asynchronous ventilations and 30:2 CPR. 30:2 CPR was associated with better outcomes than 15:2 CPR. It may be reasonable for EMS to use 10 breaths per
The patient with AHF on the ICU : Respiratory Supportdrucsamal
This document discusses respiratory support for patients with acute heart failure in the intensive care unit (ICU). It provides the following key points:
1. Noninvasive ventilation (NIV), including CPAP and bilevel PAP, should be the first-line treatment for acute pulmonary edema and can reduce intubation rates and mortality compared to conventional oxygen therapy.
2. High-flow nasal cannula oxygen is an alternative to NIV and has been shown to reduce intubation compared to conventional oxygen in patients with acute hypoxemic respiratory failure.
3. Invasive mechanical ventilation should be reserved for patients with significant hypercapnia, acidosis or respiratory distress that cannot be managed with NIV.
This document discusses the role of nuclear medicine imaging in evaluating patients presenting with acute chest pain. It outlines how nuclear imaging techniques like acute rest myocardial perfusion imaging (MPI) can help distinguish between cardiac causes like acute coronary syndrome from non-cardiac causes. MPI provides high sensitivity and negative predictive value in detecting acute myocardial ischemia. The document compares the diagnostic accuracy of MPI to electrocardiograms and cardiac biomarkers in evaluating acute chest pain.
Similar to Dobutamine stress echocardiography (20)
A 57-year-old woman was admitted to the hospital with chest pain. Electrocardiograms and troponin levels were normal. Intravascular ultrasound was performed before placing a stent in the left main coronary artery and left anterior descending artery to treat a blockage. The minimum lumen area increased to 4.24mm x 4.13mm after stenting.
Congenital defects can put a strain on the heart, causing it to work harder. To stop your heart from getting weaker with this extra work, your doctor may try to treat you with medications. They are aimed at easing the burden on the heart muscle. You need to control your blood pressure if you have any type of heart problem.
Changing your lifestyle can help control and manage high blood pressure. Your health care provider may recommend that you make lifestyle changes including:
Eating a heart-healthy diet with less salt
Getting regular physical activity
Maintaining a healthy weight or losing weight
Limiting alcohol
Not smoking
Getting 7 to 9 hours of sleep daily
CRISPR technologies have progressed by leaps and bounds over the past decade, not only having a transformative effect on
biomedical research but also yielding new therapies that are poised to enter the clinic. In this review, I give an overview of (i)
the various CRISPR DNA-editing technologies, including standard nuclease gene editing, base editing, prime editing, and epigenome editing, (ii) their impact on cardiovascular basic science research, including animal models, human pluripotent stem
cell models, and functional screens, and (iii) emerging therapeutic applications for patients with cardiovascular diseases, focusing on the examples of Hypercholesterolemia, transthyretin amyloidosis, and Duchenne muscular dystrophy.
This case report describes a patient who underwent seven operations over one year to treat recurrent pacemaker pocket infections. The patient had undergone a splenectomy seven years prior due to a splenic rupture from a traffic accident. This left the patient immunocompromised and at higher risk for infection. The patient later required a pacemaker implantation for complete heart block. The pacemaker pocket developed repeated infections, likely due to the patient's asplenic state impairing immunity. The infections were difficult to treat due to multiple complicating factors, including an abandoned pacemaker lead and reuse of a sterilized pacemaker. This highlights the influence of patient factors like asplenia on procedural outcomes like pacemaker implantation.
Transcatheter closure of patent ductus arteriosus (PDA) is feasible in low-birth-weight infants. A female baby was born prematurely with a birth weight of 924 g. She had a PDA measuring 3.7 mm. She was dependent on positive pressure ventilation for congestive heart failure in addition to the heart failure medications. She could not be discharged from the hospital even after 79 days of birth, and even though her weight reached 1.9 kg in the neonatal intensive care unit. We attempted to plug the PDA using an Amplatzer Piccolo Occluder, but the device failed to anchor. Then, the PDA was plugged using a 4-6 Amplatzer Duct Occluder using a 6-Fr sheath which was challenging.
Accidental misplacement of the limb lead electrodes is a common cause of ECG abnormality and may simulate pathology such as ectopic atrial rhythm, chamber enlargement or myocardial ischaemia and infarction
A Case of Device Closure of an Eccentric Atrial Septal Defect Using a Large D...Ramachandra Barik
Device closure of an eccentric atrial septal defect can be challenging and needs technical modifications to avoid unnecessary complications. Here, we present a case of a 45-year-old woman who underwent device closure of an eccentric defect with a large device. The patient developed pericardial effusion and left-sided pleural effusion due to injury to the junction of right atrium and superior vena cava because of the malalignment of the delivery sheath and left atrial disc before the device was pulled across the eccentric defect despite releasing the left atrial disc in the left atrium in place of the left pulmonary vein. These two serious complications were managed conservatively with close monitoring of the case during and after the procedure.
1) Bradycardia can be caused by abnormalities in the conduction system or autonomic nervous system. The conduction system includes the sinus node, AV node, His-Purkinje system and different types of heart block can occur when impulses are blocked at different locations.
2) There are three main types of AV block - first degree, second degree (Mobitz types I and II), and third degree. High grade AV block involves blockage of two or more consecutive impulses.
3) Third degree or complete heart block results in complete dissociation between the atria and ventricles with independent pacemakers. It can occur at the AV node or below in the His-Purkin
1. Bradycardia is defined as a resting heart rate below 50 beats per minute. It can be physiological or pathological.
2. Sinus bradycardia originates from the sinus node and has a normal P wave morphology with a prolonged PR interval. It can be caused by increased vagal tone, medications, or hypothyroidism.
3. Sick sinus syndrome is characterized by sinus bradycardia, sinus arrest, or combinations of sinus node and AV node dysfunction. It may involve intermittent bradycardia and tachycardia. Pacemaker implantation is usually treatment.
This document discusses ventricular arrhythmias including their origins, characteristics, classifications, and causes. It provides details on:
- The sites of origin for supraventricular tachycardia (SVT) and ventricular arrhythmias.
- Characteristics that distinguish SVT from ventricular arrhythmias such as QRS width.
- Classifications of ventricular arrhythmias including premature ventricular complexes, ventricular tachycardia, fibrillation, and electrical storm.
- Causes and characteristics of different types of ventricular tachycardia such as monomorphic VT, polymorphic VT, and torsades de pointes.
- Investigations and treatments for ventricular arrhythmias including cardiac imaging
This document provides information on supraventricular tachycardia (SVT), including:
- The anatomy and conduction system of the heart that is relevant to SVT.
- The mechanisms that can cause cardiac arrhythmias, including disorders of impulse formation, conduction, and combinations of the two.
- Characteristics used to classify different types of arrhythmias based on rate, rhythm, site of origin, and QRS morphology.
- Specific types of SVT like atrial fibrillation, AV nodal reentry tachycardia, and accessory pathway mediated tachycardias.
- Methods for diagnosing and treating SVT such as electrophysiology studies, catheter ablation
Trio of Rheumatic Mitral Stenosis, Right Posterior Septal Accessory Pathway a...Ramachandra Barik
A 57-year-old male presented with recurrent palpitations. He was diagnosed with rheumatic mitral stenosis, right posterior septal accessory pathway and atrial flutter. An electrophysiological study after percutaneous balloon mitral valvotomy showed that the palpitations were due to atrial flutter with right bundle branch aberrancy. The right posterior septal pathway was a bystander because it had a higher refractory period than the atrioventricular node.
This document discusses anticoagulation therapy options during pregnancy for different cardiac conditions. It notes that vitamin K antagonists (VKAs) should be avoided in the first trimester due to risk of embryopathy but can be used in the second and third trimester with risks of 0.7-2% of foetopathy. Unfractionated heparin does not cross the placenta but its use throughout pregnancy is not recommended due to risk of foetopathy. Low molecular weight heparin is considered the safest option for anticoagulation in weeks 6-12 when risk of embryopathy is a concern and has not been associated with risk of foetopathy. Fondaparinux use should be limited
Percutaneous balloon dilatation, first described by
Andreas Gruentzig in 1979, was initially performed
without the use of guidewires.1 The prototype
balloon catheter was developed as a double lumen
catheter (one lumen for pressure monitoring or
distal perfusion, the other lumen for balloon inflation/deflation) with a short fixed and atraumatic
guidewire at the tip. Indeed, initially the technique
involved advancing a rather rigid balloon catheter
freely without much torque control into a coronary
artery. Bends, tortuosities, angulations, bifurcations,
and eccentric lesions could hardly, if at all, be negotiated, resulting in a rather frustrating low procedural success rate whenever the initial limited
indications (proximal, short, concentric, noncalcified) were negated.2 Luck was almost as
important as expertise, not only for the operator,
but also for the patient. It is to the merit of
Simpson who, in 1982, introduced the novelty of
advancing the balloon catheter over a removable
guidewire, which had first been advanced in the
target vessel.3 This major technical improvement
resulted overnight in a notable increase in the procedural success rate. Guidewires have since evolved
into very sophisticated devices.
Optical coherence tomography-guided algorithm for percutaneous coronary intervention. Vessel diameter should be assessed using the external elastic lamina (EEL)-EEL diameter at the reference segments, and rounded down to select interventional devices (balloons, stents). If the EEL cannot be identified, luminal measures are used and rounded up to 0.5 mm larger for selection of the devices. Optical coherence tomography (OCT)-guided optimisation strategies post stent implantation per EEL-based diameter measurement and per lumen-based diameter measurement are shown. For instance, if the distal EEL-EEL diameter measures 3.2 mm×3.1 mm (i.e., the mean EEL-based diameter is 3.15 mm), this number is rounded down to the next available stent size and post-dilation balloon to be used at the distal segment. Thus, a 3.0 mm stent and non-compliant balloon diameter is selected. If the proximal EEL cannot be visualised, the mean lumen diameter should be used for device sizing. For instance, if the mean proximal lumen diameter measures 3.4 mm, this number is rounded up to the next available balloon diameter (within up to 0.5 mm larger) for post-dilation. MLA: minimal lumen area; MSA: minimal stent area;NC: non-compliant
Brugada syndrome (BrS) is an inherited cardiac disorder,
characterised by a typical ECG pattern and an increased
risk of arrhythmias and sudden cardiac death (SCD).
BrS is a challenging entity, in regard to diagnosis as
well as arrhythmia risk prediction and management.
Nowadays, asymptomatic patients represent the majority
of newly diagnosed patients with BrS, and its incidence
is expected to rise due to (genetic) family screening.
Progress in our understanding of the genetic and
molecular pathophysiology is limited by the absence
of a true gold standard, with consensus on its clinical
definition changing over time. Nevertheless, novel
insights continue to arise from detailed and in-depth
studies, including the complex genetic and molecular
basis. This includes the increasingly recognised
relevance of an underlying structural substrate. Risk
stratification in patients with BrS remains challenging,
particularly in those who are asymptomatic, but recent
studies have demonstrated the potential usefulness
of risk scores to identify patients at high risk of
arrhythmia and SCD. Development and validation of
a model that incorporates clinical and genetic factors,
comorbidities, age and gender, and environmental
aspects may facilitate improved prediction of disease
expressivity and arrhythmia/SCD risk, and potentially
guide patient management and therapy. This review
provides an update of the diagnosis, pathophysiology
and management of BrS, and discusses its future
perspectives.
The Human Developmental Cell Atlas (HDCA) initiative, which is part of the Human Cell Atlas, aims to create a comprehensive reference map of cells during development. This will be critical to understanding normal organogenesis, the effect of mutations, environmental factors and infectious agents on human development, congenital and childhood disorders, and the cellular basis of ageing, cancer and regenerative medicine. Here we outline the HDCA initiative and the challenges of mapping and modelling human development using state-of-the-art technologies to create a reference atlas across gestation. Similar to the Human Genome Project, the HDCA will integrate the output from a growing community of scientists who are mapping human development into a unified atlas. We describe the early milestones that have been achieved and the use of human stem-cell-derived cultures, organoids and animal models to inform the HDCA, especially for prenatal tissues that are hard to acquire. Finally, we provide a roadmap towards a complete atlas of human development.
The treatment of patients with advanced acute heart failure is still challenging.
Intra-aortic balloon pump (IABP) has widely been used in the management of
patients with cardiogenic shock. However, according to international guidelines, its
routinary use in patients with cardiogenic shock is not recommended. This recommendation is derived from the results of the IABP-SHOCK II trial, which demonstrated
that IABP does not reduce all-cause mortality in patients with acute myocardial infarction and cardiogenic shock. The present position paper, released by the Italian
Association of Hospital Cardiologists, reviews the available data derived from clinical
studies. It also provides practical recommendations for the optimal use of IABP in
the treatment of cardiogenic shock and advanced acute heart failure.
Left ventricular false tendons (LVFTs) are fibromuscular
structures, connecting the left ventricular
free wall or papillary muscle and the ventricular
septum.
There is some discussion about safety issues during
intense exercise in athletes with LVFTs, as these
bands have been associated with ventricular arrhythmias
and abnormal cardiac remodelling. However,
presence of LVFTs appears to be much more common
than previously noted as imaging techniques
have improved and the association between LVFTs
and abnormal remodelling could very well be explained
by better visibility in a dilated left ventricular
lumen.
Although LVFTsmay result in electrocardiographic abnormalities
and could form a substrate for ventricular
arrhythmias, it should be considered as a normal
anatomic variant. Persons with LVFTs do not appear
to have increased risk for ventricular arrhythmias or
sudden cardiac death.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
Our backs are like superheroes, holding us up and helping us move around. But sometimes, even superheroes can get hurt. That’s where slip discs come in.
2. Al-Lamee et al Stress Echocardiography-Stratified ORBITA Analysis
December 10, 2019 Circulation. 2019;140:1971–1980. DOI: 10.1161/CIRCULATIONAHA.119.0429181972
ORIGINALRESEARCH
ARTICLE
T
he primary results of the ORBITA trial (Objective
Randomised Blinded Investigation With Optimal
Medical Therapy of Angioplasty in Stable Angina)
showed a smaller-than-expected effect size of percuta-
neous coronary intervention (PCI) in comparison with
placebo in single-vessel stable coronary artery disease
on the primary end point of change in treadmill exer-
cise time.1
These findings of ORBITA contrasted with
those of previous unblinded trials which showed that
patients aware that they had received PCI had a clear
improvement in exercise time, reduction in angina, and
improved quality of life, in comparison with patients
aware that they had not received PCI.2–7
Although there was no significant difference be-
tween PCI and placebo groups in the patient-reported
and physician-assessed symptom and quality-of-life end
points, ischemia as assessed by dobutamine stress echo-
cardiography (DSE) wall motion score index showed a
clear reduction with PCI (prerandomization to follow-
up increment: –0.07 in the PCI arm versus 0.02 in the
placebo arm, P0.0001).
Building on the primary analysis, the physiology-strati-
fied analysis of ORBITA found that the severity of ischemia
assessed by prerandomization fractional flow reserve (FFR)
and instantaneous wave-free ratio (iFR) predicted the
degree of improvement of ischemia as assessed by DSE
score in the 196 patients with prerandomization invasive
physiology data.8
However, there was no detectable in-
teraction between invasive physiology and the placebo-
controlled effect of PCI on symptoms or exercise time.
Again, these findings contrasted with those of unblinded
studies.9,10
Without placebo control, and with staff aware
of measurements, there was a clear relationship between
FFR or iFR and symptoms or exercise time.
In previous data sets11
and in ORBITA, PCI almost com-
pletely normalizes any left ventricular wall motion abnor-
malities detected by DSE. However, there has been no
assessment of whether the magnitude of baseline stress
echocardiography ischemia determines the magnitude
of symptom relief from PCI, beyond any placebo effect.
In the present analysis of patients who had preran-
domization DSE data, we stratified by the prerandom-
ization stress echocardiography score and assessed its
impact on the placebo-controlled effect of PCI on the
primary and secondary end points of ORBITA.
METHODS
The data, analytical methods, and study materials will not be
made available to other researchers for purposes of repro-
ducing the results or replicating the procedure. The London
Central Research Ethics Committee (reference 13/LO/1340)
approved the study and written consent was obtained from
all patients before their enrollment.
Study Design
The design of the ORBITA trial has been reported previously.1
In brief, the ORBITA trial was a double-blind randomized,
controlled trial comparing PCI with a placebo procedure in
patients with stable angina and angiographically severe sin-
gle-vessel coronary artery disease. Intensive medical therapy
was given to both groups. Before randomization, patients
had assessment of symptom and quality-of-life question-
naires, cardiopulmonary exercise testing using a smoothed
modified Bruce protocol, DSE, and FFR and iFR measurement.
Blinding and Randomization
Patients were randomly assigned 1:1 to PCI or a placebo
procedure. Patients and the medical team outside the cath-
eterization laboratory were blinded to treatment allocation as
previously described.1
Study End Points and Follow-Up
At the end of the 6-week blinded period, patients returned
for the repeat of all prerandomization tests including symp-
tom and quality-of-life questionnaires, cardiopulmonary exer-
cise testing, and DSE.
DSE Assessment
Patients were instructed to omit β-blockers for at least 24
hours before DSE. The test was performed by a physician and
Clinical Perspective
What Is New?
• This report of ORBITA (Objective Randomised
Blinded Investigation With Optimal Medical Ther-
apy of Angioplasty in Stable Angina), stratified
by ischemia assessed by stress echocardiography,
provides the first placebo-controlled evidence of
an association between stress echocardiography
ischemia and the magnitude of placebo-controlled
benefit attributable to percutaneous coronary
intervention.
• Prerandomization stress echocardiography score pre-
dicts the placebo-controlled effect of percutaneous
coronary intervention on angina frequency score.
What Are the Clinical Implications?
• Although in ORBITA there was no detectable pla-
cebo-controlled reduction in angina frequency with
percutaneous coronary intervention, this analysis
shows that the greater the prerandomization stress
echocardiography score, the greater the placebo-
controlled reduction in angina.
• For patients with a stress echocardiography score
of at least 1, there is a clear placebo-controlled
reduction in patient-reported symptoms with per-
cutaneous coronary intervention.
• This dependence of symptomatic relief on preran-
domization ischemia was evident with stress echo-
cardiography, but not with invasive physiology.
Downloadedfromhttp://ahajournals.orgbyonDecember11,2019
3. Al-Lamee et al Stress Echocardiography-Stratified ORBITA Analysis
Circulation. 2019;140:1971–1980. DOI: 10.1161/CIRCULATIONAHA.119.042918 December 10, 2019 1973
ORIGINALRESEARCH
ARTICLE
a sonographer. The patient, physician, and sonographer were
all blinded to allocation arm.
Echocardiography was performed using contrast for all
studies. The contrast agent used was a commercially avail-
able sulfur hexafluoride microbubble preparation, SonoVue
(Bracco Imaging SpA). This agent was administered in 0.3-
mL bolus doses intravenously for each image acquisition
followed by 1 to 2 mL of saline flush. After acquisition of
resting images to exclude significant valvular disease, intrave-
nous dobutamine was infused at a starting dose of 10 µg·kg–
1
·min–1
followed by increasing doses of 20 µg·kg–1
·min–1
, 30
µg·kg–1
·min–1
, up to a maximum of 40 µg·kg–1
·min–1
in 3-min-
ute stages. Intravenous atropine was administered in 300-μg
boluses up to a maximum of 1200 μg for those patients not
achieving 85% of the predicted maximal heart rate. Images
were taken in the apical 2-chamber, 3-chamber, 4-chamber,
and parasternal short-axis views at baseline, low-dose stress,
high-dose stress, and recovery.
DSE Reporting
Analysis was also performed with reporters blinded to treat-
ment allocation and phase (prerandomization or follow-up),
using an online reporting tool.
Each scan was examined twice by 6 imaging consultants
(R.A., D.P.F., G.C., G.K., J.S., and N.G.K.) who were blinded to
treatment allocation, time point of the scan, their colleagues’
opinions, and their own first opinion.
Stress echocardiography results are presented in a man-
ner that represents the number of hypokinetic segments
(with akinetic segments scoring double, dyskinetic segments
scoring triple, and aneurysmal segments scoring quadruple).
The left ventricle was divided into the standard 17-segment
model. Wall motion was scored as follows: normal=0, hypoki-
netic=1, akinetic=2, dyskinetic=3, or aneurysmal=4. Individual
wall abnormality scores at peak stress were summed. Both
opinions from all 6 consultants were averaged. The stress
echocardiography score8
can be broadly converted to clas-
sical wall motion score index as follows: wall motion score
index=1+(stress echocardiography score)/17. More details are
provided in the online-only Data Supplement.
Statistical Analysis
Summary statistics were presented as appropriate for baseline
characteristics. To assess the observer variability of the stress
echocardiography score, we calculated the mean inter- and
intraobserver absolute differences.12
Models were fitted for each end point. Models using ordi-
nary least squares were used for the continuous variables:
Seattle Angina Questionnaire (SAQ) physical limitation and
quality-of-life score, EuroQOL 5 (EQ-5D-5L) descriptive score,
and exercise time. Proportional odds logistic models were
used for ordinal variables: SAQ angina frequency score and
freedom from angina, and Canadian Cardiovascular Society
angina class. For each of the components of the SAQ, and
freedom from angina, as well, a higher score represents a bet-
ter health state; therefore, an odds ratio 1 suggests that a
better health state was achieved with PCI over placebo.
To assess the interaction of prerandomization stress echo-
cardiography score with each continuous and categorical out-
come variable, the follow-up value was modeled conditioned
on the prerandomization value transformed by a restricted
cubic spline with 3 parameters, and randomization arm. A
model was then fitted with prerandomization stress echo-
cardiography score interacting with the randomization arm
with a restricted cubic spline with 3 parameters. Knots were
placed at the standard positions of 25th, 50th, and 75th per-
centiles of the covariate distribution. Therefore, the shape
of the effect was allowed to vary over treatments.13
Graphs
are shown of the end points against prerandomization stress
echocardiography score. The contrast between the arms
was generated with an adjustment for the median value of
the prerandomization value. The vertical coordinate of the
graphs is the difference in end value between the 2 arms,
conditioned on their prerandomization value. We report the
interaction with treatment as the P value (Pinteraction
) from the
combined main effect and interaction effect.
Analyses were performed using the open-source statistical
environment R,14
with the package rms for regression model-
ing15
and ggplot2 for graphs.16
RESULTS
Prerandomization stress echocardiography scores were
available for 183 patients (98 PCI and 85 placebo) of
the 200 patients randomly assigned in ORBITA. Of the
remaining 17 patients, 1 had poor-quality echocardio-
graphic imaging windows, 6 had a previous adverse
reaction to dobutamine (5 minor but limiting reac-
tions, 1 severe life-threatening reaction), 6 had a clini-
cal contraindication to dobutamine administration,
and in 4 there were logistical reasons as to why the
test was not performed.
Patient Demographics
Table 1 shows the patient demographic data. The ma-
jority of patients had normal left ventricular systolic
function (94.9% in the PCI arm and 90.6% in the pla-
cebo arm). Median angina duration was 5 months in
the PCI arm (interquartile range, 4–10) and 6 months in
the placebo arm (interquartile range, 4–9).
Procedural Demographics
Table 2 shows the procedural demographic data. The ma-
jority of lesions were in the left anterior descending artery
(68.4% PCI and 69.4% placebo); 16.3% (16/98) patients
in the PCI arm and 11.8% (10/85) patients in the placebo
arm had serial lesions in a single coronary artery. The mean
diameter stenosis by quantitative coronary angiography
was 64.3±13.9% in the PCI arm and 64.1±13.4% in the
placebo arm. The mean prerandomization stress echo-
cardiography score was 1.56±1.77 in the PCI arm and
1.61±1.73 in the placebo arm. The distribution of pre-
randomization stress echocardiography scores is shown in
Figure I in the online-only Data Supplement. The preran-
domization mean stress wall motion score for each seg-
Downloadedfromhttp://ahajournals.orgbyonDecember11,2019
4. Al-Lamee et al Stress Echocardiography-Stratified ORBITA Analysis
December 10, 2019 Circulation. 2019;140:1971–1980. DOI: 10.1161/CIRCULATIONAHA.119.0429181974
ORIGINALRESEARCH
ARTICLE
ment as associated with target vessel coronary territory
is shown in Table I in the online-only Data Supplement.
The mean inter- and intraobserver absolute differences of
the stress echocardiography score were 1.4 and 1.0 stress
echocardiography units, respectively. The mean FFR was
0.69±0.16 for the PCI arm and 0.69±0.16 for the pla-
cebo arm, and the mean iFR was 0.76±0.22 for the PCI
arm and 0.77±0.20 for the placebo arm. After interven-
tion with drug-eluting stents implanted in the PCI arm,
the mean FFR increased to 0.90±0.05 and iFR increased to
0.95±0.04. The change in stress echocardiography score
from prerandomization to follow-up in 161 patients with
stress echocardiography data at both time points is shown
in Figure II in the online-only Data Supplement.
Table 1. Patient Demographics at Enrollment
Demographics
PCI (n=98)
n (%)
Placebo
(n=85)
n (%)
Complete
Group
(n=183)
n (%)
Age, y
Mean (SD) 65.9±9.6 65.8±8.5 65.9±9.1
Median (IQR) 66 (60–74) 67 (60–71) 66 (60–73)
Male 68 (69.4) 65 (76.5) 133 (72.7)
Hypertension 65 (66.3) 58 (68.2) 123 (67.2)
Hypercholesterolemia 74 (75.5) 57 (67.1) 131 (71.6)
Diabetes mellitus 14 (14.3) 19 (22.4) 33 (18.0)
Previous MI 4 (4.1) 7 (8.2) 11 (6.0)
Previous PCI 9 (9.2) 15 (17.6) 24 (13.1)
CCS class
I 2 (2.0) 3 (3.5) 5 (2.7)
II 61 (62.2) 48 (56.4) 109 (59.6)
II 35 (35.7) 34 (40.0) 69 (37.7)
Left ventricular systolic function
Normal 93 (94.9) 77 (90.6) 170 (92.9)
Mild impairment 3 (3.1) 5 (5.9) 8 (4.4)
Moderate impairment 2 (2.0) 3 (3.5) 5 (2.7)
Severe impairment 0 (0) 0 (0) 0 (0)
Angina duration, mo
Mean (SD) 9.7 (16.2) 8.4 (7.7) 9.1 (12.9)
Median (IQR) 5 (4–10) 6 (4–9) 6 (4–9)
Preenrollment clinical positive
functional test
52 (53.1) 36 (42.4) 88 (48.1)
ETT 24 (24.5) 15 (17.6) 39 (21.3)
MIBI 10 (10.2) 8 (9.4) 18 (9.8)
DSE 18 (18.4) 12 (14.1) 30 (16.4)
MRI perfusion 0 (0) 1 (1.2) 1 (0.5)
CCS indicates Canadian Cardiovascular Society angina class; DSE, dobutamine
stress echocardiography; ETT, exercise tolerance test; IQR, interquartile range;
MI, myocardial infarction; MIBI, nuclear medicine myocardial perfusion scan;
MRI, magnetic resonance imaging; and PCI, percutaneous coronary intervention.
Table 2. Procedural Demographics
Demographics
PCI (n=98)
n (%)
Placebo
(n=85) n (%)
Complete
Group
(n=183) n (%)
Target vessel
Left anterior
descending
67 (68.4) 59 (69.4) 126 (68.9)
Right coronary 16 (16.3) 13 (15.3) 29 (15.8)
Circumflex 9 (9.2) 9 (10.6) 18 (9.8)
First obtuse marginal 3 (3.1) 0 (0) 3 (1.6)
First diagonal 2 (2.0) 2 (2.4) 4 (2.2)
Intermediate 1 (1.0) 2 (2.4) 3 (1.6)
Serial lesions 16 (16.3) 10 (11.8) 26 (14.2)
No. pts with diameter
stenosis ≥50% by QCA
84 (85.7) 73 (85.9) 157 (85.8)
No. pts with area
stenosis ≥70% by QCA
92 (93.9) 78 (91.8) 170 (92.9)
Diameter stenosis by QCA
Mean (SD) 64.3±13.9 64.1±13.4 64.2±13.6
Median (IQR) 63.9 (53.5–74.1) 62.8 (53.2–74.9) 63.4 (53.3–74.2)
Prerandomization stress echocardiography score
Mean (SD) 1.56±1.77 1.61±1.73 1.58±1.75
Median (IQR) 1 (0.42–2.15) 1 (0.42–2.00) 1 (0.42–2.08)
FFR n=97 n=82 n=179
Mean (SD) 0.69±0.16 0.69±0.16 0.69±0.16
Median (IQR) 0.72 (0.57–0.82) 0.73 (0.59–0.80) 0.72 (0.58–0.81)
iFR n=97 n=84 n=181
Mean (SD) 0.76±0.22 0.77±0.20 0.76±0.21
Median (IQR) 0.85 (0.68–0.92) 0.85 (0.70–0.89) 0.85 (0.69–0.90)
No. pts with FFR
≤0.80
n=97 n=82 n=179
71 (73.2) 63 (76.8) 134 (74.9)
No. pts with iFR ≤0.89 n=97 n=84 n=181
63 (64.9) 62 (73.8) 125 (69.1)
Stent length (mm)
Median (IQR) 24 (18–33) NA NA
Stent diameter (mm)
Median (IQR) 3 (2.75–3.5) NA NA
FFR post PCI n=96 NA NA
Mean (SD) 0.90±0.05
Median (IQR) 0.90 (0.87–0.93)
iFR post PCI n=97 NA NA
Mean (SD) 0.95±0.04
Median (IQR) 0.95 (0.92–0.97)
No. pts with post
FFR0.80
n=96 NA NA
91 (94.8)
No. pts with post
iFR0.89
n=97 NA NA
94 (96.9)
FFR indicates fractional flow reserve; iFR, instantaneous wave-free ratio; IQR,
interquartile range; NA, not available; PCI, percutaneous coronary intervention;
pts, patients; and QCA, quantitative coronary angiography.
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5. Al-Lamee et al Stress Echocardiography-Stratified ORBITA Analysis
Circulation. 2019;140:1971–1980. DOI: 10.1161/CIRCULATIONAHA.119.042918 December 10, 2019 1975
ORIGINALRESEARCH
ARTICLE
Relationship Between FFR and iFR and
Stress Echocardiography Score
Prerandomization FFR or iFR and DSE data were avail-
able in 179 patients and 181 patients, respectively (in
2 patients we were unable to elicit a hyperemic re-
sponse to adenosine and, therefore, only iFR data are
available). Figure 1A shows the relationship between
prerandomization FFR and prerandomization stress
echocardiography score. As the stress echocardiogra-
phy score became larger with a greater number of isch-
emic myocardial segments, the FFR value decreased,
therefore showing a greater degree of ischemia (Pcor-
relation
0.0001). At a stress echocardiography score of
0 (normal), the mean FFR was 0.76±0.17 (n=16). For
scores intermediate between 0 and 1, mean FFR was
0.72±0.14 (n=72); at ≥1 to 2, 0.71±0.12 (n=45); at
≥2 to 3, 0.65±0.17 (n=21); and at ≥3, 0.55±0.18
(n=25). Figure 1B shows the relationship between pre-
randomization iFR and prerandomization stress echo-
cardiography score. Similarly, as the stress echocardiog-
raphy score became larger with a greater number of
ischemic myocardial segments, the iFR also decreased,
showing a greater degree of ischemia (P0.0001). At a
stress echocardiography score of 0 (normal), the mean
iFR was 0.85±0.16 (n=16). For scores intermediate be-
tween 0 and 1, mean iFR was 0.82±0.16 (n=73); at
≥1 to 2, 0.80±0.16 (n=45); at ≥2 to 3, 0.67±0.26
(n=21); and at ≥3, 0.57±0.27 (n=26).
Patient-Reported Symptoms
SAQ Angina Frequency Score and Freedom From
Angina
Paired SAQ angina frequency data were available for
176 patients in the stress echocardiography–stratified
analysis of ORBITA (96 in the PCI arm and 80 in the
placebo arm). Overall, there was little evidence that PCI
improved angina frequency score more than placebo
(odds ratio [OR], 1.68 [95% CI, 0.96–2.95], P=0.069)
in this DSE subset (Table 3). However, there was a de-
tectable interaction between prerandomization stress
echocardiography score and the effect of PCI on an-
gina frequency score with a larger placebo-controlled
effect of PCI in patients with the highest stress echocar-
diography score (Pinteraction
=0.031; Figure 2). This interac-
tion resulted in patients with a prerandomization stress
echocardiography score of ≥1 being more likely to have
a lower angina frequency score with PCI than with pla-
cebo (OR, 3.18 [95% CI, 1.38–7.34], P=0.007; Table II
in the online-only Data Supplement).
Paired angina freedom data were available for
175 patients in the stress echocardiography–stratified
analysis of the ORBITA (95 in the PCI arm and 80 in
the placebo arm). PCI was more likely to result in pa-
tient-reported freedom from angina than placebo (OR,
3.01 [95% CI, 1.51–6.03], P=0.002) in this DSE sub-
set (Table 3). There was no detectable interaction be-
tween prerandomization stress echocardiography score
and the effect of PCI on freedom from angina (Pinterac-
tion
=0.116; Figure 3). Patients with a prerandomization
stress echocardiography score of ≥1 were more likely
to be free from angina with PCI than with placebo (OR,
4.62 [95% CI, 1.70–12.60], P=0.003; Table III in the
online-only Data Supplement).
SAQ Physical Limitation Score and Quality-of-Life
Score and EQ-5D-5L Score
Paired SAQ physical limitation data, SAQ quality of life,
and EQ-5D-5L data were available for 171 patients (93
in the PCI arm and 78 in the placebo arm), 175 patients
(96 in the PCI arm and 79 in the placebo arm), and 175
Figure 1. Relationship between prerandomization stress echocardiography score and prerandomization FFR and iFR.
A, Relationship between prerandomization stress echocardiography score and prerandomization FFR. B, Relationship between prerandomization stress echocar-
diography score and prerandomization iFR. echo indicates echocardiography; FFR, fractional flow reserve; and iFR, instantaneous wave-free ratio.
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6. Al-Lamee et al Stress Echocardiography-Stratified ORBITA Analysis
December 10, 2019 Circulation. 2019;140:1971–1980. DOI: 10.1161/CIRCULATIONAHA.119.0429181976
ORIGINALRESEARCH
ARTICLE
patients (96 in the PCI arm and 79 in the placebo arm),
respectively, in the stress echocardiography–stratified
analysis of the ORBITA. There was no evidence that PCI
improved physical limitation score more than placebo
(1.02 [95% CI, –4.65 to 6.68], P=0.724 in this DSE
subset, quality-of-life score more than placebo (0.14
[95% CI, –5.80 to 6.07], P=0.964 in this DSE subset
or EQ-5D-5L quality-of-life score more than placebo
(–0.007 [95% CI, –0.048 to 0.034], P=0.73; Table 3).
There was no detectable interaction between preran-
domization stress echocardiography score and the ef-
fect of PCI on physical limitation score (Pinteraction
=0.461;
Figure 4), quality-of-life score (Pinteraction
=0.689; Figure III
in the online-only Data Supplement) or quality of life as
assessed by EQ-5D-5L (Pinteraction
=0.789; Figure IV in the
online-only Data Supplement).
Physician-Assessed Symptoms
Paired Canadian Cardiovascular Society class data were
available for 179 patients (98 in the PCI arm and 81
in the placebo arm). There was no evidence that PCI
improved Canadian Cardiovascular Society class more
than placebo (OR, 0.85 [95% CI, 0.49–1.47], P=0.552;
Table 3). There was no detectable interaction between
prerandomization stress echocardiography score and
the effect of PCI on Canadian Cardiovascular Society
class (Pinteraction
=0.693; Figure V in the online-only Data
Supplement).
Exercise Time
Paired exercise time data were available for 177 patients
(97 in the PCI arm and 80 in the placebo arm). The esti-
mated effect of PCI over placebo on exercise time using
regression modeling was 17.0 seconds (95% CI, –8.22
to 42.2; P=0.19) in this DSE subset (Table 3). There was
no detectable interaction between prerandomization
stress echocardiography score and the effect of PCI on
exercise time (Pinteraction
=0.426; Figure 5). There was no
evidence that patients with a prerandomization stress
echocardiography score of ≥1 were more likely to have
more exercise time improvement with PCI that with pla-
Table 3. End Point Analysis
End Point
ANCOVA Estimate With the Covariate
Modeled as a Restricted Cubic Spline
(PCI Over Placebo)
Primary end point:
Exercise time 17.01 s (95% CI, –8.22 to 42.24;
P=0.185)
Secondary end points:
EQ-5D-5L –0.007 (95% CI, –0.048 to 0.034;
P=0.730)
SAQ physical limitation score 1.02 (95% CI, –4.65 to 6.68; P=0.724)
SAQ quality-of-life score 0.14 (95% CI −5.80 to 6.07; P = 0.964)
Logistic (Proportional Odds) Ordinal
Regression Model Estimate (PCI Over
Placebo)
SAQ angina frequency score OR, 1.68 (95% CI, 0.96 to 2.95;P=0.069)
SAQ freedom from angina OR, 3.01 (95% CI, 1.51 to 6.03;
P=0.002)
CCS class OR, 0.85 (95% CI, 0.49 to 1.47;
P=0.552)
Treatment effect estimates obtained using modeling. The follow-up value is
dependent on prerandomization value and treatment arm. ANCOVA indicates
analysis of covariance; CCS, Canadian Cardiovascular Society angina class; EQ-
5D-5L, EuroQOL 5 questionnaire; OR, odds ratio; PCI, percutaneous coronary
intervention; and SAQ, Seattle Angina Questionnaire.
Figure 2. Relationship of treatment difference in Seattle Angina Ques-
tionnaire (SAQ) angina frequency score at follow-up to prerandomiza-
tion stress echocardiography score by randomization arm.
There is a significant interaction between stress echocardiography score and
Seattle Angina Frequency score with a progressive tendency for larger effects
on angina frequency score with higher stress echocardiography score
(Pinteraction
=0.031). echo indicates echocardiography; and PCI, percutaneous
coronary intervention.
Figure 3. Relationship of treatment difference in freedom from angina
and prerandomization stress echocardiography by randomization arm.
There is no discernible dependence on prerandomization stress echocardiogra-
phy score. echo indicates echocardiography; and PCI, percutaneous coronary
intervention.
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7. Al-Lamee et al Stress Echocardiography-Stratified ORBITA Analysis
Circulation. 2019;140:1971–1980. DOI: 10.1161/CIRCULATIONAHA.119.042918 December 10, 2019 1977
ORIGINALRESEARCH
ARTICLE
cebo (18.4 seconds [95% CI, –18.3 to 55.1], P=0.322;
Table IV in the online-only Data Supplement).
DISCUSSION
This is the first placebo-controlled analysis of the relation-
ship between ischemia assessed by DSE and the efficacy
of PCI in stable coronary artery disease. The prerandom-
ization stress echocardiography score significantly pre-
dicted the placebo-controlled impact of PCI on patient-
reported angina frequency. The greater the ischemia, the
greater the symptom improvement. Second, although a
greater proportion of patients became free from angina
in the PCI arm than in the placebo arm, there was no evi-
dence of interaction between this effect and the preran-
domization stress echocardiography score. Finally, there
was strong correlation between prerandomization stress
echocardiography score and invasive physiology mea-
sured by FFR and iFR. The greater the number of ischemic
regional wall segments, the lower the FFR and iFR.
We propose an explanation for these and previously
reported results from the ORBITA trial.1,8
The progres-
sive decline in strengths of association may result from
the sequence of steps in the pathway of ischemia, with
the signal becoming increasingly dilute at later steps in
the chain (Figure 6). PCI immediately relieves the angio-
graphic stenosis (step A). As a result, the intracoronary
physiology improves (step B). This in turn can reduce
myocardial ischemia, resolving wall motion abnormali-
ties (step C). Angina, which is presumably a sensation
arising from ischemia, can be alleviated by this and re-
ported by the patient (step D). The physician, who relies
on the patient’s verbal and nonverbal cues, is one step
further removed (step E).
In the primary analysis of ORBITA,1
PCI had an ex-
tremely clear effect on anatomy (step A, P 0.001 for
anatomical stenosis). There was a very clear effect on
physiology (step B, P 0.001 for FFR and P 0.001 for
iFR). The effect on myocardial wall motion abnormality
was still clear (step C, P 0.001). One step further, and
there was no longer a clear effect on angina (step D),
with the preplanned analysis of SAQ angina frequency
showing no detectable change (P=0.260) and a post
hoc analysis showing a clearer effect on the dichoto-
mous end point of freedom from angina (P=0.006).8
Although the relatively weak effects on steps D to
E in Figure 6 were a surprise in the context of exten-
sive previous experience,2,7,17,18
the previous experience
was unblinded. Clinical staff are trained to interpret
the information in steps A, B, and C and explain to the
patient that the problem has been resolved. Therefore,
the impact of reassurance alone and simply being told
that their lesion was not flow-limiting dramatically re-
duced angina rates from 88% to 54% in the DEFER trial
(Deferral of PTCA Versus Performance of PTCA) and
64% to 15% in the FAME-2 trial (Fractional Flow Re-
serve-Guided Percutaneous Coronary Intervention Plus
Optimal Medical Treatment Versus Optimal Medical
Treatment Alone in Patients With Stable Coronary Ar-
tery Disease).17,19
An unblinded PCI procedure gives this
reassurance, that there is now no significant lesion, but
also gives patients an expectation that the symptoms
were attributable to the treated lesion and should now
resolve. Because of this powerful reassurance effect, it
is not possible to gauge how much of the symptom
relief from unblinded PCI is purely attributable to the
physiological effect of stenosis relief20–22
and how much
may be attributable to the placebo component of un-
blinded PCI.7,18
Figure 4. Relationship of treatment difference in Seattle Angina Ques-
tionnaire (SAQ) physical limitation score and prerandomization stress
echocardiography by randomization arm.
There is no discernible dependence on prerandomization stress echocar-
diography score. echo indicates echocardiography; and PCI, percutaneous
coronary intervention.
Figure 5. Relationship of treatment difference in exercise time and
prerandomization stress echocardiography by randomization arm.
There is no discernible dependence on prerandomization stress echocardiogra-
phy score. echo indicates echocardiography; and PCI, percutaneous coronary
intervention.
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8. Al-Lamee et al Stress Echocardiography-Stratified ORBITA Analysis
December 10, 2019 Circulation. 2019;140:1971–1980. DOI: 10.1161/CIRCULATIONAHA.119.0429181978
ORIGINALRESEARCH
ARTICLE
This stress echocardiography–stratified analysis shows
the link between stress-induced myocardial wall motion
abnormalities (step C) and patient-reported angina fre-
quency (step D). The greater the ischemia on DSE, the
greater the placebo-controlled angina relief from PCI.
The invasive physiology measures, FFR and iFR, are
further upstream (step B). This may explain why they
were not as strongly associated as DSE with the mag-
nitude of placebo-controlled angina relief from PCI.8
Physiological features other than the transstenotic
pressure gradient may affect whether the myocardium
experiences sufficient ischemia to manifest stress echo-
cardiography abnormalities or symptoms. For example,
there may be microvascular dysfunction or differential
sensitivity of the myocardium to intracoronary pressure.
Many patients with obstructive epicardial stenoses also
have microvascular disease. ORBITA did not acquire
coronary microvascular function to distinguish between
the various possibilities.
Another alternative proposed explanation might be
that the conventional cut points for ischemia with FFR
and iFR may not correspond to those of stress echo-
cardiography. However, the threshold of FFR was de-
fined by reference to tests such as stress echocardiogra-
phy.23
Moreover, the differences in sensitivity/specificity
cannot be the explanation, because, in both our FFR/
iFR-stratified analysis8
and our present stress echocar-
diography–stratified analysis, the variables were treated
continuously across their entire spectrum and not as a
mere dichotomy.24
In ORBITA the research stress echocardiography
(and the previously reported research FFR/iFR) were
performed after the clinical decision to revascularize.
These research assessments were not made available to
the clinicians. Therefore, as might be expected in a trial
of single-vessel coronary stenoses, many patients had a
low stress echocardiography score. Nevertheless, there
was not only a clear reduction of stress echocardiogra-
phy score by PCI, but also a relationship between the
prerandomization stress echocardiography score and
the degree of angina relief beyond placebo from PCI.
PCI is known to improve ischemia as assessed by
DSE.1,11
The COURAGE trial (Clinical Outcomes Utiliz-
ing Revascularization and Aggressive Drug Evaluation),
which confirmed that PCI reduced ischemia on myo-
cardial perfusion scans,25
showed that the baseline ex-
tent of ischemia did not predict the efficacy of PCI in
reducing death or myocardial infarction.26
No previous
studies have assessed the impact of prerandomization
noninvasive ischemia on the placebo-controlled efficacy
of PCI on symptom relief. The present analysis shows
that the greater the degree of stress echocardiography
ischemia preintervention, the greater the angina relief
from PCI beyond placebo.
Limitations of This Study
This analysis addresses only the 183 patients from the
200-patient ORBITA trial with prerandomization DSE.
There is potential for bias if the remaining 17 patients
differed in some way.
Our original expectation had been of a large PCI ef-
fect on exercise time. Because this expectation was not
realized, there is reduced power to detect variation in
exercise time effect across different prerandomization
strata. Despite this, there was still a surprisingly clear
relationship between prerandomization DSE and place-
bo-controlled angina relief.
The follow-up period may be considered short at 6
weeks. However, the effect of PCI on both angiographic
and physiological improvement of a stenosis is immedi-
ate, and the primary results of ORBITA showed virtually
complete normalization of stress echocardiography (as-
sessed blinded to time point) at the 6-week follow-up
scan. In previous trials, angina relief was seen a month
post-PCI.2
Therefore, we believe that we should not re-
gard 6-week data as premature.
Stress echocardiography assessment is known to
have interobserver27
and intraobserver variability.28
To
reduce the impact of this variability, each scan was re-
ported twice by 6 different operators who were each
blinded to the treatment allocation and time point of
the scan and to their own and each other’s opinions.
Each scan was therefore summarized as the mean of
12 opinions.
Conclusions
Stratification of the primary and secondary end points
of ORBITA by prerandomization DSE showed that the
higher the stress echocardiography score, the greater
the placebo-controlled efficacy of PCI on improvement
in patient-reported frequency of angina.
Figure 6. A proposed sequence of steps in the pathway of ischemia.
Coronary stenosis (step A) causes coronary hemodynamic insufficiency (step B)
which leads to stress-induced myocardial ischemia. This manifests as wall mo-
tion abnormalities on imaging tests (step C) and causes pain that is verbalized
by the patient (step D) and recorded by the physician (step E). The magnitude
of association between measurements is likely to be stronger between adja-
cent steps than steps further apart.
Downloadedfromhttp://ahajournals.orgbyonDecember11,2019
9. Al-Lamee et al Stress Echocardiography-Stratified ORBITA Analysis
Circulation. 2019;140:1971–1980. DOI: 10.1161/CIRCULATIONAHA.119.042918 December 10, 2019 1979
ORIGINALRESEARCH
ARTICLE
In ORBITA, the effect of PCI was progressively less
clear at each step in the chain from anatomy, to invasive
hemodynamics, to stress echocardiography ischemia,
and then to the frequency of angina.
We have previously found that there is a clear
relationship between invasive physiology and stress
echocardiography score, but no relationship be-
tween invasive physiology and placebo-controlled
symptom improvement. The present analysis shows
that there is clear evidence of a relationship be-
tween ischemia on stress echocardiography and the
placebo-controlled efficacy of PCI on the frequency
of angina.
ARTICLE INFORMATION
Received July 25, 2019; accepted September 24, 2019.
Continuing medical education (CME) credit is available for this article. Go to
http://cme.ahajournals.org to take the quiz.
The online-only Data Supplement is available with this article at https://www.
ahajournals.org/doi/suppl/10.1161/CIRCULATIONAHA.119.042918.
Authors
Rasha K. Al-Lamee, MA, MBBS, PhD; Matthew J. Shun-Shin, MA, BMBCh,
PhD; James P. Howard, MA, MBBChir; Alexandra N. Nowbar, BSc, MBBS;
Christopher Rajkumar, BSc, MBBS; David Thompson, MBBS, PhD; Sayan Sen,
BSc, MBBS, PhD; Sukhjinder Nijjer, BSc, MBBS, PhD; Ricardo Petraco, MBBS,
PhD; John Davies, BSc, MBBS, PhD; Thomas Keeble, BSc, MBBS, MD; Kare Tang,
MBBS; Iqbal Malik, MBBChir, MA, PhD; Nina Bual, MSc; Christopher Cook, BSc,
MBBS; Yousif Ahmad, BSc, MBBS; Henry Seligman, BA, MBBS; Andrew S.P.
Sharp, MBChB, MD; Robert Gerber, BSc, MBBS, PhD; Suneel Talwar, MBBS,
MD; Ravi Assomull, MA, MBBChir, MD; Graham Cole, MA, MBBChir, PhD;
Niall G. Keenan, MA, BMBCh, MD; Gajen Kanaganayagam, BSc, MBBS, PhD;
Joban Sehmi, BSc, MBBS, PhD; Roland Wensel, MD, PhD; Frank E. Harrell, Jr,
PhD; Jamil Mayet, MBChB, MD; Simon Thom, MBBS, MD; Justin E. Davies, BSc,
MBBS, PhD; Darrel P. Francis, MA, MBBChir, MD
Correspondence
Rasha Al-Lamee, MA, MBBS, PhD, National Heart and Lung Institute, Impe-
rial College London, Hammersmith Hospital, Du Cane Rd, London W10 0HS,
United Kingdom. Email r.al-lamee13@imperial.ac.uk
Affiliations
National Heart and Lung Institute, Imperial College London, UK (R.K.A-L.,
M.J.S.-S., J.P.H., A.N.N., C.R., D.T., S.S., S.N., R.P., I.M., C.C., Y.A., H.S., G.C.,
R.W., J.M., S. Thom, D.P.F.). Imperial College Healthcare NHS Trust, London, UK
(R.K.A-L., M.J.S.-S., J.P.H., A.N.N., C.R., S.S., S.N., R.P., I.M., C.C., Y.A., H.S.,
R.A., G.C., G.K., J.M., J.E.D., D.P.F.). Essex Cardiothoracic Centre, Basildon, UK
(J.D., T.K., K.T.). Anglia Ruskin University, Chelmsford, UK (J.D., T.K.). Cardiff
Royal Infirmary, UK (A.S.P.S.). East Sussex Healthcare NHS Trust, Hastings, UK
(R.G.). Royal Bournemouth and Christchurch NHS Trust, UK (S. Talwar). West
Hertfordshire Hospitals NHS Trust, Watford, UK (N.G.K., J.S.). Vanderbilt Uni-
versity School of Medicine, Department of Biostatistics, Nashville, TN (F.E.H.).
Acknowledgments
ORBITA was an investigator-led trial sponsored by Imperial College London. We
thank our patients and their families for their dedication and support for the
ORBITA trial. Special thanks to N. Bual for performing the stress echocardiogra-
phy investigations. We thank the research and administrative teams at Imperial
College Healthcare NHS Trust, Essex Cardiothoracic Centre, East Sussex Health-
care NHS Trust, Royal Devon and Exeter NHS Trust, and Royal Bournemouth and
Christchurch NHS Trust for their dedication and support.
Sources of Funding
The trial was funded by grants from National Institute for Health Research
(NIHR) Imperial Biomedical Research Centre, Foundation for Circulatory Health,
and Imperial College Healthcare Charity. Dr Howard is a PhD Training Fellow at
the Wellcome Trust. Philips Volcano supplied the coronary pressure wires. We
acknowledge the support of the NIHR Clinical Research Network (NIHR CRN).
Disclosures
Drs J. E. Davies and Mayet hold patents pertaining to the iFR technology. Drs J.
E. Davies and Sharp are consultants for Philips Volcano. Drs Al-Lamee, Sen, Pe-
traco, Cook, and Nijjer have received speaker’s honoraria from Philips Volcano.
Drs J. E. Davies and Keeble have received research grants from Philips Volcano.
The other authors report no conflicts.
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