Acute Myocardial Infarction Imaging
Acute myocardial infarction (MI), commonly known as a heart attack, is a condition characterized by ischemic injury and necrosis of the cardiac muscle. Ischemic injury occurs when the blood supply is insufficient to meet the tissue demand for metabolism. More than two thirds of myocardial infarctions occur in lesions that are less than 60% severe. (See the images below.) Almost all MIs are caused by rupture of coronary atherosclerotic plaques with superimposed coronary thrombosis. Patients with MI usually present with signs and symptoms of crushing chest pressure, diaphoresis, malignant ventricular arrhythmias, heart failure (HF), or shock. MI may also manifest itself as sudden cardiac death, which may not be apparent on autopsy (because necrosis takes time to develop). MI is clinically silent in as many as 25% of elderly patients, a population in whom 50% of MIs occur; in such patients, the diagnosis is often established only retrospectively by applying electrocardiographic criteria  or by performing imaging with 2-dimensional (2-D) echocardiography or magnetic resonance imaging (MRI). [1, 2, 3, 4, 5]
Coronary thrombolysis and mechanical revascularization have revolutionized the primary treatment of acute MI, largely because they allow salvage of the myocardium when implemented early after the onset of ischemia. The modest prognostic benefit of an opened infarct-related artery may be realized even when recanalization is induced only 6 hours or later after the onset of symptoms, that is, when the salvaging of substantial amounts of jeopardized ischemic myocardium is no longer likely. The opening of an infarct-related artery may improve ventricular function, collateral blood flow, and ventricular remodeling, and it may decrease infarct expansion, ventricular aneurysm formation, left ventricular (LV) dilatation, late arrhythmia associated with ventricular aneurysms, and mortality. (See the image below.) [6, 7, 8, 9, 10] Evidence suggests a benefit from the use of beta blockers, angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARB), and possibly insulin infusion (with potassium and glucose) to inhibit apoptosis (cell death).
Chest radiography is useful in determining the presence of cardiomegaly, pulmonary edema, pleural effusions, Kerley B lines, and other criteria of HF. In some patients, cephalization (evidence of vascular congestion) may be associated with peripheral pulmonary arterial pruning (decreased prominence). Chest roentgenographic findings are usually nonspecific.
A small cardiac silhouette and clear lung fields in a patient with systemic hypotension may indicate relative or absolute hypovolemia. A large cardiac silhouette with similar hemodynamics may reflect hemopericardium and tamponade or right ventricular (RV) MI that is compromising cardiac output.
Chest radiographic findings indicative of pulmonary venous hypertension may occur late and persist because of delay in fluid shifts among vascular, interstitial, and alveolar spaces.
Multidetector-row computed tomography (CT) scanning (ie, CT scanning with 16-64 detectors) is emerging as a useful means of identifying blockages of the coronary arteries. However, it involves substantial exposure to ionizing radiation and iodinated contrast agent (more so than with cardiac catheterization).
The preferred noninvasive modality for evaluating regional wall motion and overall ventricular performance is usually color-flow Doppler transthoracic echocardiography. If image quality is good and if the apex is visualized, the sensitivity and specificity of abnormal wall motion for diagnosing acute MI exceeds 90%, particularly in patients without previous MI.
Assessment of segmental function and overall LV performance provides prognostic information and is essential when MI is extensive, as judged by use of enzymatic criteria, or when MI is complicated by shock or profound HF. In part, this assessment is done to identify potentially surgically correctable complications and to detect true ventricular aneurysms, false ventricular aneurysms, or thrombi.
Imaging is also useful in detecting pericardial effusion, concomitant valvular or congenital heart disease, and marked depression of ventricular function that may interdict treatment in the acute phase with beta-adrenergic blockers. Echocardiography is also helpful in delineating recovery of stunned or hibernating myocardium.
Doppler echocardiography is particularly useful in estimating the severity of mitral or tricuspid regurgitation; in detecting ventricular septal defects secondary to rupture; in assessing diastolic function; in monitoring cardiac output, as calculated from flow velocity and aortic outflow tract area estimates; and in estimating pulmonary artery systolic pressure. For dobutamine echocardiography, images are acquired during an infusion of dobutamine, which is increased from 0 to 40 mcg/kg/min in 10-mcg/kg/min increments. If target stress is not achieved (>85% of the age-predicted maximum heart rate) and if the patient does not have glaucoma, atropine may be added to augment the peak heart rate.
Normal walls show a progressive increase in contractility (motion and thickening). Dead segments have poor motion and no thickening, and contractility fails to increase with high stimulation. Viable but jeopardized myocardium (ischemic myocardium) shows a biphasic response, wherein the contractility increases at lower doses of dobutamine and declines with perceptible wall-motion abnormalities at high doses of dobutamine. This kind of response is characteristic of ischemic myocardium and is most often the result of coronary stenosis.
With echocardiography, endocardial dropout is common, because not all parts of the heart are seen. In 1 in 10 patients, the views are inadequate, most often because of lung disease.
Positron-emission tomography (PET) scanning performed with the use of tracers of intermediary metabolism, perfusion, or oxidative metabolism permits quantitative assessment of the distribution and extent of impairment of myocardial oxidative metabolism and regional myocardial perfusion. It may also be used to assess the effectiveness of therapeutic interventions intended to salvage myocardium, and it has been used to diagnostically differentiate reversible injury from irreversible injury in hypoperfused zones.  Resolution is a frequent problem. Also, a glucose load is required, and patients with diabetes need an insulin-glucose lock to ensure adequate myocardial uptake.
In patients with MI, portable radiography is almost always performed in the emergency department or CCU.
When present, prominent pulmonary vascular markings on the radiograph reflect an elevation in LV end-diastolic pressure (LVEDP), but clinically significant temporal discrepancies may occur because of diagnostic and posttherapeutic lags. Up to 12 hours may elapse before pulmonary edema accumulates after ventricular filling pressure becomes elevated. The posttherapeutic phase lag is even longer; up to 2 days are required for pulmonary edema to resorb and for the radiographic signs of pulmonary congestion to clear after ventricular filling pressure returns toward normal.
The degree of congestion and the size of the left side of the heart on the chest radiograph are useful for identifying patients with MI who are at increased risk for dying after the acute event.
Radiographic findings are nonspecific. The degree of confidence is low. If findings from transthoracic echocardiography are not diagnostic, transesophageal echocardiography may be necessary. False-positive and false-negative findings occur frequently.
When CHF persists despite treatment, certain complications of MI must be excluded. These include aneurysm, pseudoaneurysm, rupture of the ventricular wall or papillary muscle, and interventricular septal defect. In converse, MI may occur as a complication of aortic dissection.
An interventricular septal defect occurs in 0.5-1.0% of patients with recent septal infarction; it is characterized by cardiomegaly, pulmonary edema, and poor myocardial contractility. On the plain radiograph, the typical shunt pattern may not be appreciated because of pulmonary edema, but it may emerge months later if the patient survives. Such defects usually involve the muscular septum; they occur within 7-12 days after MI.
The radiographic picture of post-MI syndrome (ie, Dressler syndrome) is that of a heart that is enlarged because of pericardial effusion. Unilateral pleural effusions are common, though bilateral effusions may also occur; lower-lobe consolidation, particularly on the left side, occurs in less than 20% of patients. These findings generally appear 2-6 weeks after MI and are analogous to postpericardiotomy syndrome.
Aneurysm of the LV is an abnormal bulge or outpouching of the myocardial wall that develops in 12-15% of patients after MI. It most commonly occurs at the cardiac apex or along the anterior free wall of the LV. A true aneurysm is lined with myocardium; a false aneurysm is a contained rupture in which at least part of the wall is typically pericardium. In some cases, a false aneurysm is lined with thrombus. False aneurysm or pseudoaneurysm often has a narrow entrance to a large cavity.
The chest radiograph may show a localized bulge along the ventricular wall, with or without a thin rim of calcification. CT, MRI, and echocardiography may all demonstrate differences in dyskinesis of the damaged wall. High resolution may be needed to distinguish some cases of pseudoaneurysm from true aneurysm; for this purpose, MRI is preferred.
The differential diagnosis of LV aneurysm includes other deformities of the left heart border caused by pericardial cysts, mediastinal or pleural tumor, thymoma, and other mediastinal masses.
Cardiac rupture usually occurs in patients who have had an acute transmural infarction. Most such patients die immediately; in a few such patients, surrounding extracardiac soft tissue contains or encloses the rupture, and a pseudoaneurysm forms.
Radiographs show a paracardiac mass with sharply marginated edges free of calcification. On the lateral projection, the mass is usually posterior; by contrast, a true aneurysm appears in a relatively anterior position.
Papillary muscle rupture follows MI in approximately 1% of patients. Plain radiographic findings vary from that of a normal chest to that of gross cardiomegaly with left atrial and ventricular enlargement and pulmonary edema. Left ventriculography, MRI, and Doppler echocardiography demonstrate the flail leaflets of the mitral valve and help in estimating the degree of mitral regurgitation.
CT scanning may provide useful cross-sectional information for patients with MI. In addition to helping in the assessment of cavity dimensions and wall thickness, CT depicts LV aneurysms and intracardiac thrombi, which are particularly important in MI. New multidetector-row CT provides 3-dimensional (3-D) visualization of the coronary artery anatomy and ramifications, its calcifications, stenoses, and even the presence of soft plaque in the wall of the coronary artery. [12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22]
Complications of MI, such as pseudoaneurysm, are confirmed by means of echocardiography, MRI, or contrast-enhanced CT. Imaging of a pseudoaneurysm typically shows a relatively narrow neck and a complete absence of muscle in the wall of the pseudoaneurysm, unlike a true aneurysm, which has a rim of myocardial wall that may be identified on angiograms by the presence of mural vessels.
CT angiography (CTA) may lead to an overestimation of obstructions. The degree of confidence is lower than that with MRI for assessing mural thrombi and the locations of infarcts. Although cardiac CT is less convenient than echocardiography, it is probably more sensitive than echocardiography for detecting thrombi.  False-positive and false-negative findings occur frequently.
MRI enables direct visualization of the myocardium with excellent delineation of the epicardial and endocardial interfaces.  As a consequence, it may be used to accurately define segmental wall thinning indicative of previous MI. In some patients with a clinical history of transmural infarction, residual myocardium may be demonstrated at the site of the infarction. In other patients, MRI shows virtually complete replacement of muscle by scar.
Direct visualization of the myocardium may be used to determine whether sufficient residual myocardium remains in the region jeopardized by a coronary arterial lesion to warrant bypass grafting.
The recognition of decreased signal intensity of the myocardial wall at the site of an old MI suggests that MRI may demonstrate replacement of myocardium by fibrous scar. MRI scar maps may be generated through the use of delayed enhancement, which consists of T1-sensitive imaging performed 10-20 minutes after the administration of a gadolinium-based contrast agent (diethylenetriamine penta-acetic acid [DPTA]; in typical adults, 0.1 mM/kg, 20 mL); it indicates early myocardial injury. [25, 26, 27, 28] Damaged cells and collagen in scar tissue retain the contrast material; this causes the scar to appear white, whereas normal wall appears dark. [5, 28]
With scars measuring less than one third the thickness of the wall, there is good potential for improvement with revascularization, whereas with scars measuring more than one third the thickness of the wall, the potential for recovery with therapy is limited (except in cases involving research cell therapies or surgical scar revision). (See the image below.)
Electrocardiogram (ECG)- and respiratory-gated MRI may demonstrate complications of MIs, such as LV thrombus and aneurysms. Transverse or short-axis tomography facilitates the recognition of the small ostium that connects the LV chamber and the false aneurysm; this is a distinguishing feature of the false LV aneurysm, as compared to the true LV aneurysm.
MIs have been demonstrated on gated MRI. The region of ischemically damaged myocardium has increased signal intensity, as compared to normal myocardium. Contrast between infarcted and normal myocardium increases on images, with increased T2 contribution to signal intensity. The administration of contrast medium (gadolinium chelates) with T1-weighted spin-echo imaging increases enhancement of infarcted myocardium, with increased signal intensity, as compared to normal myocardium.
Regional wall thickening may also be assessed during MRI with dynamic movies or grid-tag strain maps. A wall that is thinner than 6 mm at end diastole and wall thickening of less than 1 mm correspond to a myocardial scar, as defined by lack of uptake of technetium-99m sestamibi single-photon emission CT (SPECT) or FDG glucose on PET. Furthermore, MRI is a good predictor of recovery of regional function after myocardial revascularization.
In a study of 25 patients who underwent prospective cardiac PET/MRI after acute coronary occlusion and interventional reperfusion, the area of reduced FDG uptake correlated with the area at risk, as determined with the endocardial surface area (ESA) method, and was localized in the perfusion territory of the culprit artery in the absence of necrosis. However, the area of reduced FDG uptake largely overestimated the size of the infarct and the ESA-based area at risk. 
Native T1 mapping and late gadolinium enhancement have been shown to offer detailed characterization of the myocardium after acute MI. One study, by Robbers et al, found that microvascular injury after acute MI affects local T1 and T2* values, infarct zone T1 values are lower in the presence of microvascular injury, T2* mapping suggests that hemorrhage is likely in the case of low infarct T1 values, and T1 and T2* values are complementary in the correct assessment post-infarct myocardium.
Gadolinium-based contrast agents have been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic Nephrogenic Systemic Fibrosis. The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans. For more information, see Medscape.
MRI is generally excluded for patients with pacemakers, defibrillators, and other select metallic implants. Echocardiography is inferior to MRI in image quality, especially for the apex and for the RV, but it is portable. Although MRI can precisely depict the location of infarct and the percentage of wall thickness involved, echocardiography is generally used to estimate the location on the basis of wall motion and/or wall thickening. MRI is generally superior for evaluating complications of MI, such as VSD and pseudoaneurysm.
The degree of confidence is typically high unless arrhythmia impairs image quality. MRI is the most accurate test for identifying MIs and for delineating the size and depth of wall-thickness involvement. The modality is attractive because of its ability to show the following:
Perfusion of infarcted and noninfarcted tissue
Areas of jeopardized but not infarcted myocardium
Myocardial edema, fibrosis, wall thinning, and hypertrophy
Ventricular chamber size and segmental wall motion
Temporal transition between ischemia and infarction
Complications of MI
MRI may also be used to image wall motion after dobutamine or adenosine infusion to assess ischemia. Dobutamine stress MRI, using a low dose (5-15 mcg/kg/min), may be performed after a recent MI. The rationale for the use of this study is that contractile function of viable tissue improves after inotropic stimulation, whereas scarred tissue does not. Criteria for viability include end-diastolic wall thickness (EDWT) of 5.5 mm or less and dobutamine-induced systolic wall thickness (SWT) of 2 mm or more. In patients with an acute MI or recent MI, dobutamine stress MRI has a sensitivity of approximately 91% and a specificity of approximately 70%. For cardiac ischemia, dobutamine, 10 to 40 mg/kg/min, is used.
However, dobutamine stress MRI has several limitations. First, ECG changes resulting from ischemia cannot be detected reliably with standard ECG monitoring in the high-field MRI environment. Instead, wall-motion abnormalities are visually and subjectively detected to ensure the patient’s safety during stress testing. Also, wall thickening in response to dobutamine is not entirely specific for ischemia.
The rates of false-positive and false-negative findings are low.
The portability of echocardiographic equipment makes this the preferred technique for the assessment of patients with MI who are hospitalized in the CCU or the emergency department before admission. For patients with chest pain that is compatible with MI but whose ECG is not diagnostic, a distinct segment of abnormal contraction on echocardiography indicates ischemic impairment (see the image below).
The degree of confidence is moderately high; if adequate stress is achieved, findings are 85% accurate. In one study of patients with acute ST-segment elevation myocardial infarction (STEMI), qualitative and quantitative myocardial contrast echocardiography (MCE) helped predict cardiac events (after adjustment for cardiovascular risk factors) after patients underwent reperfusion. Perfusion score index (PSI) and Aβ were identified as independent predictors of cardiac events, with an adjusted hazard ratio of 3.41 (1.19-12.27) and 4.19 (1.3-19.09), respectively. Patients with cardiac events had a higher PSI and lower A, β and Aβ parameters compared to patients without events.  The rate of false-positive findings is low. False-negative results occur when the peak stress level is marginal, when rest and stress views do not match, or when views do not cover the entire heart. Poor views are acquired in about 10% of patients. Echocardiography requires a lung-free window that commonly excludes the true apex of the LV and that offers limited views of the RV. 
Complete 2-D echocardiographic examination typically includes color-coded assessment of blood movement (red indicates movement toward the transducer; blue, away), which reveals valvular leaks and septal defects. Continuous and pulsed Doppler likewise help in evaluating blood movement by using shifts in sound frequency to measure velocity anywhere along a column or at a specific location Because a pressure drop across a passage, such as a valve or VSD, is predominantly the result of change in kinetic energy (½ MV2), Doppler imaging may be used to estimate pressure gradients. Furthermore, equations that are based on conservation (ie, the observed fluid is neither created nor destroyed) may be used in a number of ways to estimate the severity of pressures, stenoses, and leakages.
Echocardiography is also useful in evaluating patients with chest pain in whom an aortic dissection is suspected. Identification of an intimal flap that is consistent with aortic dissection is a crucial observation because it represents a major contraindication to thrombolytic therapy. Transthoracic echocardiography offers a limited view of the aorta; its usefulness is increased by including views from the suprasternal notch. The views are improved through the use of transesophageal echocardiography, but portions of the aorta, particularly in the arch, may still be missed. CT and MRI are equally good and enable complete examination of the aorta.
Areas of abnormal regional wall motion are almost universally observed in patients with MI; the degree of wall-motion abnormality may be categorized by use of a semiquantitative wall-motion score. Of note, infarcts may be missed during echocardiography when the infarction is small or when it involves just the apex. MRI is the best modality for examining the apex and small or partial-thickness infarctions.
LV function, as estimated with the use of 2-D echocardiography, is well correlated with angiographic measurements; 2-D echocardiography is useful in establishing the patient’s prognosis after MI. Furthermore, early use of echocardiography may aid in the detection of potentially viable but stunned myocardium (contractile reserve). Stress echocardiography is as good as nuclear imaging for detecting inducible ischemia.
Although transthoracic imaging is adequate in many patients, 10-20% have poor echocardiographic windows; windows may be especially poor in patients with lung disease or in those who require a ventilator. In such patients, transesophageal echocardiography or MRI may be used. [30, 31, 32, 33, 34, 35, 36]
Computer-controlled rotation of the transducer used for 2-D echocardiography may be used to generate 3-D movies. This technique has advantages for the evaluation of a diseased mitral valve and, potentially, in other situations in which 3-D tissue relationships may clarify the character and severity of an abnormality. 
Echocardiography is frequently used to assess myocardial ischemia by providing images at rest and during stress. A typical treadmill or bicycle ergometer may be used as means of exercise. In patients who cannot exercise, chemical stress may be induced with dobutamine. During dobutamine-stress echocardiography, images are acquired during an infusion of dobutamine, which is given in increments of 10 mcg/kg/min to a dosage of 40 mcg/kg/min. Normal walls show progressively increasing contractility (motion and thickening). In necrotic segments, motion is reduced or reversed motion, and thickening is absent; in addition, in necrotic segments, contractility fails to increase with increased stimulation. Viable but jeopardized myocardium (ie, ischemic myocardium) shows a biphasic response. With low doses of dobutamine, its contractility increases; with high doses, it declines, and wall-motion abnormalities are perceptible. 
Radionuclide angiography, perfusion imaging, infarct-avid scintigraphy, and PET have been used to evaluate patients with MI.
Nuclear cardiac-imaging techniques may be useful for detecting MI; assessing infarct size, collateral flow, and jeopardized myocardium; determining the effects of the infarct on ventricular function; and establishing the prognosis of patients with MI. However, the necessity of moving a critically ill patient from the CCU to the nuclear medicine department limits practical application of this study unless a portable gamma camera is available.
For the diagnosis of MI, cardiac radionuclide imaging should be restricted to special, limited situations in which the triad of the patient’s clinical history, ECG findings, and serum marker measurements is unavailable or unreliable.
Radionuclides, such as thallium, sestamibi, and tetrofosmin, are used along with mechanical (treadmill or bicycle) or pharmacologic (dobutamine or adenosine) stress testing. Images are obtained at rest and during stress and are compared to look for inducible ischemia (decreased counts with stress). When thallium is used, images must be obtained within a few minutes of infusion. Images obtained at rest sometimes do not show adequate redistribution, and reinjection and imaging performed at 24 hours reveals viability that was missed during immediate imaging. Background correction is performed by acquiring images before perfusion or by estimating, using low-resolution CT or other imaging means.
Selective coronary angiography requires the injection of a material that is opaque on radiography; typically, iodine is administered through a catheter that is threaded through an artery to the aorta and to the origin of each coronary artery. Coronary angiography is the criterion standard for identifying coronary blockages. 
The degree of confidence is high. False findings are extremely rare. Additional procedures may be required to determine the hemodynamic significance of observed lesions. Microvascular disease may cause ischemia with no obstructions evident on angiography. Catheterization may cause dissection of an artery (bleeding into the vessel lining), resulting in obstruction and an MI in a patient with normal coronary arteries. Catheterization may also cause a perforation with associated bleeding into the pericardial space. Either of these events may cause death.
Viability studies, such as MRI with delayed enhancement, PET, nuclear medicine studies, or dobutamine echocardiography, may be needed to determine whether damaged tissue located beyond a blockage can recover. However, the open-artery hypothesis is that opening all blocked arteries, even if the muscle they supply cannot recover function, may be best. Extensions of the catheterization technique needed for coronary angiography enable treatment to be accomplished by inserting balloons or stents and/or by locally delivering medications. These therapies are collectively known as percutaneous coronary interventions (PCIs).
PCI is used instead of thrombolytic therapy to clear a blockage early in the course of an acute MI (primary angioplasty), as adjunctive therapy with thrombolysis, as a management strategy in the subacute phase of acute MI (days 2-7), or late after MI. In the early stages of MI, intervention is typically limited to the infarct-related lesion.
Coronary arteriography should be performed in patients with Q-wave or non-Q-wave MI who develop spontaneous ischemia; in those who have ischemia with a minimal workload; and in those who have MI that is complicated by CHF, hemodynamic instability, cardiac arrest, mitral regurgitation, or ventricular septal rupture. Patients who experience angina or provocable ischemia after MI should also undergo coronary arteriography because revascularization may reduce the high risk of repeat infarction in these patients.
Guidelines from the American College of Cardiology/American Heart Association (ACC/AHA) list classes of indications for coronary angiography  :
Class I indications are as follows:
Spontaneous myocardial ischemia or ischemia provoked with minimal exertion
Presurgical therapy for acute MI, ventricular septal defect, true aneurysm, or pseudoaneurysm
Persistent hemodynamic instability
Class IIA indications are as follows:
Suspected MI caused by coronary embolism, arteritis, trauma, certain metabolic diseases, or coronary spasm
Survivors of acute MI with LV ejection fraction (LVEF) of less than 0.40, CHF, previous PCI or coronary artery bypass grafting (CABG), or malignant ventricular arrhythmias
Class IIB indications are as follows:
Suspected persistent occlusion of the IRA to perform delayed PCI
Coronary arteriography performed without risk stratification to identify the presence of left main or 3-vessel coronary artery disease
All patients after non–Q-wave MI
Recurrent ventricular tachycardia despite antiarrhythmic therapy without ongoing ischemia
No absolute contraindications are described for coronary arteriography.
Relative contraindications include the following:
Severe anemia with hemoglobin level less than 8 g/dL
Severe electrolyte imbalance
Severe active bleeding
Uncontrolled systemic hypertension
Previous allergy to contrast material but no pretreatment with corticosteroids
Acute renal failure
Diabetic patients with Cr greater than 2
Patients on metformin (Glucophage) or other oral hypoglycemic agents
Risk factors for clinically significant complications after catheterization include advanced age, hemodynamic instability, multisystemic disease, large infarctions, bleeding disorders, and extensive atherosclerosis in the aorta or access arteries.
Contrast-enhanced magnetic resonance angiography (MRA) is a fast-growing, noninvasive modality for vascular imaging. Current clinical applications of MRI of the coronary arteries include evaluations of anomalous coronary arteries, Kawasaki disease, and bypass-graft patency. MRI of native coronary arteries remains the most challenging area of cardiac MRI. Several factors contribute to this difficulty. The coronary arteries are small (2-4 mm in diameter) and are frequently tortuous. They have continuous inherent cardiac and respiratory motions that cause motion artifact. Both black-blood and bright-blood techniques with 2-D or 3-D linear and nonlinear acquisitions during breath holding or free breathing with navigators have been used with limited success. ECG- and respiratory-gated MRI have decreased the overall severity of these artifacts.
CTA is widely used to examine the peripheral arteries and grafts. Previously, however, motion artifact hindered coronary angiography, as with MRI of the coronary arteries. Newer, faster 64-section CT angiography has substantially resolved this problem and is proving to be a convenient and useful test for confirming the absence of coronary artery disease and for constructing 3-D models of coronary obstructions and calcifications. In addition, soft plaque within arterial walls appear as areas of distinctly decreased Hounsfield attenuation.
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Vibhuti N Singh, MD, MPH, FACC, FSCAI Clinical Assistant Professor, Division of Cardiology, University of South Florida College of Medicine; Director, Cardiology Division and Cardiac Catheterization Lab, Chair, Department of Medicine, Bayfront Medical Center, Bayfront Cardiovascular Associates; President, Suncoast Cardiovascular Research
Vibhuti N Singh, MD, MPH, FACC, FSCAI is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, Florida Medical Association
Disclosure: Nothing to disclose.
Kul Aggarwal, MD, FACC Professor of Clinical Medicine, Department of Internal Medicine, Division of Cardiology, University of Missouri-Columbia School of Medicine; Chief, Cardiology Section, Harry S Truman Veterans Hospital
Disclosure: Nothing to disclose.
Bernard D Coombs, MB, ChB, PhD Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.
David S Levey, MD Musculoskeletal and Neurospinal Forensic Radiologist; President, David S Levey, MD, PA, San Antonio, Texas
David S Levey, MD is a member of the following medical societies: American Roentgen Ray Society, Bexar County Medical Society, Forensic Expert Witness Association, International Society of Forensic Radiology and Imaging, International Society of Radiology, Technical Advisory Service for Attorneys, Texas Medical Association
Disclosure: Nothing to disclose.
Eugene C Lin, MD Attending Radiologist, Teaching Coordinator for Cardiac Imaging, Radiology Residency Program, Virginia Mason Medical Center; Clinical Assistant Professor of Radiology, University of Washington School of Medicine
Eugene C Lin, MD is a member of the following medical societies: American College of Nuclear Medicine, American College of Radiology, Radiological Society of North America, Society of Nuclear Medicine and Molecular Imaging
Disclosure: Nothing to disclose.
Justin D Pearlman, MD, ME, PhD, FACC, MA Chief, Division of Cardiology, Director of Cardiology Consultative Service, Director of Cardiology Clinic Service, Director of Cardiology Non-Invasive Laboratory, Chair of Institutional Review Board, University of California, Los Angeles, David Geffen School of Medicine
Justin D Pearlman, MD, ME, PhD, FACC, MA is a member of the following medical societies: American College of Cardiology, International Society for Magnetic Resonance in Medicine, American College of Physicians, American Federation for Medical Research, Radiological Society of North America
Disclosure: Nothing to disclose.
Acute Myocardial Infarction Imaging
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