Myocardial Infarction Images Download

processing.... Drugs & Diseases > Radiology Acute Myocardial Infarction Imaging Updated: Aug 09, 2018 Author: Vibhuti N Singh, MD, MPH, FACC, FSCAI; Chief Editor: Eugene C Lin, MD more... Share Print Feedback Close Facebook Twitter LinkedIn WhatsApp Email webmd.ads2.defineAd({id: 'ads-pos-421-sfp',pos: 421}); Sections Acute Myocardial Infarction Imaging Sections Acute Myocardial Infarction Imaging Practice Essentials Radiography Computed Tomography Magnetic Resonance Imaging Ultrasonography Nuclear Imaging Angiography Show All Media Gallery References Practice Essentials 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 [1] or by performing imaging with 2-dimensional (2-D) echocardiography or magnetic resonance imaging (MRI). [1, 2, 3, 4, 5]

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.

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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. [11] 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.

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.

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.

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.

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.

MRI enables direct visualization of the myocardium with excellent delineation of the epicardial and endocardial interfaces. [24] 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.

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]

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.

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.

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. [37]

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.

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.

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.

Ethics committees approved human and animal study components; informed written consent was provided (prospective human study [20 men; mean age, 62 years]) or waived (retrospective human study [16 men, four women; mean age, 59 years]). The purpose of this study was to prospectively evaluate a clinically applicable method, accounting for the partial volume effect, to automatically quantify myocardial infarction from delayed contrast material-enhanced magnetic resonance images. Pixels were weighted according to signal intensity to calculate infarct fraction for each pixel. Mean bias +/- variability (or standard deviation), expressed as percentage left ventricular myocardium (%LVM), were -0.3 +/- 1.3 (animals), -1.2 +/- 1.7 (phantoms), and 0.3 +/- 2.7 (patients), respectively. Algorithm had lower variability than dichotomous approach (2.7 vs 7.7 %LVM, P < .01) and did not differ from interobserver variability for bias (P = .31) or variability (P = .38). The weighted approach provides automatic quantification of myocardial infarction with higher accuracy and lower variability than a dichotomous algorithm. 006ab0faaa