Cardiovascular Imaging Flashcards
Normal aortic arch branching
The normal aortic branching pattern is seen 66% of the time and features three arteries arising from the aortic arch; Brachiocephalic trunk (inominante artery), left common carotid, and left subclavian artery.
Common origin of the brachiocephalic artery and left common carotid artery
A common origin of the brachiocephalic artery and left common carotid artery is seen in 13% of patients (most commonly in blacks) and is often incorrectly referred to as a “bovine aortic arch”. The term “bovine aortic arch” is a misnomerand is not the preferred description of this anomaly, as a true bovine arch in cattle features a single great vessel arising from the aortic arch.
Aberrant right subclavian
An aberrant right subclavian is seen in 1% of patients. The right subclavian artery arises directly from the aortic arch distal to the left subclavian and loops behind the esophagus on its way into the right arm.
It is very uncommon for an aberrant right subclavian artery to cause symptoms, but this anomaly may rarely be a cause of dysphagia via esophageal compression, called dysphagia lusoria. Barium esophagram features a posterior indentation on the esophagus. Although usually incidental, it is important to mention the presence of an aberrant right subclavian artery when reading a CT neck. If thyroid surgery is planned, then the recurrent laryngeal nerve will not be in its usual location.
A diverticulum of Kommerel represents a small bulge at the origin of the aberrant subclavian artery.
Left vertebral orign off aorta
A four vessel arch with direct origin of the vertebral artery off of the aorta is seen in 6% of the population. The left vertebral is the third aortic branch, proximal ot the left subclavian.
Overview of acute aortic syndrome
Acute aortic syndrome represents a clinical spectrum of three related diseases that are characterized by damage to at least one component of the aortic wall, and presents as severe chest pain.
A defect primarily in the intima is seen in penetrating atherosclerotic ulcer (PAU).
A defect in the media only describes intramural hematoma (IMH).
A defect in the intima extending to media is the hallmark of aortic dissection.
A defect in all three layers (aortic transection) is almost always due to trauma and is considered a separate entity.
The treatment of acute aortic syndrome depends primarily on the location (ascending versus descending aorta) and is often the same regardless of the underlying etiology. Ascending aorta: Treatment is most commonly surgical. Descending aorta: Treatment is most commonly medical (blood pressure control).
Imaging of the full aorta is generally required in any acute aortic pathology.
Aortic dissection
The key feature of dissection is a disruption in the intima, which allows high-pressure blood to infiltrate and expand the media.
The most common risk factor for aortic dissection is hypertension, but other risk factors include connective tissue disorders (especially Marfan syndrome), cocaine use, aortopathy associated with a bicuspid aortic valve, weight lifting, and sudden deceleration injury.
The classification of aortic dissection is the Stanford classification, which divides dissection into types A (ascending aorta) and B (non-ascending aorta). Type A is typically treated surgically, and type B is typicaly treated medically. Aortic dissection secondary to atherosclerosis is more commonly type B (descending aorta).
Intramural hematoma
Intramural hematoma (IMH) is a variant of dissection where blood collects within the media, without an intimal flap to connect the intramural hematoma with the aortic lumen. IMH is thought to be due to rupture of the vasa vasorum, which are small blood vessels that supply the aortic wall.
Similar to dissection, IMH may be secondary to hypertension or trauma.
Clinically, IMH can present identically to aortic dissection with acute tearing back pain. The treatment recommendations for IMH are the same as dissection regarding involvement of the ascending versus descending aorta.
The key imaging finding of IMH is a faint peripheral hyperattenuating (45-50 HU) crescent within the aorta, best seen on noncontrast CT. In high-risk patients, the aortic dissection CT protocol typically includes an unenchanced CT prior to CTA to evaluate specifically for IMH. An alternative strategy in low-risk patients is to perform unenchanced CT only if there is suspicion of IMH on the CTA in order to decrease radiation exposure.
Penetrating athersclerotic ulcer (PAU)
Penetrating atherosclerotic ulcer (PAU) is a focal defect in the intima that occurs at the site of an atherosclerotic plaque. PAU may lead to saccular aneurysm formation.
In contrast to dissection and IMH, PAU tends to be caused by atherosclerosis rather than hypertension. One of the theories of dissection secondary to atherosclerosis is that it begins as a penetrating ulcer
On imaging, PAU appears as contrast ulcerating beyond the expected contour of the aortic wall. The primary differential would be a simple ulcerated atherosclerotic plaque, which would not extend beyond the expected contour of the aortic wall. Atherosclerotic plaque represents chronic atherosclerotic disease and is not an acute aortic syndrome.
Multiple ulcers may be present throught the thoracoabdominal aorta, and as with all acute aortic pathologies, imaging of the full aorta is recommended if a PAU is seen.
Aortic trauma
There are three relatively fixed levels fo the aorta where traumatic aortic injuries occur secondary to deceleration injury, which are the aortic root, isthmus, and hiatus. The resulting pseudoaneurysm is held in place by the surrounding connective tissues. In the small percentage of patients who survive blunt aortic trauma, injury occurs at the isthmus in 95% of cases. Associated injury to the origins of the brachiocephalic, left carotid, or left subclavian arteries is frequently present.
CTA is the gold standard for evaluation of suspected traumatic aortic injury.
Traumatic mediastinal hemorrhage is often venous; however, aortic injury is the primary concern. Direct CT signs of traumatic injury include a dissection flap, pseudoaneurysm, and intramural hematoma. Mediastinal hemorrhage that is separated from an intact aorta by a fat plane can be presumed to be venous, and treatment is conservative. In contrast, hemorrhage in contact with the aortic wall is suggestive of aortic injury and necessitates surgical treatment.
Thoracic aortic aneurysm
A thoracic aortic aneurysm (TAA) is defined as an ascending aortic diameter >4 cm or a descending thoracic aorta >3 cm in diameter. Aortic size may also be normalized to body surface area and compared to reference values.
Double-oblique short-axis multiplanar reformatted images perpendicular to teh aortic lumen (i.e., true short-axis) should always be used to measure aortic diameter.
Most thoracic aortic aneurysms are caused by atherosclerosis, with the descending thoracic aorta affected more commonly. Almost one third of patients with atherosclerotic TAA will have an associated abdominal aortic aneurysm.
Non-atherosclerotic causes of TAA include connective tissue disorders (such as Marfan and Ehlers-Danlos syndromes), bicuspid aortic valve (BAV) associated aortopathy, vasculitis (including Takayasu arteritis, giant cell arteritis, ankylosing spondylitis, and relapsing polychondritis), cystic medial necrosis, and infectious aortitis.
Annuloaortic ectasia represents dilated sinuses of Valsalva and ascending aorta with effacement of the sinotubular junction, resulting in a tulip bulb-shaped aorta. Annuloaortic ectasia is associated with Marfan and Ehlers-Danlos syndromes.
Surgical treatment is recommended for an ascending TAA >5.5 cm in diameter and a descending TAA >6 cm in diameter. However, patients with connective tissue disorders and BAV aortopathy (meeting criteria for valve replacement) have a lower surgical threshold of 4.5 cm. Beyond simple size criteria, annual growth rate >1 cm/year (or >5 mm/6 months) is an indication for surgical repari.
A sign of impending rupture is the draped aorta sign, which describes drooping of the posterior aorta against the spine on an axial image.
Complications of TAA treatment include rupture, dissection, infection, endoleak, and paraplegia (caused by artery of Adamkiewicz occlusion).
Abdominal aortic aneurysm (AAA)
Abdominal aortic aneurysm (AAA) is relatively prevalent in older men (seen in up to 5.9% of men by age 80) and less common in women. Rupture of abdominal aortic aneurysms is the 13th leading cause of death in older men. Risk factors for development of an abdominal aortic aneurysm include age, male sex, smoking, and family history.
An abdominal aortic aneurysm is defined as an aortic diameter >/= 3 cm. Similar to measurement of thoracic aortic aneurysms, double-oblique reformatted images should be used to obtain a true cross-sectional diameter. Volume measurement can also be used to monitor for endoleak on follow-up.
The natural history of abdominal aortic aneurysm is progressive enlargement and eventual rupture. The annual risk of rupture for an AAA between 5.5 and 5.9 cm is 9.4%. The annual risk of rupture for an AAA between 6.0 and 6.5 cm is 10.2%. The annual risk of rupture for AAA between 6.5 adn 6.9 cm is 19.2%. The annual risk of rupture for an AAA greater than 7.0 cm is 32.5%.
Ultrasound screening of high-risk patients is approved by Medicare in the US for patients older than age 65. If an aneurysm is detected on screening, follow-up imaging is recommended: Aneurysm <4 cm: Follow-up in 6 months; if no change -> annual surveillance. Aneurysm 4-4.5 cm: Follow-up in 6 months; if no change -> 6-month surveillance. Aneurysm 5-5.5 cm: Consider surgery. Aneursym >5.5 cm: Surgery recommended.
In addition to a size >5.5 cm, repair is recommended when the AAA is expanding at a rapid rate (>5 mm/year) or is symptomatic.
The mortality of elective open AAA repair is >3%, while the mortality for urgent repair is 19%. A ruptured AAA has a mortality of at least 50%.
Repair of abdominal aortic aneurysm can be performed with a traditional open or endovascular technique. Endovascular repair is preferred for patients with high surgical risks and is associated with reductions in major morbidity and hospital time. Long-term outcomes are equivalent between endovascular and open repair, but endovascular repair often requires repeat interventions.
Complications of endovascular repair of AAA include rupture, dissection, infection, endoleak, and aorto-enteric fistula.
Type I endoleak: Inadequate seal of graft
Type I endoleak is inadequate graft seal. Type IA is a proximal leak and IB is distal.
Type II endoleak: Persistent collateral flow to excluded aneurysm
Type II endoleak is persistent collateral flow to the excluded aneurysm sac, which typically arises from the lumbar arteries or the inferior emsenteric artery (IMA).
Type III endoleak: Device failure causing leakage
Type III endoleak represents device failure causing leakage through graft fabric or segments of a modular graft.
Type IV and V endoleaks
Both type IV and V endoleaks are diagnoses of exlusion as no endoleak can be visualized by imaging although the sac continues to increase in size.
Type IV endoleak: Type IV endoleak is caused by a porous graft and is seen typically transient and seen intraprocedurally. Type IV endoleak usually resolves within one month after withdrawal of anticoagulation. It is rarely seen with modern grafts.
Type V endoleak: Also called endotension, type V endoleak is continued expansion of the aneursym without any endoleak present, thought to be due to an endoleak below the resolution of imaging.
Aortitis
Aortitis in inflammation of the aorta, which may be either infectious or inflammatory. A complication of infectious aortitis is the development of a mycotic aneurysm.
Inflammatory aortitis can be due to Takayasu arteritis, giant cell arteritis, ankylosing spondylitis, polyarteritis nodosa, rheumatoid arthritis, and immune complex disease. Inflammatory aortitis is treated with corticosteroids.
The acute phase of aortitis will show circumferential mural thickening and enhancement. There may be an associated aneurysm, dissection, or intramural hematoma. In contrast to intramural hematoma, aortitis tends to cause circumferential thickening rather than the eccentric, crescentic thickening of IMH. MRI findings of active aortitis include an aortic wall thickness >2 mm and enhancement of the aortic wall.
In the chronic phase of the disease, there can be long segmental stenoses and/or aneurysms.
Takayasu arteritis
Also known as pulseless disease, Takayasu arteritis is an idiopathic, inflammatory, large-vessel vasculitis that involves the thoracic and abdominal aorta, subclavian arteries, carotid arteries, pulmonary arteries, and large mesenteric arteries.
Takayasu arteritis typically affects young to middle-aged women.
On imaging, long smooth stenoses are classic. Imaigng is often indistinguishable from giant cell artertiis, with the patient’s age being the main distinguishing factor. Takayasu arteritis occurs in relatively younger patients and giant cell arteritis is rare in patients under age 50.
During the acute phase, treatment is with steroids. If symptomatic stensoses occur, endovascular treatment can be performed, but only when the active inflammation has resolved, as measured by normalization of the erthyrocyte sedimentation rate.
Aortic coarctation
Aortic coarctation is congenital focal narrowing of the proximal descending aorta.
The adult form of coarctation is usually juxtaductal (at the junction of the ductus arteriosus), leading to upper extremity hypertension. In contrast, an infant presenting with congestive heart failure due to coarctation is usually due to a preductal variant, which functions as a left ventricular obstructive lesion.
In the setting of coarctation, prominent collaterals develop between the internal thoracic arteries to both the epigastric vessels and intercostal arteries.
The radiographic findings of coarctation include the 3 sig of the left upper heart border, which represents a double bulge from the focal aortic narrowing and post-stenotic dilation. Rib notching is frequently seen from collateral intercostal vessels.
Phase contrast-MRI can be used to measure the gradient of flow across the coarctation. Calculatin of the flow differential between the proximal descending aorta and the aorta at the hiatus aids in determining hemodynamic significance.
A pseudocoarctaion represents focal narrowing of the aorta, similar in morphology to a true coarctation; however, there is no pressure differential and thus no collaterals.
Evidence for using coronary CT to evaluate for ischemic cardiac disease
Coronary CT angiography (CCTA) is an excellent test to rule out hemodynamically significant coronary artery disease. Meta-analyses of multiple trials have shown the negative predictive value for CCTA to be in the high 90s.
The ACRIN-PA and ROMICAT-II clinical trials (both published in 2012 NEJM) evaluate the use of CCTA in teh emergency room setting for acute chest pain in low to medium risk patients. Both trials conclude that early CCTA improves efficiency, clinical decision making, and leads to a shorter hospitilization, although the ROMICAT-II trial did note increased radiation exposure in the CCTA group and no significant cost difference.
Coronary CT is very sensitive for hemodynamically significant (>50% lumenal diameter) stenoses; however, a stenosis found on CT may be overcalled, especially if there is calcified plaque, which can cause a blooming artifact.
ECG gating and radiation dose
ECG gating is used to minimize cardiac motion. The choice of ECG gating has a large effect on patient radiation dose. To estimate the radiation dose, the dose-length product (DLP) should be multiplied by a conversion factor of 0.017 to arrive at the dose in millisieverts.
In a retrospectively gated exam continuos CT scanning is performed throughout the cardiac cycle and the images are correlated to the ECG cycle arterwards. The main advantage of retrospective gating is the ability to evaluate cardiac and valvular function, typically with 10-20 frames per cardiac cycle. The main disadvantage of retrospective gating is a signficant increase in radiation exposure compared to a prospectively gated study.
For prospective gating, the ECG is used to time image acquisition at a specific phase of the cardiac cycle, exposing the patient to radiation only during this segment of the cardiac cycle. The main advantage of prospective gating is decreased radiation exposure. However, since only a fraction of the cardiac cycle is acquired, cine reconstructions are not possible.
Spatial resolution and grading of stenoses
Coronary arteries have an average luimnal diameter of approximately 3 mm.
CT has an isotropic voxel resolution of 0.35 to 0.5 mm, which allows only 6 to 9 voxels to image the entire coronary artery lumen. This is insufficient resolution to grade a stenosise with accuracy greater than approximately 20% of the diameter.
In contrast, catheter angiography has a spatial resolution of approximately 18 pixels.
Due to the limited spatial resolution of CT, a stenosis is classified into categories: <20%; 20-50%; 50-70%, or >70%. A >50% stenossi is considered potentially hemodynamically significant. Conversely, a <50% stenosis is considered not hemodynamically significant.
Temporal resolution and “freezing” of cardiac motion
A CT scanner requires slightly more than 180 degrees of gantry rotation for image acquisition: For a complete rotation time of 330 ms, the temporal resolution is ~175 ms.
Dual source CT has two X-rays oriented 90 degrees to each other and needs to rotate only 90 degrees to complete a reconstruction, with a temporal resolution of ~75 ms.
CCTA Procedure
A low heart rate (typically below 60 bpm) is desired in order to maximize the R-R interval.
Beta-blockade is usually necessary to achieve the this target heart rate. Oral metroprolol is administered (between 5 and 25 mg, typically administered in 5 mg doses). Oral beta blocker gives better heart rate control and decreased heart rate variability compared to IV.
Just prior to scanning, sublingual nitroglycerin (0.5-0.8 mg) is administered to dilate the coronary arteries.
Coronary artery anatomy
The diagram is in anatomic orientation, as if one were looking directly at the patient from the front.
Coronary artery origination
Most commonly, there are two coronary artery origins off the proximal aorta at the sinuses of Valsalva. The most common anomaly is a high take-off from the sinotubular junction or above.
There are three coronary sinuses. The right coronary artery arises from the right coronary sinus (located anteriorly); the left main coronary artery arises from the left coronary sinus (located left-posterior); and no coronary artery arises from the noncoronary sinus (located right-posterior).
Left main coronary artery (LMCA)
The left main coronary artery (LMCA) courses between the pulmonary artery and the left atrial appendage (LAA).
The LMCA bifurcates into left anterior descending (LAD) and left circumflex (LCx) arteries. A ramus branch may be present to form a trifurcation.
Left anterior descending (LAD) coronary artery
The left anterior descending (LAD) coronary artery courses in teh anterior interventricular groove, which is the anatomic groove between the right and left ventricles.
The LAD gives off the diagonal branches (LAD-Diagnoal) and septal branches, whic penetrate the interventricular septum to supply blood to the anterior half of the septum.
Left circumflex (LCx) coronary artery
The left circumflex (LCx) coronary artery courses underneath the left atrial appendage (LAA) in the left atrioventricular groove (between the left ventricle and left atrium).
The LCx artery gives off the obtuse marginal (OM; cirOMflex) branch, which supplies the posterolateral wall of the left ventricle. The angle of the lateral wall of the obtuse marginal artery is obtuse, hence the name.
The LCx uncommonly (~7%) supplies the posterior descending artery (PDA), which is criteria for a left-dominant system. In the anatomic diagram on the previous page, the more common right-dominant system is shown, where the right coronary artery supplies the PDA.
Malignant coronary artery anomaly
Anomalous origin of the left coronary arter arising from the right coronary sinus, passign between the aorta and the PA.
Anomalous origin of right coronary artery arising from the left coronary sinus, passing between the aorta and the PA.
Anomalous interarterial (between the pulmonary artery or right ventricular outflow tract and the aorta) course of a coronary artery carries a high risk of sudden death of up to 40%, associated with exercise. It is thought that dilation of the aorta occurs during exercise, which may compress the anomalous vessel resulting in myocardial infarction.
Either an anomalous left coronary artery or anomalous right coronary artery may take a malignant interarterial course.
Treatment is surgical bypass grafting.
Summary of delayed enhancement MRI
