Term used to describe a constellation of symptoms resulting from acute myocardial ischemia.

Two major groups: (1) ST elevation myocardial infarct (STEMI) and (2) non-ST elevation myocardial infarction (NSTEMI and unstable angina).

Treatments: (1) STEMI, reperfusion therapy; (2) NSTEMI, not treated with thrombolysis.

Vasodilator agent used in myocardial stress perfusion.

Most commonly used stress agent due to its ultrashort half-life (<10 s).

Dose: 140 μg/kg/min for 3–6 min.

Caffeine or other methylxanthines should be avoided for 24 h before the administration.

Contraindications: (1) high-grade AV block; (2) asthma or COPD; (3) sinus bradycardia; (4) systemic hypotension (BP < 90 mmHg); (5) severe carotid stenosis.

Side effects: transient heart block, transient hypotension, transient tachycardia, bronchospasm.

Antagonist: aminophylline, 50–100 mg over 1 min, injection can be repeated up to 250 mg total dose.

See also “Perfusion imaging, myocardial”.

Procedures that utilize ionizing radiation should be performed according to the As Low As Reasonably Achievable (ALARA) principles, and physicians prescribing and performing cardiac imaging should be very confidential with the radiation dose delivered and strategies able to minimize radiation dose exposure.

HCM treatment in patients with severe LVOT dynamic obstruction consisting in the injection of alcohol into the septal perforator arteries to induce localized infarct of the hypertrophied segment.

Complications: AV block and increased risk of ventricular arrhythmias.

Characteristics: (1) deposition of amyloid protein in any organ; (2) hereditary or acquired; (3) cardiac involvement frequent in primary AL amyloid including myeloma and lymphoma; rare in AA amyloid secondary to chronic infection.

MR: (1) LV concentric hypertrophy, heart failure (restrictive pattern with atrial dilatation followed by systolic dysfunction); (2) LE, subendocardial ring pattern or diffuse transmural pattern, involves both ventricles; (3) in late enhancement, can be difficult to suppress the myocardial signal due to extensive amyloid deposition.

Differential diagnosis: hypertrophic cardiomyopathy, Anderson–Fabry disease, hypertensive hypertrophy.

Tips and tricks: Amyloidosis is associated with renal failure; look for renal morphological alteration using coronal single-shot turbo spin-echo sequence with large FoV.

Characteristics: X-linked lysosomal storage disease for the lack of alpha-galactosidase A.

MR: (1) LV concentric hypertrophy; (2) intramural LE (inferolateral wall); (3) valvular thickening (aortic and mitral); (4) conduction abnormalities.

Differential diagnosis: hypertrophic cardiomyopathy, amyloidosis, sarcoidosis, hypertensive hypertrophy.

Chest pain caused by myocardial ischemia.

Causes: coronary stenosis, tachycardia, anemia, aortic stenosis, left ventricular hypertrophy, syndrome X, coronary artery spasm.

Classification: (1) stable angina, pain occurring after constant level of exercise; (2) unstable angina, pain on minor exercise or at rest which is of new onset or a worsening angina.

Most common primary cardiac malignant tumor.

Two forms: (1) focal, usually in the right atrium; (2) diffuse, with pericardial infiltration.

MR: heterogeneous intracardiac mass with extensive myocardial infiltration.

Aortic values should be normalized for patient BSA.

A diameter >40 mm for ascending aorta is considered dilated.

Ascending aorta should be less than twice the diameter of the descending.

CT/MR: To accurately evaluate ascending aorta and aortic annulus dimensions, use cardiac gating.

Surgical repair should be considered in (1) asymptomatic patients with ascending aorta or aortic sinus diameter >5.5 cm, (2) patients with Marfan syndrome or other genetically mediated disorders (vascular Ehlers–Danlos syndrome, Turner’s syndrome, bicuspid aortic valve, or familial thoracic aortic aneurysm and dissection) with ascending aorta or aortic sinus diameter >4.0 or 5.0 cm depending on the condition, (3) patients with a growth rate of more than 0.5 cm/year in an aorta that is less than 5.5 cm, and (4) patients undergoing aortic valve repair or replacement and who have an ascending aorta or aortic root >4.5 cm should be considered for concomitant repair of the aortic root or replacement of the ascending aorta.

Impending signs of rupture: (1) Maximal diameter, the most important factor to predict likelihood of aneurysmal rupture; of patients suffering for aneurysms >5 cm, an aneurysmal rupture within 5 years has a likelihood of 25–41 %; a 5–7 cm and >7 cm sized aneurysms have annual risks of rupture of 6–11 % and 20 %; (2) expansion rate, if higher than 1 cm/6 months, might be a reasonable criterion of impending rupture, and an enlargement rate of 10 mm or more per year is also considered as an indication for surgical repair; (3) hyperdense aortic wall crescent, appreciated on unenhanced CT and represents an internal dissection of blood into the peripheral thrombus or into aneurysm wall; (4) infected aneurysm, more prone to rupture (rate of 53–75 % at surgical repair); (5) thrombus and calcification, thick circumferential thrombus has a protective value against rupture, and a focal discontinuity in circumferential wall calcifications is more commonly observed in unstable or ruptured aneurysms.

Congenital variant in which the aortic arch course is higher than normal and lies behind the left clavicle.

Clinical consequences if central venous cannulation is required.

Congenital variant with the thoracic aorta lying on the right side (0.5 % of population).

Abdominal aorta usually normal.

No clinical consequences.

Focal transverse outpouching of the aortic wall.

Impending sign of aneurysm rupture.

CT: use multiplanar reconstruction and volume rendering algorithm to detect aortic bleb.

The left common carotid artery has a common origin with the innominate artery.

A similar but less common variant occurs when the left common carotid artery originates directly from the innominate artery rather than as a common trunk.

No clinical consequences.

Narrowing of the aorta just distal to the left subclavian artery due to ductus arteriosus abnormalities and remnants.

Isolated or in combination with other anomalies (bicuspid aortic valve, VSD, mitral disease, intracranial aneurysms, Turner’s syndrome, Shone’s syndrome).

Discrete or segmental.

Poststenotic dilatation of the proximal descending aorta.

Always look at the transverse arch caliber (exclude hypoplasia) and branches, particularly the position of the left subclavian artery related to the site of coarctation.

50 % patients with bicuspid aortic valve.

Aortic coarctation and bicuspid aortic valve are considered by many authors as a diffuse aortopathy.

In native severe coarctation the amount of flow at the level of minimum caliber is very low and there might be no pressure gradient. This is in keeping with dominant collateral flow.

Maximum gradient >20 mmHg indicates need for surgical treatment.

Postsurgical complications: (1) isthmic aneurysms; (2) recoarctation, maximum gradient >20 mmHg; (3) endocarditis; (4) bicuspid aortic valve: ascending aorta dilatation; (5) intracranial arterial aneurysms; (6) coronary artery disease.

MR: (1) Use black blood imaging on the arch (“candle stick” view), particularly for stents; (2) “diastolic tail” is a sign of coarctation with competent aortic valve and good elastance of the thoracic aorta; (3) flow of the descending aorta at the diaphragm in through plane with “diastolic tail”; the aortic valve must be competent; (4) peak velocity measured with a through-plane flow immediately after the site of maximum stenosis; (5) quantification of collaterals by measuring flow volume of descending aorta at the level of coarctation and at the diaphragm. In normal subject a flow reduction is observed due to orthodromic outflow in intercostal arteries. In coarctation there is a flow increment for the presence of retrograde inflow from the intercostal arteries; (6) reporting: site, morphology, extension, gradient, collaterals, LV function and dimensions (hypertrophy), mitro-aortic disease.

CT: can be useful in postsurgical evaluation, stent, and coronary assessment.

Differential diagnosis: (1) pseudocoarctation, tortuous aorta without stenosis; (2) hypoplastic aortic arch, with or without coarctation.

Stanford classification: (1) Type A: involves the ascending aorta and/or aortic arch and possibly the descending aorta. The tear can originate in the ascending aorta, in the aortic arch, or in the descending aorta. Requires primary surgical treatment because ascending aortic dissections often involve the aortic valve; (2) type B: involves the descending aorta or the arch (distal to right brachiocephalic artery origin), without involvement of the ascending aorta. Medically as initial treatment with surgery reserved for any complications.

CT: It is a fast noninvasive test that will give an accurate three-dimensional view of the aorta.

MR: Time-consuming procedure with inferior spatial resolution. Second-line technique. Useful in postsurgical follow-up.

Normal annulus area: 2 cm² in adults, varying from 2.5 to 4.0 cm².

CT: Planimetry is best achieved in axial MIP reformatted image during midsystole (approximately 20 % of the R-R interval or 50–100 ms from the R-wave peak depending on heart rate) to minimize artifacts.

MR: (1) LVOT (oblique axial) and LVIT/OT (oblique coronal) views; (2) short axis through aortic valve cusps, perpendicular to both the precedent views and at the level of the tips; (3) planimetry is achieved in an imaging plane through the valve tips in systole and acquiring multiple thin (4–5 mm) slices parallel to the valve orifice.

The most common congenital cardiac defect (1–2 % of population).

Two types: (1) two morphological and functional cusps and (2) three cusps, two of which are fused to a single aberrant one with the development of a raphe.

Association with aortic coarctation, PDA, and coronary artery anomalies.

Dilatation of sinus of Valsalva and ascending aorta.

CT: Can be difficult to differentiate the two types, because at diastole the raphe can be mistaken as a normal commissure. Reconstructions during systole are required.

MR: Permits to visualize the aortic valve morphology in axial image in systole. For quantification velocity mapping in systole shows the forward flow and peak velocity.