Ischemic heart disease

CMR can be uniquely helpful in differentiating between ischemic and various nonischemic forms of acute myocardial injury. Even after the diagnosis of myocardial infarction (MI) has been made, CMR may be helpful in identifying residual viability, stunning, and microvascular damage. In addition, post-MI sequelae, including LV thrombus, LV aneurysm or pseudoaneurysm formation, and pericarditis are easily identified.

Acute MI or acute coronary syndromes 1.

LV structure and function

2.

Advanced tissue characterization - optional, although frequently used to assess edema/inflammation that can accompany acute necrotic injury

3.

Optional - First pass perfusion (only at rest). Consider stress if culprit vessel has already been revascularized to evaluate for ischemia in the non-infarct territories

4.

Optional - Early gadolinium enhancement, i.e. within the first 1–3 min after contrast infusion to look for early microvascular obstruction (MVO)

5.

LGE

Chronic ischemic heart disease and viability

General purpose of CMR is to document baseline LV morphology, contractility, viability, and (often) ischemia. Follow-up imaging can be helpful in assessing changes in ventricular remodeling as well as scar and/or ischemia burden following clinical events and/or medical therapeutic interventions. Detection of LV thrombi is also important.

1.

LV structure and function

2.

Advanced tissue characterization - optional, although may be used to exclude other potential pathologies

3.

Optional - low dose dobutamine with 5–10 min infusion of 2.5–10 μg/kg/min of dobutamine to assess contractile reserve identified as improvement in wall thickening

4.

Optional - vasodilator stress-rest perfusion or high dose dobutamine functional imaging to determine the presence of inducible ischemia

5.

LGE

Nonischemic heart diseaseHypertrophic cardiomyopathy (HCM)

Goals of imaging HCM include measuring LV mass and volumes, global function, and maximal wall thickness (by cine imaging), assessing scar (LGE and T1 mapping) and measuring the LVOT gradient if present.

1.

LV structure and function

2.

LVOT flow imaging using bSSFP cine imaging in a 3-chamber view examining for turbulence and systolic anterior motion of the mitral valve or chordae, and phase velocity measurements for gradient (using either in-plane phase-velocity imaging in the 3-chamber view, or through plane phase-velocity measurements perpendicular to the LVOT) if LVOT obstruction is present

3.

Advanced tissue characterization - optional, although frequently used

4.

Optional – consider vasodilator stress perfusion if underlying ischemia is being considered

5.

LGE

Hypertensive heart disease

Goals of imaging hypertensive heart disease include assessing LV mass, wall thickness, volumes, global function (by cine imaging), and scar (LGE and T1 mapping).LV structure and function

1.

Advanced tissue characterization - optional, although frequently used

2.

Optional - vasodilator stress-rest perfusion or high dose dobutamine functional imaging to determine the presence of inducible ischemia

3.

Optional – aortic imaging and renal MRA to exclude secondary causes of hypertension

4.

LGE

Left ventricular non-compaction

Goals of imaging LV noncompaction include assessing trabeculations and measuring the wall thickness of compacted and noncompacted segments as well as LV volumes and global function, and assessing for thrombi and scar (LGE)

1.

LV structure and function

2.

Advanced tissue characterization - optional, although frequently used to exclude other potential etiologies.

3.

Optional - vasodilator stress-rest perfusion or high dose dobutamine functional imaging to determine the presence of inducible ischemia

4.

LGE

Dilated cardiomyopathy

Goals of imaging dilated cardiomyopathy include measuring LV mass, volumes, and global function (by cine imaging), and assessing scar (LGE and T1 mapping).

1.

LV structure and function

2.

Advanced tissue characterization - optional, although frequently used

3.

Optional - vasodilator stress-rest perfusion or high dose dobutamine functional imaging to determine the presence of inducible ischemia

4.

LGE

Arrhythmogenic ventricular cardiomyopathy (AVC)

Goals of imaging AVC include measuring RV and LV volumes and global and regional function (by cine imaging), and assessing RV and LV scar (LGE).

1.

LV structure and function – consider 5–6 mm slice thickness

2.

Transaxial or oblique transaxial bSSFP cine images (slice thickness 5–6 mm) covering the RV including RV outflow tract (RVOT). An RV vertical long-axis view aligned with tricuspid inflow is recommended

3.

Optional sequences

a.

Selected transaxial or oblique transaxial black blood images (double inversion recovery T1-weighted (T1w) FSE)

b.

Repeat same geometry with fat suppression

4.

LGE. Consider T1 nulling for RV

Siderotic cardiomyopathy

Goals of imaging siderotic cardiomyopathy include measuring LV mass, volumes, and global function (by cine imaging), and assessing for iron overload (T2* imaging).

1.

LV structure and function

2.

Advanced tissue characterization using T2* mapping

3.

Optional - vasodilator stress-rest perfusion or high dose dobutamine functional imaging to determine the presence of inducible ischemia

4.

Optional - LGE (to be consider if LV or RV ejection fraction is abnormal)

Restrictive cardiomyopathy

Goals of imaging restrictive cardiomyopathy include measuring LV mass, volumes, and global function (by cine imaging), and assessing scar and infiltration (LGE and T1 mapping)

1.

LV structure and function

2.

Advanced tissue characterization - optional, although frequently used

3.

LGE

4.

Optional (to exclude constrictive physiology) - real time cine imaging, mid-left ventricular short axis, during dynamic breathing manoeuvres for abnormal ventricular interdependence

Cardiac sarcoidosis

Goals of imaging sarcoidosis include measuring LV mass, volumes, and global function (by cine imaging), and assessing scar (LGE and T1 mapping), and inflammation/edema (T2w imaging or T2 mapping).

1.

LV structure and function

2.

Advanced tissue characterization

3.

LGE

Myocarditis

Goals of imaging myocarditis include measuring LV mass, volumes, and global and regional function (by cine imaging), and assessing for inflammation/edema (T2w imaging or T2 mapping), and increased interstitial space (T1 mapping, LGE).

1.

LV structure and function

2.

Advanced tissue characterization including techniques listed above

3.

Optional - Early Gadolinium Enhancement

4.

LGE

Cancer-related cardiomyopathies

Goals of imaging cancer-related cardiomyopathy include measuring LV mass and volumes, global function, and maximal wall thickness (by cine imaging), and assessing scar (LGE and T1 mapping). When cardiomyopathy or myocarditis due to chemotherapeutic agents are in consideration, acute/subacute assessment for inflammation/edema (T2w imaging or T2 mapping) may be included.

1.

LV structure and function

2.

Advanced tissue characterization - optional, although frequently used

3.

Optional - vasodilator stress-rest perfusion or high dose dobutamine functional imaging to determine the presence of inducible ischemia

4.

LGE

Recreational drug-induced cardiomyopathies

Goals of imaging recreational drug-induced cardiomyopathy include measuring LV mass, volumes, and global function (by cine imaging), and assessing scar (LGE and T1 mapping).

1.

LV structure and function

2.

Advanced tissue characterization - optional, although frequently used

3.

Optional - vasodilator stress-rest perfusion or high dose dobutamine functional imaging to determine the presence of inducible ischemia

4.

LGE

Post-heart transplantation

Goals of imaging post-heart transplantation cardiomyopathy include measuring LV mass, volumes, and global function (by cine imaging), and assessing scar (LGE and T1 mapping) and inflammation/edema (T2w imaging or T2 mapping).

1.

LV structure and function

2.

Advanced tissue characterization - optional, although frequently used

3.

Optional - vasodilator stress-rest perfusion imaging to determine the presence of inducible ischemia

4.

LGE

Vascular diseasePeripheral MRA 1.

Peripheral vascular coil, or combination of coils, as available

2.

Transaxial, low-resolution, vessel scouting with time-of-flight MRA or bSSFP

3.

Gadolinium timing

a.

Option 1 –A test bolus (transaxial or coronal) at level of distal abdominal aorta. 2 ml injection of GBCA, followed by 20 ml saline. Determine time to peak enhancement following injection using a single-shot bolus tracking sequence

b.

Option 2 – Bolus trigger technique to time start of scan

4.

Stepping-table, GBCA-enhanced MRA performed in the coronal projection from the mid abdominal aorta to the feet.

a.

Two volumetric acquisitions – one pre-contrast (for subtraction) and one during contrast administration

b.

GBCA injected in 2 phases to minimize venous contamination followed by saline bolus. See Table 1

c.

Slice thickness 1–1.5 mm; acquired spatial resolution in-plane 0.8–1.5 mm

d.

Slices – typically 60–100, as needed to accommodate vessels of interest

e.

Volumes obtained of abdomen/pelvis and thighs may be coarser spatial resolution (larger vessels), while those of the legs preferably are sub-millimeter spatial resolution. The former acquisitions typically require 15–20 s, while the leg acquisition may take 60–90 s for increased spatial resolution. Elliptical centric k-space acquisition is advantageous for the legs. If available, time-resolved acquisitions are preferred for the legs.

f.

Parallel acquisition recommended (multichannel surface coil needed)

Alternative: dual injection protocol

1.

Single dose of GBCA: time-resolved MRA of the calf and foot vessels

2.

Single dose of GBCA: abdominal and thigh vessels

Alternative: Non-contrast MRA technique

Non-contrast MRA is rapidly evolving and modifications of older methods as well as new techniques are constantly proposed. Some techniques are available for most clinical CMR systems; however as with other sequences, a vendor-specific nomenclature makes general statements difficult. Additionally, many newer techniques are only offered by a limited number of vendors as commercial products.

1.

“Fresh Blood Imaging” where two ECG-triggered 3D fast (turbo) spin-echo sequences are performed with the first gated to systole and the second to diastole. Subtraction of the systolic image from the diastolic image set results in an arterial-only image dataset. This is techniques is available for most clinical CMR systems using different vendor-specific acronyms.

a.

Slice thickness ~ 2 mm; acquired spatial resolution in-plane 0.6–0.8 mm

b.

Slices – typically 40, as needed to accommodate vessels of interest

c.

Parallel acquisition recommended (multichannel surface coil needed)

2.

3D bSSFP with an inversion preparation pulse, which provides suppression of background tissue, and with an appropriate TI, allows for the inflow of arterial blood from outside the inversion recovery prepared volume and into the region of interest providing high arterial signal. This is more suited toward smaller volume acquisitions

a.

Volume acquired: ~ 340 × 300 × 70; acquired spatial resolution ~ 1.3 × 1.3 × 1.4

b.

Parallel acquisition recommended (multichannel surface coil needed)

3.

Quiescent Interval slice selective (QISS) MRA is a cardiac gated 2D multi-slice inflow technique, acquired in multiple groups of axial slices with incremental table movement and coverage from pelvis to feet. The sequence uses magnetization preparation pulses to suppress venous flow and stationary tissue and the arterial signal is acquired using a single-shot balanced steady state free precession sequence.

a.

Slice thickness 2–3 mm, in plane resolution 1.0–1.2 mm

b.

Parallel acquisition routine

Thoracic aortic MRA 1.

Localizer, 3 orientations

2.

Single shot black blood or bSSFP (one breathhold, entire thorax) Transaxial orientation

3.

Transaxial T1w FSE or spoiled GRE through aorta (for intramural hematoma, dissection)

4.

bSSFP cine imaging in parasagittal plane parallel to and along midline of aorta Option – use 3-point piloting

5.

Evaluate aortic valve as per valvular protocol

6.

Contrast timing

a.

Option 1 -Transaxial/sagittal oblique test bolus in thoracic aorta. 2 ml injection of GBCA, followed by 20 ml saline. Determine time to peak enhancement following injection

b.

Option 2 – Bolus triggering technique to time start of scan

c.

Option 3 – Rapid multiphase 3D acquisitions without timing

7.

3D GBCA enhanced MRA (0.1–-0.2 mmol/kg

a.

Use spatial resolution of at least 1–-1.5 mm

b.

Parallel acquisition if available

c.

Use ECG gating, if available

d.

At least 2 acquisitions after contrast injection

8.

Optional - transaxial T1w imaging with fat suppression post-contrast for aortitis

9.

Optional – see section 3.2.1 above (Peripheral MRA) for noncontrast MRA techniques

Coronary arteries 1.

LV structure and function to look for wall motion abnormalities

a.

Add repeat horizontal long-axis with high temporal resolution sequence (< < 20 ms per phase) to accurately determine quiescent period of right coronary artery (RCA)

2.

Navigator-gated, 3D, free-breathing, MRA sequence:

a.

Transaxial slices spanning from level of proximal main pulmonary artery down to the middle of the right atrium (entire cardiac coverage if desired). Slice thickness 1–-1.5 mm; acquired spatial resolution in-plane of 1.0 mm or less. Fat suppression is typically used.

b.

Slices – typically 50–-80, as needed to encompass vessels of interest

c.

Adjust trigger delay and acquisition window according to observed quiescent coronary period

d.

Parallel acquisition preferred

e.

Navigator placed over the right hemi-diaphragm

f.

Optional – GBCA may increase vessel conspicuity if the contrast agent was administered previously as part of the scan. Due to the relatively long scan time of coronary artery imaging with CMR, a bolus injection is not recommended.

3.

Optional –

a.

Breathhold techniques if poor image quality or navigators unavailable or of poor quality

b.

T2-prepared sequence may be useful to suppress myocardial and venous signal

Pulmonary vein evaluation – pre- and post-ablation 1.

LV structure and function (optional)

2.

Breathheld 3D contrast-enhanced MRA performed in the coronal projection encompassing the pulmonary veins and left atrium (greater anterior coverage if breathholding permits)

a.

Optional – oblique plane centering the pulmonary veins can reduce slab thickness and therefore breath hold time but will lead to less coverage of the left atrium

b.

Optional - ECG-gating. When patient has irregular rhythm, readout should be synchronized with systole (i.e. no trigger delay)

c.

2–3 volumetric acquisitions – one pre-contrast (for subtraction), one during the first pass of contrast administration, one (optional) after contrast administration

d.

Time-resolved multiphase MRA – acquisition and contrast started simultaneously; this can provide isolated pulmonary venous phase image for reconstruction and integration with ablation mapping software

e.

GBCA (0.1–0.2 mmol/kg) injected at 2–3 ml/s

f.

Slice thickness 1–2 mm; acquired spatial resolution in-plane 1–1.5 mm

g.

Slices – typically 60–80, as needed to encompass region of interest

3.

Optional – through plane phase contrast flow analysis through each pulmonary vein

4.

Optional - LGE of the left atrial wall

OtherValvular disease

Patients with artificial valves can safely undergo CMR at 1.5 and 3 T. The force exerted by the beating heart is many-fold higher than the force exerted by the magnetic field.

1.

General approach

a.

Valve morphology assessment with bSSFP cine in the plane of the valve in question. Care must be taken to optimize the level and angle of imaging as described below

b.

Note – if planimetry of a stenotic valve is to be attempted, a contiguous or slightly overlapping stack of cine imaging transecting the line of the jet and moving from orifice level to immediately downstream is recommended. Planimetry is most likely to be valid where the cross section of the orifice, or rather of the jet, is clearly delineated.

c.

GRE or hybrid GRE-EPI may visualize regurgitant jets with a higher sensitivity (for qualitative purposes only)

d.

Velocity encoded imaging to measure velocities and direction quantitatively. Adapt velocity encoding to actual velocity (using lowest velocity without aliasing)

e.

Use lowest TE possible for high velocity jet flows

2.

Specific approaches by valve

a.

Mitral

i.

Regurgitation

1.

LV structure and function

2.

Velocity encoded imaging in a plane perpendicular to the aortic valve, at the sinotubular junction level, at end diastole. Retrospectively-gated acquisition is essential to cover the entire cardiac cycle

ii.

Stenosis

1.

Velocity encoded imaging (though-plane encoding) in a plane parallel to the mitral valve and at the point of peak flow disturbance identified on a long-axis cine image through the mitral valve

2.

Alternatively, velocity encoded imaging (in-plane) along an imaging plane parallel to and in line with the mitral valve jet of flow disturbance

b.

Aortic

i.

Regurgitation

1.

LV structure and function

a.

Further imaging planned using the planes of the aortic valve and aortic root visualized from LVOT and coronal views.

2.

Velocity encoded imaging in a plane perpendicular to the aortic valve, approximately 5 mm superior to the valve plane at end diastole. Retrospective acquisition is essential to cover the entire cardiac cycle

3.

Velocity encoded imaging in a plane perpendicular to the descending aorta at the level of the main pulmonary artery to examine for diastolic flow reversal

ii.

Stenosis

1.

Velocity encoded imaging (through plane encoding) in a plane parallel to the aortic valve and at the point of peak flow disturbance identified on a long-axis cine image through the aortic valve

2.

Alternatively, velocity encoded imaging (in-plane encoding) along an imaging plane parallel to and in line with the aortic valve jet of flow disturbance

c.

Tricuspid

i.

Regurgitation

1.

RV structure and function

2.

Velocity encoded imaging in a plane perpendicular to the pulmonic valve, approximately 5 mm superior to the valve plane, at end diastole. Retrospective acquisition is essential to cover the entire cardiac cycle

ii.

Stenosis

1.

Velocity encoded imaging (through plane encoding) in a plane parallel to the tricuspid valve and at the point of peak flow disturbance identified on a long axis cine image through the tricuspid valve

2.

Alternatively, velocity encoded imaging (in-plane encoding) along an imaging plane parallel to and in line with the tricuspid valve jet of flow disturbance

d.

Pulmonic

i.

Regurgitation

1.

RV structure and function

a.

Further imaging planned off of pulmonic valve and pulmonic root visualization from RVOT and coronal views

2.

Velocity encoded imaging in a plane perpendicular to the pulmonic valve, approximately 5 mm superior to the valve plane, at end diastole. Retrospective acquisition is essential to cover the entire cardiac cycle

ii.

Stenosis

1.

Velocity encoded imaging (through plane encoding) in a plane parallel to the pulmonic valve and at the point of peak flow disturbance identified on a long-axis cine image through the pulmonic valve

2.

Alternatively, Velocity encoded imaging (in-plane encoding) along an imaging plane parallel to and in line with the pulmonic valve jet of flow disturbance

Pericardial disease 1.

LV structure and function

2.

T1 or T2-weighted FSE images (optional, with or without fat saturation)

a.

2–-3 representative long-axis images and 3–-4 representative short-axis images to measure pericardial thickness (normal ≤3 mm)

b.

If pericardial cyst is suspected, refer to masses protocol

3.

Optional - iIf regions of thickened pericardium noted – GRE myocardial tagged cine sequences to demonstrate presence or absence of epicardial/pericardial slippage (2–-3 long axis images and 1–-2 short axis images)

4.

Real-time imaging during dynamic breathing manoeuvres is valuable for evaluation of ventricular interdependence

a.

Mid-ventricular short-axis plane is preferred

b.

Cine imaging temporal resolution is preferably below 60 ms

c.

Patients are instructed to breathe deeply in and out and the total imaging period should be at least 2 complete respiratory cycles

d.

Abnormal septal motion (early diastolic septal flattening or inversion) during onset of inspiration is consistent with a constrictive physiology

5.

LGE

a.

Acquisition with and without fat saturation is helpful to distinguish pericardial inflammation from epicardial or pericardial fat

Cardiac and paracardiac masses, including thrombi 1.

LV structure and function

2.

T1w FSE - slices through the mass and surrounding structures (number of slices depends on size of the mass)

3.

T2w FSE with fat suppression (optional - without fat suppression) - through the mass and surrounding structures as above

4.

First pass perfusion module with slices through mass

5.

Repeat T1w FSE with fat suppression (early after GBCA)

6.

Optional - Repeat selected bSSFP cine images post-contrast

7.

LGE

a.

Images with the TI set to null thrombus (approximately 500–-550 ms at 1.5 T, 850–-900 ms at 3 T) will help differentiate thrombus from tumor as well as delineate thrombus surrounding or associated with tumor

b.

Serial imaging can help distinguish hypoperfused tumor necrotic core from thrombus