---

Cardiac MRI (CMR): A Comprehensive Reference for the Cardiovascular Radiologist

---

SECTION 1: FUNDAMENTALS OF CARDIAC MRI

1.1 Why Cardiac MRI?

• True 3D volumetric data for LV/RV ejection fraction, volumes, and mass
• Tissue characterization via T1 mapping, T2 mapping, T2* mapping, and Late Gadolinium Enhancement (LGE)
• Flow quantification via phase-contrast velocity encoding
• Perfusion imaging with first-pass gadolinium kinetics
• Myocardial stress testing via dobutamine or vasodilator pharmacological stress

---

1.2 Core CMR Sequences - The Radiologist's Toolkit

A. Cine Imaging - SSFP (Steady-State Free Precession)

• Also known as: TrueFISP (Siemens), FIESTA (GE), BFFE (Philips)
• Principle: Exploits the T2/T1 ratio of tissues. Blood pool appears bright (high T2/T1), myocardium appears intermediate gray - creating excellent blood-myocardium contrast without contrast agent
• Clinical use: The cornerstone sequence. Used for biventricular function, EF, volumes, wall motion analysis, valve assessment, and morphology
• ECG-gating: Retrospective ECG gating is standard; allows reconstruction of the complete cardiac cycle
• Standard planes acquired:
  • 2-chamber (vertical long axis)
  • 4-chamber (horizontal long axis)
  • 3-chamber (left ventricular outflow tract, LVOT)
  • Short-axis stack (base to apex, typically 10-12 slices)
• Artifacts: Dark banding artifacts (off-resonance artifact) - correctable with frequency adjustment. Susceptibility artifacts from metallic implants

---

B. Black-Blood Sequences (Dark Blood)

• Technique: Double inversion recovery (DIR) fast spin-echo (FSE/TSE). Two radiofrequency pulses null the blood pool signal - blood appears dark, myocardium and vessel wall appear bright
• T1-weighted black-blood: Best for morphology, fat (appears bright), hemorrhage (subacute - bright), fibrosis
• T2-weighted STIR (Short Tau Inversion Recovery): Fat suppressed T2. Edema and inflammation appear hyperintense (bright). Critical for myocarditis, acute MI, and cardiac masses
• Applications: Pericardial thickness, intracardiac masses, vessel wall imaging, myocardial edema

---

C. Late Gadolinium Enhancement (LGE)

• Principle: Gadolinium-based contrast agent (GBCA) distributes into the extracellular space. Normal myocardium with intact cell membranes has a small extracellular volume (ECV ~25%). In necrotic or fibrotic tissue, cell membranes rupture or collagen replaces cells - ECV expands dramatically. Gadolinium accumulates here and washes out slowly
• Technique: Phase-sensitive inversion recovery (PSIR) or magnitude IR sequence, acquired 10-15 minutes post-contrast. The inversion time (TI) is set to null normal myocardium (myocardium appears black); fibrosis/necrosis appears bright white
• TI scout: A TI-scout sequence (Look-Locker) is run first to identify the optimal TI (~240-300 ms typically, but varies with time post-injection, renal function, heart rate)
• Planes: Short axis stack + two- and four-chamber long axis views
• Patterns of LGE and their diagnostic significance (detailed below)

---

D. T1 Mapping and Extracellular Volume (ECV) Quantification

• Native T1 mapping: Quantifies myocardial T1 relaxation time without contrast. Uses Modified Look-Locker Inversion Recovery (MOLLI) or ShMOLLI sequences. Elevated native T1 = edema, inflammation, fibrosis, infiltration
• Post-contrast T1 mapping: T1 shortens after gadolinium. Combined with native T1 and hematocrit:
  • ECV = (1 - hematocrit) × (ΔR1 myocardium / ΔR1 blood)
  • Normal ECV ~25%; elevated ECV indicates expanded extracellular space
• Clinical use: Amyloidosis (markedly elevated ECV), myocarditis, diffuse fibrosis in cardiomyopathies, monitoring treatment response

---

E. T2 Mapping

• Quantitative T2 relaxation time without the confounders of T2-STIR (signal normalization, heterogeneity). Normal myocardial T2 ~50 ms
• Elevated T2 = myocardial edema (acute MI, myocarditis, transplant rejection)
• Advantages over T2-STIR: No reference tissue needed, more reproducible, captures diffuse edema

---

F. T2* Mapping (Myocardial Iron Quantification)

• Based on gradient-echo multi-echo technique
• T2 is shortened by iron*: Ferromagnetic iron deposits act as local field inhomogeneities accelerating T2* decay
• T2 <20 ms* = iron overload; T2 <10 ms* = severe iron overload with high arrhythmia risk
• Primary indication: Thalassemia major, hemochromatosis, sideroblastic anemia, repeated transfusions
• Liver T2* is acquired simultaneously for comparison

---

G. Phase-Contrast (PC) Flow Imaging / Velocity Encoding (VENC)

• Principle: Spins moving through a bipolar gradient accumulate phase proportional to velocity. Phase difference maps encode velocity
• VENC setting: Set slightly above peak expected velocity to avoid aliasing
• Applications:
  • Aortic/pulmonary flow quantification (forward and regurgitant volumes, regurgitant fraction)
  • Shunt quantification (Qp:Qs ratio) - pulmonary-to-systemic flow ratio in ASD, VSD
  • Stenotic jet velocity measurement
  • 4D flow: Time-resolved 3D PC imaging of the great vessels

---

H. First-Pass Perfusion Imaging

• Technique: Fast spoiled gradient-echo or EPI sequence acquired during bolus injection of GBCA (0.05-0.1 mmol/kg). Images acquired at 3 standard short-axis levels (basal, mid, apical) every cardiac cycle
• Rest perfusion: Detects severe resting ischemia, subendocardial hypoperfusion
• Stress perfusion: Vasodilator stress (adenosine at 140 µg/kg/min, or regadenoson) - coronary hyperemia unmasks relative perfusion defects in territory of stenosed coronary arteries
• Visual analysis: Dark subendocardial rim at peak enhancement = inducible perfusion defect
• Quantitative perfusion: Myocardial blood flow (mL/g/min) can be calculated using signal-time curves

---

I. Stress Cine (Dobutamine CMR)

• Dobutamine infused at 10-40 µg/kg/min with atropine if needed
• Assessment: New wall motion abnormalities (hypokinesia, akinesia) at stress = inducible ischemia
• Superior specificity compared with dobutamine echo in technically challenging windows
• Also used to assess contractile reserve in low-flow low-gradient aortic stenosis

---

J. Coronary MRA (Non-invasive)

• Navigator-gated, free-breathing, whole-heart coronary MRA
• Limited spatial resolution compared to CTA
• Used primarily for anomalous coronary artery course (avoids radiation), coronary aneurysms in Kawasaki disease

---

1.3 Standard CMR Protocol

---

SECTION 2: STANDARD CARDIAC ANATOMY ON CMR

2.1 Planes and Structures

---

SECTION 3: CMR IN SPECIFIC CARDIAC CONDITIONS

---

3.1 Ischemic Heart Disease

Acute Myocardial Infarction

• Transmural extent of LGE predicts functional recovery: <25% transmural = high likelihood of recovery; >75% transmural = unlikely to recover even after revascularization
• Microvascular obstruction (MVO): Dark core within the enhancing territory on LGE images (also called "no-reflow"). Represents zones of hemorrhagic necrosis with impaired gadolinium delivery. On T2*, it appears hypointense due to iron from degraded hemoglobin. MVO on LGE is an adverse prognostic marker

Chronic MI / Hibernating Myocardium

• LGE <50% transmural + wall motion abnormality = hibernating/stunned myocardium (viable - likely to recover with revascularization)
• LGE >50% transmural = transmural scar (non-viable)
• Fat deposition within old LGE territory (bright on T1, suppressed on STIR) = chronic lipomatous metaplasia of scar

---

3.2 Cardiomyopathies

3.2.1 Hypertrophic Cardiomyopathy (HCM)

• LV hypertrophy - asymmetric septal hypertrophy (ASH) most common. CMR precisely measures maximum wall thickness in all segments (more accurate than echo, especially for lateral wall, apex)
• Apical HCM (Yamaguchi variant): Apical cavity obliteration, "ace of spades" configuration on 4-chamber cine at end-diastole
• Systolic anterior motion (SAM) of the anterior mitral leaflet - visible on 3-chamber cine
• LVOT obstruction: turbulent jet (signal void) in LVOT on cine

• Pattern: Mid-wall / intramural hyperintensity, predominantly at the RV insertion points (anterior and inferior septum-RV junction), also in hypertrophied segments. Characteristically spares the subendocardium (distinguishing from ischemic pattern)
• Extent of LGE correlates with arrhythmia risk and SCD risk - used for ICD risk stratification
• Diffuse or large-foci intramural LGE = fibrosis

---

3.2.2 Dilated Cardiomyopathy (DCM)

• Global LV (and often RV) dilatation
• Reduced LVEF, global hypokinesia
• Spherical LV remodeling
• Functional mitral regurgitation jet (signal void into LA)

• Non-ischemic DCM: LGE absent (most common, ~60%) OR faint mid-wall / mesocardial enhancement in the interventricular septum (stripe pattern). Subendocardium is spared - this distinguishes it from ischemic DCM
• Ischemic DCM: Subendocardial or transmural LGE in a coronary territory distribution
• The presence of any LGE in DCM independently predicts SCD and adverse events (18% SCD rate with LGE vs 2% without, over 4.6 years follow-up) - Braunwald's Heart Disease

---

3.2.3 Arrhythmogenic Cardiomyopathy (ACM / ARVC)

• RV dilatation (RVEDV index ≥110 mL/m² men, ≥100 mL/m² women per Task Force Criteria)
• Reduced RVEF (<40% major, 40-45% minor)
• Regional RV wall motion abnormalities: dyskinesia/akinesia of RVOT, RV apex, or subtricuspid region (the "triangle of dysplasia")
• LV involvement in biventricular ACM

• RV free wall fibrofatty replacement: Thin, hyperenhancing RV free wall, most prominent in RVOT
• LV involvement: Mid-wall LGE in the inferolateral wall in left-dominant or biventricular ACM

---

3.2.4 Cardiac Amyloidosis

• Concentrically thickened LV walls (can mimic HCM)
• Biatrial dilatation
• Diastolic dysfunction pattern
• Granular sparkling appearance on echo; less specific on CMR

• Diffuse subendocardial enhancement in a non-coronary distribution, affecting all segments globally - the classic "zebra striping" pattern
• In advanced disease, transmural enhancement
• Abnormal gadolinium kinetics: Blood pool and myocardium both null abnormally - difficult to set an appropriate TI. The "inverted" LGE appearance (where the blood pool nulls before the myocardium) is a diagnostic hallmark
• ECV is markedly elevated (often >40-50%, normal ~25%)

---

3.2.5 Cardiac Sarcoidosis

• Variable - can be normal or show regional/global LV dysfunction
• Wall thinning in areas of granulomatous replacement
• Aneurysmal dilatation in burnt-out disease

• Focal or patchy mid-wall (intramural) enhancement - most common in the basal and mid-interventricular septum and basal inferolateral wall
• Enhancement does not follow a coronary territory
• Can also show subepicardial enhancement, mimicking myocarditis
• Perilesional transmural extension possible

---

3.3 Myocarditis

Lake Louise Criteria (2018 Updated CMR Criteria)

1. LGE in a non-ischemic pattern: typically subepicardial or mid-wall distribution, most commonly lateral wall, inferior wall, or septal involvement. The subendocardium is characteristically spared (key differentiator from MI)
2. Elevated native T1 (globally or regionally above vendor/center normal values)
3. Elevated ECV

1. Regional or global T2 signal increase on T2-STIR (T2 ratio myocardium/skeletal muscle >1.9)
2. Elevated regional T2 on T2 mapping (>59 ms at 1.5T)

• Acute: Subepicardial LGE + T2 hyperintensity (edema) in the same region - lateral wall most common
• Chronic: LGE without edema, often mesocardial/septal - associated with new-onset arrhythmias. Septal LGE is the most arrhythmogenic substrate

---

3.4 Pericardial Disease

Pericardial Effusion

Pericarditis / Myopericarditis

• Pericardial enhancement: the inflamed, vascular pericardium enhances avidly on early post-contrast imaging (delayed gadolinium with shorter TI, or dedicated early enhancement sequences)
• Pericardial enhancement on LGE correlates with active inflammation and predicts response to anti-inflammatory therapy
• Enhancement extending into subepicardial myocardium = myopericarditis

Constrictive Pericarditis

• Pericardial thickening >4 mm (normal <2 mm) - but constriction can occur with normal thickness in up to 20% cases
• Black-blood sequences: Low T1 and T2 signal in fibrous/calcified pericardium (note: CMR cannot detect calcification as reliably as CT - CT is preferred for calcification assessment)
• Pericardial adhesions may be seen

• Septal bounce / interventricular dependence: On cine imaging, paradoxical septal motion - the interventricular septum flattens or shifts leftward during inspiration as RV filling increases at the expense of LV filling. This exaggerated septal motion is the MRI equivalent of the echocardiographic "septal bounce"
• Dilated IVC and hepatic veins
• Flat diaphragmatic descent pattern

---

3.5 Valvular Heart Disease

Aortic Regurgitation

• Cine SSFP: Signal void (flow turbulence) jet extending from the aortic valve into the LV during diastole. LV dilatation (volume overload pattern)
• Phase-contrast at the aortic valve: Quantifies regurgitant volume (mL/beat) and regurgitant fraction (%). Gold standard method for AR quantification when echo is discordant
• LGE: Mid-wall fibrosis in LV may indicate advanced disease with irreversible myocardial injury

Aortic Stenosis

• Cine SSFP: Thickened, restricted aortic leaflets. Systolic signal void jet through the stenotic orifice (jet size correlates with severity). LV hypertrophy (concentric)
• Planimetry of aortic valve area (AVA): Using cine or phase-contrast - provides "anatomical orifice area (AOA)"
• Phase-contrast: Measures peak systolic velocity for gradient estimation
• LGE / T1 mapping: Myocardial fibrosis assessment in AS is a major emerging indication - mid-wall fibrosis predicts worse outcomes post-TAVI/SAVR. ECV elevation even before LVEF reduction

Mitral Regurgitation

• Cine: Signal void jet into the LA during systole. Eccentric jets harder to grade than central
• Phase-contrast: Indirect calculation of regurgitant volume = LV stroke volume - aortic forward flow
• LGE: Fibrosis patterns in myxomatous/ischemic MR

Mitral Stenosis

• Cine: Thickened, restricted mitral leaflets, reduced mitral valve area (planimetry), diastolic jet signal void. LA dilatation
• Phase-contrast: Mean transmitral gradient

---

3.6 Iron Overload Cardiomyopathy

• T2* >20 ms: Normal cardiac iron
• T2* 10-20 ms: Mild-moderate iron overload
• T2* <10 ms: Severe iron overload - high risk of LV dysfunction and arrhythmia
• T2* <6 ms: Critical - imminent heart failure

---

3.7 Cardiac Masses and Tumors

Tissue characterization sequences:

• Myxoma: T1 intermediate, T2 bright, heterogeneous LGE; pedunculated from fossa ovalis; mobile
• Lipoma: T1 bright, T2 moderate; signal drops on fat saturation; no LGE
• Fibroelastoma: Usually valve-associated; small; T2 intermediate
• Rhabdomyoma: Neonates; T1 iso, T2 bright; multiple; associated with tuberous sclerosis

• Angiosarcoma: RA most common. T1 intermediate with areas of high signal (hemorrhage). T2 heterogeneous. Avid, heterogeneous LGE. Pericardial invasion
• Rhabdomyosarcoma: Any age, any chamber. T1 iso, T2 high. Aggressive LGE
• Metastases: History of primary tumor. Multiple lesions. Pericardial effusion common

---

3.8 Congenital Heart Disease (CHD)

• Cine: Direct visualization of shunt flow (signal void through defect)
• Phase-contrast Qp:Qs >1.5 = significant shunt
• RV volume overload (dilated RV on SAx)

• Phase-contrast Qp:Qs ratio
• LV volume overload

• Primary indication for repeat CMR
• RVEF and RVEDV indexed - determines timing of pulmonary valve replacement
• Pulmonary regurgitation quantification (phase-contrast)
• RVOT aneurysm assessment
• Residual VSD

---

3.9 Aortic Disease

• Aortic root dimensions, ascending aorta, arch, descending aorta
• Aortic dissection: True vs. false lumen (cine shows differential flow); intimal flap
• Aortic wall hematoma: T1 hyperintense crescentic wall thickening (no dissection flap)
• Penetrating aortic ulcer

---

3.10 Takotsubo Syndrome (Stress Cardiomyopathy)

---

SECTION 4: LGE PATTERN SUMMARY - QUICK REFERENCE

---

SECTION 5: CONTRAINDICATIONS AND SAFETY

• Non-MRI-conditional pacemakers/ICDs (though many modern devices are now MRI-conditional at 1.5T)
• Cochlear implants (most; check manufacturer)
• Certain intracranial aneurysm clips
• Metallic foreign bodies in or near the eye

• Severe claustrophobia
• Inability to breath-hold (degrades image quality; free-breathing navigator sequences available)
• Renal impairment (eGFR <30 mL/min): gadolinium risk of Nephrogenic Systemic Fibrosis (NSF) with older Group 1 agents; modern macrocyclic agents (gadobutrol, gadoteridol) have excellent safety profiles
• Pregnancy: avoid gadolinium in first trimester unless absolutely necessary

• Macrocyclic chelates (gadobutrol, gadoterate) are preferred for cardiac imaging due to superior thermodynamic stability
• Group 1 linear agents (gadodiamide, gadopentetate) are associated with gadolinium deposition in brain and bone - avoid where possible

---

SECTION 6: QUANTITATIVE REFERENCE VALUES

---

SECTION 7: CONDITION-SPECIFIC ADDITIONAL SEQUENCES SUMMARY

---