Download Cardiac MRI in Left Ventricular Hypertrophy: From the Etiological

Cardiac MRI in Left Ventricular Hypertrophy: From the
Etiological Diagnosis to the Prognosis
Poster No.:
C-0611
Congress:
ECR 2011
Type:
Educational Exhibit
Authors:
J. Caudron, J. Fares, J.-N. Dacher; Rouen/FR
Keywords:
Cardiac, MR, Diagnostic procedure
DOI:
10.1594/ecr2011/C-0611
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Page 1 of 31
Learning objectives
1. To define and quantify left ventricular hypertrophy (LVH) by cardiac MR (CMR).
2. To describe the diagnostic approach when investigating a patient with LVH.
3. To discuss and illustrate the usefulness of CMR in identifying the cause and prognosis
of LVH.
Background
Main causes of LVH
Main causes of LVH are summarized in Table 1 and can be classified as primitive
(Hypertrophic cardiomyopathy, HCM) vs. secondary. LVH can be the consequence of an
increased afterload or an infiltration of the myocardium. The LVH associated with practice
of sport ("Athlete's heart") is a different condition.
Differential diagnosis is foreground and often challenging because associations are so
frequent: Hypertension with aortic stenosis, HCM with hypertension, amyloidosis with
aortic stenosis, sport and hypertension, sport and HCM…
Table 1: Main causes of LVH
Primitive
Hypertrophic Cardiomyopathy
Secondary
Afterload elevation
- Hypertension
- Aortic Stenosis
- Aortic Coarctation
Myocardial infiltration
- Cardiac Amyloidosis
- Sarcoidosis and other granulomatosis
Page 2 of 31
- Fabry Disease
- Cardiac Tumors
Sport's related LVH: "Athlete's Heart"
LVH - Two Definitions
- 1. Thickening of the LV wall >11 mm,
•
•
Measured at end-diastole on short axis balanced Steady State Free
Precession (bSSFP) images (3 or 4-chamber views for the apex)
LV and RV trabeculations should be excluded from measurements
- 2. Increased LV Mass
•
2
Inferred from measurements indexed to body surface area (>113g/m in
2
men and >95 g/m in women in our center)
Differentiate these 2 definitions is essential because LV mass may be normal in case
of focused LVH (typically in case of HCM)
Several types of LV geometry have been described by TTE in case of LVH secondary to
afterload elevation (Figure 1 on page 4):
- Concentric LVH
- Eccentric LVH
- Concentric remodeling
Evaluation of LVH
Diagnostic Approach
A basic diagnostic approach of LVH is presented in Figure 2 on page 5
Diagnostic Procedures
- ECG
•
•
QRS axis normal or deviated to the left
Sokolow index (SV1 + RV5 or RV6) >35mm
Page 3 of 31
- TTE
•
•
First-line technique
•
Estimation of LVH
•
Assessment of systolic and diastolic function
•
Assessment of valvular function
Limitations
•
Acoustic window
•
Exhaustive segmental analysis difficult (apex, anterior and basal
segments)
•
LV mass not reliable
•
Limited for tissue characterization and causative diagnosis
- Cardiac MRI
•
•
Allows a comprehensive assessment of the hypertrophied myocardium
•
Exhaustive LV covering with precise assessment of thickened areas
•
Reproducible and accurate measurement of LV mass [1], EF and
volumes
•
Basic diastolic function evaluation feasible [2]
•
Myocardial First-pass perfusion imaging
•
Late gadolinium enhancement sequences useful for tissue
characterization, causative diagnosis, and prognostic stratification
[3-4]
Cardiac MRI is a key tool for assessing LVH, in addition to ECG and TTE
Cardiac MRI protocol
- bSSFP CINE sequences in conventional planes (2, 3, 4-chamber views, short axis views
from base to apex, LVOT views) to assess LV wall thickness, volumes and LVEF.
- T1/T2 morphological sequences depending on the clinical indication
- Phase contrast sequence perpendicular to LV inflow to assess transmitral flow for
diastolic function assessment
- First pass perfusion imaging
- Late gadolinium enhancement/Phase sensitive inversion recovery sequences
Images for this section:
Page 4 of 31
Fig. 1: Figure 1: LV geometry
Page 5 of 31
Fig. 2: Figure 2: Basic diagnostic approach of LVH
Page 6 of 31
Imaging findings OR Procedure details
Hypertrophic Cardiomyopathy (Figure 3 on page 16)
Background [5]
- Abnormal primitive LVH associated with cardiomyocytes disorganization and interstitial
fibrosis
- Predominant in the interventricular septum
- Mostly familial forms (>150 genetic mutations described)
- Phenotypic prevalence # 0.2% but >50% asymptomatic
- Annual risk of sudden death #1-4%, mostly related to ventricular arrhythmias, with
identified risk factors:
•
•
•
•
•
•
History of missed sudden death or sustained ventricular tachycardia
Family history of multiple sudden death
History of unexplained syncope
LV wall thickness >30mm
Hypertension on exercise
Non-sustained ventricular tachycardia on 24-hour Holter ECG
- Therapeutic options
•
•
Medical treatment: # Blockers or Calcium Channel Blockers
Treatment of obstructive HCM: Double-chamber pacing, surgical myectomy,
alcohol septal ablation [6]
Cardiac MRI Findings
- Morphological/Functional Findings
•
LVH
•
LV wall thickness #15mm, most often >20mm (>30 mm in 12% of
cases) [7]
•
Cardiac MRI is more accurate than TTE to detect LVH,
particularly for the anterior-lateral free wall and for the apex [8]
•
LV mass is normal in 20% of patients with documented HCM,
but correlates with risk of sudden death [9]
•
Five phenotypic forms of HCM were described [10] (Panel A)
•
Reverse curvature septum (1), strongly associated with
myofilament mutation
Page 7 of 31
•
•
•
Sigmoid septum (2)
•
Neutral septum (3)
•
Apical (4)
•
Mid-ventricular (5)
Systolic Function
•
Increased LVEF is common with global hyperkinesia and
disappearance of the LV cavity during end-systole (Panel B)
•
Most thickened areas are hypokinetic as demonstrated by Tagging
sequences (Panel C)
Diastolic Function
•
Left atrium most often not dilated
•
Transmitral flow abnormal: Relaxation (Panel D) >> Restrictive
pattern in severe ("burn-out") forms
- Enhancement Findings
•
•
First Pass Perfusion
•
Rest: most often normal
•
Stress (Adenosine, Dipyridamole): subendocardial hypoperfusion
related to microvascular dysfunction and correlated to LV wall
thickness, risk of sudden death, LV systolic dysfunction, and extent of
LGE [11-13]
Delayed Enhancement
•
Very common in HCM (40-80% of patients) [14-16]
•
Most often intramyocardial and predominant in most thickened areas
(Panel E)
•
Prognostic factor: independent predictor of adverse outcome [14-16]
- Specific Cardiac MR Findings: Intraventricular Obstruction
•
•
25% of cases, most often located at LV outflow tract. Association with
systolic anterior motion and mitral regurgitation [17] (Panel F, Pre)
Cardiac MRI can assess the efficacy of alcohol septal ablation [18] (Panel F,
Post)
Cardiac Amyloidosis (Figure 4 on page 17)
Background [19]
- LVH related to extra cellular amyloid deposits, predominantly in subendocardial layers
- Several types of amyloidosis:
•
Primary AL amyloidosis, most often with multiple myeloma or monoclonal
gammopathy. Light chain deposits in tissues: cardiac disease predominates
(poor prognosis)
Page 8 of 31
•
•
Secondary AA amyloidosis, related to chronic inflammatory diseases
(rheumatoid arthritis, tuberculosis…): renal disease predominates
(Senile amyloidosis, hereditary amyloidosis)
- Clinical settings
•
•
History of Multiple myeloma, monoclonal gammopathy…
Restrictive cardiomyopathy, systolic heart failure, orthostatic hypotension
(autonomic nervous system and/or vessels infiltration), conduction or rhythm
abnormalties
- Diagnosis
•
•
•
ECG: microvoltage or pseudo infarction with Q waves
TTE: Massive LVH with hyperechogenic myocardium, diastolic dysfunction
Standard of reference: endomyocardial biopsies
Cardiac MRI Findings
- Morphological/Functional Findings
•
•
•
LVH
•
Concentric LVH (Panel A)
•
Possibly associated with interatrial septum (>6mm), right
atrium free wall (>6mm), and RV free wall thickening [20, 21]
•
Pericardial and pleural effusion frequent
•
Increase of LV T1 and T2 relaxation times [22, 23]
Systolic Function (Panel B)
•
± altered depending on the stage of the disease
Diastolic Function
•
Bi atrial dilatation
•
Transmitral flow: restrictive pattern (Panel C)
- Enhancement Findings
•
•
First Pass Perfusion
•
Rest: most often normal but possible subendocardial defect due to
subendocardial vessels infiltration [24] (Panel D)
Delayed Enhancement
•
Time of Inversion (TI) difficult to determine (Panel E) [25, 26]
•
Diffuse enhancement, involving both ventricles and atria (Panel F)
[25-27]
•
Rather subendocardial if early sequence (5 min)
•
Rather diffuse and heterogeneous if more delayed acquisition
(15 min)
Page 9 of 31
•
Prognostic implications: gadolinium kinetics was shown to be
a predictor of death [28] but the prognostic significance of the
presence of LGE remains debated [29]
Aortic Stenosis (Figure 5 on page 18)
Background [30]
- Most frequent heart valve disease in western countries (calcified aortic stenosis +++)
- Diagnosis based on TTE and invasive cardiac catheterism
Cardiac MRI Findings
- Morphological/Functional Findings
•
•
•
LVH
•
Concentric LVH, sometimes very important (wall thickness >20 mm)
(Panel A)
Systolic Function
•
Longtime preserved
Diastolic Function
•
Frequently impaired relaxation but pseudo normal or restrictive
pattern possible in patients with dyspnea (Panel B)
•
Diastolic dysfunction is a frequent mode of revelation of aortic
stenosis
- Enhancement Findings
•
•
First Pass Perfusion
•
Most often normal
Delayed Enhancement
•
Diffuse myocardial fibrosis frequent but poorly evaluable with LGE
sequences: T1 mapping sequences [31]
•
Focal myocardial fibrosis: Intramyocardial patchy enhancement has
been described in up to 25% of cases, especially when wall thickness
>18mm [32] (Panel C)
•
Prognosis: Extent of LGE was shown to correlate with clinical
evolution after aortic valve replacement [33]
- Specific Cardiac MR Findings: Stenosis surface area
•
Stenosis surface area correlates well with TTE and catheterism, whichever
planimetry or continuity equation was being used [34-36] (Panel D)
Page 10 of 31
Sport's related LVH: "Athlete's Heart" (Figure 6 on page 19)
Background [37]
- Risk of sudden death is low in athletes (<1/200,000)
- >90% of deaths occur during training or competition
- Most frequent causes of sudden death:
•
•
•
•
HCM +++
Coronary implantation anomalies
Arrhythmogenic right ventricular dysplasia/cardiomyopathy
Others: myocarditis, congenital aortic stenosis, myocardial bridging, long QT
syndrome, dilated cardiomyopathy
- Screening these anomalies is essential and very variable from one country to another
•
ECG is first line in Italy, not in the USA
- Difficulty of screening: athlete's heart can mimic disease such as HCM or dilated
cardiomyopathy. Indeed, 2% of highly trained athletes present with [38]:
•
•
•
LVH with wall thickening >13mm but normally <16mm (if >16 mm
complementary exams are required to eliminate HCM)
LVH with increased LV mass
Increased left and right cardiac chambers volumes (ventricles and/or atria)
- During the screening, some arguments are in favor of physiological sport's related LVH
•
•
•
First-line screening
•
No familial history of HCM
•
No abnormalities on clinical examination
•
Normal ECG [39]
Second-line screening (TTE)
•
No systolic anterior motion of the mitral valve
•
No diastolic dysfunction (Normal relaxation)
•
Proportional increase of LV volume and wall thickness
•
Normal metabolic stress test
In doubtful cases, deconditioning (complete cessation of sport) helps to
distinguish physiological from pathological LVH [39]
- Role of cardiac MRI: useful in third-line screening, in addition to TTE
Cardiac MRI Findings
- Morphological/Functional Findings
Page 11 of 31
•
LVH
•
•
Symmetric hypertrophy with LV wall Thickness <16mm (Panel A)
Proportional increase of LV volume and wall thickness [41, 42]
•
Ratio LV end-diastolic wall thickness (in mm)/ LV indexed end2
•
•
diastolic volume (mL/m ) <0.15 (Se=80%, Spe=99%)
Systolic Function
•
Normal
•
LV may be dilated and LVEF may be low at rest in highly trained
athletes
Diastolic Function
•
Normal relaxation pattern (Panel B)
•
Left atrium can be dilated in highly trained athletes
- Enhancement Findings
•
•
First Pass Perfusion
•
Normal
Delayed Enhancement
•
Normal (Panel C)
•
Absence of delayed enhancement does not exclude HCM
•
Prognosis: Recently, it was demonstrated that healthy marathon
runners had an unexpectedly high rate of myocardial LGE, with
potential diagnostic and prognostic relevance [43]
Cardiac Sarcoidosis (Figure 7 on page 20)
Background [44]
- Systemic granulomatosis
- Associated with cardiac involvement
•
•
•
25% of patients in autopsy series but…
…Only 5% of patients have clinical and/or ECG signs of myocardial
involvement
Cardiac involvement: major prognostic factor
•
Most cases of death are related to rhythm or conduction abnormalities
- Diagnosis
•
•
•
TTE, ECG and isotopic methods not enough sensitive to confirm cardiac
involvement
Reference method: endomyocardial biopsies showing noncaseating
granulomas, but invasive and limited by the sample-size
Cardiac MRI can confirm the diagnosis with an excellent sensitivity/
specificity, and track disease progression [45-47]
Page 12 of 31
- Treatment: corticosteroid therapy indicated in case of cardiac localization
Cardiac MRI Findings
- Morphological/Functional Findings [48, 49]
•
•
•
LVH
•
•
•
Frequent, can mimic HCM with asymmetric focal LVH (Panel A)
T2 hypersignal in thickened areas at inflammatory phase
Myocardial thinning at fibrous phase. Possible evolution: dilated
cardiomyopathy
Systolic Function
•
Most often preserved (Panel B)
•
Impairment possible in advanced fibrous forms (Panel B)
Diastolic Function
•
Variable, from normal to restrictive pattern in severe forms
- Enhancement Findings
•
•
First Pass Perfusion
•
Normal or decreased in fibrous segments, increased in inflammatory
segments
Delayed Enhancement [46-50] (Panel C)
•
Intramyocardial or subepicardial location (>>subendocardial), most
often at basal septum and lateral wall
•
Rather nodular at inflammatory phase, linear at fibrous phase
•
Prognostic implications: LGE extent correlates with NT-proBNP
levels, end-diastolic volumes, decreased LVEF [50], and future
cardiac events including death [51]
- Specific Cardiac MR Findings: Associated thoracic anomalies
•
•
•
Mediastinal/Hilar adenomegalies
RV dilatation or wall-thickening, most-often related to pulmonary
parenchymal disease (Panel D)
Pericardial involvement: pericardial effusion and/or thickening
Fabry Disease (Figure 8 on page 21)
Background [52]
- X linked recessive lysosomal storage disease
•
•
Related to deficiency of enzyme alpha-galactosidase A
Leads to an accumulation of glycosphingolipid in various tissues
Page 13 of 31
- Clinical manifestations: various
•
Renal (failure), neurological (stroke), cardiac (LVH, valvular thickening,
angina, conduction or rhythm disorders).
- Diagnosis
•
•
•
Blood test: measurement of alpha-galactosidase activity
Mutation detection possible in almost 100% of men (>250 mutations
described)
#1% of patients referred for HCM suspicion [53]
- Treatment
•
Enzyme replacement therapies
Cardiac MRI Findings
- Morphological/Functional Findings [54]
•
•
•
LVH
•
Important symmetric and concentric LVH (Panel A). Cardiac MRI is
useful for monitoring LV mass regression under treatment
•
Rarely asymmetric septal LVH (5%) mimicking HCM
•
Increase of LV T2 relaxation time [55]
•
RV often hypertrophied without clinical consequence
Systolic Function
•
Most often normal
Diastolic Function
•
Relaxation impaired
•
Restrictive pattern in case of important myocardial fibrosis
- Enhancement Findings
•
•
First Pass Perfusion
•
Rest: most often normal
•
Stress: possible reduction of coronary flow reserve, secondary to
microvascular infiltration
Delayed Enhancement [54, 56]
•
Intra or subepicardial enhancement predominant at inferior-basal and
lateral-basal segments (Panel B)
Hypertension
Background [57]
Page 14 of 31
- High prevalence = the most frequent cause of LVH
- LVH is a independent predictor of morbidity and mortality in patients with hypertension
- Cardiomyocytes hypertrophy associated with diffuse interstitial myocardial fibrosis and
microvascular impairment
Cardiac MRI Findings
- Morphological/Functional Findings
•
•
•
LVH
•
•
Symmetric and concentric LVH with variable myocardial thickening
Increased LV mass in 28% of Caucasian patients but 62% of Black
patients
•
Cardiac MRI is clearly more sensitive than TTE (Se=30%) and ECG
(Se=10%) to detect a LVH in hypertensive patients
Systolic Function
•
Most often normal
•
Alteration possible if associated with ischemic cardiomyopathy
Diastolic Function
•
Diastolic dysfunction is very common: hypertension is one of the main
cause of heart failure with preserved ejection fraction [2]
- Enhancement Findings
•
•
First Pass Perfusion
•
Rest: Most often normal
•
Stress: possible reduction of coronary flow reserve, secondary to
microvascular lesions, leading to subendocardial ischemia
Delayed Enhancement
•
Diffuse myocardial fibrosis frequent but poorly evaluable with LGE
sequences: interest of T1 mapping sequences [31]
•
Focal myocardial fibrosis with Intramyocardial patchy enhancement
described [58]
Cardiac Tumors located to the LV (Figure 9 on page 22)
Background
- Primary or secondary tumors located to the LV
- Leading to localized LVH
- Etiology
Page 15 of 31
•
•
Cardiac Metastasis +++ (Most frequent primary tumor: lung, breast,
melanoma, lymphoma, leukemia, kidney, and liver)
Primary cardiac tumor rare: benign (fibroma, rhabdomyoma, angioma) or
malignant (rhabdomyosarcoma, angiosarcoma)
Cardiac MRI Findings [59]
•
An exhaustive illustration of cardiac tumor located to the LV is beyond the
scope of this educational exhibit. Some examples are illustrated in Figure 9:
•
Non Hodgkin lymphoma with LV metastasis (Panel A1)
•
Melanoma with LV metastasis (Panel A2)
•
Cardiac fibroma (Panel A3)
Pitfalls (Figure 9 on page 22)
Cardiac MRI is very useful in some situations that may mimic a LVH in TTE
- Mural Thrombus of the LV: LGE sequences have a better sensitivity and specificity than
TTE for the diagnosis [60, 61] (Figure 9, Panel B)
- LV non-compaction [62] defined as:
•
•
TTE: ratio non-compacted/compacted myocardium >2 in end-systole [63]
Cardiac MRI (Figure 9, Panel C):
•
Ratio non-compacted/compacted myocardium >2.3 in end-diastole
[64]
•
Non-compacted LV mass above 20% of the global LV mass [65]
Images for this section:
Page 16 of 31
Fig. 1: Figure 3: Hypertrophic Cardiomyopathy
Page 17 of 31
Fig. 2: Figure 4: Cardiac Amyloidosis
Page 18 of 31
Fig. 3: Figure 5: Aortic Stenosis
Page 19 of 31
Fig. 4: Figure 6: Sport's related LVH: "Athlete's Heart"
Page 20 of 31
Fig. 5: Figure 7: Cardiac Sarcoidosis
Page 21 of 31
Fig. 6: Figure 8: Fabry Disease
Page 22 of 31
Fig. 7: Figure 9: Cardiac Tumors located to the LV - Pitfalls
Page 23 of 31
Conclusion
LVH is a frequent indication of cardiac MRI. Whereas identifying LVH causes
is sometimes challenging with echocardiography, cardiac MRI is an important
complementary tool, which offers morphological and functional evaluation of the whole
heart. Recognizing LVH, depicting its topography and evaluating myocardial mass
are fundamental steps which require a thorough MR examination. Evaluation of the
myocardial perfusion and late gadolinium enhancement were shown to contribute to
the prognostic stratification in certain diseases.
Personal Information
Jérôme Caudron, MD, MSc
Department of Radiology, University Hospital of Rouen, Rouen, France
INSERM U644, University of Rouen, Rouen, France
e-mail: [email protected]
Jeannette Fares, MD
Departments of Radiology and Internal Medicine, University Hospital of Rouen, Rouen,
France
e-mail: [email protected]
Jean-Nicolas Dacher, MD, PhD
Department of Radiology, University Hospital of Rouen, Rouen, France
INSERM U644, University of Rouen, Rouen, France
e-mail: [email protected]
Page 24 of 31
Page 25 of 31
Fig.: Claude Monet: Cathédrale de Rouen
References: Musée des Beaux Arts de Rouen
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