- Open Access
Left ventricular apical diseases
© European Society of Radiology 2011
- Received: 18 October 2010
- Accepted: 1 April 2011
- Published: 18 April 2011
There are many disorders that may involve the left ventricular (LV) apex; however, they are sometimes difficult to differentiate. In this setting cardiac imaging methods can provide the clue to obtaining the diagnosis. The purpose of this review is to illustrate the spectrum of diseases that most frequently affect the apex of the LV including Tako-Tsubo cardiomyopathy, LV aneurysms and pseudoaneurysms, apical diverticula, apical ventricular remodelling, apical hypertrophic cardiomyopathy, LV non-compaction, arrhythmogenic right ventricular dysplasia with LV involvement and LV false tendons, with an emphasis on the diagnostic criteria and imaging features.
- Cardiac aneurysm
- Left ventricular remodelling
- Left ventricular hypertrophy
- Tako-Tsubo cardiomyopathy
- Isolated non-compaction of the ventricular myocardium
The left ventricle (LV) is affected by many diseases with different clinical and morphological features. Within this broad spectrum, a subset of heterogeneous diseases is characterised as preferentially affecting the LV apex. Generally LV assessment begins with echocardiography because of its wide availability and because it is fast, low-priced, portable and robust in experienced hands. However, because of intrinsic or technical limitations (limited field of vision, inadequate acoustic window, inability to definitively depict the endocardial border, especially the anterolateral free wall of the left ventricle in the parasternal short-axis view and the apex) [1, 2] and technical artefacts (reverberations, near-field artefacts), in such cases further investigation, usually with magnetic resonance (MR) imaging, which is the method of choice for the diagnosis of myocardial diseases, may be necessary. MR imaging is less dependent on the operator and is not subject to acoustic window limitations . Due to their high spatial and temporal resolution, MR and CT can clearly visualise the apex of the LV, but CT is not yet recommended as the method of primary choice in the case of suspected left ventricular apical disease. Cine MR imaging with the steady-state free precession pulse sequence can offer the advantages of multiplanar imaging, complete coverage of the entire myocardium without obliquity, and excellent soft-tissue contrast between the myocardial border and the blood pool [4, 5]. In addition, the status of myocardial blood flow can be assessed by using adenosine stress cardiac MR imaging. Delayed enhancement MR imaging techniques can provide unique information for tissue characterisation, specifically for the identification of myocardial fibrosis or scarring [6, 7]. CT has also emerged as a novel technique for evaluating cardiac morphology and function, as well as the coronary artery. Compared with the spatial resolution of MR imaging, that of multidetector CT is usually higher . Therefore, cardiac multidetector CT can offer anatomical and functional information about the cardiac chambers and a high-quality non-invasive coronary angiography [9, 10]. Multidetector CT would be more appropriate in those cases for which there are specific requests to exclude coronary artery disease and in those with contraindications for MR imaging, such as the patient having a pacemaker .
Therefore, radiologists play an increasing role in the evaluation of LV apical abnormalities, thus requiring a greater awareness and familiarity with this diseases.
The aim of this paper is to illustrate the spectrum of diseases that most frequently affect the apex of the LV, with an emphasis on the diagnostic criteria and imaging features.
Myocardial thinning (one of the principal signs of myocardial injury) is an important observation in patients suspected of having had ischaemic insults to the heart. However, thinning of the LV apex has been described by anatomists as a normal feature. With the advent of motion-gated cross-sectional cardiac imaging, normal apical thinning can be quite noticeable, especially on computed tomography (CT) in which the spatial resolution is submillimetre [12, 13].
Differences among aneurysms, pseudoaneurysms and congenital diverticula
All layers of the ventricular myocardium
Organized hematoma and pericardium
All layers of the ventricular myocardium
Akinetic dyskinetic segment
Akinetic or dyskinetic segment
Shows contraction during systole
Myocardial late enhancement
No, only the border of the pseudoaneurysm will show enhancement
Pericardial late enhancement
No or faint
Conversely, a true aneurysm, which occurs in 5–10% of patients with acute myocardial infarction, contains the endocardium, epicardium and a predominantly fibrous tissue that has replaced myocardium in its wall . An important difference is the lower rupture potential of a true aneurysm compared with a pseudoaneurysm. Surgical repair is the treatment of choice for pseudoaneurysms, while true aneurysms, in the absence of other surgical indications (i.e. refractory angina pectoris, congestive heart failure, systemic embolisation or refractory arrhythmia) are treated medically [18, 19]. Cine MR and cine CT imaging reveal, in both aneurysms and pseudoaneurysms, an akinetic/dyskinetic segment in the LV wall [18, 19]. A typical feature of pseudoaneurysm is that it has a narrow ostium connecting them to the ventricle. In most cases, the maximal width of the ostium is less than the maximal parallel internal diameter .
Apical diverticulum is a finger-like contractile pouch with connection to the ventricle . It is important to differentiate apical diverticula from aneurysm and pseudoaneurysm. Ventricular diverticula are congenital, often asymptomatic and are usually incidentally found while performing diagnostic imaging procedures for other reasons . The wall of the diverticulum contains all layers of the ventricular myocardium with preserved myocardial architecture . Contrary to a LV aneurysm, this diverticulum shows contraction during systole, because it contains a muscular wall [19, 20]. Delayed enhancement is not seen.
In children, apical diverticula can be associated with Cantrell’s syndrome, which is a rare syndrome characterised by a partial sternal cleft, anterior abdominal wall defects, anterior diaphragmatic defect and intracardiac defects of which the ventricular septal defect is the most common and is invariably present. LV diverticulum is present in 20% to 50% of these cases .
Hypertrophic cardiomyopathy (HCM) is a primary and genetic myocardial disease characterised by a hypertrophied, non-dilated LV in the absence of another systemic or cardiac disease (e.g. systemic hypertension, aortic valve stenosis) capable of producing LV hypertrophy [1, 24].
There are several distinctive involvement patterns, one variant being the apical hypertrophic cardiomyopathy (AHC). Unlike usual HCM, AHC possesses typical clinical features and has a relatively good prognosis. However, it seems that the clinical course is less benign in western countries than in Japan .
Relative merits of each non-invasive imaging technique for the assessment of hypertrophic cardiomyopathy (HCM)
LV filling pressure
The diagnosis is primarily based on the demonstration of localised apical hypertrophy, defined as an end-diastolic LV apical wall thickness greater than 15 mm or a ratio comparing apical LV and basal LV wall thicknesses of ≥1.3–1.5 .
More subjective criteria for the diagnosis of AHC include: obliteration of the LV apical cavity in systole, failure to identify a normal progressive reduction in LV wall thickness towards the apex  and apical aneurysm formation with delayed enhancement [25, 26]. The formation of apical aneurysm is thought to be due to ischaemia, which results from reduced capillary density, hyperplasia of the arterial media, increased perivascular fibrosis and myocardial bridging. This process usually occurs in the presence of normal epicardial coronary arteries .
There are three types of apical HCM: (1) true apical form (“spade-like” configuration), (2) involvement of the apex and symmetric hypertrophy of the four ventricular wall segments, and (3) involvement of the apex with asymmetric involvement of the wall segments (“non-spade” apical HCM) .
Most frequent primary and secondary cardiomyopathies 
Primary cardiomyopathies (mostly confined to the heart)
Secondary cardiomyopathies (cardiac involvement is a part of systemic disease)
Systemic lupus erythematosis
Differences among Tako-Tsubo, acute myocardial infarction (AMI) and myocarditis
Hyperintensity distribution in T2-STIR
Transmural or diffuse
Transmural or subendocardial
Medium or subepicardic
Apical and mid ventricular segments without vascular distribution
Patchy, without vascular distribution
Hyperintensity durability in T2-STTR
More than 2 weeks
Another characteristic feature of TSC is the lack of hypoperfusion on the first-pass imaging and at rest and of late enhancement on the delayed contrast sequence (Fig. 6) in the LV segments where there is STIR spotted oedema, which allows the differentiation from anterior ST elevation myocardial infarction. A rare but serious complication is the thrombus formation in the LV. The LV wall thickness is normal .
In combination with clinical history and catheterisation findings, cardiac MR imaging can be useful in supporting the diagnosis and monitoring functional recovery . MRI is also useful in differentiating Tako-Tsubo cardiomyopathy from myocardial infarction and myocarditis. Although coronary CT angiography is not indicated in the initial evaluation of patients with Tako-Tsubo cardiomyopathy, reports are emerging of the use of coronary CT angiography in the subsequent evaluation of patients with TSC .
LV non-compaction (LVNC) may be an isolated finding (isolated left ventricular non-compaction) or may be associated with other congenital heart anomalies (left ventricular non-compaction). It is a congenital cardiomyopathy  characterised by a thickened wall with multiple prominent ventricular trabeculations and deep intertrabecular recesses (sinusoids) in communication with the ventricular cavity, resulting in systolic and diastolic ventricular dysfunction. Non-compaction involves predominantly the apical portion of the LV chamber, with or without right ventricular involvement, due to an arrest in the normal embryogenesis [32–34].
Although ventricular non-compaction can appear similar to ventricular diverticula or prominent trabeculations (while virtually always <3 in number in normal variants), diagnosis of ventricular non-compaction usually requires the finding of more than three deep intertrabecular recesses in one imaging plane apically from the insertion of the papillary muscles [20, 32, 36]. False tendons, dilated cardiomyopathy, endocardial fibroelastosis and cardiac metastases are other important differential diagnostic considerations [34, 36].
Although echocardiography has been the diagnostic test of choice for non-compaction, other techniques have been used for the diagnosis, including CT and MRI . Echocardiography may not visualise the apical region optimally, leading to underestimation of the degree of left ventricular non-compaction . MRI provides good correlation with echo for the localisation and extent of non-compaction, and is useful in cases of poor echocardiographic image quality. In addition, the demonstration of differences in MRI signal intensity in non-compacted myocardium may help identify substrates for potentially lethal arrhythmias .
Arrhythmogenic right ventricular dysplasia (ARVD) is an uncommon form of inheritable cardiomyopathy  and is characterised by progressive loss of myocytes and fibrofatty replacement of the right ventricular myocardium [24, 38–41].
The diagnosis of ARVD is based on established criteria determined by a task force comprising the European Society of Cardiology and the International Society and Federation of Cardiology .
Diagnostic criteria for arrhythmogenic right ventricular dysplasia (ARVD)
I. Global and/or regional dysfunction and structural alterations
—Severe dilatation and reduction of right ventricular ejection fraction with no (or only mild) left and ventricular impairment
—Localized right ventricular aneurysms (akinetic or dyskinetic areas with diastolic bulging)
—Severe segmental dilatation of the right ventricle
—Mild global right ventricular dilatation and/or ejection fraction reduction with normal left ventricle
—Mild segmental dilatation of the right ventricle
—Regional right ventricular hypokinesia
II. Tissue characterisation of walls
—Fibrofatty replacement of myocardium at endomyocardial biopsy
III. Repolarisation abnormalities
—Inverted T waves in right precordial leads (V2 and V3) (people >12 years old; in absence of right bundle branch block)
IV. Depolarisation of conduction abnormalities
—Epsilon waves or localised prolongation (>110 ms) of the QRS complex in right precordial leads (V1—V3)
—Late potentials (signal-averaged ECG)
—Left bundle branch block type ventricular tachycardia (sustained or nonsustained; ECO, Holter, exercise testing)
—Frequent ventricular extrasystoles on Holter (>1,000/24 h)
VI. Family history
—Familial disease confirmed at necropsy or surgery
—Familial history of premature sudden death (at <35 years) due to suspected right ventricular cardiomyopathy
—Familial history (clinical diagnosis based on present criteria)
Reports of left ventricular involvement have led to the recognition of ARVD as a diffuse disease of the heart muscle affecting both ventricles [40, 41, 45, 46]. There is evidence of LV involvement with fibrofatty replacement, chamber enlargement and myocarditis in up to 75% of patients . Focal left ventricular dyskinesia can also be present in the setting of fatty infiltration within the left ventricle . Late left ventricular enhancement has also been described in patients with ARVD [39, 47]. In addition, these changes can definitely affect the LV apex.
The diagnosis of diseases affecting the apex of the LV can be challenging. This is mainly caused by the technical limitations of echocardiography. CT and MRI are non-invasive techniques that, because of their high temporal and spatial resolution, are valuable in assessing the apex of the LV, overcoming the technical limitations of echocardiography and contributing to the differential diagnosis (i.e. apical diverticula, aneurysms and pseudoaneurysms).
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