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 Table of Contents  
REVIEW ARTICLE
Year : 2018  |  Volume : 28  |  Issue : 1  |  Page : 9-17

Multimodality Imaging and Clinical Significance of Congenital Ventricular Outpouchings: Recesses, Diverticula, Aneurysms, Clefts, and Crypts


1 Department of Cardiology, Misericordia Hospital, Grosseto, Italy
2 Department of Radiology, University of Siena, Siena, Italy
3 Department of Internal Medicine, Misericordia Hospital, Grosseto, Italy
4 Department of Radiology, Misericordia Hospital, Grosseto, Italy

Date of Web Publication6-Mar-2018

Correspondence Address:
Dr. Alberto Cresti
Via Etiopia, 131, Grosseto 58100
Italy
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jcecho.jcecho_72_17

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  Abstract 


The high spatial resolution of cardiac computed tomography (CT) and cardiac magnetic resonance (CMR) permit the diagnosis of congenital ventricular outpouchings (CVOs), including congenital ventricular diverticula (CVD), congenital ventricular aneurysms (CVA), clefts, and crypts. A unique classification has not been established, and these terms are used interchangeably with confounding terminology. Moreover, their significance is not univocal. A research was performed using PubMed on six subjects: (1) congenital left ventricular outpouchings; (2) congenital ventricular diverticulum; (3) congenital ventricular aneurysm; (4) ventricular clefts; (5) ventricular crypts; and (6) ventricular crevices. Usually, CVOs are small with a preserved contraction and in asymptomatic patients, the clinical relevance may be minimal, although electrocardiographic anomalies are often present. CVA and diverticula may carry an embolic risk and cases of arrhythmia and rupture are described. In the presence of clefts, or crypts a cardiomyopathy should be excluded. A simple classification can be proposed: CVD extend beyond the myocardial wall and fibrous type may be termed CVA, acquired forms should be kept distinct. Clefts, or crypts, are small recesses extending for more than 50% of the ventricular wall but not beyond its margin. The presence of fibrosis may be evaluated by CMR. A multicenter prospective registry would be helpful to investigate potential clinical implications and to exclude dubious forms of hypertrophic cardiomyopathy or ventricular noncompaction. In conclusion, CVOs have been described with different terminologies and classifications. Their significance needs to be interpreted in the clinical setting and with the help of a multimodality imaging, particularly of CMR.

Keywords: Aneurysm, cardiac diverticulum, false aneurysm, myocardial crypt, pseudoaneurysm, ventricular diverticula


How to cite this article:
Cresti A, Cannarile P, Aldi E, Solari M, Sposato B, Franci L, Limbruno U. Multimodality Imaging and Clinical Significance of Congenital Ventricular Outpouchings: Recesses, Diverticula, Aneurysms, Clefts, and Crypts. J Cardiovasc Echography 2018;28:9-17

How to cite this URL:
Cresti A, Cannarile P, Aldi E, Solari M, Sposato B, Franci L, Limbruno U. Multimodality Imaging and Clinical Significance of Congenital Ventricular Outpouchings: Recesses, Diverticula, Aneurysms, Clefts, and Crypts. J Cardiovasc Echography [serial online] 2018 [cited 2018 Sep 25];28:9-17. Available from: http://www.jcecho.org/text.asp?2018/28/1/9/226686




  Introduction Top


The high spatial resolution of cardiac computed tomography (CT) and cardiac magnetic resonance (CMR) enable the diagnosis of congenital ventricular recesses and congenital ventricular outpouchings (CVOs), including congenital ventricular diverticula (CVD), congenital ventricular aneurysms (CVA), clefts, and crypts. Nowadays, these anomalies seem to be more frequent than previously thought. The presence of a myocardial “crypt” is reported in up to 6.7% of all the cardiac CT scans.[1]

A unique definition and classification of different types of ventricular outpouchings have not been established yet and the terms diverticula, aneurysm, crypts are often used interchangeably with confounding terminology.[2]

Among CVOs, some Authors include accessory ventricles and chambers, the so-called double-chambered left ventricle (DCLV),[2] while other Authors have introduced the term pseudodiverticulum[3] to define the fibrous subtype. These different terminologies and classifications are confusing, and agreement among experts is warranted as already suggested by several investigators.[1],[2],[3]

The clinical relevance of CVOs is a clinical dilemma, especially when electrocardiographic anomalies are present in asymptomatic patients. Which level of physical activity or competitive sport can be prescribed still need an answer.

Performing a review on the diagnostic criteria of all types of CVOs, our aim was to evaluate the definitions that have been used in recent literature to invite an expert consensus for a standardized and comprehensive classification with prognostic implications. A simple classification is proposed.


  Methods Top


A research was performed using PubMed electronic database on five subjects: (1) congenital left ventricular outpouchings (LVO); (2) congenital ventricular diverticulum; (3) CVA; (4) ventricular clefts; (5) ventricular crypts; and (6) ventricular crevices. The last search was performed on March 2017.

Review articles, case series and relevant isolated case reports with important clinical points were evaluated. All patients with all types of CVOs from prenatal to geriatric age range were investigated. In case of multiple papers published by the same Author, the largest and newest database was evaluated.

We reviewed a total of 110 studies including review articles and case series. Whether all reported cases should be really considered true congenital outpouchings is not always discernible and some papers have not been included in the final analysis. As an example, Chen et al.[4] included in his study acquired cases of ventricular outpouchings. In the review process, the PRISMA guidelines were followed.[5]

The largest case-series from prenatal age to adulthood, about 500 cases, was presented by Ohlow.[6]


  Current Definitions and Classification Top


Congenital ventricular diverticula

CVD are rare cardiac malformations described for the first time by O'Bryan in 1838.[7] They are characterized by an outpouching of the entire ventricular wall[8] and a corresponding finger-like protrusion from the internal cavity extending outside the epicardium margin[1] and a narrow connection to the cavity.[9]

Depending on the amount of myocardial fibers involved, diverticula may be classified in muscular or fibrous.[10] Muscular diverticula contain all layers of the ventricular myocardium with the myocardial architecture preserved and minimal fibrous tissue.[11] [Table 1] shows the main diagnostic features of muscular and fibrous diverticula are summarized. Muscular forms tend to show a contractile function synchronous with the ventricle. Fibrous diverticula have connective tissue composed of reticulin and muscle fibers are few or absent. Fibrous forms show either an akinetic or dyskinetic contractile function and usually a wider neck. Nam et al. divided CVD in apical and nonapical.[12] The term pseudodiverticulum has been used by some Authors to define the fibrous type of CVD recommending delayed enhancement CMR imaging to differentiate pseudodiverticulum from true diverticulum.[13] In our opinion, this definition adds a further element of terminological confusion and should be avoided.
Table 1: Differential diagnosis between muscular and fibrous diverticula

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Fibrous diverticula seem to be indistinguishable from congenital aneurysm and carry the same clinical significance. The term fibrous diverticulum is less used in recent literature.

CVD may be isolated or associated to midline thoraco-abdominal congenital abnormalities. CVD as part of a complex malformation syndrome are usually detected in children and have been described in detail by Cantrell et al.[14] in 1958 as part of a pentalogy including (1) median line abdominal wall defects (omphalocele); (2) inferior sternal defects (aplasia and cleft sternum); (3) anterior diaphragmatic defects; (4) diaphragmatic pericardium defects (absence of the inferolateral pericardium); and (5) complex cardiac abnormalities. Cantrell's pentalogy may be underreported as phenotypic expression is often incomplete. However, diverticula without midline abnormalities are increasingly reported and nowadays are by far the most common in the adult population.

CVD are typically single but may be multiple.[15] Diverticula diameter may range from 0.5 to 9 cm.[6] They are most often found in the LV,[16] but all chambers may be affected[5] and rarely may be multiple (“ventricular diverticulosis”).[17]

Although diverticula can theoretically be found in any segment, they are generally reported in the apex and perivalvular area; they have never been found in the ventricular septum.[10]

CVD not associated with congenital malformations, namely, isolated left ventricular diverticulum, represent an underestimated anomaly whose prevalence in the general population is not known. Shauq reported CVD as 0.05% of all congenital heart malformations,[18] but the prevalence varies according to different imaging modalities, ranging from 0.4% in autoptic series,[19] to 0.26%[20] - 0.76[6] in patients undergoing cardiac ventricular angiography. Aquaro, in a population of patients who underwent CMR, found a prevalence of isolated CVD of 0,75%.[20] Nakazono et al. reported an incidence of left and right ventricular diverticula on 256-slice CT of 3.4% and 0.6%, respectively.[21] [Table 2] shows LVO frequencies reported from different studies are summarized.
Table 2: Incidence of ventricular outpouchings according to different diagnostic studies

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  Congenital Ventricular Aneurysms Top


From a histological point of view, VA lack completely the myocardial layer; they also show akinetic or dyskinetic wall with asynchronous or paradoxical contraction and may exhibit multiple necks.[22]

The term CVA has been used when the morphology of the ventricular outpouching resembled an acquired aneurysm, with a wide connection to the ventricular cavity and without midline thoraco-abdominal defects.[23] It has been proposed to use the term aneurysm only for acquired forms of ventricular outpouchings, secondary to a myocardial damage (myocardial infarction, myocarditis, cardiomyopathy, trauma, tuberculosis, connective tissue disease, and ventricular dysplasia) and to define congenital outpouchings diverticula.[8] On the contrary, other Authors proposed to identify CVD only with the muscular types and use the term aneurysms for the fibrous type.[6] CVA are probably the same entity as CVD of the fibrous type.

Myocardial crypts and clefts

Myocardial crypts are narrow, deep invaginations within the myocardium localized predominantly in the basal posterior septum and LV-free wall. They are congenital fissures related to the disarray of the myocardial fibers.

Crypts have been defined as “a discrete approximately V- or U-shaped extension of blood signal, considered on cine viewing to penetrate more than 50% of the thickness of the adjoining compact myocardium in diastole” narrowing or completely occluding in systole, without segmental contractility defects.[24],[26]

The term “partial crypts” has been proposed to define recesses penetrating 25%–50% of the wall thickness, but they may represent just irregularities due to trabeculations arising from the endocardial contour without any clinical significance.[24]

Myocardial crypts have been described for the first time at autopsy in patients with hypertrophic cardiomyopathy (HCM).[25] They are generally localized between the muscle bundles of the junctional regions between the ventricles. The crossing and interdigitation of myocytes in this location may predispose to myocardial splitting.[24]

The term “myocardial cleft” has been used especially in the context of HCM, to define narrow invaginations within the left ventricular myocardium.

CMR has enabled in vivo detection of clefts in carriers of HCM mutations[27] and healthy volunteers.[26] Among 16 HCM mutation carriers, who had not yet developed frank hypertrophy, Germans et al. found similar recesses in 13 (81%) and called them crypts.[27] The Author postulated that crypts may have a potential pathological significance as they could precede the phenotypic evidence of HCM. In contrast, Petryka et al. reported a prevalence of 15.6% in HCM, 13.6% of hypertensive patients and 6% of healthy volunteers,[24] suggesting them to be, in most of the cases, only “innocent bystanders.”

A similar incidence has been reported by Erol et al.[1] 6.7% ventricular clefts among 2093 patients undergoing cardiac CT scan while Ozturk et al., in a similar population, found an incidence of 3.05%.[28]

In unselected patients undergoing a cardiac CT scan for suspected coronary disease the prevalence was 2.2%.[10]

The terms cleft and crypt have been used interchangeably to describe such recesses containing luminal blood into the otherwise normal compact myocardium, with a systolic narrowing or obliteration. In literature, small muscular diverticula have been sometimes (be) termed “crypts,” as it may not be easy to detect the exact percentage of myocardial fibers surrounding the recess.

Although crypts may be significant findings in a familial context with a high pretest probability of HCM, their clinical significance is doubtful when isolated findings in asymptomatic patients, probably representing, in these cases, only incidental variants of local myocardial structure.[24],[29],[30],[31]

According to Erol et al.,[1] we believe that all these fissure-like lesions, sometimes called recesses, crypts or clefts are the same entity and maybe only the term crypts should be used to avoid confounding terminology but, again, an agreement is warranted.

Basso et al., in an Editorial comment to Petryka's paper, added the term “crevices,” but this definition of myocardial fissures does not seem to differ from clefts or crypts and has quite never been used according to the results of our PubMed research.[32]


  Etiology Top


CVD are developmental anomalies arising during the fourth embryonic week.[33] The etiology of nonapical, isolated CVD and CVA has been attributed to a focal defect of the muscular ventricular wall due to intrinsic abnormality in embryogenesis.[23] Congenital outpouchings may be acquired during foetal or neonatal period, due to a viral infection,[34] coronary anomalies or vasculitis[35] or arrhythmia-related vascular accidents,[34] which may result in a localized weakness of the LV wall with gradual protrusion, due to the high intraventricular pressure.

Ventricular clefts, crypts, crevices, or fissures most frequently represent “a failure to resorb the trabeculated wall during embryological development phase in which the ventricular wall consists of a spongy meshwork of fibers organized into trabeculae with deep recesses communicating with the LV cavity and enabling a direct blood supply to the myocardium.”[32] Spontaneous closure of a ventricular septal defect may resemble the diagnostic features of a septal cleft or diverticula.[36] Kantarci et al.[37] reviewed the records of 2.725 consecutive patients referred for cardiac CT scan and found septal outpouches in 18 cases. Judging from their aspect, the Authors supposed that these “pouches or sacs” may represent a consequence of spontaneous closure of muscular septal defects. Unfortunately, no further studies have investigated this topic.

Isolated ventricular noncompaction is another entity that needs to be differentiated. It is characterized by a prominent trabecular meshwork with a distinctly spongy appearance and deep inter-trabecular recesses commonly believed to be caused by an arrest in normal embryogenesis.[38],[39],[40] The imaging features of ventricular diverticula and crypts can resemble ventricular noncompaction, and it has been proposed that at least the presence of more than three deep inter-trabecular recesses are necessary to diagnose a noncompaction.[39] Moreover, Singh et al. hypothesized a continuum or a common developmental abnormality between diverticula and noncompaction.[40] Some apical outpouchings may resemble a Takotsubo cardiomyopathy[41] [Figure 1], and a differential diagnosis in the acute phase may be difficult due to the absence of delayed enhancement at CMR: The clinical setting and the reversibility of the dyskinesia are the main diagnostic features.
Figure 1: Echocardiographic images of an apical congenital aneurysm. Echocardiographic apical four-chamber views. On the left, a diastolic still image displaying a congenital apical aneurysm with a large neck, surrounded by thin tissue, and with systolic expansion, on the right (yellow arrow). The patient was an asymptomatic 19-year-old woman with biphasic T waves on precordial leads V4–V6 and no delayed enhancement was present at cardiac magnetic resonance

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Malakan Rad et al. proposed a novel classification of LV outpouchings. According to their classification, if the normal elliptical shape of the left ventricular cavity is preserved, then the diagnosis should be DCLV.[2],[42] Apart from the complexity of this proposal, the inclusion of DCLV among CVOs is a questionable topic.


  Diagnosis Top


Symptoms

Most patients remain asymptomatic and without complications throughout their lifetime[16] and CVD, in most cases, are incidental echocardiographic findings.[34] In Ohlow's series, 60% of the patients were asymptomatic. The most common symptoms were syncope and rhythm disturbances (43%), followed by chest pain (39%) and embolic events (2%).[6] Symptomatic patients may have ventricular arrhythmias, such as sporadic premature ventricular contractions,[43],[44],[45] but sudden cardiac death was also reported.[10]

Clinical implications

CVOs can be diagnosed in any age, with clinical finding ranging from prenatal rupture and death[46],[47],[48] to completely asymptomatic presentation in late adulthood. The prognosis depends on the severity of underlying cardiac pathology and associated malformations. In adults, ventricular diverticula have usually a benign course.[6],[13],[43]

Progressive enlargement and spontaneous rupture of a diverticulum have been described. Marijon demonstrated a mortality rate of 70% in a population of neonates and pediatric patients with associated other intra- and/or extra-cardiac malformations.[23]

Ventricular arrhythmias in diverticula have been reported[44],[45],[49] and syncope may be the first symptom.[50] Ventricular tachycardia is often monomorphic with right bundle branch block morphology, often inducible during electrophysiological study and a cardioverter defibrillator may be required. Fellows et al. reported two patients with aborted sudden cardiac death and one patient who presented with syncope and documented nonsustained ventricular tachycardia.[44] Shen et al. described a male patient with a sustained ventricular tachycardia caused by a postero-basal left ventricular diverticulum.[45] Systemic embolism is a very rare complication,[51] because of blood stasis in its cavity [Figure 2].[52]
Figure 2: Three-dimensional CT scan reconstruction of an apical diverticulum. (a and c): CT scan axial and oblique diastolic image (b and d): CT scan axial and oblique systolic image showing quite complete obliteration of the diverticulum. (e): echocardiographic appearance of the apical outpoching. (f): 3D CT-scan allows a clear view of the cavity with a tortuous diverticulum (yellow arrow). The patient was asymptomatic until at 56-year-old, he had cryptogenic” ischemic stroke (same case of Figures 3 and 6). LV = Left ventricle, RC = Right coronary artery, RV = Right ventricle, CT = Computed tomography, 3D = Three-dimensional

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Electrocardiogram

Electrocardiogram (ECG) may be normal, but in about half of the cases, it shows incomplete bundle branch blocks or nonspecific ST-T changes and sometimes LV hypertrophy pattern. The largest CVD series has been described by Ohlow:[6] about 56.8% of patients have ECG abnormalities and some may rise the suspicion of ventricular diverticula: (1) repolarization pattern with inverted T wave >2 mm in ≥2 contiguous leads; (2) repolarization patterns with either flat, minimally inverted, or >15 mm tall T waves in >2 leads; (3) Q waves 2–3 mm in depth and present in >2 leads; (4) abnormal R progression in the anterior precordial leads; (5) atrial fibrillation; (6) right bundle branch block; (7) early repolarization pattern; and (8) increased PR interval duration. More frequently, ECG abnormalities are found in the apical diverticula, sometimes suggesting left ventricular hypertrophy, a challenging pattern particularly in athletes, [Figure 3]. These ECG findings are not specific but may be symptomatic of a cardiac diverticulum or aneurysm in the absence of other possible ethiologies.[49]
Figure 3: Electrocardiogram of an athlete with an apical left ventricular diverticulum and signs of left ventricle hypertrophy. Repolarization abnormalities and a pattern of left ventricular hypertrophy are present in half of the cases of ventricular diverticula. In this case, a large apical diverticulum was present (same case of Figure 2). T wave inversion in the inferior and lateral precordial leads are present without elevation of the J-point (yellow arrows), and an incomplete right bundle branch block. These abnormalities should not be confused with early repolarization pattern and with an hypertrophic cardiomyopathy

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Echocardiography

Most CVOs are incidentally found during an echocardiographic examination. Echocardiography may allow accurate detection of diverticula and assessment of their location, morphology, contractility, presence of thrombosis, and associated congenital cardiac disorders. A CVD appears as a tongue-like or finger-shaped outpouching of the ventricular wall. A narrow neck and a finger-like contractile pouch are typical characteristics of the congenital muscular ventricular diverticulum, [Figure 4]. Small muscular diverticula and clefts cavity may completely disappear during systole; therefore, only telediastolic images should be used to define diagnosis and measurement, [Figure 5]. Echocardiographic visualization can be challenging, particularly if the CVO location does not coincide with standard acquisition planes. Contrast-enhanced harmonic imaging is a very helpful tool as the contrast entering the recess clearly delineate its contour.
Figure 4: Echocardiographic displays of a left ventricular diverticulum in the inferolateral wall. On the left an apical two chamber and on the right a parasternal short axis view. The diverticulum has a narrow neck and appears as a contractile finger-like pouch in the entire left ventricular wall. The inferior, lateral wall and the apex are the preferred localization. LA = Left atrium, LV = Left ventricle, PML = Posterior mitral leaflet, RV = Right ventricle

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Figure 5: Echocardiographic characteristics of a left ventricular cleft. During diastole (left) a narrow neck deep pouch is seen in the inferior wall, but it almost disappears during systole (right) because of the contraction of the surrounding muscular fibers (yellow arrow). The indentation exceeds half the myocardial thickness without reaching the epicardium. LV = Left ventricle

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Angiography

Angiographic ventriculography offers another diagnostic option, but due to its invasive nature is less useful than other imaging modalities and it may be used to confirm diagnosis in patients with chest pain undergoing coronary angiography. Minor coronary arteries anomalies may be associated to CVD, and are described in up to 58.1% of the cases[49] with a 9-fold risk. This high percentage is somewhat surprising, and the Authors themselves admit a possible selection bias. The most frequent coronary anomaly was a splitting of the origin followed by an ectopic origin but no major anomalies, with potential lethal consequences, have been found.

Computed tomography

The high spatial and temporal resolution offered by ECG-gated cardiac CT provides a unique opportunity to evaluate the ventricular walls.[10],[21] The detection of asymptomatic clefts appearing as V-shaped perpendicular recesses penetrating more than 50% of the myocardial thickness, usually with normal adjacent muscle, seems to be particularly frequent,[1] [Figure 2]. Whether a CT scan may be always advisable in patients with ventricular outpouchings is a matter of debate. Due to high prevalence of minor coronary anomalies and in order to exclude secondary causes of ventricular aneurysms, a coronaric CT scan should be performed. Moreover, a CT scan should be performed when the echocardiographic examination is not conclusive, and CMR not available or contraindicated.

Magnetic resonance

CMR is the ideal noninvasive and nonionizing diagnostic tool. Black blood and steady-state free precession sequences respectively provide accurate definition, measurement, tissue characterization, and contractility assessment [Figure 6], [Figure 7], [Figure 8]. The depth of the outpouching in diastolic frames may be exactly evaluated in order to differentiate whether it is <50% of the wall thickness. The detection of delayed enhancement with T1-weighted sequences, allows diagnosis of fibrous or necrotic tissue and thus the differential diagnosis between diverticula and aneurysms.[20],[29],[30],[53] A pseudoaneurysm is composed only of pericardium and does not show delayed enhancement, while the presence of enhancement around outpouching indicates a peri-aneurysmal necrotic wall.[52] We, therefore, recommend performing a CMR as it is the gold standard imaging technique in the suspect of a CVO.
Figure 6: Cardiac Magnetic Resonance images of an apical ventricular diverticulum (same case of Figure 2) Panel A: T1-weighted four-chamber view Panel B: Perfusion imaging still frame four-chamber view showing the contrast media filling the diverticulum cavity Panel C: The gadolinium delayed image does not show late enhancement

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Figure 7: Cardiac magnetic resonance images of a left ventricular diverticulum localized in the inferior wall. On the left a still frame of a cine-magnetic resonance imaging sequence and on the right the late gadolinium enhancement sequence. The diverticulum is deep and extends beyond the myocardial wall, has a narrow neck and is surrounded by vital myocardial tissue, without scar as demonstrated by the absence of late gadolinium enhancement. This allows the differential diagnosis with ischemic aneurysm or pseudo-aneurysm (yellow arrow). LV = Left ventricle. The patient was an asymptomatic 15-year-old male

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Figure 8: Cardiac magnetic resonance images: left ventricular cleft of the basal inferior wall in a 69 yo woman affected by Hypertrophic Cardiomyopathy. Panel A: T1-weighted two-chamber views: the cleft extends beyond the half of the wall Panel B: Cine image still diastolic frame of the same two-chamber view Panel C: Cine image still systolic frame showing the complete disappearance of the outpouching

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  Proposed Classification Top


In addition to the anamnestic data of a previous myocardial injury, a multi-imaging approach can differentiate diverticula from aneurysms: [Table 3] and [Figure 9] shows our proposed classification: diverticula have a narrow neck and contractility, the ejection fraction is usually normal, there is a systolic flow pattern from the outpouching to the ventricle, the size is often smaller and diastolic shape more circular. In contrast, a left ventricular aneurysm has a wide neck with akinetic walls or paradoxical expansion during systole,[54] no myocardial muscle layer and a layer of fibrous tissue which may be calcified as detectable by the late gadolinium enhancement sequences [Figure 6]. The main diagnostic feature to differentiate diverticula from crypts is that CVD extend outside the epicardial border while crypts remain confined inside the myocardial margin, [Table 2].
Table 3: Differential diagnosis between congenital ventricular outpouchings

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Figure 9: Recess has narrow neck and does not reach half of myocardial wall while crypt (or cleft) goes beyond half of the wall. In systole they obliterate. Diverticulum has narrow neck, coated by thinned vital myocardium and goes beyond the myocardial wall; during systole, it contracts but does not completely disappear. The Congenital Aneurysm has broad neck, coated by fibrous tissue with systolic dyskinesia. The pseudoaneurysm is due to myocardial ischemia with wall rupture and blood in pericardium. The Double-Chambered left ventricle is a rare congenital abnormality in which left ventricle has an anomalous septum or band

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CVD and CVA must be also differentiated from pseudoaneurysms, which are acquired complication of myocardial infarction,[55] cardiac surgery,[56] trauma,[57] or infection.[58] Pseudoaneurysms, also termed false aneurysms, are the consequences of a rupture of the ventricular wall contained by overlying fibrosis and thrombosis of the adherent pericardium.[55]


  Conclusion Top


Our review confirmed the need of an expert consensus to avoid confounding terminologies used to define CVOs. A simple classification may be proposed: Diverticula extend beyond the myocardial wall, and fibrous type may be termed congenital aneurysm, acquired forms should be kept distinct; the term clefts, or crypts, might be used to describe small muscular recesses extending for more than 50% of the ventricular wall but not beyond its margin. CMR seems to be the imaging modality of choice due to the possibility of evaluating the presence of fibrosis and to exclude dubious forms of HCM or ventricular noncompaction.

A multicenter prospective registry, imaged by CMR and/or CT scans, and a long-term follow-up would be needed to investigate clinical implications.[59],[60],[61],[62]

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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    Tables

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