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 Table of Contents  
CASE REPORT
Year : 2022  |  Volume : 6  |  Issue : 4  |  Page : 276-281

Necklace pattern left ventricular noncompaction cardiomyopathy with plethora of paradoxic septal premature ventricular complexes: A case report and literature review


Department of Cardiology, All India Institute of Medical Sciences, Bhubaneswar, Odisha, India

Date of Submission25-Oct-2021
Date of Acceptance28-Mar-2022
Date of Web Publication16-Dec-2022

Correspondence Address:
Dr. Debasish Das
Department of Cardiology, All India Institute of Medical Sciences, Bhubaneswar - 751 019, Odisha
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/hm.hm_69_21

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  Abstract 

We report an extremely rare case of left ventricular noncompaction (LVNC) cardiomyopathy sparing the anterior ventricular wall in an interesting “necklace” pattern in parasternal short axis view in a 76-year-old female with frequent palpitation and shortness of breath for the last 6 months. Interestingly, the patient had a plethora of basal septal premature ventricular complexes (PVCs) both from the anterior and posterior aspects of the paradoxically thinned-out basal septum and they were not from the segment of noncompacted (NC) myocardium. Our case is unique and the first to describe the LVNC in an interesting shape of “necklace” sparing the left ventricular anterior, anteroseptal, and anterolateral wall and paradoxically arising plethora of septal PVCs from the thinned-out basal septum deteriorating the left ventricular function rapidly in an elderly female in her seventh decade of life. Although commonly in LVNC, the PVCs arise from the NC segment, in this unique case plethora of PVCs paradoxically arising from the basal septum were contributing toward rapid deterioration of left ventricular systolic function in an elderly patient in her seventh decade of life without the presence of conventional risk factors.

Keywords: Cardiomyopathy, left ventricular, necklace, noncompaction, premature ventricular complexes


How to cite this article:
Das D, Kumar A, Banerjee A, Das T, Singh S, Dixit M. Necklace pattern left ventricular noncompaction cardiomyopathy with plethora of paradoxic septal premature ventricular complexes: A case report and literature review. Heart Mind 2022;6:276-81

How to cite this URL:
Das D, Kumar A, Banerjee A, Das T, Singh S, Dixit M. Necklace pattern left ventricular noncompaction cardiomyopathy with plethora of paradoxic septal premature ventricular complexes: A case report and literature review. Heart Mind [serial online] 2022 [cited 2023 Feb 7];6:276-81. Available from: http://www.heartmindjournal.org/text.asp?2022/6/4/276/363956


  Introduction Top


Left ventricular noncompaction (LVNC) cardiomyopathy otherwise known as spongiform cardiomyopathy occurs due to embryonic arrest of compaction of cardiomyocytes into a compacted layer resulting in most of the myocardium looking spongy or noncompacted (NC) with a thin ribbon-like layer of the compacted segment. Echocardiography nicely demonstrates the same with the thickness of the NC layer to the compacted (C) layer being more than 2 and typical blood flow into the recesses is noted in color doppler during routine echocardiography. Spongiform myocytes degenerate with time and most of the spongiform cardiomyopathy present by adolescence or early adulthood. Our case is a unique description of completely normal course of spongiform cardiomyopathy till seven and half decades of life with recent deterioration by the plethora of pleomorphic septal premature ventricular complexes (PVCs) which are not routinely expected in a case of LVNC. Rather PVCs in LVNC are expected from the NC segments in salvos and runs sometimes causing a faster deterioration of left ventricular systolic function.


  Case Top


A 76-year-old female without conventional risk factors without any history of coronary artery disease in the past presented with effort intolerance Class II and palpitation for the last 6 months with faster progression of shortness of breath to Class III for the last 3 months. She was absolutely doing well before 6 months, she was able to climb two flights of stairs at a stretch without any effort angina or shortness of breath. Her baseline electrocardiogram revealed the presence of septal PVCs from the left ventricular (LV) septum with right bundle branch block (RBBB) morphology with the transition before V4 and having both positive and negative morphology in inferior leads suggestive of both anteroseptal and posteroseptal basal PVCs [Figure 1]. Her serum chemistries were within normal limits and her thyroid profile was also normal. Echocardiography revealed the presence of LVNC with the ratio of the thickness of the NC to the compacted layer being more than 2 with color Doppler clearing showing the blood flow into the recesses [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]. The parasternal short axis (PSAX) view revealed an interesting “necklace” pattern of LVNC sparing the apical septum, anterior and anterolateral wall [Figure 2]. This “necklace” pattern of LVNC sparing the anteroseptal, anterior, and anterolateral wall of the LV has not been described in the world literature so far. Uniquely, the NC layer was much thicker than the compacted layer which was like a thin rim of ribbon on the posterior, posteroseptal, and posterolateral surface. She had severe mitral regurgitation, global hypokinesia of the LV, and severe left ventricular systolic dysfunction (ejection fraction [EF] 30%). As she had a plethora of basal septal PVCs, we wanted to analyze the basal septum which was thinned out and scarred with preserved mid and apical interventricular septal thickness [Figure 7]. In view of basal thinning and scaring, assuming it to be a sequalae of coexistent previous myocardial infarction, we subjected the patient to right transradial coronary angiogram which revealed normal coronaries without any evidence of fresh or old atherosclerotic obstructive coronary lesion. The patient had a metallic prosthesis in their right leg as she had fracture tibia 6 months back for which cardiac magnetic resonance imaging (MRI) could not be accomplished. No family member had history of cardiomyopathy. The patient was also unaffordable for genetic testing. We did a Holter analysis to assess the burden of septal PVCs and the burden of septal pleomorphic PVCs was 33%. In LVNC, the PVCs are expected to arise from the noncompaction segment, but paradoxically in our case salvos of PVCs were arising from the basal septum which is extremely unusual to encounter in a case of LVNC. Those paradoxical left ventricular PVCs besides the recent increase in the severity of mitral regurgitation may be the causative factor behind rapid deterioration of left ventricular systolic function in a patient of 76 years of age who was absolutely doing well till such an elderly age without any effort intolerance or limitation of day-to-day activity. Our case is the first to illustrate a “necklace” pattern of LVNC cardiomyopathy in an extremely elderly patient of 76 years of age, in whom the paradoxically arising plethora of septal PVCs were the contributing factor toward rapid deterioration of left ventricular systolic function over the past 6 months. Because of extremely elderly age, we did not put an automated implantable cardioverter defibrillator (AICD) in this patient. The patient was put on angiotensin receptor neprilysin inhibitor, optimum beta blocker (carvedilol), amiodarone [Figure 8] and diuretics. She was advised for follow-up after 1 month.
Figure 1: Anteroseptal and posteroseptal basal premature ventricular complexes

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Figure 2: Necklace pattern of left ventricular noncompaction involving inferior, inferoseptal and inferolateral wall sparing the anteroseptal, anterior and antero lateral wall

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Figure 3: NC/C layer ratio >2

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Figure 4: A4CH view showing prominent trabeculations of left ventricle

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Figure 5: Prominent trabeculations in A2CH view

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Figure 6: Blood flow into the recesses

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Figure 7: Thinned out and scarred basal interventricular septal

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Figure 8: Summary of the index case. PVCs: Premature ventricular complexes, LVNC: Left ventricular noncompaction, MR: mitral regurgitation, LV: Left ventricular, AICD: Automated implantable cardioverter defibrillator, ACEI: Angiotensin converting enzyme inhibitor, VT: Ventricular tachycardia, LVSD: Left ventricular systolic dysfunction, CRT IF LBBB: cardiac resynchronisation therapy if left bundle branch block

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  Discussion Top


We present an extremely rare case of LVNC cardiomyopathy with index presentation in seventh decade of life which usually presents in adolescence or early adulthood due to degeneration of spongy myocardium with age. The patient had frequent PVCs with RBBB morphology suggestive of left ventricular origin, had transition before V4 suggestive of septal origin as transition beyond V4 suggests free wall origin. Across the limb leads, the PVCs had two different morphologies both being positive and negative in inferior leads suggestive of origin from both anterior and posterior parts of the septum. PVCs with positive morphology in lead II, III, and aVF suggest anterior origin while PVCs with negative morphology in II, III, aVF suggests posterior origin. In total, our case had a plethora of anteroseptal and posteroseptal PVCs.

In LVNC, we expect the PVCs from the NC myocardium but paradoxically the PVCs were originating from the basal septum. Echocardiography revealed paradoxically thin basal septum of 4.5 mm (<5 mm) with scarring and calcification. Encountering a plethora of septal PVCs in a case of LVNC cardiomyopathy is a rare phenomenon as most often they present with apical septal ventricular tachycardia or apical septal PVCs. The plethora of septal PVCs causing PVC-induced cardiomyopathy with deterioration of left ventricular systolic dysfunction and parallelly increasing the severity of mitral regurgitation may be a plausible explanation behind acute deterioration in the aforesaid patient.

The form of LVNC noted in our case spared the left ventricular anterior wall, anteroseptal wall, and anterolateral wall and had exclusively involved the left ventricular inferior, inferoseptal, and inferolateral wall mimicking a bridal “necklace” (quite thick anteriorly in the neck with a thin thread in the back). This pattern of exclusive basal septal involvement in LVNC is also not seen in routine practice. We did a coronary angiogram to rule out right coronary artery occlusion as basal septum was scarred and thinned out which came out to be normal. This necklace pattern myocardial involvement in LVNC cardiomyopathy sparing of anteroseptal, anterior and anterolateral wall with exclusively involving the basal septum has not been reported in world literature so far. Our case is the first echocardiographic illustration of the necklace pattern of LVNC in a patient in her seventh decade of life with a quite asymptomatic course. Our case is also an illustration of the origin of pathological clinical PVCs away from the site of myofiber pathology in a case of LVNC.

In echocardiography, the ratio of the thickness of the NC layer to the compacted (C) layer was more than 2 [Figure 3], i.e., the compacted layer was looking like a thin rim of ribbon and the grossly NC or spongy layer had a honeycomb appearance due to presence of numerous trabeculations. Plethora of PVCs lead to intermittent asynchronous contraction of the LV and this asynchronous contraction of the LV over a short period leads to deterioration of left ventricular systolic function or development of cardiomyopathy.

PVC-induced cardiomyopathy is a phenomenon mostly encountered in the young population and Baman et al.[1] concluded that a PVC burden of more than 24% mandates early radiofrequency ablation. As noted in our case, as the patient had pleomorphic or two different population of PVCs, we did not proceed for radiofrequency ablation. LVNC is a very rare form of congenital cardiomyopathy due to the embryonic arrest of the normal maturation process of the myocardium. It accounts for 0.05%–0.24% of all cardiomyopathies. Predominantly noncompaction involves the LV, but biventricular involvement can be seen in up 22%–38% of cases.[2] It is an autosomal dominant disorder with a single point mutation of beta myosin heavy gene; mutation in Z-band alternatively spliced PDZ motif protein (ZASP) , dystrobrevin, and taffazin have also been reported. It is otherwise known as spongy myocardium, spongiform cardiomyopathy, persisting myocardial sinusoids, or zaspopathy. It has been known to be a part of Noonan, Barth, Roifman, and Toriello Carey Syndrome.[3] In LVNC, endomyocardial trabeculations increase in number with prominence in the cardiac apex. It carries a high risk of malignant ventricular arrhythmia due to structural and electrical heterogeneity, progressive left ventricular dysfunction with the advancement of age and also carries a high risk of thromboembolism. Echocardiography plays an important role in the diagnosis of LVNC as follows:

  1. Chin Criteria: Ratio of the distance of trough of trabecular recess from epicardium (X) to distance of the peak of trabecular recess from epicardium (Y) <0.5. This can be well delineated in transthoracic echocardiography
  2. Jenni Criteria: Ratio of the thickness of the NC layer to compacted layer >2 which is well delineated in cardiac MRI in short axis view of LV in end-systole.


Heart failure is the most common presentation,[4] as noted in our case. The prognosis of the patients with LVNC is poor but asymptomatic cases have been reported to survive up to the seventh decade[5] as noted in our case. Our case may be the illustration of the asymptomatic nature of LVNC up to the seventh decade of life and maybe the description of LVNC in the most elderly patient in world literature. An AICD is always indicated in those subsets of patients to prevent Sudden Cardiac Death (SCD) in young cohorts with recurrent hemodynamically unstable ventricular tachycardia (VT).[6] We did not proceed for AICD implantation as she had no history of aborted SCD or hemodynamically unstable VT in the past requiring cardioversion and was quite elderly.

Jenni et al.[7] emphasized the morphological criteria as a maximal end-systolic ratio of NC to compacted layers of >2 with deep perfused intertrabecular recesses as a diagnostic feature of LVNC. However, this necklace-type of noncompaction confined to the inferior, inferolateral, and inferoseptal left ventricular wall with paradoxical thinning of the basal septum has not been described in the literature so far. 3D echocardiography allows for accurate diagnosis, detailed characterization, and description of the extent of the affected myocardium in LVNC as described in a case series of four patients by Baker et al.[8] Entire trabecular projections and intertrabecular recesses are well visualized simultaneously in three-dimensional echo and the distinction between the compact and noncompact LV myocardium is easily demarcated.

Koo et al.[9] performed transpulmonary contrast echocardiography with intravenous injection of perflurocarbon-exposed sonicated dextrose albumin (PESDA) (a sonicated mixture of perfluorocarbon [8 cc], 5% albumin [4 cc], and 5% dextrose water [8 cc]) which clearly defined the endocardial border. Contrast echocardiography can be helpful without further patient discomfort, and can save time and money. Involvement of the septum is much less frequent in LVNC.[10] However, in our case, it involved the basal septum and this was the site of origin of PVCs deteriorating the left ventricular systolic function rapidly. MRI is useful in cases with poor echocardiographic image quality.[11] MRI signal intensity in NC myocardium may help identify substrate for potentially lethal arrhythmias.[12] Echocardiography is generally considered the gold standard for the diagnosis of LVNC. In most cases, cardiac MRI offers no additional information except for the detection of a hidden thrombus in deep recesses.[13] Differential echocardiographic diagnosis includes prominent normal myocardial trabeculations, false tendons and aberrant bands, cardiac tumors, and left ventricular apical thrombus. Blood flow into deep intertrabecular recesses is helpful for the differentiation of LVNC from other echocardiographic differential diagnoses.[13]

Clinical morbidity includes heart failure, arrhythmias, and systemic and pulmonary embolism.[14],[15] We put the patient on low dose Rivaroxaban 10 mg once daily in view of the high likelihood of getting left ventricular thrombus as she had also left ventricular spontaneous echo contrast (LVSEC). Thrombi are very often missed when inside deep recesses.[16] Sometimes, LVSEC confuses with the apical noncompaction of the LV. Nonisolated form of LVNC exists with conotruncal anomalies, Ebstein anomaly, transposition of great arteries, pulmonary stenosis, ventricular septal defect, atrial septal defect, hypoplastic left heart syndrome and in the association of coronary anomalies.[17] Dysynchrony between the compacted and NC myocardium gives rise to global left ventricular systolic dysfunction in LVNC.[17]

They are more prone to arrhythmia in the form of polymorphic or pleomorphic PVCs, atrial fibrillation, ventricular tachycardia, and Wolf Parkinson White syndrome in children.[17] Life-threatening ventricular tachycardia occurs in 20% or more patients and serves as a risk factor for SCD.[18] Grothoff et al. concluded a trabeculated left ventricular mass >25% of the global left ventricular mass and a NC mass >15 g/m2 is highly sensitive and specific for the diagnosis of LVNC in cardiac MRI.[19] Burke et al. proposed a transmural thickness of the NC right ventricle of more than 75% is diagnostic of right ventricular noncompaction.[20] Toyono et al.[21] reported carvedilol improves the prognosis in LVNC cardiomyopathy.

Oechslin and Jenni[22] recommended anticoagulation with target prothrombin time international normalized ratio of 2–3 in patients with left ventricular systolic dysfunction (EF <40%). We managed the patient with low-dose rivaroxaban 10 mg once daily in view of extremely elderly age. They also described AICD as indicated for secondary prevention in patients with LVNC presenting with syncope, symptomatic ventricular arrhythmias, or severely impaired left ventricular systolic function. Stöllberger et al.[23] reported a case of dilated cardiomyopathy of 10 years duration with NYHA Class IV heart failure symptoms and left ventricular ejection fraction (LVEF) of 30%. The features of hyper trabeculation were shown to disappear with improvement in LVEF to 47% following implantation of a biventricular pacemaker. Trabeculations disappear with improvement in left ventricular function. Diagnostic features of LVNC have been described in cases of myocarditis,[24] peripartum cardiomyopathy,[25] and Dengue fever[26],[27] but she had none of those. Okumura and Murohara[28] concluded LVNC as a acquire cardiomyopathy, not a congenital one because trabeculae emerge as a compensation to increase endocardial surface area to optimize the stroke volume in failing hearts,[29] and when cardiac contraction improves by cardiac resynchronization therapy, the trabecular structure may become inconspicuous and no longer appear.[23] However, the supportive issue for LVNC being congenital is that according to a survey in Japan, around 40% of the patients with LVNC are affected by genetic factors with autosomal inheritance, mitochondrial gene mutation, and X-linkage.[30] We represented a unique and first illustration of LVNC cardiomyopathy involving the LV in a typical “necklace” pattern and paradoxically involving the basal septum with basal septal thinning and this was the site of origin of the plethora of PVCs deteriorating the left ventricular systolic function fairly rapidly in a 76-year-old female who was quite asymptomatic till this age with LVNC.

Overall, this is an extremely rare case of LVNC cardiomyopathy with index presentation in the seventh decade of life. Interestingly, the patient did not have PVCs from the spongy myocardium. She had plethora of anteroseptal and posteroseptal PVCs. Noncompaction spared the left ventricular anterior, anteroseptal, and anterolateral wall and had exclusively involved the left ventricular inferior, inferoseptal, and inferolateral wall mimicking a bridal “necklace” . This pattern of left ventricular non-compaction has not been described in the literature so far. Because of extremely elderly age, the patient was managed conservatively with anti-heart failure medications and amiodarone.


  Conclusion Top


Our case is the unique and first illustration of LVNC cardiomyopathy exclusively involving the inferoseptal, inferior, and inferolateral wall in an interesting “necklace” pattern with paradoxic thinning of the basal septum which was the source of the plethora of basal septal PVCs. Those paradoxic septal PVCs besides progressive left ventricular systolic dysfunction and increase in the severity of mitral regurgitation could be contributing toward rapid deterioration of left ventricular systolic function in this elderly female of 76 years without the presence of any conventional cardiac risk factors. Plethora of pleomorphic PVCs was managed with amiodarone; guarded prognosis was explained to the patient's attendants in view of presentation in extremes of age with severe left ventricular systolic dysfunction with expected survival within 2–5 years and presentation at such an extreme of age was the limitation behind implanting an AICD. Beginning from the genetics to management, LVNC has been always a disease of diversity and debate.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

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Baman TS, Lange DC, Ilg KJ, Gupta SK, Liu TY, Alguire C, et al. Relationship between burden of premature ventricular complexes and left ventricular function. Heart Rhythm 2010;7:865-9.  Back to cited text no. 1
    
2.
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Richard P, Ader F, Roux M, Donal E, Eicher JC, Aoutil N, et al. Targeted panel sequencing in adult patients with left ventricular non-compaction reveals a large genetic heterogeneity. Clin Genet 2019;95:356-67.  Back to cited text no. 3
    
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10.
Oechslin EN, Attenhofer Jost CH, Rojas JR, Kaufmann PA, Jenni R. Long-term follow-up of 34 adults with isolated left ventricular noncompaction: A distinct cardiomyopathy with poor prognosis. J Am Coll Cardiol 2000;36:493-500.  Back to cited text no. 10
    
11.
Junga G, Kneifel S, Von Smekal A, Steinert H, Bauersfeld U. Myocardial ischaemia in children with isolated ventricular non-compaction. Eur Heart J 1999;20:910-6.  Back to cited text no. 11
    
12.
Daimon Y, Watanabe S, Takeda S, Hijikata Y, Komuro I. Two-layered appearance of noncompaction of the ventricular myocardium on magnetic resonance imaging. Circ J 2002;66:619-21.  Back to cited text no. 12
    
13.
Hany TF, Jenni R, Debatin JF. MR appearance of isolated noncompaction of the left ventricle. J Magn Reson Imaging 1997;7:437-8.  Back to cited text no. 13
    
14.
Ritter M, Oechslin E, Sütsch G, Attenhofer C, Schneider J, Jenni R. Isolated noncompaction of the myocardium in adults. Mayo Clin Proc 1997;72:26-31.  Back to cited text no. 14
    
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16.
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17.
Saito K, Ibuki K, Yoshimura N, Hirono K, Watanabe S, Watanabe K, et al. Successful cardiac resynchronization therapy in a 3-year-old girl with isolated left ventricular non-compaction and narrow QRS complex: A case report. Circ J 2009;73:2173-7.  Back to cited text no. 17
    
18.
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19.
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20.
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21.
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22.
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23.
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29.
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30.
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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]



 

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