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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Left ventricular noncompaction &#40;LVNC&#41; describes a ventricular wall anatomy characterized by prominent left ventricular &#40;LV&#41; trabeculae&#44; forming a thin compacted layer&#44; and deep intertrabecular recesses that are continuous with the LV cavity and separated from the epicardial coronary arteries&#46;<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">1</span></a> In the normal heart&#44; trabeculae actively provide mechanical leverage by contracting during early systolic ejection&#46;<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">2</span></a> Trabeculae are formed during early embryonic development&#46; The origin of LVNC is attributed to an arrest in compaction of the endomyocardial layer of the heart during early embryogenesis&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">The diagnostic criteria for LVNC are based on ratios between thickness&#44; mass or volume of noncompacted and compacted left ventricle&#46; The number of noncompacted segments provides information on the extension of LVNC&#46; However&#44; this approach is highly investigator-dependent&#59; diagnosis is based on two-dimensional planes using semi-quantitative or qualitative criteria and specificity is low&#46;<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">3</span></a> Grothoff et al&#46; demonstrated that&#44; on cardiovascular magnetic resonance imaging &#40;CMRI&#41;&#44; trabeculation in segments 4-6 indicates a high probability of LVNC and distinguishes LVNC from other cardiomyopathies and normal hearts&#46;<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">4</span></a> Alternative CMRI-based methods include assessment of the global trabeculation index&#46;<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">5</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">Some authors suggest that the established diagnostic criteria are too sensitive and that LVNC is over-diagnosed&#46;<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">6</span></a> LVNC can be an incidental finding in screening studies&#44; such as for athletes&#44;<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">7</span></a> and is not associated with deterioration in LV volumes or function during long-term follow-up in the asymptomatic population&#46;<a class="elsevierStyleCrossRef" href="#bib0165"><span class="elsevierStyleSup">8</span></a> When faced with isolated LVNC morphology&#44; cardiologists must decide whether what they are observing is a cardiomyopathy or a variant LV wall anatomy&#46; In most cases&#44; especially in adult patients&#44; the key element in the diagnostic decision is not the LVNC itself&#44; but the associated LV dilation and&#47;or dysfunction&#44; hypertrophy&#44; right ventricular involvement&#44; arrhythmias and conduction disturbances&#46; The genetic basis of LVNC is an issue of ongoing research&#44; severely limited by the enrollment criteria&#44; which reflect the current heterogeneous diagnostic definitions of LVNC&#46;<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">1</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">The weakness of a diagnosis based solely on proportions or ratios is demonstrated by using Fabry disease &#40;FD&#41; as an example&#46; The hearts of patients with FD may exhibit prominent papillary muscles and trabeculae<a class="elsevierStyleCrossRef" href="#bib0170"><span class="elsevierStyleSup">9</span></a> which may reach LVNC criteria&#44;<a class="elsevierStyleCrossRefs" href="#bib0175"><span class="elsevierStyleSup">10&#44;11</span></a> which are fulfilled for trabecular thickness rather than for a thin compacted layer&#46; Similarly&#44; in patients with Danon disease with LVNC&#44;<a class="elsevierStyleCrossRef" href="#bib0185"><span class="elsevierStyleSup">12</span></a> the criteria for diagnosis of LVNC seem to be met due to the prominent trabeculae with a thickened compacted layer&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">The occurrence of hypertrabeculation and left ventricular noncompaction &#40;LVNC&#41; is increasingly reported in large echocardiographic series&#46;<a class="elsevierStyleCrossRef" href="#bib0165"><span class="elsevierStyleSup">8</span></a> LVNC can be regarded as an isolated entity or as one of the traits that may recur in cardiac and noncardiac diseases&#46;<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">1</span></a> On the basis of current definitions and terminology&#44; LVNC can occur in various settings&#44; including as an isolated finding&#44; or associated with LV dilatation and dysfunction or with cardiomyopathies or congenital heart disease&#44; or acquired and potentially reversible&#44; as has been reported in athletes&#46;<a class="elsevierStyleCrossRefs" href="#bib0130"><span class="elsevierStyleSup">1&#44;7</span></a> However&#44; the association of Fabry disease &#40;FD&#41; with LVNC has been reported in a few cases&#46;<a class="elsevierStyleCrossRefs" href="#bib0175"><span class="elsevierStyleSup">10&#44;11</span></a> It is possible that unidentified mutations in genes other than <span class="elsevierStyleItalic">GLA</span> &#40;responsible for FD&#41; may coexist&#44; which would explain the association found&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">FD is a progressive multisystemic X-linked genetic sphingolipidosis caused by deficient activity of lysosomal alpha-galactosidase A &#40;&#945;-Gal A&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0190"><span class="elsevierStyleSup">13</span></a> Accumulation of &#945;-Gal A substrates in various cells and organs produces the clinical phenotype in FD&#46;<a class="elsevierStyleCrossRef" href="#bib0195"><span class="elsevierStyleSup">14</span></a> FD can mimic other myocardial diseases&#44; including sarcomeric hypertrophic cardiomyopathy &#40;HCM&#41; and amyloid cardiomyopathy&#46; Cardiac imaging&#44; in particular echocardiography and CMRI&#44; plays an important role in detecting this peculiar disease&#46;<a class="elsevierStyleCrossRef" href="#bib0200"><span class="elsevierStyleSup">15</span></a> Although increased left ventricular &#40;LV&#41; wall thickness has traditionally been the hallmark feature of FD&#44; several other structural and functional abnormalities have been uncovered by conventional and novel echocardiographic techniques&#46; Among patients with increased LV wall thickness due to various etiologies&#44; those with FD tend to have more prominent papillary muscles&#44; in both thickness and hyperechogenicity&#46; Systolic function is generally preserved&#44; but can be reduced in advanced disease&#44; usually associated with extensive fibrosis&#46;<a class="elsevierStyleCrossRef" href="#bib0205"><span class="elsevierStyleSup">16</span></a> CMRI is an excellent method to reveal the presence of fibrosis in FD&#44; which is commonly located in the posterolateral basal and mid-level or subepicardial layers&#46;<a class="elsevierStyleCrossRef" href="#bib0190"><span class="elsevierStyleSup">13</span></a> Magnetic resonance noncontrast myocardial T1 mapping may show glycosphingolipid deposits before the onset of left ventricular hypertrophy &#40;LVH&#41;&#44; and is also a useful method for differentiating FD from other causes of LVH&#46;<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">17</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">FD is a multisystemic disease&#44; and depending on the affected organs it can result in neurological&#44; ocular&#44; skin&#44; renal or cardiac manifestations&#46; Therefore&#44; cardiologists&#44; neurologists&#44; dermatologists&#44; nephrologists and ophthalmologists should all be aware of the possibility of FD&#44; depending on the patient&#39;s clinical presentation&#46; In a cardiological setting&#44; a diagnosis of FD should be considered systematically in cases of unexplained LVH&#44; particularly when it is concentric&#44; symmetric&#44; homogeneous or non-obstructive&#46;<a class="elsevierStyleCrossRef" href="#bib0215"><span class="elsevierStyleSup">18</span></a> LVH is a key feature in FD and is reported in up to 50&#37; of male patients and one-third of female patients&#46;<a class="elsevierStyleCrossRef" href="#bib0220"><span class="elsevierStyleSup">19</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">LVH in FD typically combines concentric thickening without LV obstruction and normal LV ejection fraction&#46; However&#44; asymmetric septal or apical hypertrophy has also been described&#44; along with subaortic obstruction&#44; which may mimic the phenotypical and clinical features of sarcomeric HCM&#46;<a class="elsevierStyleCrossRef" href="#bib0225"><span class="elsevierStyleSup">20</span></a> Right ventricular hypertrophy with preserved systolic function&#44; impaired left atrial function and moderate aortic dilatation may also be observed&#44; and LV hypertrabeculation and noncompaction have been described&#46;<a class="elsevierStyleCrossRefs" href="#bib0205"><span class="elsevierStyleSup">16&#44;21</span></a> LV function may deteriorate with time&#44; leading to a restrictive cardiomyopathy pattern&#46; Other echocardiographic features include prominent papillary muscles<a class="elsevierStyleCrossRef" href="#bib0235"><span class="elsevierStyleSup">22</span></a> and a binary appearance of the LV endocardial border&#44;<a class="elsevierStyleCrossRef" href="#bib0205"><span class="elsevierStyleSup">16</span></a> although the diagnostic value of these findings is controversial&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">Specific therapy should be initiated at the earliest stage&#44; before cardiac fibrosis develops&#44; when the first structural or functional cardiac abnormalities are detected&#46; Options include enzyme replacement therapy &#40;ERT&#41; or chaperone therapy&#46; ERT with recombinant human &#945;-Gal &#40;rh-&#945;-Gal&#41; has been available to treat FD since 2001 and may improve ventricular morphology and function&#46;<a class="elsevierStyleCrossRefs" href="#bib0190"><span class="elsevierStyleSup">13&#44;23</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">In 2003&#44; St&#246;llberger et al&#46; showed that LVNC does not appear to be a manifestation of cardiac FD&#46;<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">11</span></a> They studied 26 patients with LVNC diagnosed by echocardiographic criteria and ruled out FD by assessment of clinical systemic manifestations and blood tests for &#945;-Gal A&#46; The most common detection method is the measurement of &#945;-Gal A activity by dried blood spot &#40;DBS&#41; analysis&#46; Although decreased &#945;-Gal A activity in DBS can confirm the diagnosis of FD in homozygous males&#44; this is not the most reliable diagnostic method in heterozygous females&#44; since enzyme activity may be within the normal range in around 40&#37; of this patient group&#46; Therefore&#44; women with high clinical suspicion should undergo genotyping to confirm the diagnosis&#46; Endomyocardial biopsy is the gold standard for diagnosis of cardiac involvement in doubtful cases&#46; Caution should be exercised in clinical assessment because certain drugs such as amiodarone&#44; chloroquine&#44; and tamoxifen have a storage pattern mimicking FD&#46;<a class="elsevierStyleCrossRef" href="#bib0190"><span class="elsevierStyleSup">13</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">There are three cases in the literature documenting an association of LVNC and FD in the same patient&#44; all three of them female&#46;<a class="elsevierStyleCrossRefs" href="#bib0175"><span class="elsevierStyleSup">10&#44;24</span></a> In this issue of the <span class="elsevierStyleItalic">Journal</span>&#44; Azevedo et al&#46; report a multicenter study screening for FD in 78 patients with LVNC&#46;<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">25</span></a> The diagnosis of LVNC was established by echocardiography in 91&#46;0&#37; of the patients and that of FD by &#945;-Gal A activity measured in DBS samples by fluorometry&#46; Molecular analysis of the <span class="elsevierStyleItalic">GLA</span> gene was performed in males with reduced &#945;-Gal A activity&#46; Screening of these 78 patients with LVNC did not identify any additional patients with FD&#46; This supports the hypothesis that although LVNC may occur in patients with FD&#44; this does not represent more than a coincidence of findings&#46;</p><p id="par0060" class="elsevierStylePara elsevierViewall">This article&#44; therefore&#44; strengthens the evidence that there is no pathophysiological link between these two conditions and that LV noncompaction is unlikely to be a phenotypical expression of FD&#46;</p><p id="par0065" class="elsevierStylePara elsevierViewall">In clinical practice&#44; for the management of secondary cardiomyopathies such as FD&#44; echocardiographic study has an important role in screening and diagnosis and in assessment of cardiac function and hemodynamics&#46; Since ERT is usually a major component of treatment for FD&#44; early diagnosis is essential for effective treatment&#46; Based on recent evidence&#44; caution should be exercised when using the current diagnostic criteria of LVNC as a basis for the decision to start specific therapy for FD&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0070" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare&#46;</p></span></span>"
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Editorial comment
Left ventricular noncompaction and Fabry disease: An unlikely association
Não-compactação do ventrículo esquerdo e doença de Fabry: uma associação improvável
José Ribeiro
Centro Hospitalar de Vila Nova de Gaia/Espinho EPE, Serviço de Cardiologia, Vila Nova de Gaia, Portugal
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Left ventricular noncompaction &#40;LVNC&#41; describes a ventricular wall anatomy characterized by prominent left ventricular &#40;LV&#41; trabeculae&#44; forming a thin compacted layer&#44; and deep intertrabecular recesses that are continuous with the LV cavity and separated from the epicardial coronary arteries&#46;<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">1</span></a> In the normal heart&#44; trabeculae actively provide mechanical leverage by contracting during early systolic ejection&#46;<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">2</span></a> Trabeculae are formed during early embryonic development&#46; The origin of LVNC is attributed to an arrest in compaction of the endomyocardial layer of the heart during early embryogenesis&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">The diagnostic criteria for LVNC are based on ratios between thickness&#44; mass or volume of noncompacted and compacted left ventricle&#46; The number of noncompacted segments provides information on the extension of LVNC&#46; However&#44; this approach is highly investigator-dependent&#59; diagnosis is based on two-dimensional planes using semi-quantitative or qualitative criteria and specificity is low&#46;<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">3</span></a> Grothoff et al&#46; demonstrated that&#44; on cardiovascular magnetic resonance imaging &#40;CMRI&#41;&#44; trabeculation in segments 4-6 indicates a high probability of LVNC and distinguishes LVNC from other cardiomyopathies and normal hearts&#46;<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">4</span></a> Alternative CMRI-based methods include assessment of the global trabeculation index&#46;<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">5</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">Some authors suggest that the established diagnostic criteria are too sensitive and that LVNC is over-diagnosed&#46;<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">6</span></a> LVNC can be an incidental finding in screening studies&#44; such as for athletes&#44;<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">7</span></a> and is not associated with deterioration in LV volumes or function during long-term follow-up in the asymptomatic population&#46;<a class="elsevierStyleCrossRef" href="#bib0165"><span class="elsevierStyleSup">8</span></a> When faced with isolated LVNC morphology&#44; cardiologists must decide whether what they are observing is a cardiomyopathy or a variant LV wall anatomy&#46; In most cases&#44; especially in adult patients&#44; the key element in the diagnostic decision is not the LVNC itself&#44; but the associated LV dilation and&#47;or dysfunction&#44; hypertrophy&#44; right ventricular involvement&#44; arrhythmias and conduction disturbances&#46; The genetic basis of LVNC is an issue of ongoing research&#44; severely limited by the enrollment criteria&#44; which reflect the current heterogeneous diagnostic definitions of LVNC&#46;<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">1</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">The weakness of a diagnosis based solely on proportions or ratios is demonstrated by using Fabry disease &#40;FD&#41; as an example&#46; The hearts of patients with FD may exhibit prominent papillary muscles and trabeculae<a class="elsevierStyleCrossRef" href="#bib0170"><span class="elsevierStyleSup">9</span></a> which may reach LVNC criteria&#44;<a class="elsevierStyleCrossRefs" href="#bib0175"><span class="elsevierStyleSup">10&#44;11</span></a> which are fulfilled for trabecular thickness rather than for a thin compacted layer&#46; Similarly&#44; in patients with Danon disease with LVNC&#44;<a class="elsevierStyleCrossRef" href="#bib0185"><span class="elsevierStyleSup">12</span></a> the criteria for diagnosis of LVNC seem to be met due to the prominent trabeculae with a thickened compacted layer&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">The occurrence of hypertrabeculation and left ventricular noncompaction &#40;LVNC&#41; is increasingly reported in large echocardiographic series&#46;<a class="elsevierStyleCrossRef" href="#bib0165"><span class="elsevierStyleSup">8</span></a> LVNC can be regarded as an isolated entity or as one of the traits that may recur in cardiac and noncardiac diseases&#46;<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">1</span></a> On the basis of current definitions and terminology&#44; LVNC can occur in various settings&#44; including as an isolated finding&#44; or associated with LV dilatation and dysfunction or with cardiomyopathies or congenital heart disease&#44; or acquired and potentially reversible&#44; as has been reported in athletes&#46;<a class="elsevierStyleCrossRefs" href="#bib0130"><span class="elsevierStyleSup">1&#44;7</span></a> However&#44; the association of Fabry disease &#40;FD&#41; with LVNC has been reported in a few cases&#46;<a class="elsevierStyleCrossRefs" href="#bib0175"><span class="elsevierStyleSup">10&#44;11</span></a> It is possible that unidentified mutations in genes other than <span class="elsevierStyleItalic">GLA</span> &#40;responsible for FD&#41; may coexist&#44; which would explain the association found&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">FD is a progressive multisystemic X-linked genetic sphingolipidosis caused by deficient activity of lysosomal alpha-galactosidase A &#40;&#945;-Gal A&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0190"><span class="elsevierStyleSup">13</span></a> Accumulation of &#945;-Gal A substrates in various cells and organs produces the clinical phenotype in FD&#46;<a class="elsevierStyleCrossRef" href="#bib0195"><span class="elsevierStyleSup">14</span></a> FD can mimic other myocardial diseases&#44; including sarcomeric hypertrophic cardiomyopathy &#40;HCM&#41; and amyloid cardiomyopathy&#46; Cardiac imaging&#44; in particular echocardiography and CMRI&#44; plays an important role in detecting this peculiar disease&#46;<a class="elsevierStyleCrossRef" href="#bib0200"><span class="elsevierStyleSup">15</span></a> Although increased left ventricular &#40;LV&#41; wall thickness has traditionally been the hallmark feature of FD&#44; several other structural and functional abnormalities have been uncovered by conventional and novel echocardiographic techniques&#46; Among patients with increased LV wall thickness due to various etiologies&#44; those with FD tend to have more prominent papillary muscles&#44; in both thickness and hyperechogenicity&#46; Systolic function is generally preserved&#44; but can be reduced in advanced disease&#44; usually associated with extensive fibrosis&#46;<a class="elsevierStyleCrossRef" href="#bib0205"><span class="elsevierStyleSup">16</span></a> CMRI is an excellent method to reveal the presence of fibrosis in FD&#44; which is commonly located in the posterolateral basal and mid-level or subepicardial layers&#46;<a class="elsevierStyleCrossRef" href="#bib0190"><span class="elsevierStyleSup">13</span></a> Magnetic resonance noncontrast myocardial T1 mapping may show glycosphingolipid deposits before the onset of left ventricular hypertrophy &#40;LVH&#41;&#44; and is also a useful method for differentiating FD from other causes of LVH&#46;<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">17</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">FD is a multisystemic disease&#44; and depending on the affected organs it can result in neurological&#44; ocular&#44; skin&#44; renal or cardiac manifestations&#46; Therefore&#44; cardiologists&#44; neurologists&#44; dermatologists&#44; nephrologists and ophthalmologists should all be aware of the possibility of FD&#44; depending on the patient&#39;s clinical presentation&#46; In a cardiological setting&#44; a diagnosis of FD should be considered systematically in cases of unexplained LVH&#44; particularly when it is concentric&#44; symmetric&#44; homogeneous or non-obstructive&#46;<a class="elsevierStyleCrossRef" href="#bib0215"><span class="elsevierStyleSup">18</span></a> LVH is a key feature in FD and is reported in up to 50&#37; of male patients and one-third of female patients&#46;<a class="elsevierStyleCrossRef" href="#bib0220"><span class="elsevierStyleSup">19</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">LVH in FD typically combines concentric thickening without LV obstruction and normal LV ejection fraction&#46; However&#44; asymmetric septal or apical hypertrophy has also been described&#44; along with subaortic obstruction&#44; which may mimic the phenotypical and clinical features of sarcomeric HCM&#46;<a class="elsevierStyleCrossRef" href="#bib0225"><span class="elsevierStyleSup">20</span></a> Right ventricular hypertrophy with preserved systolic function&#44; impaired left atrial function and moderate aortic dilatation may also be observed&#44; and LV hypertrabeculation and noncompaction have been described&#46;<a class="elsevierStyleCrossRefs" href="#bib0205"><span class="elsevierStyleSup">16&#44;21</span></a> LV function may deteriorate with time&#44; leading to a restrictive cardiomyopathy pattern&#46; Other echocardiographic features include prominent papillary muscles<a class="elsevierStyleCrossRef" href="#bib0235"><span class="elsevierStyleSup">22</span></a> and a binary appearance of the LV endocardial border&#44;<a class="elsevierStyleCrossRef" href="#bib0205"><span class="elsevierStyleSup">16</span></a> although the diagnostic value of these findings is controversial&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">Specific therapy should be initiated at the earliest stage&#44; before cardiac fibrosis develops&#44; when the first structural or functional cardiac abnormalities are detected&#46; Options include enzyme replacement therapy &#40;ERT&#41; or chaperone therapy&#46; ERT with recombinant human &#945;-Gal &#40;rh-&#945;-Gal&#41; has been available to treat FD since 2001 and may improve ventricular morphology and function&#46;<a class="elsevierStyleCrossRefs" href="#bib0190"><span class="elsevierStyleSup">13&#44;23</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">In 2003&#44; St&#246;llberger et al&#46; showed that LVNC does not appear to be a manifestation of cardiac FD&#46;<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">11</span></a> They studied 26 patients with LVNC diagnosed by echocardiographic criteria and ruled out FD by assessment of clinical systemic manifestations and blood tests for &#945;-Gal A&#46; The most common detection method is the measurement of &#945;-Gal A activity by dried blood spot &#40;DBS&#41; analysis&#46; Although decreased &#945;-Gal A activity in DBS can confirm the diagnosis of FD in homozygous males&#44; this is not the most reliable diagnostic method in heterozygous females&#44; since enzyme activity may be within the normal range in around 40&#37; of this patient group&#46; Therefore&#44; women with high clinical suspicion should undergo genotyping to confirm the diagnosis&#46; Endomyocardial biopsy is the gold standard for diagnosis of cardiac involvement in doubtful cases&#46; Caution should be exercised in clinical assessment because certain drugs such as amiodarone&#44; chloroquine&#44; and tamoxifen have a storage pattern mimicking FD&#46;<a class="elsevierStyleCrossRef" href="#bib0190"><span class="elsevierStyleSup">13</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">There are three cases in the literature documenting an association of LVNC and FD in the same patient&#44; all three of them female&#46;<a class="elsevierStyleCrossRefs" href="#bib0175"><span class="elsevierStyleSup">10&#44;24</span></a> In this issue of the <span class="elsevierStyleItalic">Journal</span>&#44; Azevedo et al&#46; report a multicenter study screening for FD in 78 patients with LVNC&#46;<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">25</span></a> The diagnosis of LVNC was established by echocardiography in 91&#46;0&#37; of the patients and that of FD by &#945;-Gal A activity measured in DBS samples by fluorometry&#46; Molecular analysis of the <span class="elsevierStyleItalic">GLA</span> gene was performed in males with reduced &#945;-Gal A activity&#46; Screening of these 78 patients with LVNC did not identify any additional patients with FD&#46; This supports the hypothesis that although LVNC may occur in patients with FD&#44; this does not represent more than a coincidence of findings&#46;</p><p id="par0060" class="elsevierStylePara elsevierViewall">This article&#44; therefore&#44; strengthens the evidence that there is no pathophysiological link between these two conditions and that LV noncompaction is unlikely to be a phenotypical expression of FD&#46;</p><p id="par0065" class="elsevierStylePara elsevierViewall">In clinical practice&#44; for the management of secondary cardiomyopathies such as FD&#44; echocardiographic study has an important role in screening and diagnosis and in assessment of cardiac function and hemodynamics&#46; Since ERT is usually a major component of treatment for FD&#44; early diagnosis is essential for effective treatment&#46; Based on recent evidence&#44; caution should be exercised when using the current diagnostic criteria of LVNC as a basis for the decision to start specific therapy for FD&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0070" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare&#46;</p></span></span>"
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ISSN: 08702551
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2021 Fevereiro 41 20 61
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2020 Setembro 45 16 61
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