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    "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Case report</span><p id="par0005" class="elsevierStylePara elsevierViewall">Increased ventricular wall thickness can be a physiologic response to pressure overload or to exercise&#44; but it can also be pathologic&#44; resulting from myocyte hypertrophy or deposition of an abnormal substance&#46; Finding its exact cause can be challenging&#44; but is crucial in determining the appropriate management&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">We describe the case of a 47-year-old Caucasian man complaining of tiredness and dyspnea on moderate exertion lasting several months&#44; progressively worsening and associated with orthopnea&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">A history of erectile dysfunction&#44; night sweats and paresthesias in both hands and feet was also reported&#46; He had also experienced bilateral calf pain during the previous month&#44; with no specific relieving or aggravating factors&#44; and had noted blurred vision in the left eye for the previous six months&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">He denied chest pain&#44; fever&#44; muscular weakness or other symptoms&#46; His medical history was positive for type 2 diabetes and his family history was unremarkable&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">On physical examination&#44; bilateral rales and hypoesthesia of the hands and feet were noted&#46; The chest X-ray revealed an increased cardiothoracic index and arterial blood gas analysis showed mild hypoxemia&#46; Blood analysis revealed increased proBNP &#40;1781 pg&#47;ml&#41;&#44; without anemia or renal impairment&#46; The electrocardiogram showed normal sinus rhythm&#44; QS waves in the inferior leads&#44; poor R progression in the precordial leads and T-wave inversion in I and aVL &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Figure 1</a>&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0030" class="elsevierStylePara elsevierViewall">The transthoracic echocardiogram &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Figure 2</a>&#41; showed severe biventricular concentric thickening with normal ejection fraction&#46; Diastolic assessment indicated restrictive physiology&#59; mild pericardial effusion was also noted&#46;</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0035" class="elsevierStylePara elsevierViewall">At this point&#44; our findings suggested an infiltrative cardiomyopathy&#44; such as amyloidosis&#44; Fabry disease or glycogen storage disease&#46;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;2</span></a> The neuropathy and visual changes could fit with a systemic disease&#46; Interestingly&#44; the ECG did not show decreased voltages&#44; which is common in familial amyloidosis&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">Hypertrophic cardiomyopathy was another hypothesis&#46; Against it was the ECG showing poor R-wave progression and echocardiographic findings suggestive of an infiltrative disease&#44; with symmetric biventricular wall thickening and pericardial effusion&#46; We excluded hypertensive heart disease&#44; since the patient did not have hypertension&#46; Blood analysis and thoracic computed tomography showed no changes suggestive of hemochromatosis or sarcoidosis&#46; Thyroid disease and HIV&#44; HCV or HBV infection were also excluded&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">Cardiac magnetic resonance &#40;CMR&#41; showed marked concentric left ventricular &#40;LV&#41; hypertrophy&#44; mild right ventricular &#40;RV&#41; hypertrophy and normal ejection fraction&#46; There was biatrial enlargement&#44; thickening of the interatrial septum and mild pericardial effusion &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Figure 3</a>&#41;&#46; Short-tau inversion-recovery &#40;STIR&#41; sequences showed no myocardial edema or inflammation&#46; In late gadolinium enhancement study&#44; there was difficulty in setting the optimal inversion time to correctly null the myocardium&#44; with a relatively dark blood pool and diffuse subendocardial enhancement of the interatrial septum and the LV and RV walls &#40;<a class="elsevierStyleCrossRef" href="#fig0020">Figure 4</a>&#41;&#46; The diffuse subendocardial late gadolinium enhancement&#44; coupled with abnormal myocardial and blood-pool contrast kinetics&#44; was most consistent with cardiac amyloidosis&#46; The fact that the optimal inversion time that would null the normal myocardium could not be found is an indirect sign suggesting amyloidosis&#44; because if abnormal fibrils are widespread in the intercellular space&#44; the gadolinium may not be taken up by healthy myocardium&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p><elsevierMultimedia ident="fig0015"></elsevierMultimedia><elsevierMultimedia ident="fig0020"></elsevierMultimedia><p id="par0050" class="elsevierStylePara elsevierViewall">Endomyocardial biopsies and biopsy of the salivary glands were then performed but were negative for amyloid&#46;</p><p id="par0055" class="elsevierStylePara elsevierViewall">Immunosubtraction testing for free immunoglobulin chains in serum and urine&#44; which could point to AL amyloidosis&#44; was also negative&#46;</p><p id="par0060" class="elsevierStylePara elsevierViewall">An electromyogram suggested the presence of a pressure-sensitive neuropathy of the lower limbs&#44; bilateral carpal tunnel syndrome and signs of parasympathetic dysfunction&#44; which would be compatible with amyloidosis&#46;</p><p id="par0065" class="elsevierStylePara elsevierViewall">Finally&#44; we returned to the patient&#39;s complaint of left visual impairment&#46; Vitreous opacities in the left eye were reported and&#44; after vitrectomy&#44; vitreous humor analysis confirmed the presence of amyloid&#46;</p><p id="par0070" class="elsevierStylePara elsevierViewall">Since the patient had no abnormal immunoglobulin chain production or inflammatory condition suggesting AL or AA amyloidosis&#44; we searched for the most common mutation in Portugal of a protein responsible for the production of amyloid&#44; and a mutation in the transthyretin gene &#40;TTR Val30Met&#41; was found&#44; leading to a diagnosis of familial amyloid polyneuropathy &#40;FAP&#41; with a Portuguese type 1 variant&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a></p><p id="par0075" class="elsevierStylePara elsevierViewall">The patient gradually improved and was discharged after a few days&#46; He is currently being assessed for possible heart and liver transplantation and genetic counseling has been offered to his only son&#46;</p><p id="par0080" class="elsevierStylePara elsevierViewall">To summarize&#44; when assessing a patient with increased ventricular wall thickness&#44; it is important to determine whether it is a restrictive cardiomyopathy as opposed to other types of disease&#44; such as hypertrophic cardiomyopathy or hypertensive heart disease&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> The echocardiogram is crucial&#44; raising the initial suspicion based on structural abnormalities and restrictive physiology&#46; Further study with cardiac magnetic resonance and endomyocardial biopsy can help to identify an infiltrative cardiomyopathy and usually establish the diagnosis&#46; Due to the systemic nature of these deposition diseases&#44; it is essential to investigate the involvement of other organs and to check the family history&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a></p><p id="par0085" class="elsevierStylePara elsevierViewall">Amyloidosis consists of a group of diseases characterized by changes in secondary protein structure&#44; in which insoluble extracellular fibril deposits form&#44; leading to organ dysfunction&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a></p><p id="par0090" class="elsevierStylePara elsevierViewall">FAP is usually diagnosed in the third decade of life&#46; Its predominant feature is sensorimotor neuropathy&#44;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> but patients commonly have autonomic dysfunction&#44; renal failure and cardiac involvement&#44; which is the major prognostic factor&#46;</p><p id="par0095" class="elsevierStylePara elsevierViewall">The most common mutations affect the transthyretin gene &#40;FAP-I or -II&#41;&#44; but apolipoprotein A1 &#40;FAP-III&#41; or gelsolin &#40;FAP-IV&#41; may also be involved&#46; Transthyretin is produced mainly in the liver&#44; with a small percentage in the choroid plexus and the retina&#46;</p><p id="par0100" class="elsevierStylePara elsevierViewall">Amyloidosis due to a TTR mutation is an autosomal dominant disease&#46; Many mutations have been described&#44; but the Val30Met mutation is the most frequent mutation in Portugal&#44; where it has more than 90&#37; penetrance&#46;</p><p id="par0105" class="elsevierStylePara elsevierViewall">The cornerstone of treatment has been liver transplantation&#44; particularly when there is already cardiac or renal impairment&#46; However&#44; a new drug &#40;tafamidis&#41; that promotes stabilization of the transthyretin protein has been approved in Europe and has shown promising results in halting progression of the disease at an early stage&#46;</p><p id="par0110" class="elsevierStylePara elsevierViewall">This case illustrates a highly atypical presentation of FAP&#44; with advanced heart disease and mild neurologic impairment&#44; relatively late onset and no family history&#46; In fact&#44; we believe this is the first case described so far of FAP caused by a TTR Val30Met mutation with predominantly cardiac involvement in this age-group&#46;</p><p id="par0115" class="elsevierStylePara elsevierViewall">This case is a reminder of the diagnostic limitations of endomyocardial biopsy and of the value of genetic testing in patients with cardiomyopathies&#44;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> which in this instance was crucial not only to establish a definite diagnosis&#44; but also to outline the prognosis&#44; treatment options and follow-up for the patient and his family&#46;</p><p id="par0120" class="elsevierStylePara elsevierViewall">It also highlights the importance of multimodality cardiac imaging in the diagnosis of cardiomyopathies&#46; In this case&#44; both the echocardiogram and CMR were fundamental in guiding our investigation&#46; A <span class="elsevierStyleSup">99m</span>Tc-3&#44;3-diphosphono-1&#44;2-propanodicarboxylic acid &#40;<span class="elsevierStyleSup">99m</span>Tc-DPD&#41; scintigraphy scan could also have helped to identify TTR amyloid deposition in the heart&#46;</p><p id="par0125" class="elsevierStylePara elsevierViewall">Finally&#44; this case highlights the importance of combining all the phenotypic manifestations and persevering in determining a diagnosis&#44; which is essential for deciding on the therapeutic approach and counseling&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Ethical disclosures</span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Protection of human and animal subjects</span><p id="par0130" class="elsevierStylePara elsevierViewall">The authors declare that no experiments were performed on humans or animals for this study&#46;</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Confidentiality of data</span><p id="par0135" class="elsevierStylePara elsevierViewall">The authors declare that they have followed the protocols of their work center on the publication of patient data&#46;</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Right to privacy and informed consent</span><p id="par0140" class="elsevierStylePara elsevierViewall">The authors have obtained the written informed consent of the patients or subjects mentioned in the article&#46; The corresponding author is in possession of this document&#46;</p></span></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Conflicts of interest</span><p id="par0150" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare&#46;</p></span></span>"
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          "clase" => "keyword"
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            1 => "Ventricular wall thickening"
            2 => "Infiltrative cardiomyopathy"
            3 => "Familial amyloid polyneuropathy"
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            0 => "Insufici&#234;ncia card&#237;aca"
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            2 => "Cardiomiopatia infiltrativa"
            3 => "Polineuropatia amiloid&#243;tica familiar"
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        "titulo" => "Abstract"
        "resumen" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">We describe the case of a 47-year-old man with new-onset heart failure who was found to have severe biventricular wall thickening&#46; We present comprehensive data from invasive and non-invasive multimodality imaging&#44; genetic and histologic tests&#44; and briefly describe their importance in the final diagnosis&#46;</p><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">To our knowledge&#44; this is the first case of the Portuguese variant of familial amyloid polyneuropathy presenting with heart failure in the fifth decade of life&#46;</p><p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">This is an unusual case report&#44; but also an illustration of how to approach any patient with suspected infiltrative cardiomyopathy&#46;</p>"
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        "resumen" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Descrevemos o caso de um doente do sexo masculino de 47 anos&#44; com insufici&#234;ncia card&#237;aca de novo&#44; que apresentava marcado aumento da espessura da parede de ambos os ventr&#237;culos&#46; Apresentamos dados dos exames de imagem&#44; estudo gen&#233;tico e an&#225;lise histol&#243;gica que nos guiaram no diagn&#243;stico&#44; explicando o nosso precurso pelos diagn&#243;sticos diferenciais e a interpreta&#231;&#227;o dos diferentes testes&#46;</p><p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">Tanto quanto sabemos&#44; &#233; o primeiro caso descrito de um doente com a variante portuguesa da polineuropatia amiloid&#243;tica familiar que se apresenta com insufici&#234;ncia card&#237;aca na quinta d&#233;cada de vida&#46;</p><p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">Este &#233; um caso cl&#237;nico invulgar&#44; mas tamb&#233;m um exemplo ilustrativo da abordagem de um doente com suspeita de cardiomiopatia infiltrativa&#46;</p>"
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          "en" => "<p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">12-lead electrocardiogram depicting poor R-wave progression in the precordial leads and a pseudo-infarct pattern in the inferior leads&#46;</p>"
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          "en" => "<p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">Transthoracic echocardiogram&#44; parasternal long-axis &#40;A&#41; and 4-chamber &#40;B&#41; views&#44; showing biventricular hypertrophy &#40;interventricular septum 21 mm&#59; posterior wall 19 mm&#41;&#44; increased thickness of the interatrial septum&#44; biatrial enlargement &#40;left atrial indexed volume 42 ml&#47;m<span class="elsevierStyleSup">2</span>&#41; and mild circumferential pericardial effusion&#46; Diastolic assessment shows a restrictive pattern&#58; transmitral flow &#40;C&#41; with E&#47;A ratio &#62;2 and deceleration time &#60;150 msec&#59; decreased tissue Doppler &#40;D and E&#41; E&#8242; velocities &#40;lateral E&#8242;&#58; 4&#46;6 cm&#47;s&#59; septal E&#8242;&#58; 2&#46;8 cm&#47;s&#41; and increased E&#47;E&#8242; &#40;mean E&#47;E&#8242; ratio&#58; 25&#41;&#46; Decreased myocardial velocities on pulse-wave Doppler &#40;lateral S&#8242;&#58; 3&#46;7 cm&#47;s&#44; septal S&#8242;&#58; 3&#46;3 cm&#47;s&#41; can also be observed &#40;D and E&#41;&#46;</p>"
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          "en" => "<p id="spar0055" class="elsevierStyleSimplePara elsevierViewall">Cardiac magnetic resonance&#44; 4-chamber view&#44; depicting the late phase after gadolinium injection&#44; with widespread subendocardial hyperenhancement of the left ventricle&#44; not matching any coronary artery territory&#44; but also involving the right ventricle&#44; both atria and the interatrial septum&#46;</p>"
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      "titulo" => "References"
      "seccion" => array:1 [
        0 => array:2 [
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            0 => array:3 [
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              "referencia" => array:1 [
                0 => array:2 [
                  "contribucion" => array:1 [
                    0 => array:2 [
                      "titulo" => "Diagnostic work-up in cardiomyopathies&#58; bridging the gap between clinical phenotypes and final diagnosis&#46; A position statement from the ESC Working Group on Myocardial and Pericardial Diseases"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => true
                          "autores" => array:3 [
                            0 => "C&#46; Rapezzi"
                            1 => "E&#46; Arbustini"
                            2 => "A&#46;L&#46; Caforio"
                          ]
                        ]
                      ]
                    ]
                  ]
                  "host" => array:1 [
                    0 => array:2 [
                      "doi" => "10.1093/eurheartj/ehs397"
                      "Revista" => array:6 [
                        "tituloSerie" => "Eur Heart J"
                        "fecha" => "2013"
                        "volumen" => "34"
                        "paginaInicial" => "1448"
                        "paginaFinal" => "1458"
                        "link" => array:1 [
                          0 => array:2 [
                            "url" => "https://www.ncbi.nlm.nih.gov/pubmed/23211230"
                            "web" => "Medline"
                          ]
                        ]
                      ]
                    ]
                  ]
                ]
              ]
            ]
            1 => array:3 [
              "identificador" => "bib0010"
              "etiqueta" => "2"
              "referencia" => array:1 [
                0 => array:2 [
                  "contribucion" => array:1 [
                    0 => array:2 [
                      "titulo" => "Left ventricular hypertrophy in Fabry disease&#58; a practical approach to diagnosis"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => true
                          "autores" => array:3 [
                            0 => "Z&#46; Yousef"
                            1 => "P&#46;M&#46; Elliott"
                            2 => "F&#46; Cecchi"
                          ]
                        ]
                      ]
                    ]
                  ]
                  "host" => array:1 [
                    0 => array:2 [
                      "doi" => "10.1093/eurheartj/ehs166"
                      "Revista" => array:6 [
                        "tituloSerie" => "Eur Heart J"
                        "fecha" => "2013"
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                            "url" => "https://www.ncbi.nlm.nih.gov/pubmed/22736678"
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                        ]
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                    ]
                  ]
                ]
              ]
            ]
            2 => array:3 [
              "identificador" => "bib0015"
              "etiqueta" => "3"
              "referencia" => array:1 [
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                  "contribucion" => array:1 [
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                      "titulo" => "Delayed enhancement cardiovascular magnetic resonance assessment of non-ischaemic cardiomyopathies"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => true
                          "autores" => array:3 [
                            0 => "H&#46; Mahrholdt"
                            1 => "A&#46; Wagner"
                            2 => "R&#46;M&#46; Judd"
                          ]
                        ]
                      ]
                    ]
                  ]
                  "host" => array:1 [
                    0 => array:2 [
                      "doi" => "10.1093/eurheartj/ehi258"
                      "Revista" => array:6 [
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              ]
            ]
            3 => array:3 [
              "identificador" => "bib0020"
              "etiqueta" => "4"
              "referencia" => array:1 [
                0 => array:2 [
                  "contribucion" => array:1 [
                    0 => array:2 [
                      "titulo" => "Amyloid fibril protein in familial amyloidotic polyneuropathy&#46; Portuguese type&#46; Definition of molecular abnormality in transthyretin &#40;prealbumin&#41;"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => true
                          "autores" => array:3 [
                            0 => "M&#46;J&#46; Saraiva"
                            1 => "S&#46; Birken"
                            2 => "P&#46;P&#46; Costa"
                          ]
                        ]
                      ]
                    ]
                  ]
                  "host" => array:1 [
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                ]
              ]
            ]
            4 => array:3 [
              "identificador" => "bib0025"
              "etiqueta" => "5"
              "referencia" => array:1 [
                0 => array:2 [
                  "contribucion" => array:1 [
                    0 => array:2 [
                      "titulo" => "Infiltrative cardiovascular diseases&#58; cardiomyopathies that look alike"
                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => false
                          "autores" => array:2 [
                            0 => "J&#46;B&#46; Seward"
                            1 => "G&#46; Casaclang-Verzosa"
                          ]
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                      ]
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                  ]
                  "host" => array:1 [
                    0 => array:2 [
                      "doi" => "10.1016/j.jacc.2009.12.040"
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                        "paginaInicial" => "1769"
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Case report
Facing the challenges of ventricular hypertrophy: The eyes don’t lie
Resolver os desafios da hipertrofia ventricular: os olhos não mentem?
Patrícia Rodriguesa,
Corresponding author
pfdrodrigues@gmail.com

Corresponding author.
, Mário Santosa, António Marinhob, Sofia Cabrala, Miguel Vieiraa, Hipólito Reisa, Paulo Palmaa, Severo Torresa
a Cardiology Department, Centro Hospitalar do Porto, Porto, Portugal
b Internal Medicine Department, Centro Hospitalar do Porto, Porto, Portugal
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          "en" => "<p id="spar0050" class="elsevierStyleSimplePara elsevierViewall">Cardiovascular magnetic resonance showing concentric left ventricular hypertrophy and increased right ventricular free wall thickness&#44; with decreased left ventricular volume&#46;</p>"
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    "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Case report</span><p id="par0005" class="elsevierStylePara elsevierViewall">Increased ventricular wall thickness can be a physiologic response to pressure overload or to exercise&#44; but it can also be pathologic&#44; resulting from myocyte hypertrophy or deposition of an abnormal substance&#46; Finding its exact cause can be challenging&#44; but is crucial in determining the appropriate management&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">We describe the case of a 47-year-old Caucasian man complaining of tiredness and dyspnea on moderate exertion lasting several months&#44; progressively worsening and associated with orthopnea&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">A history of erectile dysfunction&#44; night sweats and paresthesias in both hands and feet was also reported&#46; He had also experienced bilateral calf pain during the previous month&#44; with no specific relieving or aggravating factors&#44; and had noted blurred vision in the left eye for the previous six months&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">He denied chest pain&#44; fever&#44; muscular weakness or other symptoms&#46; His medical history was positive for type 2 diabetes and his family history was unremarkable&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">On physical examination&#44; bilateral rales and hypoesthesia of the hands and feet were noted&#46; The chest X-ray revealed an increased cardiothoracic index and arterial blood gas analysis showed mild hypoxemia&#46; Blood analysis revealed increased proBNP &#40;1781 pg&#47;ml&#41;&#44; without anemia or renal impairment&#46; The electrocardiogram showed normal sinus rhythm&#44; QS waves in the inferior leads&#44; poor R progression in the precordial leads and T-wave inversion in I and aVL &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Figure 1</a>&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0030" class="elsevierStylePara elsevierViewall">The transthoracic echocardiogram &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Figure 2</a>&#41; showed severe biventricular concentric thickening with normal ejection fraction&#46; Diastolic assessment indicated restrictive physiology&#59; mild pericardial effusion was also noted&#46;</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0035" class="elsevierStylePara elsevierViewall">At this point&#44; our findings suggested an infiltrative cardiomyopathy&#44; such as amyloidosis&#44; Fabry disease or glycogen storage disease&#46;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;2</span></a> The neuropathy and visual changes could fit with a systemic disease&#46; Interestingly&#44; the ECG did not show decreased voltages&#44; which is common in familial amyloidosis&#46;</p><p id="par0040" class="elsevierStylePara elsevierViewall">Hypertrophic cardiomyopathy was another hypothesis&#46; Against it was the ECG showing poor R-wave progression and echocardiographic findings suggestive of an infiltrative disease&#44; with symmetric biventricular wall thickening and pericardial effusion&#46; We excluded hypertensive heart disease&#44; since the patient did not have hypertension&#46; Blood analysis and thoracic computed tomography showed no changes suggestive of hemochromatosis or sarcoidosis&#46; Thyroid disease and HIV&#44; HCV or HBV infection were also excluded&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">Cardiac magnetic resonance &#40;CMR&#41; showed marked concentric left ventricular &#40;LV&#41; hypertrophy&#44; mild right ventricular &#40;RV&#41; hypertrophy and normal ejection fraction&#46; There was biatrial enlargement&#44; thickening of the interatrial septum and mild pericardial effusion &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Figure 3</a>&#41;&#46; Short-tau inversion-recovery &#40;STIR&#41; sequences showed no myocardial edema or inflammation&#46; In late gadolinium enhancement study&#44; there was difficulty in setting the optimal inversion time to correctly null the myocardium&#44; with a relatively dark blood pool and diffuse subendocardial enhancement of the interatrial septum and the LV and RV walls &#40;<a class="elsevierStyleCrossRef" href="#fig0020">Figure 4</a>&#41;&#46; The diffuse subendocardial late gadolinium enhancement&#44; coupled with abnormal myocardial and blood-pool contrast kinetics&#44; was most consistent with cardiac amyloidosis&#46; The fact that the optimal inversion time that would null the normal myocardium could not be found is an indirect sign suggesting amyloidosis&#44; because if abnormal fibrils are widespread in the intercellular space&#44; the gadolinium may not be taken up by healthy myocardium&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p><elsevierMultimedia ident="fig0015"></elsevierMultimedia><elsevierMultimedia ident="fig0020"></elsevierMultimedia><p id="par0050" class="elsevierStylePara elsevierViewall">Endomyocardial biopsies and biopsy of the salivary glands were then performed but were negative for amyloid&#46;</p><p id="par0055" class="elsevierStylePara elsevierViewall">Immunosubtraction testing for free immunoglobulin chains in serum and urine&#44; which could point to AL amyloidosis&#44; was also negative&#46;</p><p id="par0060" class="elsevierStylePara elsevierViewall">An electromyogram suggested the presence of a pressure-sensitive neuropathy of the lower limbs&#44; bilateral carpal tunnel syndrome and signs of parasympathetic dysfunction&#44; which would be compatible with amyloidosis&#46;</p><p id="par0065" class="elsevierStylePara elsevierViewall">Finally&#44; we returned to the patient&#39;s complaint of left visual impairment&#46; Vitreous opacities in the left eye were reported and&#44; after vitrectomy&#44; vitreous humor analysis confirmed the presence of amyloid&#46;</p><p id="par0070" class="elsevierStylePara elsevierViewall">Since the patient had no abnormal immunoglobulin chain production or inflammatory condition suggesting AL or AA amyloidosis&#44; we searched for the most common mutation in Portugal of a protein responsible for the production of amyloid&#44; and a mutation in the transthyretin gene &#40;TTR Val30Met&#41; was found&#44; leading to a diagnosis of familial amyloid polyneuropathy &#40;FAP&#41; with a Portuguese type 1 variant&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a></p><p id="par0075" class="elsevierStylePara elsevierViewall">The patient gradually improved and was discharged after a few days&#46; He is currently being assessed for possible heart and liver transplantation and genetic counseling has been offered to his only son&#46;</p><p id="par0080" class="elsevierStylePara elsevierViewall">To summarize&#44; when assessing a patient with increased ventricular wall thickness&#44; it is important to determine whether it is a restrictive cardiomyopathy as opposed to other types of disease&#44; such as hypertrophic cardiomyopathy or hypertensive heart disease&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> The echocardiogram is crucial&#44; raising the initial suspicion based on structural abnormalities and restrictive physiology&#46; Further study with cardiac magnetic resonance and endomyocardial biopsy can help to identify an infiltrative cardiomyopathy and usually establish the diagnosis&#46; Due to the systemic nature of these deposition diseases&#44; it is essential to investigate the involvement of other organs and to check the family history&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a></p><p id="par0085" class="elsevierStylePara elsevierViewall">Amyloidosis consists of a group of diseases characterized by changes in secondary protein structure&#44; in which insoluble extracellular fibril deposits form&#44; leading to organ dysfunction&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a></p><p id="par0090" class="elsevierStylePara elsevierViewall">FAP is usually diagnosed in the third decade of life&#46; Its predominant feature is sensorimotor neuropathy&#44;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> but patients commonly have autonomic dysfunction&#44; renal failure and cardiac involvement&#44; which is the major prognostic factor&#46;</p><p id="par0095" class="elsevierStylePara elsevierViewall">The most common mutations affect the transthyretin gene &#40;FAP-I or -II&#41;&#44; but apolipoprotein A1 &#40;FAP-III&#41; or gelsolin &#40;FAP-IV&#41; may also be involved&#46; Transthyretin is produced mainly in the liver&#44; with a small percentage in the choroid plexus and the retina&#46;</p><p id="par0100" class="elsevierStylePara elsevierViewall">Amyloidosis due to a TTR mutation is an autosomal dominant disease&#46; Many mutations have been described&#44; but the Val30Met mutation is the most frequent mutation in Portugal&#44; where it has more than 90&#37; penetrance&#46;</p><p id="par0105" class="elsevierStylePara elsevierViewall">The cornerstone of treatment has been liver transplantation&#44; particularly when there is already cardiac or renal impairment&#46; However&#44; a new drug &#40;tafamidis&#41; that promotes stabilization of the transthyretin protein has been approved in Europe and has shown promising results in halting progression of the disease at an early stage&#46;</p><p id="par0110" class="elsevierStylePara elsevierViewall">This case illustrates a highly atypical presentation of FAP&#44; with advanced heart disease and mild neurologic impairment&#44; relatively late onset and no family history&#46; In fact&#44; we believe this is the first case described so far of FAP caused by a TTR Val30Met mutation with predominantly cardiac involvement in this age-group&#46;</p><p id="par0115" class="elsevierStylePara elsevierViewall">This case is a reminder of the diagnostic limitations of endomyocardial biopsy and of the value of genetic testing in patients with cardiomyopathies&#44;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> which in this instance was crucial not only to establish a definite diagnosis&#44; but also to outline the prognosis&#44; treatment options and follow-up for the patient and his family&#46;</p><p id="par0120" class="elsevierStylePara elsevierViewall">It also highlights the importance of multimodality cardiac imaging in the diagnosis of cardiomyopathies&#46; In this case&#44; both the echocardiogram and CMR were fundamental in guiding our investigation&#46; A <span class="elsevierStyleSup">99m</span>Tc-3&#44;3-diphosphono-1&#44;2-propanodicarboxylic acid &#40;<span class="elsevierStyleSup">99m</span>Tc-DPD&#41; scintigraphy scan could also have helped to identify TTR amyloid deposition in the heart&#46;</p><p id="par0125" class="elsevierStylePara elsevierViewall">Finally&#44; this case highlights the importance of combining all the phenotypic manifestations and persevering in determining a diagnosis&#44; which is essential for deciding on the therapeutic approach and counseling&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Ethical disclosures</span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Protection of human and animal subjects</span><p id="par0130" class="elsevierStylePara elsevierViewall">The authors declare that no experiments were performed on humans or animals for this study&#46;</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Confidentiality of data</span><p id="par0135" class="elsevierStylePara elsevierViewall">The authors declare that they have followed the protocols of their work center on the publication of patient data&#46;</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Right to privacy and informed consent</span><p id="par0140" class="elsevierStylePara elsevierViewall">The authors have obtained the written informed consent of the patients or subjects mentioned in the article&#46; The corresponding author is in possession of this document&#46;</p></span></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Conflicts of interest</span><p id="par0150" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare&#46;</p></span></span>"
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        "resumen" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">We describe the case of a 47-year-old man with new-onset heart failure who was found to have severe biventricular wall thickening&#46; We present comprehensive data from invasive and non-invasive multimodality imaging&#44; genetic and histologic tests&#44; and briefly describe their importance in the final diagnosis&#46;</p><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">To our knowledge&#44; this is the first case of the Portuguese variant of familial amyloid polyneuropathy presenting with heart failure in the fifth decade of life&#46;</p><p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">This is an unusual case report&#44; but also an illustration of how to approach any patient with suspected infiltrative cardiomyopathy&#46;</p>"
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        "resumen" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Descrevemos o caso de um doente do sexo masculino de 47 anos&#44; com insufici&#234;ncia card&#237;aca de novo&#44; que apresentava marcado aumento da espessura da parede de ambos os ventr&#237;culos&#46; Apresentamos dados dos exames de imagem&#44; estudo gen&#233;tico e an&#225;lise histol&#243;gica que nos guiaram no diagn&#243;stico&#44; explicando o nosso precurso pelos diagn&#243;sticos diferenciais e a interpreta&#231;&#227;o dos diferentes testes&#46;</p><p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">Tanto quanto sabemos&#44; &#233; o primeiro caso descrito de um doente com a variante portuguesa da polineuropatia amiloid&#243;tica familiar que se apresenta com insufici&#234;ncia card&#237;aca na quinta d&#233;cada de vida&#46;</p><p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">Este &#233; um caso cl&#237;nico invulgar&#44; mas tamb&#233;m um exemplo ilustrativo da abordagem de um doente com suspeita de cardiomiopatia infiltrativa&#46;</p>"
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                      "titulo" => "Diagnostic work-up in cardiomyopathies&#58; bridging the gap between clinical phenotypes and final diagnosis&#46; A position statement from the ESC Working Group on Myocardial and Pericardial Diseases"
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ISSN: 21742049
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