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"referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 6 => array:3 [ "nombre" => "Joana" "apellidos" => "Trigo" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 7 => array:3 [ "nombre" => "Ana" "apellidos" => "Botelho" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 8 => array:3 [ "nombre" => "Maria" "apellidos" => "do Carmo Cachulo" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 9 => array:3 [ "nombre" => "Joana" "apellidos" => "Alves" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] 10 => array:3 [ "nombre" => "Luís" "apellidos" => "Francisco" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">c</span>" "identificador" => "aff0015" ] ] ] 11 => array:3 [ "nombre" => "António" "apellidos" => "Leitão Marques" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] ] "afiliaciones" => array:3 [ 0 => array:3 [ "entidad" => "Serviço de Cardiologia, CHUC – Hospital Geral, Coimbra, Portugal" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Serviço de Anatomia Patológica, CHUC – Hospital Geral, Coimbra, Portugal" "etiqueta" => "b" "identificador" => "aff0010" ] 2 => array:3 [ "entidad" => "Serviço de Hematologia, CHUC – Hospital Geral, Coimbra, Portugal" "etiqueta" => "c" "identificador" => "aff0015" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "pt" => array:1 [ "titulo" => "Amiloidose cardíaca – abordagem diagnóstica, a propósito de um caso clínico" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 792 "Ancho" => 1708 "Tamanyo" => 428411 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">ECG showing sinus rhythm, heart rate 67 bpm, first-degree atrioventricular block, low voltage in frontal leads and complete left bundle branch block.</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Case report</span><p id="par0005" class="elsevierStylePara elsevierViewall">A 78-year-old man, with no cardiovascular risk factors but a history of paroxysmal atrial fibrillation and chronic renal disease (National Kidney Foundation stage IV), was admitted to the cardiac care unit for acute heart failure (HF) of unknown cause, in New York Heart Association (NYHA) class IV. He reported exertional dyspnea and worsening peripheral edema over the previous two months. He now complained of dyspnea on minimal exertion, orthopnea and paroxysmal nocturnal dyspnea, peripheral edema and increased abdominal circumference, apparently decreased urine output, and upper limb paresthesia. Physical examination showed anasarca, blood pressure 114/81 mmHg, heart rate (HR) 67 bpm and 90% oxygen saturation in room air.</p><p id="par0010" class="elsevierStylePara elsevierViewall">Diagnostic exams revealed type 2 respiratory failure with acidosis (pH 7.24; PaO<span class="elsevierStyleInf">2</span> 58 mmHg, PaCO<span class="elsevierStyleInf">2</span> 55 mmHg, HCO<span class="elsevierStyleInf">3</span> 23.6 mmol/l, and lactates 2.66 mmol/l); normocytic anemia (hemoglobin 12.1 g/dl), with no increase in inflammatory markers; NT-pro-BNP 43<span class="elsevierStyleHsp" style=""></span>300 pg/ml; hyponatremia (Na+ 132.7 mmol/l); worsening of chronic renal disease (urea 24.8 mmol/l and creatinine 207.8 μmol/l); and evidence of hepatic congestion (alkaline phosphatase 183 U/l), with increased transaminases (glutamic oxaloacetic transaminase 161 U/l and glutamic pyruvic transaminase 297 U/l). The chest X-ray showed alveolar interstitial infiltrate with a butterfly pattern. The electrocardiogram (ECG) showed sinus rhythm, HR 67 bpm, first-degree atrioventricular block, low voltage in the frontal leads and complete left bundle branch block (<a class="elsevierStyleCrossRef" href="#fig0005">Figure 1</a>).</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0015" class="elsevierStylePara elsevierViewall">Transthoracic echocardiography revealed left ventricular (LV) size at the upper limit of normal (end-diastolic diameter 60 mm), with increased wall echogenicity, severe hypertrophy of the interventricular septum (20 mm) and moderate hypertrophy of the other walls (posterior wall 15 mm; LV mass index 200.1 g/m<span class="elsevierStyleSup">2</span>); severe biatrial dilatation (left atrial area 37 cm<span class="elsevierStyleSup">2</span>/m<span class="elsevierStyleSup">2</span>) (<a class="elsevierStyleCrossRef" href="#fig0010">Figure 2</a>A and B); severely impaired LV systolic function (ejection fraction 27% by Simpson's method, with global longitudinal strain of −3%); hypocontractile right ventricle (tricuspid annular plane systolic excursion 12 mm); LV filling pattern suggestive of restrictive cardiomyopathy (deceleration time 145 ms, septal E′ 3 cm/s, lateral E′ 4 cm/s, and mean E/E′ ratio 29.5); right ventricular/right atrial gradient 43 mmHg; dilated inferior vena cava (2.3 cm) without inspiratory collapse; a small circumferential pericardial effusion; and interatrial septal hypertrophy.</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">Cardiac magnetic resonance imaging (CMRI) was not performed since the patient had a hip prosthesis.</p><p id="par0025" class="elsevierStylePara elsevierViewall">Anticongestive therapy and a positive inotropic agent (levosimendan) were begun, together with noninvasive ventilation, resulting in progressive clinical improvement.</p><p id="par0030" class="elsevierStylePara elsevierViewall">Given the findings of severe LV hypertrophy and low voltage on the ECG, a diagnosis of amyloidosis was considered. Abdominal fat pad biopsy confirmed the presence of amyloid deposits, exhibiting green birefringence after staining with Congo red.</p><p id="par0035" class="elsevierStylePara elsevierViewall">Laboratory tests showed increased beta-2 microglobulin (4.98 mg/l), erythrocyte sedimentation rate 32 mm/h, C-reactive protein 5.0 mg/dl, calcium 2.07 mmol/l, phosphorus 1.05 mmol/l, parathyroid hormone 171 pg/ml, negative tumor markers and normal autoimmune parameters. Serum protein immunofixation revealed an IgG monoclonal spike (11.8 g/dl), with no changes in urine protein immunofixation. The ratio between kappa and lambda light chains was 1.22 (7.29:5.98 g/dl). After discussion with the hematology department, myelography and bone marrow biopsy were performed, which showed no plasma cell proliferation. No mutations were identified in genes coding for transthyretin proteins.</p><p id="par0040" class="elsevierStylePara elsevierViewall">Based on the above findings, a diagnosis of systemic amyloidosis with cardiac involvement was made. The type of fibril involved was not determined, and <span class="elsevierStyleSup">99m</span>Tc-DPD scintigraphy was not performed to establish the type of amyloidosis.</p><p id="par0045" class="elsevierStylePara elsevierViewall">The patient was readmitted four months later for decompensated HF in NYHA class IV, followed by progressive worsening of his general state, culminating in death due to pulseless electrical activity.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Discussion</span><p id="par0050" class="elsevierStylePara elsevierViewall">Amyloidosis is a systemic disease first described by Rudolph Virchow in 1854.<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">1</span></a> It is caused by extracellular deposition of insoluble fibrils of low molecular weight proteins<a class="elsevierStyleCrossRefs" href="#bib0165"><span class="elsevierStyleSup">2,3</span></a> that form beta sheets.<a class="elsevierStyleCrossRef" href="#bib0175"><span class="elsevierStyleSup">4</span></a> Over 30 different proteins are known to be involved in the disease,<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">5</span></a> of which the most common forms are light-chain amyloidosis (AL), amyloid A amyloidosis (AA) and transthyretin-related amyloidosis (ATTR).<a class="elsevierStyleCrossRefs" href="#bib0185"><span class="elsevierStyleSup">6,7</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">Despite the heterogeneity in their structure and function, these proteins are deposited in the form of amyloid in various organs, locally or systemically, and can cause multiple organ dysfunction (<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>).</p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><p id="par0060" class="elsevierStylePara elsevierViewall">Cardiac amyloidosis is the result of amyloid deposits in the heart,<a class="elsevierStyleCrossRef" href="#bib0195"><span class="elsevierStyleSup">8</span></a> the most common presentation in the West being restrictive cardiomyopathy, while in around 5% of cases, it may mimic hypertrophic cardiomyopathy.<a class="elsevierStyleCrossRef" href="#bib0200"><span class="elsevierStyleSup">9</span></a></p><p id="par0065" class="elsevierStylePara elsevierViewall">Cardiac involvement is found in around 50% of patients with AL amyloidosis,<a class="elsevierStyleCrossRef" href="#bib0205"><span class="elsevierStyleSup">10</span></a> in isolation in 5% of these,<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">11</span></a> but is rare in AA amyloidosis. ATTR amyloidosis also frequently affects the heart, although the endemic mutation in Portugal is more typically associated with neurological manifestations (familial amyloid polyneuropathy). Senile systemic amyloidosis (SSA), found predominantly in men over 70, mainly affects the heart.<a class="elsevierStyleCrossRef" href="#bib0190"><span class="elsevierStyleSup">7</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">Clinical presentation varies depending on the organs involved and the degree of associated dysfunction.<a class="elsevierStyleCrossRef" href="#bib0170"><span class="elsevierStyleSup">3</span></a> It is usually diagnosed late since symptoms are nonspecific and are often disregarded or confused with other conditions. Renal and heart failure of unknown cause are common forms of presentation, as in our patient. HF is found in around 60% of patients and is caused by deposition of amyloid fibrils between myocytes, resulting in diastolic dysfunction and hence exertional dyspnea.<a class="elsevierStyleCrossRef" href="#bib0215"><span class="elsevierStyleSup">12</span></a> LV systolic dysfunction, peripheral edema (81%) and ascites secondary to right ventricular dysfunction are common in later stages of the disease. The most common arrhythmia is atrial fibrillation (10–15%), and chest discomfort is found in 25% of cases.<a class="elsevierStyleCrossRef" href="#bib0205"><span class="elsevierStyleSup">10</span></a> Episodes of syncope indicate a poor prognosis, frequently culminating in sudden death.<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">11</span></a></p><p id="par0075" class="elsevierStylePara elsevierViewall">Unlike hypertrophic cardiomyopathy, amyloidosis is typically associated with low voltage on the ECG<a class="elsevierStyleCrossRef" href="#bib0220"><span class="elsevierStyleSup">13</span></a> despite the presence of ventricular hypertrophy, as in the case presented. Low voltage is caused by the loss of viable myocardium due to amyloid deposits, which are electrically inert.<a class="elsevierStyleCrossRefs" href="#bib0210"><span class="elsevierStyleSup">11,14,15</span></a></p><p id="par0080" class="elsevierStylePara elsevierViewall">Echocardiography shows diastolic dysfunction, with a restrictive pattern in 21–88% of patients.<a class="elsevierStyleCrossRef" href="#bib0235"><span class="elsevierStyleSup">16</span></a> Speckle-tracking imaging can detect reduced LV longitudinal strain at an early stage of the disease in which ejection fraction is still preserved.<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">11</span></a> In the case presented, there was biventricular systolic dysfunction as well as diastolic dysfunction, indicating an advanced stage of the disease (<a class="elsevierStyleCrossRef" href="#fig0015">Figure 3</a>).</p><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0085" class="elsevierStylePara elsevierViewall">CMRI is useful for diagnosis, since it can noninvasively detect cardiac involvement in amyloidosis, with a sensitivity of 80% and specificity of 94%, by the presence of late enhancement, most commonly subendocardial and around the entire ventricular circumference.<a class="elsevierStyleCrossRef" href="#bib0240"><span class="elsevierStyleSup">17</span></a></p><p id="par0090" class="elsevierStylePara elsevierViewall">Biopsy of the organ involved is necessary to establish a definitive diagnosis, but abdominal fat pad biopsy is the method of choice since it is less invasive. When the sample is stained with Congo red, green birefringence is observed under polarized light (sensitivity 57–85% and specificity 92–100%). An alternative is staining with sulfated Alcian blue, which has higher specificity.<a class="elsevierStyleCrossRef" href="#bib0225"><span class="elsevierStyleSup">14</span></a> In the case of localized cardiac amyloidosis, endomyocardial biopsy may be necessary, which is invasive, costly and not always available, but has virtually 100% sensitivity.<a class="elsevierStyleCrossRef" href="#bib0245"><span class="elsevierStyleSup">18</span></a></p><p id="par0095" class="elsevierStylePara elsevierViewall">The specific amyloid protein involved must be established in order to determine the appropriate treatment. In patients with cardiac amyloidosis, the most likely differential diagnosis is between AL, ATTR and SSA. Clinical differences can help in arriving at a definitive diagnosis: renal involvement is more frequent in AL, while neuropathy precedes cardiac symptoms in ATTR. Our patient had renal and heart failure as well as a history of neuropathy, and laboratory tests showed an IgG monoclonal spike, all of which pointed to AL. The myelogram and bone marrow biopsy did not reveal monoclonal plasma cells, which is the case in 10–15% of patients.<a class="elsevierStyleCrossRef" href="#bib0190"><span class="elsevierStyleSup">7</span></a> However, it should be borne in mind that 5–10% of individuals aged over 70 have monoclonal gammopathy of undetermined significance, with a normal kappa/lambda ratio.<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">11</span></a></p><p id="par0100" class="elsevierStylePara elsevierViewall">The type of amyloid protein involved can be determined by immunohistochemical study of biopsied tissue (using anti-kappa, anti-lambda, anti-amyloid A and anti-transthyretin serums) or by mass spectrophotometry.</p><p id="par0105" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleSup">99m</span>Tc-DPD scintigraphy can detect transthyretin deposits in the heart.<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">11</span></a> The technique is extremely useful in distinguishing between AL and ATTR, since in the latter there is selective <span class="elsevierStyleSup">99m</span>Tc uptake in the heart, which is not found in AL.<a class="elsevierStyleCrossRef" href="#bib0225"><span class="elsevierStyleSup">14</span></a> If scintigraphy detects transthyretin deposition, genetic study can be performed to distinguish ATTR (mutant transthyretin) from SSA (wild-type transthyretin) (<a class="elsevierStyleCrossRef" href="#fig0020">Figure 4</a>).</p><elsevierMultimedia ident="fig0020"></elsevierMultimedia><p id="par0110" class="elsevierStylePara elsevierViewall">Amyloid P scintigraphy is a noninvasive exam that provides information on the distribution and systemic extent of amyloid deposits and can also be used to assess treatment response. It cannot however detect the presence of cardiac amyloidosis due to the motion of the heart.<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">11</span></a></p><p id="par0115" class="elsevierStylePara elsevierViewall">Positron emission tomography, used in the evaluation of cerebral amyloidosis, is not a generally accepted method for detection of cardiac amyloidosis; however, studies have shown that it may be useful in assessing treatment response.<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">19</span></a></p><p id="par0120" class="elsevierStylePara elsevierViewall">Management should be coordinated by a multidisciplinary team and is mainly aimed at treatment of the underlying disease and symptom relief.</p><p id="par0125" class="elsevierStylePara elsevierViewall">HF therapy is based on diuretics, which should be administered cautiously to prevent too steep a decrease in preload, since this can lead to a marked reduction in ventricular filling pressures and severe hypotension in patients with restrictive cardiomyopathy. Vasodilators and beta-blockers are poorly tolerated due to their hypotensive effect.<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">20</span></a> Digoxin should be used with caution since it binds to amyloid fibrils, resulting in an increased risk of toxicity.<a class="elsevierStyleCrossRef" href="#bib0260"><span class="elsevierStyleSup">21</span></a></p><p id="par0130" class="elsevierStylePara elsevierViewall">The formation of atrial thrombi is common in patients with atrial fibrillation. The decision to prescribe anticoagulants should be made on an individual basis since the high risk of thromboembolism must be weighed against the increased bleeding risk due to plasma cell dyscrasia and/or renal failure.<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">22</span></a></p><p id="par0135" class="elsevierStylePara elsevierViewall">There is a high incidence of conduction disturbances in patients with cardiac amyloidosis, and dual-chamber pacemakers should be implanted when indicated.<a class="elsevierStyleCrossRefs" href="#bib0180"><span class="elsevierStyleSup">5,11</span></a></p><p id="par0140" class="elsevierStylePara elsevierViewall">Heart transplantation is a controversial option due to the shortage of donors, the risk of amyloid deposition in the transplanted organ and the fact that in systemic amyloidosis the already poor prognosis is further worsened by extracardiac involvement.<a class="elsevierStyleCrossRef" href="#bib0270"><span class="elsevierStyleSup">23</span></a> Mean survival at five years is reported as 20–30%, significantly lower than in patients transplanted for other reasons. Survival can be slightly improved (to 36%) by subsequent chemotherapy.<a class="elsevierStyleCrossRef" href="#bib0225"><span class="elsevierStyleSup">14</span></a> Young patients with limited systemic involvement may undergo heart transplantation followed by stem cell transplantation.<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">11</span></a></p><p id="par0145" class="elsevierStylePara elsevierViewall">For patients with AL, the standard treatment is chemotherapy and/or autologous stem cell transplantation, depending on the disease stage and comorbidities.<a class="elsevierStyleCrossRef" href="#bib0275"><span class="elsevierStyleSup">24</span></a></p><p id="par0150" class="elsevierStylePara elsevierViewall">In SSA, treatment is directed at symptom relief only, while individuals under 65 may be candidates for heart transplantation.</p><p id="par0155" class="elsevierStylePara elsevierViewall">Liver transplantation is the main treatment option for ATTR, since the altered protein is mainly produced by the liver.<a class="elsevierStyleCrossRef" href="#bib0280"><span class="elsevierStyleSup">25</span></a> However, recurrence of extracardiac disease is often accompanied by progressive heart disease. It has been suggested that this is due to the fact that existing deposits of the mutant protein in the heart increase deposition of the normal protein through tropism. Heart and liver transplantation is recommended in patients with severe cardiac compromise. Tafamidis is available in Europe for stabilization of mutant transthyretin.</p><p id="par0160" class="elsevierStylePara elsevierViewall">The leading causes of cardiac death are HF and sudden death due to asystole or pulseless electrical activity, against which implantable cardioverter-defibrillators are rarely effective.<a class="elsevierStyleCrossRef" href="#bib0285"><span class="elsevierStyleSup">26</span></a></p><p id="par0165" class="elsevierStylePara elsevierViewall">Mean survival in patients with untreated AL amyloidosis without cardiac involvement is 10–14 months; only 5% survive longer than 10 years, the extent of cardiac involvement being the main determinant of prognosis.<a class="elsevierStyleCrossRefs" href="#bib0290"><span class="elsevierStyleSup">27,28</span></a> The cause of death in around 50% of patients with AL amyloidosis is cardiac, due to arrhythmias or HF, with median survival of only six months from the onset of HF symptoms.<a class="elsevierStyleCrossRefs" href="#bib0210"><span class="elsevierStyleSup">11,27</span></a> An Italian study by Rapezzi et al. confirmed the expected differences in mortality and morbidity between AL, ATTR and SSA, patients with AL presenting a rather aggressive clinical course.<a class="elsevierStyleCrossRefs" href="#bib0295"><span class="elsevierStyleSup">28,29</span></a> The prognosis is more favorable in ATTR and SSA, irrespective of the extent of cardiac involvement.<a class="elsevierStyleCrossRefs" href="#bib0305"><span class="elsevierStyleSup">30,31</span></a></p><p id="par0170" class="elsevierStylePara elsevierViewall">In the case of our patient, the diagnosis was made at an advanced stage of the disease. If the proteins involved have not been identified, chemotherapy is not recommended.</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Conclusions</span><p id="par0175" class="elsevierStylePara elsevierViewall">Cardiac amyloidosis is rare, and diagnosis requires a high level of suspicion based on the clinical setting and the findings of noninvasive diagnostic exams, particularly transthoracic echocardiography and CMRI. A definitive diagnosis can only be made following histological study. Treatment is directed at the underlying disease and symptom relief. Prognosis is poor in AL amyloidosis with cardiac involvement.</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Ethical disclosures</span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Protection of human and animal subjects</span><p id="par0180" class="elsevierStylePara elsevierViewall">The authors declare that the procedures followed were in accordance with the regulations of the relevant clinical research ethics committee and with those of the Code of Ethics of the World Medical Association (Declaration of Helsinki).</p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Confidentiality of data</span><p id="par0185" class="elsevierStylePara elsevierViewall">The authors declare that no patient data appear in this article.</p></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Right to privacy and informed consent</span><p id="par0190" class="elsevierStylePara elsevierViewall">The authors declare that no patient data appear in this article.</p></span></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Conflicts of interest</span><p id="par0195" class="elsevierStylePara elsevierViewall">The authors have no conflicts of interest to declare.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:10 [ 0 => array:3 [ "identificador" => "xres827479" "titulo" => "Abstract" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0005" ] ] ] 1 => array:2 [ "identificador" => "xpalclavsec823744" "titulo" => "Keywords" ] 2 => array:3 [ "identificador" => "xres827480" "titulo" => "Resumo" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0010" ] ] ] 3 => array:2 [ "identificador" => "xpalclavsec823743" "titulo" => "Palavras-chave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Case report" ] 5 => array:2 [ "identificador" => "sec0010" "titulo" => "Discussion" ] 6 => array:2 [ "identificador" => "sec0015" "titulo" => "Conclusions" ] 7 => array:3 [ "identificador" => "sec0020" "titulo" => "Ethical disclosures" "secciones" => array:3 [ 0 => array:2 [ "identificador" => "sec0025" "titulo" => "Protection of human and animal subjects" ] 1 => array:2 [ "identificador" => "sec0030" "titulo" => "Confidentiality of data" ] 2 => array:2 [ "identificador" => "sec0035" "titulo" => "Right to privacy and informed consent" ] ] ] 8 => array:2 [ "identificador" => "sec0040" "titulo" => "Conflicts of interest" ] 9 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2013-05-01" "fechaAceptado" => "2016-01-22" "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec823744" "palabras" => array:4 [ 0 => "Amyloidosis" 1 => "Hypertrophic cardiomyopathy" 2 => "Restrictive cardiomyopathy" 3 => "Heart failure" ] ] ] "pt" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palavras-chave" "identificador" => "xpalclavsec823743" "palabras" => array:4 [ 0 => "Amiloidose" 1 => "Miocardiopatia hipertrófica" 2 => "Miocardiopatia restritiva" 3 => "Insuficiência cardíaca" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">The authors present a case of systemic amyloidosis with cardiac involvement. We discuss the need for a high level of suspicion to establish a diagnosis, diagnostic techniques and treatment options. Our patient was a 78-year-old man with chronic renal disease and atrial fibrillation admitted with acute decompensated heart failure of unknown cause. The transthoracic echocardiogram revealed severely impaired left ventricular function with phenotypic overlap between hypertrophic and restrictive cardiomyopathy. After an extensive diagnostic workup, which included an abdominal fat pad biopsy, the final diagnosis was amyloidosis.</p></span>" ] "pt" => array:2 [ "titulo" => "Resumo" "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Os autores apresentam um caso de amiloidose sistémica com envolvimento cardíaco e discutem a importância de um elevado índice de suspeição para o diagnóstico, os meios de diagnóstico e as opções terapêuticas à luz do conhecimento atual. Homem de 78 anos, com antecedentes de doença renal crónica e fibrilhação auricular, admitido por insuficiência cardíaca aguda de etiologia desconhecida. O ecocardiograma transtorácico mostrou ventrículo esquerdo não dilatado, com compromisso severo da função sistólica global com <span class="elsevierStyleItalic">overlap</span> fenotípico de miocardiopatia hipertrófica e restritiva. Após estudo complementar alargado, o diagnóstico definitivo de amiloidose foi obtido por biópsia da gordura abdominal.</p></span>" ] ] "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Fernandes A, Caetano F, Almeida I, Paiva L, Gomes P, Mota P, et al. Amiloidose cardíaca – abordagem diagnóstica, a propósito de um caso clínico. Rev Port Cardiol. 2016;35:305.e1–305.e7.</p>" ] ] "multimedia" => array:5 [ 0 => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 792 "Ancho" => 1708 "Tamanyo" => 428411 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">ECG showing sinus rhythm, heart rate 67 bpm, first-degree atrioventricular block, low voltage in frontal leads and complete left bundle branch block.</p>" ] ] 1 => array:7 [ "identificador" => "fig0010" "etiqueta" => "Figure 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 609 "Ancho" => 1507 "Tamanyo" => 99904 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Transthoracic echocardiogram showing non-dilated left ventricle with severe hypertrophy of the septum and moderate hypertrophy of the other walls, non-dilated right ventricle, and severe biatrial dilatation (A); small circumferential pericardial effusion (B).</p>" ] ] 2 => array:7 [ "identificador" => "fig0015" "etiqueta" => "Figure 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr3.jpeg" "Alto" => 1052 "Ancho" => 1405 "Tamanyo" => 135460 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">Global longitudinal strain of −3%.</p>" ] ] 3 => array:7 [ "identificador" => "fig0020" "etiqueta" => "Figure 4" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr4.jpeg" "Alto" => 1174 "Ancho" => 1610 "Tamanyo" => 209854 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">Diagnostic algorithm of cardiac amyloidosis.</p> <p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">AAB: autoantibodies; ANA: antinuclear antibodies; BM: bone marrow; ECG: electrocardiogram; MRI: magnetic resonance imaging; PEP: protein electrophoresis; RF: rheumatoid factor; TM: tumor markers; TTE: transthoracic echocardiogram; TTR: transthyretin.</p>" ] ] 4 => array:8 [ "identificador" => "tbl0005" "etiqueta" => "Table 1" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at1" "detalle" => "Table " "rol" => "short" ] ] "tabla" => array:2 [ "leyenda" => "<p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">AA: amyloid A amyloidosis; AL: light-chain amyloidosis; ATTR: transthyretin-related amyloidosis; CNS: central nervous system; GIT: gastrointestinal tract; M/F: male/female; PNS: peripheral nervous system; SSA: senile systemic amyloidosis.</p>" "tablatextoimagen" => array:1 [ 0 => array:2 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Type \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Precursor protein \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Main organs affected \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Diagnosis \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Treatment \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">Specific characteristics \t\t\t\t\t\t\n \t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">AL, primary \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">Light-chain amyloid \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">Kidney<br>Heart<br>CNS<br>GIT<br>Liver<br>Skin \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">Serum and urine protein immunofixation<br>Myelogram (5–10% plasma cells)<br>Abdominal fat pad biopsy<br>Bone marrow biopsy \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">Chemotherapy<br>Stem cell transplantation \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">M/F ratio 3:2<br>10–15% associated with multiple myeloma \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">AA, secondary \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">Amyloid A \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">Kidney \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="" valign="top"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">Treat underlying disease \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="" valign="top"> \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">ATTR, hereditary (autosomal dominant) \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">Transthyretin, mutant \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">Heart<br>Liver<br>CNS and PNS \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top"><span class="elsevierStyleSup">99m</span>Tc-DPD scintigraphy<br>Genetic study of transthyretin \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">Liver transplant<br>Tafamidis \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="" valign="top"> \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">SSA \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">Transthyretin, wild-type \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">Heart<br>Carpel tunnel syndrome<br>Heart \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top"><span class="elsevierStyleSup">99m</span>Tc-DPD scintigraphy<br>Genetic study of transthyretin<br>Linear endocardial deposits \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="" valign="top"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">M/F ratio 20:1 \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="table-entry ; entry_with_role_rowhead " align="left" valign="top">Isolated atrial amyloidosis \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">Atrial natriuretic peptide \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="" valign="top"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="" valign="top"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="" valign="top"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">Increased incidence with age and in women \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab1392130.png" ] ] ] ] "descripcion" => array:1 [ "en" => "<p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">Characteristics of different types of amyloidosis.</p>" ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:31 [ 0 => array:3 [ "identificador" => "bib0160" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Por detrás da síndroma da insuficiência cardíaca: o diagnósticos de amiloidose AL. 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Year/Month | Html | Total | |
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2024 November | 18 | 8 | 26 |
2024 October | 89 | 52 | 141 |
2024 September | 113 | 38 | 151 |
2024 August | 114 | 38 | 152 |
2024 July | 112 | 39 | 151 |
2024 June | 87 | 33 | 120 |
2024 May | 100 | 50 | 150 |
2024 April | 80 | 31 | 111 |
2024 March | 84 | 25 | 109 |
2024 February | 99 | 44 | 143 |
2024 January | 70 | 31 | 101 |
2023 December | 80 | 41 | 121 |
2023 November | 101 | 44 | 145 |
2023 October | 94 | 33 | 127 |
2023 September | 69 | 25 | 94 |
2023 August | 63 | 27 | 90 |
2023 July | 70 | 21 | 91 |
2023 June | 94 | 30 | 124 |
2023 May | 97 | 38 | 135 |
2023 April | 92 | 15 | 107 |
2023 March | 103 | 29 | 132 |
2023 February | 100 | 40 | 140 |
2023 January | 108 | 31 | 139 |
2022 December | 102 | 29 | 131 |
2022 November | 99 | 29 | 128 |
2022 October | 117 | 33 | 150 |
2022 September | 85 | 43 | 128 |
2022 August | 92 | 61 | 153 |
2022 July | 137 | 54 | 191 |
2022 June | 99 | 47 | 146 |
2022 May | 87 | 54 | 141 |
2022 April | 126 | 57 | 183 |
2022 March | 130 | 49 | 179 |
2022 February | 122 | 43 | 165 |
2022 January | 130 | 39 | 169 |
2021 December | 81 | 45 | 126 |
2021 November | 181 | 63 | 244 |
2021 October | 194 | 71 | 265 |
2021 September | 142 | 41 | 183 |
2021 August | 159 | 46 | 205 |
2021 July | 113 | 42 | 155 |
2021 June | 138 | 45 | 183 |
2021 May | 150 | 63 | 213 |
2021 April | 401 | 117 | 518 |
2021 March | 232 | 63 | 295 |
2021 February | 181 | 31 | 212 |
2021 January | 171 | 35 | 206 |
2020 December | 154 | 34 | 188 |
2020 November | 130 | 29 | 159 |
2020 October | 182 | 14 | 196 |
2020 September | 134 | 31 | 165 |
2020 August | 100 | 26 | 126 |
2020 July | 124 | 10 | 134 |
2020 June | 136 | 19 | 155 |
2020 May | 153 | 18 | 171 |
2020 April | 135 | 18 | 153 |
2020 March | 133 | 33 | 166 |
2020 February | 256 | 43 | 299 |
2020 January | 141 | 20 | 161 |
2019 December | 149 | 23 | 172 |
2019 November | 116 | 25 | 141 |
2019 October | 159 | 11 | 170 |
2019 September | 218 | 30 | 248 |
2019 August | 135 | 14 | 149 |
2019 July | 165 | 14 | 179 |
2019 June | 108 | 31 | 139 |
2019 May | 121 | 17 | 138 |
2019 April | 136 | 40 | 176 |
2019 March | 212 | 32 | 244 |
2019 February | 160 | 36 | 196 |
2019 January | 149 | 26 | 175 |
2018 December | 155 | 17 | 172 |
2018 November | 270 | 25 | 295 |
2018 October | 586 | 40 | 626 |
2018 September | 186 | 17 | 203 |
2018 August | 230 | 26 | 256 |
2018 July | 66 | 11 | 77 |
2018 June | 80 | 9 | 89 |
2018 May | 112 | 13 | 125 |
2018 April | 99 | 16 | 115 |
2018 March | 143 | 14 | 157 |
2018 February | 67 | 6 | 73 |
2018 January | 128 | 22 | 150 |
2017 December | 223 | 15 | 238 |
2017 November | 86 | 13 | 99 |
2017 October | 40 | 10 | 50 |
2017 September | 47 | 15 | 62 |
2017 August | 32 | 13 | 45 |
2017 July | 38 | 8 | 46 |
2017 June | 53 | 13 | 66 |
2017 May | 70 | 9 | 79 |
2017 April | 48 | 4 | 52 |
2017 March | 83 | 54 | 137 |
2017 February | 180 | 4 | 184 |
2017 January | 56 | 10 | 66 |
2016 December | 68 | 17 | 85 |
2016 November | 93 | 17 | 110 |
2016 October | 132 | 20 | 152 |
2016 September | 190 | 14 | 204 |
2016 August | 30 | 3 | 33 |
2016 July | 32 | 17 | 49 |
2016 June | 19 | 42 | 61 |
2016 May | 7 | 84 | 91 |