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"documento" => "article" "crossmark" => 1 "subdocumento" => "rev" "cita" => "Med Clin. 2021;156:609-14" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:1 [ "total" => 0 ] "en" => array:12 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Review</span>" "titulo" => "Microvascular thrombosis and clinical implications" "tienePdf" => "en" "tieneTextoCompleto" => "en" "tieneResumen" => array:2 [ 0 => "en" 1 => "es" ] "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "609" "paginaFinal" => "614" ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Trombosis microvascular y sus implicaciones clínicas" ] ] "contieneResumen" => array:2 [ "en" => true "es" => true ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "José A. 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Heart disease can occur in patients with an established rheumatic disease diagnosis, or it can be the initial manifestation in patients without a prior diagnosis. The spectrum of cardiovascular manifestations associated with rheumatic diseases is quite extensive, as rheumatological disorders can directly affect the myocardium, endocardium, heart valves, pericardium, conduction system and blood vessels<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> (<a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>). Cardiovascular manifestations may be mild and clinically silent, but they can also increase morbidity and mortality substantially, so early diagnosis and treatment is especially important. This document offers an updated review of the main cardiac manifestations of the most common rheumatic diseases.</p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Rheumatoid arthritis</span><p id="par0010" class="elsevierStylePara elsevierViewall">RA is a systemic, chronic, and universally distributed inflammatory disease whose prevalence in Spain is estimated to be around 0.9% (95% confidence interval [CI]: 0.7–1.3) of the population.<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> Although it can occur at any age, there is a peak incidence between the fourth and fifth decades of life, with women being 2.5 times more likely to suffer from it than men. In recent years, an increasing body of evidence suggests that RA patients have higher mortality compared to subjects of the same age and sex in the general population, and this excess mortality is mainly due to cardiovascular disease, responsible for about half of the premature deaths observed.<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> Detecting subclinical cardiac involvement is essential to ensure adequate long-term treatment, since early detection of mild cardiac lesions and the use of therapies at a preclinical stage can limit long-term morbidity and mortality.</p><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Pericardial disease</span><p id="par0015" class="elsevierStylePara elsevierViewall">Pericarditis is one of the most common cardiac manifestations of RA. Although clinically symptomatic pericarditis occurs in less than 5% of patients, evidence of pericardial involvement is observed in between 20% and 50% of cases through echocardiography and in autopsy series.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">Pericarditis is often seen in men, those with positive rheumatoid factor, and those with severe or active disease. The pericardial fluid has a variable white blood cell count (usually greater than 30,000/mm<span class="elsevierStyleSup">3</span> and a prevalence of neutrophils), high proteins, low complement, low glucose, high cholesterol, presence of rheumatoid factor and immune complexes, with the absence of pathogens. Hemodynamic compromise caused by pericardial disease is rare, observed in approximately 0.5% of patients.<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> Pericarditis is not always parallel to joint inflammation. Uncommonly, patients may have pericarditis in the setting of positivity for rheumatoid factor and/or anti-cyclic citrullinated peptide antibodies, in the absence of significant joint symptoms.<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">Treatment includes the use of non-steroidal anti-inflammatory drugs, colchicine, glucocorticoids, and disease-modifying antirheumatic drugs. There is evidence to suggest that biological therapy reduces the occurrence of extra-articular manifestations in RA.<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> Patients with hemodynamic compromise or recurrence of a pericardial effusion may require a pericardiocentesis or pericardial window.</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Valve involvement</span><p id="par0030" class="elsevierStylePara elsevierViewall">Although valvular disease has not been considered a significant cardiac manifestation in RA, echocardiographic studies have shown a higher-than-expected incidence of asymptomatic valvular involvement, around 24–39%.<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> Mitral valve involvement is the most common. Histologically, the valves may show fibrosis or nodules.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> In a study that used transoesophageal echocardiography, mitral regurgitation was detected in 80% of patients with RA compared to 37% in the control group; no differences were observed in the prevalence of aortic or tricuspid regurgitation between the two groups.<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a></p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Myocardial involvement</span><p id="par0035" class="elsevierStylePara elsevierViewall">Patients with RA are at increased risk of myocardial dysfunction and congestive heart failure.<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> The aetiology of heart failure is unknown, but both systolic and diastolic dysfunction have been described.<a class="elsevierStyleCrossRefs" href="#bib0045"><span class="elsevierStyleSup">9,10</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">In addition, a population-based study has shown that patients with positive rheumatoid factor had an increased risk of developing congestive heart failure, independent of the presence of ischaemic heart disease and traditional cardiovascular risk factors.<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> Secondary amyloidosis may occur in RA patients as a result of long-term uncontrolled inflammation, although this finding is rare.<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">Another aspect of myocardial dysfunction in RA is drug toxicity, described with anti-tumour necrosis factor (anti-TNF) therapies and antimalarial agents. Most of the cardiotoxicity associated with antimalarial drugs is due to the use of chloroquine,<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a> but cardiotoxicity has also been reported with hydroxychloroquine.<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">12,13</span></a> In most cases, the phenotype of restrictive cardiomyopathy with increased wall thickness is described as the most common structural condition, with the phenotype of dilated ventricles with normal wall thickness being less relevant. Reliable diagnosis of hydroxychloroquine-induced cardiomyopathy requires the presence of the pathognomonic curvilinear bodies on an endomyocardial biopsy.</p><p id="par0050" class="elsevierStylePara elsevierViewall">Cardiotoxicity has also been reported in association with anti-TNFs. The alert issued on cardiovascular safety in the use of anti-TNF is based on the preliminary results of two clinical trials with etanercept<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a> and a pilot study with infliximab<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a> for the treatment of patients with moderate and severe heart failure, in whom there was an increase in the incidence of serious cardiovascular events (hospitalization and death), especially in the group of those who received higher doses. However, these results disagree with the findings of observational studies and several registries of RA patients that do not show an increased risk of heart failure in RA patients treated with anti-TNF. A recent meta-analysis of data from these registries<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">16</span></a> also concludes that RA patients treated with anti-TNFs have a lower incidence of heart failure than patients who did not receive these agents. Based on the available evidence, the use of anti-TNF agents is contraindicated in patients with moderate-to-severe heart failure (class III/IV according to the New York Heart Association classification) and should be used with caution in patients in functional class I and II.</p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Coronary heart disease</span><p id="par0055" class="elsevierStylePara elsevierViewall">Patients with RA have a higher risk of developing coronary heart disease, and this risk increases with the duration of the disease.<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> It has been calculated that the relative risk of developing a cardiovascular event in subjects with RA is around twice that of people without this pathology of the same age and same sex. Furthermore, ischemic heart disease secondary to coronary atherosclerosis represents the leading cause of cardiovascular mortality in patients with RA.<a class="elsevierStyleCrossRefs" href="#bib0085"><span class="elsevierStyleSup">17,18</span></a> The increase in cardiovascular events in these patients is independent of the presence of traditional cardiovascular risk factors.<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">19</span></a> Genetic factors and persistent chronic inflammation favour the development of cardiovascular events.<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">20</span></a></p><p id="par0060" class="elsevierStylePara elsevierViewall">Active treatment of the disease has been shown to reduce the risk of cardiovascular mortality and, as a consequence of more intensive treatment of this rheumatic disease, mortality in these patients is reduced due to a decreased incidence of myocardial infarction.<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">21</span></a></p><p id="par0065" class="elsevierStylePara elsevierViewall">It has been observed that subjects with RA who had a good clinical response to treatment with methotrexate also had a lower cardiovascular mortality than those who were refractory to this treatment.<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">22</span></a> Population studies have shown that the use of biological treatments in subjects with RA refractory to conventional treatment reduces overall mortality and, in particular, cardiovascular mortality.<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">23</span></a> Regarding the use of glucocorticoids, it is recommended to prescribe them at low doses and for as short a period of time as possible, as they may promote atherogenesis by inducing negative effects on glucose metabolism, lipids, and blood pressure; however, when used acutely and for short periods, they may be beneficial by reducing inflammation and improving mobilisation.</p></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Rhythm disorders</span><p id="par0070" class="elsevierStylePara elsevierViewall">Rhythm disorders, particularly tachycardias, are common in RA and contribute significantly to the high cardiovascular morbidity and mortality observed in these patients. Although the underlying mechanisms are unknown, the main role seems to be played by chronic systemic inflammation, which may induce arrhythmogenicity indirectly by accelerating the development of structural heart disease, and directly, by affecting the conduction system.<a class="elsevierStyleCrossRef" href="#bib0120"><span class="elsevierStyleSup">24</span></a> From this point of view, reducing the inflammatory burden through an increasingly strict control of the disease activity may constitute the most effective intervention to reduce arrhythmic risk and prevent life-threatening complications.</p></span></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Systemic lupus erythematosus</span><p id="par0075" class="elsevierStylePara elsevierViewall">SLE is a relatively common autoimmune systemic inflammatory disease. The prevalence in Spain is estimated to be around 0.2% of the population (CI<span class="elsevierStyleHsp" style=""></span>95%: 0.1−0.4).<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> It predominantly affects women, with a 9:1 ratio compared to men, generally black and young, although it can occur at any age. Cardiac involvement is common; the current prevalence varies according to the population studied and may be greater than 50%.<a class="elsevierStyleCrossRef" href="#bib0125"><span class="elsevierStyleSup">25</span></a> All cardiac structures can be affected.</p><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Pericardial disease</span><p id="par0080" class="elsevierStylePara elsevierViewall">Pericarditis and pericardial effusion are the most common cardiac manifestations in patients with SLE.<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> In several clinical studies, between 20% and 50% of patients had pericardial involvement,<a class="elsevierStyleCrossRefs" href="#bib0045"><span class="elsevierStyleSup">9,26–30</span></a> and autopsy series have described an even higher prevalence of pericardial involvement (≥<span class="elsevierStyleHsp" style=""></span>60% of patients).<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">28</span></a> Pericarditis is included in the SLE classification criteria, both those prepared by the <span class="elsevierStyleItalic">American College of Rheumatology</span> in 1982 and revised in 1997, as well as the <span class="elsevierStyleItalic">Systemic Lupus International Collaborating Clinics Classification Criteria</span> (SILCC) of 2012.</p><p id="par0085" class="elsevierStylePara elsevierViewall">Pericardial effusion is usually mild and, in most cases, does not cause cardiac tamponade or haemodynamic compromise.<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">29</span></a> The pericardial fluid test shows a neutrophil-predominant exudate, high protein levels, and normal or low glucose levels<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">28</span></a>; antinuclear antibodies and complement levels can be detected, but their determination is not routinely indicated. Histologically, the presence of haematoxylin bodies may be the only specific finding of lupus pericarditis, although fibrous pericarditis with pericardial thickening is common, which can subsequently lead to focal or diffuse adhesion of the parietal and visceral layers.<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">31</span></a> Constrictive pericarditis is rare.</p><p id="par0090" class="elsevierStylePara elsevierViewall">Mild cases of lupus pericarditis are treated with anti-inflammatory drugs and colchicine, although most patients will require glucocorticoids, as well as treatment optimisation with disease-modifying antirheumatic drugs.</p></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0070">Valve involvement</span><p id="par0095" class="elsevierStylePara elsevierViewall">SLE is associated with both endocarditis and the presence of valve nodules. Transoesophageal echocardiography studies have revealed that ><span class="elsevierStyleHsp" style=""></span>50% of patients with SLE have valvular abnormalities.<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">32</span></a> Valve nodules are fairly common on autopsy reports, but clinically irrelevant. The prevalence of non-bacterial vegetations, also called Libman-Sacks vegetations, is estimated at 11–74%. These vegetations usually involve the mitral valve, are often associated with the presence of antiphospholipid antibodies, and rarely cause significant valve dysfunction or embolic events.</p><p id="par0100" class="elsevierStylePara elsevierViewall">Other valve manifestations include valvulitis and valve insufficiency and stenosis. Surgical indications for valve disease are not different in SLE. However, these patients are at higher surgical risk, especially if they receive immunosuppressive therapy. Transcatheter valve replacement may be a safer option in certain cases, although we have limited data.<a class="elsevierStyleCrossRef" href="#bib0165"><span class="elsevierStyleSup">33</span></a></p></span><span id="sec0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0075">Myocardial involvement</span><p id="par0105" class="elsevierStylePara elsevierViewall">Myocarditis prevalence is low in SLE patients.<a class="elsevierStyleCrossRefs" href="#bib0170"><span class="elsevierStyleSup">34,35</span></a> However, patients with myositis may be at increased risk of developing myocarditis. Histological findings are nonspecific, but mononuclear infiltrates are common, with perivascular immune complex deposition, necrosis, and fibrosis. The standard treatment is high doses of glucocorticoids in combination with immunosuppressive drugs such as azathioprine, cyclophosphamide, rituximab, or intravenous immunoglobulins. In patients taking chloroquine or hydroxychloroquine, cardiotoxicity from these drugs should be ruled out.<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">12,13</span></a> In addition to myocarditis, patients with SLE can develop cardiomyopathy a multifactorial aetiology cardiomyopathy.<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">32</span></a></p></span><span id="sec0060" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0080">Coronary heart disease</span><p id="par0110" class="elsevierStylePara elsevierViewall">Coronary atherosclerosis is a common manifestation in patients with SLE, associated with significant morbidity and mortality. SLE, regardless of traditional risk factors, has been shown to be a substantial risk factor for the development of atherosclerosis.<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">32</span></a> Older age at diagnosis, longer duration of disease and immunosuppressive therapy, and high homocysteine levels have been associated with subclinical atherosclerosis.<a class="elsevierStyleCrossRef" href="#bib0175"><span class="elsevierStyleSup">35</span></a> Other forms of coronary involvement, although less common, include vasculitis and thrombosis.</p><p id="par0115" class="elsevierStylePara elsevierViewall">The effect of different drugs on the risk of cardiovascular disease is variable. Glucocorticoids appear as a risk factor for atherosclerosis in SLE patients in several studies, but the results are not consistent. Although glucocorticoids decrease systemic inflammation and may reduce the atherogenic burden, their use is associated with exacerbation of multiple traditional risk factors and may therefore have opposing effects on the development of coronary atherosclerosis that are not yet well defined. On the other hand, hydroxychloroquine improves the lipid and glycaemic profile, but it is currently unknown if it can protect patients with SLE from the development of atherosclerosis.<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">36</span></a></p></span><span id="sec0065" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0085">Rhythm disorders</span><p id="par0120" class="elsevierStylePara elsevierViewall">SLE can predispose to the occurrence of tachyarrhythmias, the most common being atrial fibrillation and atrial extrasystoles. Supraventricular tachycardia episodes are often associated with myocarditis or with periods of SLE exacerbation.<a class="elsevierStyleCrossRef" href="#bib0185"><span class="elsevierStyleSup">37</span></a> Patients receiving hydroxychloroquine and those with anti-small cytoplasmic ribonucleoprotein antibodies are at increased risk of sinus bradycardia and QT prolongation.<a class="elsevierStyleCrossRef" href="#bib0175"><span class="elsevierStyleSup">35</span></a> Malignant ventricular arrhythmias are rare.<a class="elsevierStyleCrossRef" href="#bib0185"><span class="elsevierStyleSup">37</span></a></p><p id="par0125" class="elsevierStylePara elsevierViewall">Newborns of mothers with SLE are at higher risk of developing complete atrioventricular block due to the deposition of autoantibodies in the conduction system, which is related to the presence of anti-Ro antibodies. In these patients, hydroxychloroquine has shown a protective effect against this cardiac manifestation.<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">27</span></a></p></span></span><span id="sec0070" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0090">Primary antiphospholipid syndrome</span><p id="par0130" class="elsevierStylePara elsevierViewall">Primary APS is a systemic autoimmune disease characterized by the presence of antiphospholipid antibodies, which has been defined clinically by the presence of arterial and venous thromboses and obstetric problems (recurrent miscarriages). Due to its vascular nature, it can affect any organ or tissue, including the heart.<a class="elsevierStyleCrossRef" href="#bib0190"><span class="elsevierStyleSup">38</span></a></p><span id="sec0075" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0095">Valve involvement</span><p id="par0135" class="elsevierStylePara elsevierViewall">Valve involvement is the most common cardiac manifestation in APS. It has been defined as the presence of valvular morphological lesions (global leaflet thickening, localised thickening of the proximal or middle portion of the leaflet, or irregular nodules and/or non-bacterial vegetations on the valve leaflets, known as Libman-Sacks vegetations) and/or moderate or severe valvular dysfunction, in the absence of a history of rheumatic fever and infective endocarditis.<a class="elsevierStyleCrossRef" href="#bib0195"><span class="elsevierStyleSup">39</span></a> The pathogenic mechanisms involved in the development of valvular heart disease are unknown, but there is evidence that antiphospholipid antibodies play a role in the development of these lesions.<a class="elsevierStyleCrossRef" href="#bib0200"><span class="elsevierStyleSup">40</span></a></p><p id="par0140" class="elsevierStylePara elsevierViewall">Surgical indications for valvular heart disease are no different in APS. It is not clear whether glucocorticoids should be used in valvular heart disease associated with antiphospholipid antibodies due to the lack of studies in this context. Anticoagulant treatment is indicated in patients with valvulopathy and systemic embolism, but not for the treatment of the valve lesion itself. Patients with vegetations and/or valvular heart disease without thrombosis may receive acetylsalicylic acid, although there are no data to validate this strategy.<a class="elsevierStyleCrossRef" href="#bib0200"><span class="elsevierStyleSup">40</span></a></p></span><span id="sec0080" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0100">Myocardial involvement</span><p id="par0145" class="elsevierStylePara elsevierViewall">Ventricular dysfunction in APS is probably an underestimated condition, and its pathogenesis is still unclear. Histologically, microvascular thrombosis, intramyocardial arteriolar immune deposits, disseminated thrombosis, with diffuse microinfarctions and endomyocardial fibrosis have been described.<a class="elsevierStyleCrossRef" href="#bib0200"><span class="elsevierStyleSup">40</span></a></p><p id="par0150" class="elsevierStylePara elsevierViewall">In the event that systolic dysfunction is detected, the neurohormonal treatment recommended in the clinical practice guidelines should be instituted. In addition, APS patients with myocardial dysfunction require long-term anticoagulation therapy to reduce the risk of large vessel thromboembolism and thrombotic microangiopathy.<a class="elsevierStyleCrossRef" href="#bib0205"><span class="elsevierStyleSup">41</span></a></p></span><span id="sec0085" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0105">Coronary heart disease</span><p id="par0155" class="elsevierStylePara elsevierViewall">Acute coronary syndrome may be the first thrombotic manifestation in APS.<a class="elsevierStyleCrossRef" href="#bib0200"><span class="elsevierStyleSup">40</span></a> The association between antiphospholipid antibodies and myocardial infarction is more common in women. About 2.8–5.5% of myocardial infarction cases in young patients are secondary to APS.<a class="elsevierStyleCrossRef" href="#bib0205"><span class="elsevierStyleSup">41</span></a> Myocardial ischemia in APS can be due to multiple mechanisms, such as coronary embolism, accelerated coronary atherosclerosis, vasospasm, and microvascular damage. The most common cause of acute coronary syndrome in young patients with APS is coronary embolism of undetermined origin.<a class="elsevierStyleCrossRef" href="#bib0205"><span class="elsevierStyleSup">41</span></a></p><p id="par0160" class="elsevierStylePara elsevierViewall">The optimal management of acute coronary syndrome in APS is a matter of debate. Patients with APS undergoing primary angioplasty seem to have worse long-term clinical outcomes compared to patients without APS, with high rates of thrombotic recurrence.<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">42</span></a></p></span><span id="sec0090" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0110">Pulmonary hypertension</span><p id="par0165" class="elsevierStylePara elsevierViewall">In patients with APS, pulmonary arterial hypertension can occur secondary to recurrent pulmonary embolism or microthrombosis of the pulmonary vessels. Pulmonary thromboembolic disease is a common manifestation of APS.<a class="elsevierStyleCrossRef" href="#bib0215"><span class="elsevierStyleSup">43</span></a> However, chronic thromboembolic pulmonary hypertension is less common. Indefinite anticoagulation is always indicated.<a class="elsevierStyleCrossRef" href="#bib0205"><span class="elsevierStyleSup">41</span></a></p></span></span><span id="sec0095" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0115">Systemic sclerosis</span><p id="par0170" class="elsevierStylePara elsevierViewall">SSc is a chronic, generalized, and progressive connective tissue disease characterized by vascular dysfunction and microvascular abnormalities that lead to ischemia and fibrosis in various tissues and organs. Its clinical manifestations include Raynaud's phenomenon, hardening of the skin (scleroderma) and internal organ involvement, including the gastrointestinal tract, lungs, kidneys, and heart. Although cardiac involvement can be detected early in the course of the disease, clinical manifestations usually appear in advanced stages of the disease and are associated with a poor prognosis.<a class="elsevierStyleCrossRef" href="#bib0220"><span class="elsevierStyleSup">44</span></a></p><span id="sec0100" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0120">Pericardial disease</span><p id="par0175" class="elsevierStylePara elsevierViewall">Pericardial involvement in SSc is usually mild and asymptomatic.<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">32</span></a> Symptomatic pericardial disease affects 7–20% of patients; however, autopsy series have found pericardial involvement in 33–72% of patients with SSc.<a class="elsevierStyleCrossRef" href="#bib0225"><span class="elsevierStyleSup">45</span></a> Mild pericardial effusions are a common finding.<a class="elsevierStyleCrossRef" href="#bib0230"><span class="elsevierStyleSup">46</span></a> There is no specific treatment for pericardial disease in SSc, so it should be managed as recommended in clinical practice guidelines.</p></span><span id="sec0105" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0125">Valve involvement</span><p id="par0180" class="elsevierStylePara elsevierViewall">Due to the low prevalence of valve involvement in patients with SSc, it is not considered a typical manifestation.<a class="elsevierStyleCrossRef" href="#bib0225"><span class="elsevierStyleSup">45</span></a> The mitral valve is the most commonly affected valve.<a class="elsevierStyleCrossRef" href="#bib0230"><span class="elsevierStyleSup">46</span></a></p></span><span id="sec0110" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0130">Myocardial involvement</span><p id="par0185" class="elsevierStylePara elsevierViewall">Myocardial fibrosis is an important cardiac manifestation of SSc and can cause coronary vasospasm as well as systolic and diastolic dysfunction. Pulmonary involvement in SSc can cause pulmonary hypertension and associated myocardial changes, while renal involvement can cause hypertension and left ventricular hypertrophy. Nearly half of the autopsies in SSc patients reveal contraction band necrosis, reperfusion injury and fibrosis in both ventricles, despite the absence of coronary lesions.<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">32</span></a></p></span><span id="sec0115" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0135">Coronary heart disease</span><p id="par0190" class="elsevierStylePara elsevierViewall">The prevalence of atherosclerotic coronary artery disease increases in SSc.<a class="elsevierStyleCrossRef" href="#bib0235"><span class="elsevierStyleSup">47</span></a> In patients with scleroderma and coronary artery disease, the likelihood of coronary vasospasm occurring is significantly higher than in the general population.<a class="elsevierStyleCrossRef" href="#bib0240"><span class="elsevierStyleSup">48</span></a></p></span><span id="sec0120" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0140">Rhythm disorders</span><p id="par0195" class="elsevierStylePara elsevierViewall">Conduction disorders and arrhythmias are common in these patients and are believed to occur as a consequence of fibrosis or ischemia in conduction tissues.<a class="elsevierStyleCrossRef" href="#bib0240"><span class="elsevierStyleSup">48</span></a> Supraventricular tachycardias have been reported in up to 30% of cases and ventricular arrhythmias have been described in up to 67% of patients.<a class="elsevierStyleCrossRefs" href="#bib0160"><span class="elsevierStyleSup">32,37</span></a> SSc is also associated with an increased risk of conduction disorders due to sinus node and His bundle fibrosis. The treatment of conduction disorders and arrhythmias does not differ from that used in the general population.<a class="elsevierStyleCrossRef" href="#bib0225"><span class="elsevierStyleSup">45</span></a></p></span><span id="sec0125" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0145">Pulmonary hypertension</span><p id="par0200" class="elsevierStylePara elsevierViewall">SSc is the connective tissue disease with the highest risk of developing pulmonary hypertension, which is one of the most severe manifestations in these patients, occurring mostly in the limited variant of the disease (CREST syndrome). May be due to an intrinsic pulmonary artery disease or to interstitial fibrosis.<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">26</span></a> Echocardiography is the technique of choice for pulmonary hypertension screening, and if suspected by echocardiography, it should be confirmed by right catheterization.<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">26</span></a></p></span></span><span id="sec0130" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0150">Spondyloarthropathies</span><p id="par0205" class="elsevierStylePara elsevierViewall">The term spondyloarthropathy encompasses a group of diseases characterised by inflammation of the joints of the spine and limbs, including ankylosing spondylitis (AS), reactive arthritis, arthritis associated with inflammatory bowel diseases, psoriatic arthritis, undifferentiated spondylarthritis and juvenile-onset AS.</p><p id="par0210" class="elsevierStylePara elsevierViewall">AS is the most common and characteristic disease in this group. The prevalence in Spain is estimated at around 0.4% of the population (CI<span class="elsevierStyleHsp" style=""></span>95%: 0.3−0.7).<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> It is a chronic systemic inflammatory disease, of unknown aetiology, involving primarily the axial skeleton and entheses. Cardiac involvement is common, but generally subclinical.</p><p id="par0215" class="elsevierStylePara elsevierViewall">One of the cardiac manifestations of AS is aortic regurgitation,<a class="elsevierStyleCrossRefs" href="#bib0245"><span class="elsevierStyleSup">49,50</span></a> due to the thickening and shortening caused by leaflet retraction, caudal displacement of the leaflets due to the formation of a fibrous protrusion below the valve plane resulting in leaflet retraction and the dilatation of the ascending aorta.<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">51</span></a></p><p id="par0220" class="elsevierStylePara elsevierViewall">AS is also associated with the occurrence of conduction disorders.<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> The most common manifestation is first-degree atrioventricular block,<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">32</span></a> but cases of advanced atrioventricular block have also been described, as well as intraventricular blocks.<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a></p><p id="par0225" class="elsevierStylePara elsevierViewall">Involvement of the myocardium and pericardium is very rare.</p></span><span id="sec0135" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0155">Vasculitis</span><p id="par0230" class="elsevierStylePara elsevierViewall">Vasculitis is defined as inflammation or necrosis of the blood vessels that can destroy the vessel wall and cause bleeding and/or ischemia. Many diseases are involved, with polyarteritis nodosa (PAN), Wegener’s granulomatosis, eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome) and Takayasu's arteritis being the most representative. Almost all primary vasculitis can affect the heart.</p><span id="sec0140" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0160">Polyarteritis nodosa</span><p id="par0235" class="elsevierStylePara elsevierViewall">Clinically manifest cardiac involvement occurs in 5–20% of patients with PAN.<a class="elsevierStyleCrossRef" href="#bib0260"><span class="elsevierStyleSup">52</span></a> Inflammatory cardiac manifestations include coronary arteritis, fibrinous pericarditis, and, rarely, myocarditis. These patients can also develop ventricular dysfunction as a consequence of myocardial ischemia or in the context of severe hypertension.<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">53</span></a></p><p id="par0240" class="elsevierStylePara elsevierViewall">Fibrinoid necrosis, in association with acute and chronic inflammatory infiltrates and fibrosis can cause wall thickening, luminal stenosis, thrombosis, dissection, or aneurysmal dilatations in PAN coronary lesions. In cases of isolated microvascular disease, the angiography may be completely normal. Coronary arteritis requires aggressive immunosuppression with high doses of glucocorticoids and cyclophosphamide and, often, revascularization.<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">53</span></a></p><p id="par0245" class="elsevierStylePara elsevierViewall">Treatment of cardiomyopathy includes immunosuppressive therapy for patients with active vasculitis.<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">53</span></a></p></span><span id="sec0145" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0165">Eosinophilic granulomatosis with polyangiitis</span><p id="par0250" class="elsevierStylePara elsevierViewall">Cardiac involvement is common, occurs in 15–60% of cases, and is often severe. The presence of cardiomyopathy has been shown to be the most important predictor of mortality.<a class="elsevierStyleCrossRef" href="#bib0270"><span class="elsevierStyleSup">54</span></a> The most common cardiac manifestations are pericarditis and cardiomyopathy. Valvular lesions, detected in up to 30% of cases, are often asymptomatic. Coronary vasculitis and conduction disorders are rare.<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">53</span></a></p><p id="par0255" class="elsevierStylePara elsevierViewall">Because cardiac involvement is associated with significant mortality, these patients should be treated with glucocorticoids and an additional immunosuppressant, generally cyclophosphamide, mycophenolate, or rituximab. Immunosuppressive therapy has been associated with improvement in cardiac function and arrhythmic events.<a class="elsevierStyleCrossRef" href="#bib0275"><span class="elsevierStyleSup">55</span></a> Patients with isolated pericarditis can be treated with glucocorticoids alone, although more than 50% will require additional immunosuppression during the course of their disease.<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">53</span></a></p></span><span id="sec0150" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0170">Takayasu arteritis</span><p id="par0260" class="elsevierStylePara elsevierViewall">Cardiac involvement is an important cause of morbidity and mortality in Takayasu arteritis. Any cardiac structure can be potentially affected, and almost half of all patients develop cardiac involvement at some point. Volume overload (aortic regurgitation), pressure overload (hypertension caused by renal artery stenosis), myocardial ischemia (coronary arteritis), and myocarditis can lead to ventricular dysfunction. Other manifestations include pericarditis, ischemic heart disease secondary to accelerated atherosclerosis, pulmonary hypertension-induced right heart failure, arrhythmias, and sudden death.<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">53</span></a></p><p id="par0265" class="elsevierStylePara elsevierViewall">Aortic regurgitation is described in 15–50% of patients<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">53</span></a> and it usually occurs as a consequence of annular dilatation and leaflet separation occurring in the context of aortitis and aortic aneurysm formation. Depending on the severity of the valvular heart disease, treatment will include valve replacement, along with aortic root replacement and immunosuppression according to disease activity.<a class="elsevierStyleCrossRef" href="#bib0280"><span class="elsevierStyleSup">56</span></a></p><p id="par0270" class="elsevierStylePara elsevierViewall">Coronary artery disease is angiographically proven in up to 60% of patients but is symptomatic in 5–20% of cases. Vascular inflammation is the main mechanism of coronary artery disease; however, premature atherosclerosis secondary to hypertension and chronic inflammatory state is an important contributing factor.<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">53</span></a> Glucocorticoids combined with immunosuppressants are indicated when active vasculitis is considered to be the aetiology of coronary artery involvement. Should revascularisation be required, adequate control of disease activity is essential to maintain long-term patency of coronary grafts or stents.<a class="elsevierStyleCrossRefs" href="#bib0285"><span class="elsevierStyleSup">57,58</span></a></p></span><span id="sec0155" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0175">Wegener’s granulomatosis</span><p id="par0275" class="elsevierStylePara elsevierViewall">Symptomatic cardiac involvement is seen in a small percentage of patients with Wegener’s granulomatosis; however, subclinical involvement can be much more common.<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">53</span></a> Pericarditis, conduction disorders, and supraventricular tachycardias are the most common manifestations.<a class="elsevierStyleCrossRef" href="#bib0295"><span class="elsevierStyleSup">59</span></a> Myocarditis, coronary arteritis, and cardiac thrombi have been described in less than 1–2% of patients.<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">53</span></a> Valvular involvement cases have also been reported, especially in the aortic valve.</p><p id="par0280" class="elsevierStylePara elsevierViewall">Without immunosuppressive therapy, Wegener’s patients have a poor prognosis. The combination of immunosuppressive drugs, including biological agents such as rituximab, has considerably improved the prognosis.<a class="elsevierStyleCrossRef" href="#bib0300"><span class="elsevierStyleSup">60</span></a></p></span></span><span id="sec0160" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0180">Funding</span><p id="par0285" class="elsevierStylePara elsevierViewall">This research has not received specific support from public sector agencies, the commercial sector, or non-profit organisations.</p></span><span id="sec0165" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0185">Conflict of interests</span><p id="par0290" class="elsevierStylePara elsevierViewall">None.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:14 [ 0 => array:3 [ "identificador" => "xres1526954" "titulo" => "Abstract" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0005" ] ] ] 1 => array:2 [ "identificador" => "xpalclavsec1384391" "titulo" => "Keywords" ] 2 => array:3 [ "identificador" => "xres1526955" "titulo" => "Resumen" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0010" ] ] ] 3 => array:2 [ "identificador" => "xpalclavsec1384392" "titulo" => "Palabras clave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Introduction" ] 5 => array:3 [ "identificador" => "sec0010" "titulo" => "Rheumatoid arthritis" "secciones" => array:5 [ 0 => array:2 [ "identificador" => "sec0015" "titulo" => "Pericardial disease" ] 1 => array:2 [ "identificador" => "sec0020" "titulo" => "Valve involvement" ] 2 => array:2 [ "identificador" => "sec0025" "titulo" => "Myocardial involvement" ] 3 => array:2 [ "identificador" => "sec0030" "titulo" => "Coronary heart disease" ] 4 => array:2 [ "identificador" => "sec0035" "titulo" => "Rhythm disorders" ] ] ] 6 => array:3 [ "identificador" => "sec0040" "titulo" => "Systemic lupus erythematosus" "secciones" => array:5 [ 0 => array:2 [ "identificador" => "sec0045" "titulo" => "Pericardial disease" ] 1 => array:2 [ "identificador" => "sec0050" "titulo" => "Valve involvement" ] 2 => array:2 [ "identificador" => "sec0055" "titulo" => "Myocardial involvement" ] 3 => array:2 [ "identificador" => "sec0060" "titulo" => "Coronary heart disease" ] 4 => array:2 [ "identificador" => "sec0065" "titulo" => "Rhythm disorders" ] ] ] 7 => array:3 [ "identificador" => "sec0070" "titulo" => "Primary antiphospholipid syndrome" "secciones" => array:4 [ 0 => array:2 [ "identificador" => "sec0075" "titulo" => "Valve involvement" ] 1 => array:2 [ "identificador" => "sec0080" "titulo" => "Myocardial involvement" ] 2 => array:2 [ "identificador" => "sec0085" "titulo" => "Coronary heart disease" ] 3 => array:2 [ "identificador" => "sec0090" "titulo" => "Pulmonary hypertension" ] ] ] 8 => array:3 [ "identificador" => "sec0095" "titulo" => "Systemic sclerosis" "secciones" => array:6 [ 0 => array:2 [ "identificador" => "sec0100" "titulo" => "Pericardial disease" ] 1 => array:2 [ "identificador" => "sec0105" "titulo" => "Valve involvement" ] 2 => array:2 [ "identificador" => "sec0110" "titulo" => "Myocardial involvement" ] 3 => array:2 [ "identificador" => "sec0115" "titulo" => "Coronary heart disease" ] 4 => array:2 [ "identificador" => "sec0120" "titulo" => "Rhythm disorders" ] 5 => array:2 [ "identificador" => "sec0125" "titulo" => "Pulmonary hypertension" ] ] ] 9 => array:2 [ "identificador" => "sec0130" "titulo" => "Spondyloarthropathies" ] 10 => array:3 [ "identificador" => "sec0135" "titulo" => "Vasculitis" "secciones" => array:4 [ 0 => array:2 [ "identificador" => "sec0140" "titulo" => "Polyarteritis nodosa" ] 1 => array:2 [ "identificador" => "sec0145" "titulo" => "Eosinophilic granulomatosis with polyangiitis" ] 2 => array:2 [ "identificador" => "sec0150" "titulo" => "Takayasu arteritis" ] 3 => array:2 [ "identificador" => "sec0155" "titulo" => "Wegener’s granulomatosis" ] ] ] 11 => array:2 [ "identificador" => "sec0160" "titulo" => "Funding" ] 12 => array:2 [ "identificador" => "sec0165" "titulo" => "Conflict of interests" ] 13 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2020-11-12" "fechaAceptado" => "2021-01-19" "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec1384391" "palabras" => array:3 [ 0 => "Rheumatic diseases" 1 => "Autoimmune diseases" 2 => "Cardiac disease" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec1384392" "palabras" => array:3 [ 0 => "Enfermedades reumáticas" 1 => "Enfermedades autoinmunitarias" 2 => "Cardiopatía" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Autoimmune rheumatic diseases are inflammatory disorders that can involve multiple organs, including the heart. The high risk of cardiovascular pathology in these patients is not only due to traditional cardiovascular risk factors, but also to chronic inflammation and autoimmunity. All cardiac structures may be affected during the course of systemic autoimmune diseases (valves, the conduction system, the myocardium, endocardium and pericardium, and coronary arteries), and the cardiac complications have a variety of clinical manifestations. As these are all associated with an unfavourable prognosis, it is essential to detect subclinical cardiac involvement in asymptomatic systemic autoimmune disease patients and begin adequate management and treatment early. In this review, we examine the multiple cardiovascular manifestations in patients with rheumatological disorders and available management strategies.</p></span>" ] "es" => array:2 [ "titulo" => "Resumen" "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Las enfermedades reumáticas autoinmunes son trastornos inflamatorios que pueden afectar a múltiples órganos, entre los que se incluye el corazón. El elevado riesgo de aparición de patología cardiovascular en estos pacientes no solo se debe a la presencia de factores de riesgo cardiovascular tradicionales, sino también a la inflamación crónica y la autoinmunidad. Todas las estructuras cardíacas pueden verse afectadas durante el curso de la enfermedad (válvulas, sistema de conducción, miocardio, endocardio, pericardio y arterias coronarias), por lo que las complicaciones cardíacas incluyen una amplia variedad de manifestaciones clínicas. La afectación cardíaca se asocia con un pronóstico desfavorable, por lo que es esencial detectar la lesión cardíaca subclínica en pacientes asintomáticos e instaurar el tratamiento de forma precoz. Este documento ofrece una revisión actualizada de las principales manifestaciones cardíacas de las enfermedades reumáticas, así como su manejo terapéutico.</p></span>" ] ] "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Méndez Eirín E, Suárez Ouréns Y, Guerra Vázquez JL. Manifestaciones cardíacas de las enfermedades reumáticas. Med Clin (Barc). 2021;156:615–621.</p>" ] ] "multimedia" => array:1 [ 0 => array:8 [ "identificador" => "tbl0005" "etiqueta" => "Table 1" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0005" "detalle" => "Table " "rol" => "short" ] ] "tabla" => array:2 [ "leyenda" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">SLE: systemic lupus erythematosus; PAN: polyarteritis nodosa.</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="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Disease \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Pericardium \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Valves \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Myocardium \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Coronary arteries \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Conduction system \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Pulmonary hypertension \t\t\t\t\t\t\n \t\t\t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Rheumatoid arthritis \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">++++ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">++++ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">++ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+ \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">SLE \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">++++ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">++++ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">++ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">++++ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">++++ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+++ \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Antiphospholipid syndrome \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">++++ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">++++ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">++++ \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Systemic sclerosis \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">++++ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">++ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">++++ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">++++ \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Ankylosing spondylitis \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+++ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">++++ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">++++ \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">PAN \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">++ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Churg-Strauss syndrome \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">++ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">++ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Takayasu arteritis \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+++ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td-with-role" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Wegener’s granulomatosis \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">+ \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t"> \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab2624481.png" ] ] ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Most common cardiological manifestations in rheumatic diseases.</p>" ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:60 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Cardiac involvement in rheumatoid disease" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "G. 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Cardiac manifestations of rheumatic diseases
Manifestaciones cardíacas de las enfermedades reumáticas
a Servicio de Cardiología, Complejo Hospitalario Universitario de A Coruña, Instituto de Investigación Biomédica de A Coruña (INIBIC), A Coruña, Spain
b Servicio de Traumatología, Complejo Hospitalario Universitario de Ferrol, Ferrol, A Coruña, Spain
c Servicio de Reumatología, Complejo Hospitalario Universitario de Ferrol, Ferrol, A Coruña, Spain