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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Kawasaki disease &#40;KD&#41; is widely regarded as an acute autoinflammatory condition in children presenting with high-grade and persistent fever&#44; in association with a variety of multi-organ manifestations&#46;<a class="elsevierStyleCrossRefs" href="#bib0035"><span class="elsevierStyleSup">1&#8211;3</span></a> Of note&#44; coronary arteritis has been the most dangerous manifestation&#44; mainly due to its potential association with subsequent complications&#44; including coronary artery aneurysms &#40;CAAs&#41; and stenoses&#44; which have long-term clinical implications&#46;<a class="elsevierStyleCrossRefs" href="#bib0035"><span class="elsevierStyleSup">1&#8211;3</span></a> In their recently published article&#44; Magro et al&#46; &#40;1&#41; described a case of KD complicated by giant CAAs and critical left anterior descending &#40;LAD&#41; artery stenosis&#44; managed with coronary artery bypass grafting &#40;CABG&#41;&#46; In this context&#44; we would like to comment on this interesting case together with a couple of specific considerations in the management of emerging coronary sequelae associated with KD&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">First&#44; evolution of coronary artery stenosis has been mechanistically ascribed to the process of luminal myofibroblastic proliferation&#44; which also accounts for CAA regression in a large portion of patients with KD&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">2</span></a> In other terms&#44; gradual reduction in luminal CAA diameter generally comes at the cost of progressive stenotic lesions surrounding the CAAs&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">2</span></a> Consistent with this&#44; temporal regression of the LAD artery aneurysm &#40;during a period of about two and a half years&#41; seems to be associated with the emergence of a severely stenotic lesion just distal to the aneurysm in the patient&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">1</span></a> Importantly&#44; success of percutaneous coronary interventions &#40;PCIs&#41; might be relatively low in the management of these stenotic lesions due to their challenging morphological features &#40;highly fibroproliferative and&#47;or calcified&#41; and specific predilection sites &#40;mostly located at the proximal or distal part of the CAAs and potentially leading to stent malapposition&#44; etc&#46;&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0035"><span class="elsevierStyleSup">1&#44;2&#44;4</span></a> Therefore&#44; CABG in the present case appears to be a reasonable strategy at first glance&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">However&#44; coronary stenotic lesions can also arise due to a classical atheroma formation as a consequence of endothelial dysfunction<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">2&#44;3</span></a> associated with the impact of generalized vascular inflammation and disturbed rheological kinetics &#40;including slow and turbulent flow associated with the aneurysmal sac&#40;s&#41;&#41; along the coronary arteries in certain KD cases&#46; Interestingly&#44; these lesions can be relatively soft in nature&#44; and can also be located distant from the co-existing CAAs &#40;as may have also arisen in the present case<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">1</span></a> the long-term&#41;&#44; potentially rendering them more amenable to PCIs&#46; Therefore&#44; identification of plaque morphology with the guidance of certain imaging modalities &#40;intravascular ultrasound&#44; optic coherence tomography&#44; etc&#46;&#41; may help determine the subsequent management strategy &#40;CABG&#44; PCI&#44; rotational atherectomy&#44; etc&#46;<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">2&#44;4</span></a>&#41;&#46; Accordingly&#44; we wonder whether the authors considered these imaging modalities before CABG&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">Second&#44; CAA evolution following KD episodes has been a more recognized phenomenon and is generally attributed to acute multi-layer necrotizing vasculitis&#46;<a class="elsevierStyleCrossRefs" href="#bib0035"><span class="elsevierStyleSup">1&#44;2&#44;4</span></a> In this setting&#44; CAAs&#44; if present&#44; generally reach their maximum diameter around six weeks after the onset of KD&#46;<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">2&#44;3</span></a> Established CAAs have been universally managed with antiaggregant or anticoagulant medications &#40;or both&#41; together with certain antiatherogenic drugs in the setting of KD&#46;<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">2&#44;3</span></a> On the other hand&#44; most complications including fistula formation&#44; rupture&#44; recurrent coronary ischemic events etc&#46; generally take place in the setting of giant CAAs&#44; characterized by a diameter of &#62;8 mm or a Z score of &#8805;10&#46;<a class="elsevierStyleCrossRefs" href="#bib0035"><span class="elsevierStyleSup">1&#8211;5</span></a> Accordingly&#44; even though the CAAs in the patient<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">1</span></a> might be regarded as giant ones based on their aneurysmal diameters&#44; we wonder about the values of more objective parameters including Z score&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">In terms of radical management&#44; it is highly recommended that persistently large CAAs &#40;whether stable or progressively expanding&#41; be treated with elective operations including aneurysmectomy&#44; graft stents or coil embolization etc&#46;<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">2&#44;3</span></a> even if they are totally asymptomatic under optimal medical therapy&#46; Moreover&#44; indication for excision of giant CAAs seems to be even stronger during elective cardiac operations performed for concomitant pathologies including valve disease&#44;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">2</span></a> coronary stenosis &#40;as in the present case<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">1</span></a>&#41;&#46; Therefore&#44; we wonder why the surgeons exclusively performed CABG&#44; and left the giant CAAs surgically untreated&#46; Performing a more radical operation could have solved the problem in a single attempt&#46; Was there a technical failure or an anatomical obstacle &#40;including involvement of the diagonal branch by the aneurysmal sac&#44; etc&#46;&#41; potentially hampering excision or modification of CAAs&#63; Unfortunately&#44; the patient may still experience recurrent coronary ischemic events &#40;due to coronary embolization&#44; compression on the left internal mammary artery graft by the expanding CAA&#44; etc&#46;&#41; and serious mechanical complications &#40;CAA rupture&#44; fistula formation&#41; potentially requiring re-operation in the long-term&#46; On the other hand&#44; we also are of the opinion that certain giant CAAs with a clear-cut temporal regression might be watchfully monitored under optimal medical therapy&#46; Accordingly&#44; we wonder about the initial dimensions of the giant CAAs in the patient &#40;the values around six weeks after KD onset when the patient&#39;s CAAs were supposed to have maximum diameters&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">1</span></a> Were the giant CAAs progressive&#44; regressive or stable in time according to the Z score values&#63; Based on temporal changes in CAA diameters&#44; CAA involving the LAD artery seems to have a regressive nature as opposed to the CAA of the right coronary artery with a potential tendency to expand in time&#46; We also wonder whether the authors would consider renin-angiotensin system blockade &#40;particularly with captopril&#41; that might have a favorable impact on CAA progression&#44; largely through the inhibition of certain key mediators of arterial remodeling&#44; including matrix metalloproteinases&#63;<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">2&#44;6</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">Finally&#44; this case report clearly supports the strong association between the evolution of coronary sequelae and the failure to administer disease-modifying agents &#40;intravenous immunoglobulin &#40;IVIG&#41;&#44; etc&#46;&#41; in a timely manner in the setting of acute KD episodes&#46;<a class="elsevierStyleCrossRefs" href="#bib0035"><span class="elsevierStyleSup">1&#8211;4</span></a> This also suggests there is a need to further heighten clinical awareness of KD symptoms among parents<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">1</span></a> and even clinicians for the prevention of these potentially fatal sequelae&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">In summary&#44; Magro et al&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">1</span></a> should be congratulated for their didactic article&#46; In the setting of KD&#44; management of coronary sequelae primarily need to be individualized according to patient characteristics&#46; In KD patients undergoing cardiac surgery&#44; management of all the existing coronary sequelae at a single time &#40;where applicable&#41; appears to be a reasonable strategy in clinical practice&#46; Nevertheless&#44; prevention of these sequelae with the timely initiation of disease-modifying agents should still be regarded as the primary goal in KD management&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0040" class="elsevierStylePara elsevierViewall">The authors have no conflicts of interest to declare&#46;</p></span></span>"
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Letter to the Editor
Kawasaki disease: Specific considerations in the management of coronary artery sequelae
Doença de Kawasaki: Considerações específicas no tratamento de sequelas nas artérias coronárias
Kenan Yaltaa,
Autor para correspondência
kyalta@gmail.com

Corresponding author.
, Ugur Ozkana, Tulin Yaltab, Ertan Yetkınc
a Trakya University, Cardiology Department, Edirne, Turkey
b Trakya University, Pathology Department, Edirne, Turkey
c Derindere Hospital, Cardiology Department, Istanbul, Turkey
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Kawasaki disease &#40;KD&#41; is widely regarded as an acute autoinflammatory condition in children presenting with high-grade and persistent fever&#44; in association with a variety of multi-organ manifestations&#46;<a class="elsevierStyleCrossRefs" href="#bib0035"><span class="elsevierStyleSup">1&#8211;3</span></a> Of note&#44; coronary arteritis has been the most dangerous manifestation&#44; mainly due to its potential association with subsequent complications&#44; including coronary artery aneurysms &#40;CAAs&#41; and stenoses&#44; which have long-term clinical implications&#46;<a class="elsevierStyleCrossRefs" href="#bib0035"><span class="elsevierStyleSup">1&#8211;3</span></a> In their recently published article&#44; Magro et al&#46; &#40;1&#41; described a case of KD complicated by giant CAAs and critical left anterior descending &#40;LAD&#41; artery stenosis&#44; managed with coronary artery bypass grafting &#40;CABG&#41;&#46; In this context&#44; we would like to comment on this interesting case together with a couple of specific considerations in the management of emerging coronary sequelae associated with KD&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">First&#44; evolution of coronary artery stenosis has been mechanistically ascribed to the process of luminal myofibroblastic proliferation&#44; which also accounts for CAA regression in a large portion of patients with KD&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">2</span></a> In other terms&#44; gradual reduction in luminal CAA diameter generally comes at the cost of progressive stenotic lesions surrounding the CAAs&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">2</span></a> Consistent with this&#44; temporal regression of the LAD artery aneurysm &#40;during a period of about two and a half years&#41; seems to be associated with the emergence of a severely stenotic lesion just distal to the aneurysm in the patient&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">1</span></a> Importantly&#44; success of percutaneous coronary interventions &#40;PCIs&#41; might be relatively low in the management of these stenotic lesions due to their challenging morphological features &#40;highly fibroproliferative and&#47;or calcified&#41; and specific predilection sites &#40;mostly located at the proximal or distal part of the CAAs and potentially leading to stent malapposition&#44; etc&#46;&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0035"><span class="elsevierStyleSup">1&#44;2&#44;4</span></a> Therefore&#44; CABG in the present case appears to be a reasonable strategy at first glance&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">However&#44; coronary stenotic lesions can also arise due to a classical atheroma formation as a consequence of endothelial dysfunction<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">2&#44;3</span></a> associated with the impact of generalized vascular inflammation and disturbed rheological kinetics &#40;including slow and turbulent flow associated with the aneurysmal sac&#40;s&#41;&#41; along the coronary arteries in certain KD cases&#46; Interestingly&#44; these lesions can be relatively soft in nature&#44; and can also be located distant from the co-existing CAAs &#40;as may have also arisen in the present case<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">1</span></a> the long-term&#41;&#44; potentially rendering them more amenable to PCIs&#46; Therefore&#44; identification of plaque morphology with the guidance of certain imaging modalities &#40;intravascular ultrasound&#44; optic coherence tomography&#44; etc&#46;&#41; may help determine the subsequent management strategy &#40;CABG&#44; PCI&#44; rotational atherectomy&#44; etc&#46;<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">2&#44;4</span></a>&#41;&#46; Accordingly&#44; we wonder whether the authors considered these imaging modalities before CABG&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">Second&#44; CAA evolution following KD episodes has been a more recognized phenomenon and is generally attributed to acute multi-layer necrotizing vasculitis&#46;<a class="elsevierStyleCrossRefs" href="#bib0035"><span class="elsevierStyleSup">1&#44;2&#44;4</span></a> In this setting&#44; CAAs&#44; if present&#44; generally reach their maximum diameter around six weeks after the onset of KD&#46;<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">2&#44;3</span></a> Established CAAs have been universally managed with antiaggregant or anticoagulant medications &#40;or both&#41; together with certain antiatherogenic drugs in the setting of KD&#46;<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">2&#44;3</span></a> On the other hand&#44; most complications including fistula formation&#44; rupture&#44; recurrent coronary ischemic events etc&#46; generally take place in the setting of giant CAAs&#44; characterized by a diameter of &#62;8 mm or a Z score of &#8805;10&#46;<a class="elsevierStyleCrossRefs" href="#bib0035"><span class="elsevierStyleSup">1&#8211;5</span></a> Accordingly&#44; even though the CAAs in the patient<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">1</span></a> might be regarded as giant ones based on their aneurysmal diameters&#44; we wonder about the values of more objective parameters including Z score&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">In terms of radical management&#44; it is highly recommended that persistently large CAAs &#40;whether stable or progressively expanding&#41; be treated with elective operations including aneurysmectomy&#44; graft stents or coil embolization etc&#46;<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">2&#44;3</span></a> even if they are totally asymptomatic under optimal medical therapy&#46; Moreover&#44; indication for excision of giant CAAs seems to be even stronger during elective cardiac operations performed for concomitant pathologies including valve disease&#44;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">2</span></a> coronary stenosis &#40;as in the present case<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">1</span></a>&#41;&#46; Therefore&#44; we wonder why the surgeons exclusively performed CABG&#44; and left the giant CAAs surgically untreated&#46; Performing a more radical operation could have solved the problem in a single attempt&#46; Was there a technical failure or an anatomical obstacle &#40;including involvement of the diagonal branch by the aneurysmal sac&#44; etc&#46;&#41; potentially hampering excision or modification of CAAs&#63; Unfortunately&#44; the patient may still experience recurrent coronary ischemic events &#40;due to coronary embolization&#44; compression on the left internal mammary artery graft by the expanding CAA&#44; etc&#46;&#41; and serious mechanical complications &#40;CAA rupture&#44; fistula formation&#41; potentially requiring re-operation in the long-term&#46; On the other hand&#44; we also are of the opinion that certain giant CAAs with a clear-cut temporal regression might be watchfully monitored under optimal medical therapy&#46; Accordingly&#44; we wonder about the initial dimensions of the giant CAAs in the patient &#40;the values around six weeks after KD onset when the patient&#39;s CAAs were supposed to have maximum diameters&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">1</span></a> Were the giant CAAs progressive&#44; regressive or stable in time according to the Z score values&#63; Based on temporal changes in CAA diameters&#44; CAA involving the LAD artery seems to have a regressive nature as opposed to the CAA of the right coronary artery with a potential tendency to expand in time&#46; We also wonder whether the authors would consider renin-angiotensin system blockade &#40;particularly with captopril&#41; that might have a favorable impact on CAA progression&#44; largely through the inhibition of certain key mediators of arterial remodeling&#44; including matrix metalloproteinases&#63;<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">2&#44;6</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">Finally&#44; this case report clearly supports the strong association between the evolution of coronary sequelae and the failure to administer disease-modifying agents &#40;intravenous immunoglobulin &#40;IVIG&#41;&#44; etc&#46;&#41; in a timely manner in the setting of acute KD episodes&#46;<a class="elsevierStyleCrossRefs" href="#bib0035"><span class="elsevierStyleSup">1&#8211;4</span></a> This also suggests there is a need to further heighten clinical awareness of KD symptoms among parents<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">1</span></a> and even clinicians for the prevention of these potentially fatal sequelae&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">In summary&#44; Magro et al&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">1</span></a> should be congratulated for their didactic article&#46; In the setting of KD&#44; management of coronary sequelae primarily need to be individualized according to patient characteristics&#46; In KD patients undergoing cardiac surgery&#44; management of all the existing coronary sequelae at a single time &#40;where applicable&#41; appears to be a reasonable strategy in clinical practice&#46; Nevertheless&#44; prevention of these sequelae with the timely initiation of disease-modifying agents should still be regarded as the primary goal in KD management&#46;</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0040" class="elsevierStylePara elsevierViewall">The authors have no conflicts of interest to declare&#46;</p></span></span>"
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ISSN: 08702551
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Revista Portuguesa de Cardiologia
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