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which identified mild coronary calcification &#40;calcium score 54 Agatston units&#41; with no endoluminal obstruction&#44; and also revealed thickening &#40;22 mm&#41; of the interventricular septum &#40;IVS&#41;&#46; Suspicion of HCM prompted investigation by magnetic resonance imaging &#40;MRI&#41;&#44; which confirmed the diagnosis of asymmetric HCM with hypertrophy of the basal and mid IVS &#40;22 mm&#41;&#44; all other walls being of normal thickness&#59; non-dilated LV with ejection fraction of 69&#37; and LV mass index of 78 g&#47;m<span class="elsevierStyleSup">2</span>&#59; moderately dilated left atrium &#40;area 33 cm<span class="elsevierStyleSup">2</span>&#41;&#59; and no late gadolinium enhancement &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Figure 2</a>&#41;&#46; The patient presented no risk factors for sudden cardiac death and genetic study for Fabry disease was negative&#59; screening for classic mutations in sarcomere protein genes is in progress&#46;</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0035" class="elsevierStylePara elsevierViewall">At 18-month follow-up she presented worsening functional capacity with dyspnea on moderate exertion &#40;New York Heart Association class II&#41;&#46; TTE was repeated and showed marked LV hypertrophy of the basal IVS and good global systolic function&#59; an apparently tricuspid AV&#44; calcified&#44; with reduced opening&#44; that could not be assessed by planimetry&#59; and a calcified mitral valve with systolic anterior motion &#40;SAM&#41;&#46; Doppler study revealed accelerated flow beginning in the LVOT&#44; with peak velocity at mid-systole and peak and mean LV&#47;Ao gradient of 49 mmHg and 32 mmHg&#44; respectively&#44; supporting the hypothesis of a fixed obstruction &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Figure 3</a>&#41;&#46; No late-systolic velocity peak was observed&#44; with or without the Valsalva maneuver&#46;</p><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0040" class="elsevierStylePara elsevierViewall">In view of the limitations of TTE&#44; transesophageal echocardiography &#40;TEE&#41; was performed&#44; which revealed a malformed AV with marked calcification and fusion of the noncoronary and left coronary leaflets&#44; with an area estimated by planimetry of 0&#46;6 cm<span class="elsevierStyleSup">2</span> &#40;0&#46;27 cm<span class="elsevierStyleSup">2</span>&#47;m<span class="elsevierStyleSup">2</span>&#41; &#40;<a class="elsevierStyleCrossRef" href="#fig0020">Figure 4</a>&#41;&#46; Color Doppler study clearly differentiated laminar flow in the LVOT and turbulent flow through the AV throughout systole&#44; confirming the suspicion of obstruction of the valve only &#40;<a class="elsevierStyleCrossRef" href="#fig0020">Figure 4</a>&#41;&#46;</p><elsevierMultimedia ident="fig0020"></elsevierMultimedia><p id="par0045" class="elsevierStylePara elsevierViewall">Invasive hemodynamic study showed a peak-to-peak LV&#47;Ao gradient of 52 mmHg and no intraventricular gradient&#44; and excluded significant coronary artery disease&#46;</p><p id="par0050" class="elsevierStylePara elsevierViewall">A 22-mm Medtronic Hall mechanical valve was implanted surgically in aortic position&#46; At six-month follow-up the patient presented improved functional capacity and TTE revealed a normally functioning aortic valve&#46;</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Discussion</span><p id="par0055" class="elsevierStylePara elsevierViewall">This case report highlights the difficulties of investigating a patient with both HCM and AS&#44; particularly in assessing the severity of each condition and determining which is functionally more important&#46; Identifying the cause of the high LVOT gradient as AS led to the patient being referred for valve replacement surgery&#44; which resolved the obstruction and improved symptoms&#46;</p><p id="par0060" class="elsevierStylePara elsevierViewall">Assessment of such patients is based on a thorough echocardiographic assessment of the LVOT region&#46;<a class="elsevierStyleCrossRefs" href="#bib0105"><span class="elsevierStyleSup">4&#44;5</span></a> Color and pulse wave Doppler study are essential to locate the level at which flow acceleration occurs&#44;<a class="elsevierStyleCrossRef" href="#bib0125"><span class="elsevierStyleSup">8</span></a> but TTE does not always provide definitive information&#46;</p><p id="par0065" class="elsevierStylePara elsevierViewall">Continuous-wave Doppler can quantify the obstruction&#44; and the shape of the velocity waveform is particularly useful in differentiating fixed and dynamic obstruction&#46;<a class="elsevierStyleCrossRefs" href="#bib0130"><span class="elsevierStyleSup">9&#44;10</span></a> Obstructive HCM is characterized by an LVOT or&#44; less commonly&#44; a midventricular gradient<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">11</span></a> that changes with variations in preload&#44; afterload and contractility&#46;<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">12</span></a> Since it is predominantly dynamic&#44; the gradient develops at end-systole and the waveform is dagger-shaped&#46; By contrast&#44; AS results in a fixed obstruction to LV outflow throughout systole with peak velocity at mid-systole&#44; giving a bell-shaped waveform&#46;<a class="elsevierStyleCrossRefs" href="#bib0110"><span class="elsevierStyleSup">5&#44;9&#44;10</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">In the case presented&#44; continuous-wave Doppler study indicated the presence of a fixed obstruction&#59; however&#44; the existence of SAM and marked septal hypertrophy raised the suspicion of a dynamic subaortic obstruction&#46; When assessing these patients&#44; particular care should be taken in interpreting the Doppler waveform&#44; since the two patterns may overlap and the presence of a second gradient may be overlooked&#46;<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">4</span></a> If the level of suspicion is high&#44; and TTE study is inconclusive&#44; TEE should be used&#46;<a class="elsevierStyleCrossRefs" href="#bib0105"><span class="elsevierStyleSup">4&#44;13</span></a></p><p id="par0075" class="elsevierStylePara elsevierViewall">TEE also plays an important role in screening for other conditions that can cause a fixed LVOT obstruction&#44; such as HCM itself &#40;due to fibrous tissue formation caused by contact between the mitral valve and the IVS&#41;&#44; accessory mitral tissue&#44; subaortic ridge&#44; and tunnel subaortic stenosis&#46;<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">12</span></a> In the present case&#44; TEE was crucial in identifying flow acceleration at the valve and in excluding other conditions&#46;</p><p id="par0080" class="elsevierStylePara elsevierViewall">The use of cardiac MRI to measure LVOT velocities has been described&#44; but Doppler TTE has been more thoroughly validated&#46;<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">13</span></a> In some cases an accurate hemodynamic study can only be obtained by invasive means&#46;<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">14</span></a></p><p id="par0085" class="elsevierStylePara elsevierViewall">Assessment of the severity of AS in patients with suspected obstructive HCM poses particular challenges and there is little information available on the subject&#46;<a class="elsevierStyleCrossRefs" href="#bib0110"><span class="elsevierStyleSup">5&#44;9&#44;14</span></a> Use of the modified Bernoulli equation &#40;&#916;P&#61;4v<span class="elsevierStyleSup">2</span>&#41; is based on certain assumptions that mean it cannot be used in patients with serial stenoses&#46;<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">14</span></a> When flow velocity exceeds 1&#46;0 m&#47;s&#44; the peak gradient can be estimated using the formula 4&#40;v<span class="elsevierStyleSup">2</span>max&#8722;v<span class="elsevierStyleSup">2</span> proximal&#41;&#44; but calculating the mean gradient is more complex and is not easy to apply in clinical practice&#46;<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">9</span></a> Accurate measurement of gradients may only be possible by means of an invasive hemodynamic study&#46;<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">14</span></a></p><p id="par0090" class="elsevierStylePara elsevierViewall">The continuity equation for measuring valve area cannot be used in the presence of LVOT obstruction&#46;<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">9</span></a> Planimetry is the recommended method&#44; ideally by TEE&#46;<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">13</span></a> In our patient&#44; the presence of valve malformation with marked calcification and an anatomical area of 0&#46;6 cm<span class="elsevierStyleSup">2</span> led to a diagnosis of severe AS&#46;</p><p id="par0095" class="elsevierStylePara elsevierViewall">Diagnosis of HCM in a patient with significant AS is also not straightforward&#46; It is based on the presence of LV hypertrophy&#44; frequently asymmetric and involving the IVS&#44; in the absence of other causes&#46;<a class="elsevierStyleCrossRefs" href="#bib0125"><span class="elsevierStyleSup">8&#44;11&#44;13&#44;15</span></a> AS is usually associated with a uniform or symmetric &#40;i&#46;e&#46; concentric&#41; distribution of LV hypertrophy&#44;<a class="elsevierStyleCrossRef" href="#bib0165"><span class="elsevierStyleSup">16</span></a> although an asymmetric septal distribution is reported in around 10&#37; of cases&#46;<a class="elsevierStyleCrossRefs" href="#bib0105"><span class="elsevierStyleSup">4&#44;16&#44;17</span></a> This makes diagnosis more difficult&#58; is the hypertrophy an adaptive response to AS or is it due to concomitant HCM&#63; In the case described here&#44; the presence of marked septal hypertrophy and SAM favored a diagnosis of concomitant HCM&#46; Genetic study and assessment of the evolution of ventricular hypertrophy following valve surgery may support the diagnosis&#46; Some authors have suggested other characteristics that corroborate a diagnosis of HCM&#44; including mitral valve abnormalities &#40;such as lengthening of the anterior leaflet&#41;&#44; hypertrophied or bifid papillary muscles or anteroapical displacement&#44; and family history&#46;<a class="elsevierStyleCrossRefs" href="#bib0105"><span class="elsevierStyleSup">4&#44;8&#44;14</span></a> MRI can have an important role in assessing some of these characteristics&#46;<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">14</span></a></p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Conclusions</span><p id="par0100" class="elsevierStylePara elsevierViewall">This paper highlights the complexity of assessing patients with HCM and severe symptomatic AS with high LVOT gradients&#46; Echocardiographic study is a challenge&#44; but thorough assessment is important due to its direct effect on choice of therapeutic strategy and thus on prognosis&#46;</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Ethical disclosures</span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Protection of human and animal subjects</span><p id="par0105" class="elsevierStylePara elsevierViewall">The authors declare that no experiments were performed on humans or animals for this investigation&#46;</p></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Confidentiality of data</span><p id="par0110" class="elsevierStylePara elsevierViewall">The authors declare that no patient data appear in this article&#46;</p></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Right to privacy and informed consent</span><p id="par0115" class="elsevierStylePara elsevierViewall">The authors declare that no patient data appear in this article&#46;</p></span></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Conflicts of interest</span><p id="par0120" class="elsevierStylePara elsevierViewall">The authors have no conflicts of interest to declare&#46;</p></span></span>"
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            0 => "Aortic valve stenosis"
            1 => "Hypertrophic cardiomyopathy"
            2 => "Left ventricular outflow tract obstruction"
            3 => "Echocardiography"
            4 => "Doppler echocardiography"
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            0 => "Estenose a&#243;rtica"
            1 => "Cardiomiopatia hipertr&#243;fica"
            2 => "Obstru&#231;&#227;o do trato de sa&#237;da do ventr&#237;culo esquerdo"
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        "titulo" => "Abstract"
        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">The authors report the case of a patient diagnosed with both hypertrophic cardiomyopathy and aortic stenosis&#46; Due to clinical deterioration&#44; additional investigation was performed&#44; and a high left ventricular outflow tract gradient was identified&#46; Correct identification of the condition causing the symptoms was challenging&#44; and involved several imaging techniques&#44; the contribution of transesophageal echocardiography being crucial&#46; The final diagnosis of severe aortic stenosis led to successful valve replacement surgery&#46; The presence of these two conditions in the same patient has been documented&#44; although it is uncommon&#46; This association poses particular diagnostic and therapeutic challenges&#44; which are discussed in this paper&#46;</p></span>"
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        "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Os autores apresentam o caso de uma doente com os diagn&#243;sticos de miocardiopatia hipertr&#243;fica e estenose a&#243;rtica&#44; na qual foi identificada a presen&#231;a de um gradiente elevado ao n&#237;vel do trato de sa&#237;da do ventr&#237;culo esquerdo&#46; O reconhecimento da patologia respons&#225;vel pela sintomatologia foi desafiante&#44; com envolvimento de v&#225;rias t&#233;cnicas de imagem&#44; tendo sido fundamental a contribui&#231;&#227;o do ecocardiograma transesof&#225;gico&#46; O diagn&#243;stico final de estenose a&#243;rtica severa conduziu &#224; referencia&#231;&#227;o para cirurgia de substitui&#231;&#227;o valvular&#44; com sucesso&#46; A presen&#231;a destas duas patologias em simult&#226;neo num mesmo doente &#233; conhecida&#44; embora incomum&#46; A sua combina&#231;&#227;o cria importantes desafios diagn&#243;sticos e terap&#234;uticos&#44; os quais ser&#227;o objeto de discuss&#227;o neste artigo&#46;</p></span>"
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        "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as&#58; Almeida I&#44; Caetano F&#44; Trigo J&#44; et al&#46; Gradiente elevado no trato de sa&#237;da do ventr&#237;culo esquerdo&#58; estenose a&#243;rtica&#44; miocardiopatia hipertr&#243;fica obstrutiva ou ambas&#63; Rev Port Cardiol&#46; 2015&#59;34&#58;357&#46;</p>"
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          "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Electrocardiogram showing sinus rhythm&#44; heart rate 75 bpm&#44; voltage criteria for left ventricular hypertrophy&#44; without overload&#46;</p>"
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          "en" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Cardiac magnetic resonance imaging showing marked hypertrophy of the basal and mid interventricular septum &#40;22 mm&#41; and moderately dilated left atrium &#40;area 33 cm<span class="elsevierStyleSup">2</span>&#41;&#46;</p>"
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          "en" => "<p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">Transthoracic echocardiography&#58; &#40;left&#41; color Doppler showing turbulent flow beginning in the left ventricular outflow tract&#59; &#40;right&#41; continuous-wave Doppler showing rounded waveform with mid-systolic peak &#40;bell-shaped&#41; and peak and mean left ventricular&#47;aortic gradient of 49 mmHg and 32 mmHg&#44; respectively&#46;</p>"
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Case report
High left ventricular outflow tract gradient: Aortic stenosis, obstructive hypertrophic cardiomyopathy or both?
Gradiente elevado no trato de saída do ventrículo esquerdo: estenose aórtica, miocardiopatia hipertrófica obstrutiva ou ambas?
Inês Almeida
Corresponding author
inesalm@gmail.com

Corresponding author.
, Francisca Caetano, Joana Trigo, Paula Mota, António Leitão Marques
Serviço de Cardiologia, Centro Hospitalar e Universitário de Coimbra – Hospital Geral, Coimbra, Portugal
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    "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">Aortic stenosis &#40;AS&#41; and hypertrophic cardiomyopathy &#40;HCM&#41; are two conditions that can cause hemodynamic gradients in the left ventricular outflow tract &#40;LVOT&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">1</span></a> In both cases the presence of significant obstruction has clinical&#44; therapeutic and prognostic implications&#46;<a class="elsevierStyleCrossRefs" href="#bib0090"><span class="elsevierStyleSup">1&#8211;3</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">The presence of both of these conditions in the same patient has been documented&#44; although it is uncommon&#46; This association poses particular diagnostic and therapeutic challenges&#46;<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">4</span></a> Meticulous echocardiographic assessment is required for correct identification of the cause of the obstruction&#44;<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">5</span></a> although this can be complicated&#44; and the result can lead to different therapeutic options&#46;<a class="elsevierStyleCrossRefs" href="#bib0115"><span class="elsevierStyleSup">6&#44;7</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">This case report aims to discuss the complexity of such cases&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Case report</span><p id="par0020" class="elsevierStylePara elsevierViewall">A 68-year-old woman&#44; with a history of hypertension&#44; dyslipidemia&#44; obesity and breast cancer &#40;treated by left mastectomy and adjuvant chemotherapy and radiotherapy in 1998&#41;&#44; was referred for cardiology consultation in April 2011 to investigate chest pain&#59; she had no other cardiovascular symptoms&#46; On physical examination&#44; auscultation revealed a grade III&#47;VI systolic murmur audible at the right second intercostal space&#44; crescendo-decrescendo and radiating to the carotids&#59; the murmur became less intense with the Valsalva maneuver and on standing up&#44; and increased with squatting&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">A previous electrocardiogram had shown sinus rhythm with voltage criteria for left ventricular hypertrophy without overload &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Figure 1</a>&#41;&#44; while transthoracic echocardiography &#40;TTE&#41; &#40;described as &#8220;technically very difficult&#8221;&#41; had revealed concentric hypertrophy of the left ventricle &#40;LV&#41; with no wall motion abnormalities and with preserved global systolic function and a calcified aortic valve &#40;AV&#41; with moderate stenosis &#40;mean left ventricle&#47;aorta &#91;LV&#47;Ao&#93; gradient of 21 mmHg&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0030" class="elsevierStylePara elsevierViewall">Given the patient&#39;s low pretest probability of coronary artery disease&#44; coronary computed tomography angiography was performed&#44; which identified mild coronary calcification &#40;calcium score 54 Agatston units&#41; with no endoluminal obstruction&#44; and also revealed thickening &#40;22 mm&#41; of the interventricular septum &#40;IVS&#41;&#46; Suspicion of HCM prompted investigation by magnetic resonance imaging &#40;MRI&#41;&#44; which confirmed the diagnosis of asymmetric HCM with hypertrophy of the basal and mid IVS &#40;22 mm&#41;&#44; all other walls being of normal thickness&#59; non-dilated LV with ejection fraction of 69&#37; and LV mass index of 78 g&#47;m<span class="elsevierStyleSup">2</span>&#59; moderately dilated left atrium &#40;area 33 cm<span class="elsevierStyleSup">2</span>&#41;&#59; and no late gadolinium enhancement &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Figure 2</a>&#41;&#46; The patient presented no risk factors for sudden cardiac death and genetic study for Fabry disease was negative&#59; screening for classic mutations in sarcomere protein genes is in progress&#46;</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0035" class="elsevierStylePara elsevierViewall">At 18-month follow-up she presented worsening functional capacity with dyspnea on moderate exertion &#40;New York Heart Association class II&#41;&#46; TTE was repeated and showed marked LV hypertrophy of the basal IVS and good global systolic function&#59; an apparently tricuspid AV&#44; calcified&#44; with reduced opening&#44; that could not be assessed by planimetry&#59; and a calcified mitral valve with systolic anterior motion &#40;SAM&#41;&#46; Doppler study revealed accelerated flow beginning in the LVOT&#44; with peak velocity at mid-systole and peak and mean LV&#47;Ao gradient of 49 mmHg and 32 mmHg&#44; respectively&#44; supporting the hypothesis of a fixed obstruction &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Figure 3</a>&#41;&#46; No late-systolic velocity peak was observed&#44; with or without the Valsalva maneuver&#46;</p><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0040" class="elsevierStylePara elsevierViewall">In view of the limitations of TTE&#44; transesophageal echocardiography &#40;TEE&#41; was performed&#44; which revealed a malformed AV with marked calcification and fusion of the noncoronary and left coronary leaflets&#44; with an area estimated by planimetry of 0&#46;6 cm<span class="elsevierStyleSup">2</span> &#40;0&#46;27 cm<span class="elsevierStyleSup">2</span>&#47;m<span class="elsevierStyleSup">2</span>&#41; &#40;<a class="elsevierStyleCrossRef" href="#fig0020">Figure 4</a>&#41;&#46; Color Doppler study clearly differentiated laminar flow in the LVOT and turbulent flow through the AV throughout systole&#44; confirming the suspicion of obstruction of the valve only &#40;<a class="elsevierStyleCrossRef" href="#fig0020">Figure 4</a>&#41;&#46;</p><elsevierMultimedia ident="fig0020"></elsevierMultimedia><p id="par0045" class="elsevierStylePara elsevierViewall">Invasive hemodynamic study showed a peak-to-peak LV&#47;Ao gradient of 52 mmHg and no intraventricular gradient&#44; and excluded significant coronary artery disease&#46;</p><p id="par0050" class="elsevierStylePara elsevierViewall">A 22-mm Medtronic Hall mechanical valve was implanted surgically in aortic position&#46; At six-month follow-up the patient presented improved functional capacity and TTE revealed a normally functioning aortic valve&#46;</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Discussion</span><p id="par0055" class="elsevierStylePara elsevierViewall">This case report highlights the difficulties of investigating a patient with both HCM and AS&#44; particularly in assessing the severity of each condition and determining which is functionally more important&#46; Identifying the cause of the high LVOT gradient as AS led to the patient being referred for valve replacement surgery&#44; which resolved the obstruction and improved symptoms&#46;</p><p id="par0060" class="elsevierStylePara elsevierViewall">Assessment of such patients is based on a thorough echocardiographic assessment of the LVOT region&#46;<a class="elsevierStyleCrossRefs" href="#bib0105"><span class="elsevierStyleSup">4&#44;5</span></a> Color and pulse wave Doppler study are essential to locate the level at which flow acceleration occurs&#44;<a class="elsevierStyleCrossRef" href="#bib0125"><span class="elsevierStyleSup">8</span></a> but TTE does not always provide definitive information&#46;</p><p id="par0065" class="elsevierStylePara elsevierViewall">Continuous-wave Doppler can quantify the obstruction&#44; and the shape of the velocity waveform is particularly useful in differentiating fixed and dynamic obstruction&#46;<a class="elsevierStyleCrossRefs" href="#bib0130"><span class="elsevierStyleSup">9&#44;10</span></a> Obstructive HCM is characterized by an LVOT or&#44; less commonly&#44; a midventricular gradient<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">11</span></a> that changes with variations in preload&#44; afterload and contractility&#46;<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">12</span></a> Since it is predominantly dynamic&#44; the gradient develops at end-systole and the waveform is dagger-shaped&#46; By contrast&#44; AS results in a fixed obstruction to LV outflow throughout systole with peak velocity at mid-systole&#44; giving a bell-shaped waveform&#46;<a class="elsevierStyleCrossRefs" href="#bib0110"><span class="elsevierStyleSup">5&#44;9&#44;10</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">In the case presented&#44; continuous-wave Doppler study indicated the presence of a fixed obstruction&#59; however&#44; the existence of SAM and marked septal hypertrophy raised the suspicion of a dynamic subaortic obstruction&#46; When assessing these patients&#44; particular care should be taken in interpreting the Doppler waveform&#44; since the two patterns may overlap and the presence of a second gradient may be overlooked&#46;<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">4</span></a> If the level of suspicion is high&#44; and TTE study is inconclusive&#44; TEE should be used&#46;<a class="elsevierStyleCrossRefs" href="#bib0105"><span class="elsevierStyleSup">4&#44;13</span></a></p><p id="par0075" class="elsevierStylePara elsevierViewall">TEE also plays an important role in screening for other conditions that can cause a fixed LVOT obstruction&#44; such as HCM itself &#40;due to fibrous tissue formation caused by contact between the mitral valve and the IVS&#41;&#44; accessory mitral tissue&#44; subaortic ridge&#44; and tunnel subaortic stenosis&#46;<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">12</span></a> In the present case&#44; TEE was crucial in identifying flow acceleration at the valve and in excluding other conditions&#46;</p><p id="par0080" class="elsevierStylePara elsevierViewall">The use of cardiac MRI to measure LVOT velocities has been described&#44; but Doppler TTE has been more thoroughly validated&#46;<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">13</span></a> In some cases an accurate hemodynamic study can only be obtained by invasive means&#46;<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">14</span></a></p><p id="par0085" class="elsevierStylePara elsevierViewall">Assessment of the severity of AS in patients with suspected obstructive HCM poses particular challenges and there is little information available on the subject&#46;<a class="elsevierStyleCrossRefs" href="#bib0110"><span class="elsevierStyleSup">5&#44;9&#44;14</span></a> Use of the modified Bernoulli equation &#40;&#916;P&#61;4v<span class="elsevierStyleSup">2</span>&#41; is based on certain assumptions that mean it cannot be used in patients with serial stenoses&#46;<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">14</span></a> When flow velocity exceeds 1&#46;0 m&#47;s&#44; the peak gradient can be estimated using the formula 4&#40;v<span class="elsevierStyleSup">2</span>max&#8722;v<span class="elsevierStyleSup">2</span> proximal&#41;&#44; but calculating the mean gradient is more complex and is not easy to apply in clinical practice&#46;<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">9</span></a> Accurate measurement of gradients may only be possible by means of an invasive hemodynamic study&#46;<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">14</span></a></p><p id="par0090" class="elsevierStylePara elsevierViewall">The continuity equation for measuring valve area cannot be used in the presence of LVOT obstruction&#46;<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">9</span></a> Planimetry is the recommended method&#44; ideally by TEE&#46;<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">13</span></a> In our patient&#44; the presence of valve malformation with marked calcification and an anatomical area of 0&#46;6 cm<span class="elsevierStyleSup">2</span> led to a diagnosis of severe AS&#46;</p><p id="par0095" class="elsevierStylePara elsevierViewall">Diagnosis of HCM in a patient with significant AS is also not straightforward&#46; It is based on the presence of LV hypertrophy&#44; frequently asymmetric and involving the IVS&#44; in the absence of other causes&#46;<a class="elsevierStyleCrossRefs" href="#bib0125"><span class="elsevierStyleSup">8&#44;11&#44;13&#44;15</span></a> AS is usually associated with a uniform or symmetric &#40;i&#46;e&#46; concentric&#41; distribution of LV hypertrophy&#44;<a class="elsevierStyleCrossRef" href="#bib0165"><span class="elsevierStyleSup">16</span></a> although an asymmetric septal distribution is reported in around 10&#37; of cases&#46;<a class="elsevierStyleCrossRefs" href="#bib0105"><span class="elsevierStyleSup">4&#44;16&#44;17</span></a> This makes diagnosis more difficult&#58; is the hypertrophy an adaptive response to AS or is it due to concomitant HCM&#63; In the case described here&#44; the presence of marked septal hypertrophy and SAM favored a diagnosis of concomitant HCM&#46; Genetic study and assessment of the evolution of ventricular hypertrophy following valve surgery may support the diagnosis&#46; Some authors have suggested other characteristics that corroborate a diagnosis of HCM&#44; including mitral valve abnormalities &#40;such as lengthening of the anterior leaflet&#41;&#44; hypertrophied or bifid papillary muscles or anteroapical displacement&#44; and family history&#46;<a class="elsevierStyleCrossRefs" href="#bib0105"><span class="elsevierStyleSup">4&#44;8&#44;14</span></a> MRI can have an important role in assessing some of these characteristics&#46;<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">14</span></a></p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Conclusions</span><p id="par0100" class="elsevierStylePara elsevierViewall">This paper highlights the complexity of assessing patients with HCM and severe symptomatic AS with high LVOT gradients&#46; Echocardiographic study is a challenge&#44; but thorough assessment is important due to its direct effect on choice of therapeutic strategy and thus on prognosis&#46;</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Ethical disclosures</span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Protection of human and animal subjects</span><p id="par0105" class="elsevierStylePara elsevierViewall">The authors declare that no experiments were performed on humans or animals for this investigation&#46;</p></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Confidentiality of data</span><p id="par0110" class="elsevierStylePara elsevierViewall">The authors declare that no patient data appear in this article&#46;</p></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Right to privacy and informed consent</span><p id="par0115" class="elsevierStylePara elsevierViewall">The authors declare that no patient data appear in this article&#46;</p></span></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Conflicts of interest</span><p id="par0120" class="elsevierStylePara elsevierViewall">The authors have no conflicts of interest to declare&#46;</p></span></span>"
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            0 => "Aortic valve stenosis"
            1 => "Hypertrophic cardiomyopathy"
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            2 => "Obstru&#231;&#227;o do trato de sa&#237;da do ventr&#237;culo esquerdo"
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        "titulo" => "Abstract"
        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">The authors report the case of a patient diagnosed with both hypertrophic cardiomyopathy and aortic stenosis&#46; Due to clinical deterioration&#44; additional investigation was performed&#44; and a high left ventricular outflow tract gradient was identified&#46; Correct identification of the condition causing the symptoms was challenging&#44; and involved several imaging techniques&#44; the contribution of transesophageal echocardiography being crucial&#46; The final diagnosis of severe aortic stenosis led to successful valve replacement surgery&#46; The presence of these two conditions in the same patient has been documented&#44; although it is uncommon&#46; This association poses particular diagnostic and therapeutic challenges&#44; which are discussed in this paper&#46;</p></span>"
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        "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Os autores apresentam o caso de uma doente com os diagn&#243;sticos de miocardiopatia hipertr&#243;fica e estenose a&#243;rtica&#44; na qual foi identificada a presen&#231;a de um gradiente elevado ao n&#237;vel do trato de sa&#237;da do ventr&#237;culo esquerdo&#46; O reconhecimento da patologia respons&#225;vel pela sintomatologia foi desafiante&#44; com envolvimento de v&#225;rias t&#233;cnicas de imagem&#44; tendo sido fundamental a contribui&#231;&#227;o do ecocardiograma transesof&#225;gico&#46; O diagn&#243;stico final de estenose a&#243;rtica severa conduziu &#224; referencia&#231;&#227;o para cirurgia de substitui&#231;&#227;o valvular&#44; com sucesso&#46; A presen&#231;a destas duas patologias em simult&#226;neo num mesmo doente &#233; conhecida&#44; embora incomum&#46; A sua combina&#231;&#227;o cria importantes desafios diagn&#243;sticos e terap&#234;uticos&#44; os quais ser&#227;o objeto de discuss&#227;o neste artigo&#46;</p></span>"
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        "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as&#58; Almeida I&#44; Caetano F&#44; Trigo J&#44; et al&#46; Gradiente elevado no trato de sa&#237;da do ventr&#237;culo esquerdo&#58; estenose a&#243;rtica&#44; miocardiopatia hipertr&#243;fica obstrutiva ou ambas&#63; Rev Port Cardiol&#46; 2015&#59;34&#58;357&#46;</p>"
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          "en" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Cardiac magnetic resonance imaging showing marked hypertrophy of the basal and mid interventricular septum &#40;22 mm&#41; and moderately dilated left atrium &#40;area 33 cm<span class="elsevierStyleSup">2</span>&#41;&#46;</p>"
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          "en" => "<p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">Transthoracic echocardiography&#58; &#40;left&#41; color Doppler showing turbulent flow beginning in the left ventricular outflow tract&#59; &#40;right&#41; continuous-wave Doppler showing rounded waveform with mid-systolic peak &#40;bell-shaped&#41; and peak and mean left ventricular&#47;aortic gradient of 49 mmHg and 32 mmHg&#44; respectively&#46;</p>"
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Revista Portuguesa de Cardiologia (English edition)
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