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it was noted that the patient had ketone breath and was hypotensive &#40;non-invasive arm blood pressure measurement of 77&#47;52&#8239;mmHg&#41;&#44; tachycardic &#40;heart rate &#91;HR&#93; 102&#8239;bpm&#41;&#44; polypneic &#40;respiratory rate 30&#8239;cpm&#41;&#44; and hypothermic &#40;axillary body temperature 35&#46;8&#8239;&#176;C&#41;&#46; Capillary testing revealed unmeasurable blood glucose &#40;HIGH test result&#41; and increased ketonemia &#40;3&#59; normal &#60;1&#46;2&#41;&#46; Arterial blood gas analysis demonstrated severe metabolic acidosis &#40;pH 7&#46;1&#44; pCO<span class="elsevierStyleInf">2</span> 9&#46;2&#8239;mmHg&#44; pO<span class="elsevierStyleInf">2</span> 139&#8239;mmHg&#44; HCO<span class="elsevierStyleInf">3</span>- 2&#46;9&#8239;mmol&#47;l&#41;&#44; hyperlactacidemia &#40;lactates 9&#8239;mmol&#47;l&#41;&#44; hyperkalemia &#40;K<span class="elsevierStyleSup">&#43;</span> 7&#46;52 mEq&#47;l&#41; and hyponatremia &#40;Na<span class="elsevierStyleSup">&#43;</span> 126 mEq&#47;l&#41; considered pseudohyponatremia and when corrected for blood glucose estimated to be 500&#8239;mg&#47;dl &#40;HIGH capillary test result&#41;&#44; giving a figure of 136 mEq&#47;l&#46; A diagnosis of diabetic ketoacidosis &#40;DKA&#41; was made and therapy was begun with rapid intravenous &#40;IV&#41; insulin in continuous perfusion and IV hydration with sodium chloride 0&#46;9&#37; at 100 cc&#47;hour and external warming&#46; The decompensating factor was failure to administer insulin in the previous two days&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">The first venous blood analysis showed elevated troponin I &#40;2&#46;01&#8239;ng&#47;ml&#59; normal &#60;0&#46;02&#8239;ng&#47;ml&#41;&#44; with a peak of 3&#46;23&#8239;ng&#47;ml 12&#8239;hours after admission&#46; N-terminal pro-brain natriuretic peptide &#40;NT-proBNP&#41; was 17316&#8239;pg&#47;ml &#40;normal &#60;125&#41;&#46; The patient reported no current or previous chest pain or any symptoms of HF&#46; Physical examination showed no signs of cardiovascular disease&#59; there were no murmurs or extra heart sounds on cardiac auscultation&#44; no rales on pulmonary auscultation&#44; no enlarged organs on abdominal examination and no lower limb edema&#46; The electrocardiogram showed sinus tachycardia &#40;HR 109 bpm&#41; with ST-segment flattening in V5&#44; V6&#44; I and aVL&#46; A transthoracic echocardiogram &#40;TTE&#41; performed on the day of admission using a GE Vivid I portable ultrasound machine revealed a non-dilated and non-hypertrophied left ventricle with severe left ventricular systolic dysfunction &#40;ejection fraction &#91;EF&#93; estimated at 26&#37;&#41; due to diffuse hypokinesia&#59; no significant aortic or mitral valve disease&#59; preserved right ventricular longitudinal systolic function&#59; inferior vena cava 17&#8239;mm with preserved respiratory kinetics and pulmonary artery pressure estimated at 28&#8239;mmHg &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Figure 1</a>&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0030" class="elsevierStylePara elsevierViewall">At 48&#8239;hours of hospitalization&#44; and with his DKA resolved&#44; the patient was transferred to the cardiology ward to investigate the etiology of his left ventricular dysfunction&#46; During the investigation it transpired that he had been hospitalized about 15 months before&#44; also with a setting of diabetic ketacidosis&#46; At that time troponin I was also elevated and a rapid TTE performed in the ED demonstrated severe global left ventricular systolic dysfunction&#44; but a second TTE performed in the echocardiographic laboratory eight days after admission was normal&#46; It was assumed that the first exam had been incorrectly reported and no follow-up was scheduled&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">During the patient&#8217;s stay in the cardiology ward&#44; diagnostic cardiac catheterization revealed coronary arteries without lesions &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Figure 2</a>&#41;&#46; There was no history of HF&#44; cardiomyopathy or sudden death&#44; and the patient denied recent viral or bacterial infection and had never traveled abroad&#46; Laboratory tests were negative&#44; including for human immunodeficiency virus and hepatotropic viruses&#46; Thyroid function tests were normal&#44; as they had been throughout his follow-up in the diabetes clinic&#44; although antithyroid antibodies were not assessed&#46; Other laboratory parameters measured during hospital stay included hemoglobin 15&#8239;g&#47;dl at admission &#40;nadir 13&#8239;g&#47;dl&#41;&#44; no blood loss being documented&#59; no functional or absolute iron deficiency &#40;ferritin 326&#8239;ng&#47;ml&#41; and no folic acid or vitamin B<span class="elsevierStyleInf">12</span> deficiency &#40;5&#46;9&#8239;ng&#47;ml and 590&#8239;pg&#47;ml&#44; respectively&#41;&#59; and vitamin B<span class="elsevierStyleInf">1</span>&#44; routinely assessed in patients with HF or left ventricular dysfunction&#44; 28&#8239;ng&#47;ml &#40;normal 16&#8211;48&#41;&#46;</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0040" class="elsevierStylePara elsevierViewall">Seven days after admission&#44; a new TTE showed a non-dilated left ventricle&#44; with mild systolic dysfunction &#40;estimated EF 46&#37;&#41; and slightly reduced global longitudinal strain &#40;&#8722;16&#37;&#41; &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Figure 3</a>&#41;&#46; Cardiac magnetic resonance was proposed but the patient refused&#46; At hospital discharge he was in New York Heart Association class I&#44; with NT-proBNP 448&#8239;pg&#47;ml&#44; medicated with ramipril 2&#46;5&#8239;mg&#47;day and bisoprolol 5&#8239;mg&#47;day&#44; as well as slow-release insulin administered twice a day&#44; and was referred for cardiology and diabetes consultations&#46;</p><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0045" class="elsevierStylePara elsevierViewall">A third TTE&#44; scheduled for one week after discharge&#44; showed preserved global left ventricular systolic function &#40;EF 52&#37;&#41; and normal global longitudinal strain &#40;&#8722;20&#46;2&#37;&#41; &#40;<a class="elsevierStyleCrossRef" href="#fig0020">Figure 4</a>&#41;&#46; At eight months of follow-up&#44; the patient had not been readmitted and had no cardiovascular symptoms&#46;</p><elsevierMultimedia ident="fig0020"></elsevierMultimedia></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Discussion</span><p id="par0050" class="elsevierStylePara elsevierViewall">DKA is characterized by the triad of high blood glucose&#44; ketosis and metabolic acidemia resulting from a relative or absolute deficiency of insulin and excess of counter-regulatory hormones&#44; associated with severe electrolyte abnormalities&#46; Patients with DKA usually have mild to moderate hyperkalemia on initial assessment&#44; despite total-body potassium deficiency&#46;</p><p id="par0055" class="elsevierStylePara elsevierViewall">According to international guidelines&#44;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> our patient presented moderate to severe DKA &#40;pH 7&#46;1&#44; HCO<span class="elsevierStyleInf">3</span>- 2&#46;3 and altered mental status&#41;&#46; Thanks to rapid initiation of recommended treatment&#44; including insulin therapy and IV hydration&#44; no life-threatening complications occurred&#44; even though mortality in this entity ranges between 1&#37; and 5&#37; in different registries&#44; depending on age and comorbidities&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> Although our patient presented hyperkalemia&#44; no specific treatment was instituted for this condition&#44; in view of the knowledge that these patients in fact have a total-body K<span class="elsevierStyleSup">&#43;</span> deficiency and that beginning IV insulin therapy causes an inflow of K&#43; into cells&#44; thereby reducing kalemia&#46;</p><p id="par0060" class="elsevierStylePara elsevierViewall">In 2004 Stentz et al&#46; published a study<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> aiming to analyze the status of proinflammatory cytokines and markers of oxidative stress and cardiovascular risks associated with the known proinflammatory states of acute and chronic hyperglycemia&#44; in both DKA and nonketotic hyperglycemia&#46; They concluded that both conditions are associated with elevation of proinflammatory cytokines&#44; reactive oxygen species &#40;ROS&#41;&#44; and cardiovascular risk factors&#44; including C-reactive protein&#44; homocysteine and plasminogen activator inhibitor-1&#46; They also showed that values of these parameters returned to normal levels &#40;in the absence of obvious infection or cardiovascular pathology&#41; with insulin therapy&#44; and therefore characterize these two conditions as inflammatory diseases&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> Evidence from other studies reveals a significant and independent link between inflammation&#44; sepsis&#44; insulin resistance and cardiac dysfunction&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a> The classic outcome of this relationship is systemic inflammatory response syndrome &#40;SIRS&#41;&#44; which is found in many conditions&#44; the best-known being sepsis&#44; but also in non-infectious acute inflammatory settings such as acute pancreatitis&#44; trauma and burns&#46; It is defined by the presence of two or more of the following criteria&#58; temperature &#62;38&#8239;&#176;C or &#60;36&#8239;&#176;C&#44; HR&#8239;&#62;&#8239;90 bpm&#44; respiratory rate &#62;20&#8239;cpm or PaCO<span class="elsevierStyleInf">2</span> &#60;32&#8239;mmHg&#44; and white blood cell count &#62;12 000&#47;mm<span class="elsevierStyleSup">3</span> or &#60;4000&#47;mm<span class="elsevierStyleSup">3</span> or &#62;10&#37; immature bands&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> Our patient thus fulfilled criteria for SIRS in the setting of acute inflammation due to acute decompensation of diabetes &#40;DKA&#41;&#46;</p><p id="par0065" class="elsevierStylePara elsevierViewall">Myocardial dysfunction is a common complication in patients with SIRS due to sepsis and is associated with increased mortality&#44; which can reach 70-90&#37;&#44;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> as well as in SIRS due to trauma or burns&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">The initial TTE in the case presented was performed urgently but after intensive hydration as part of the routine treatment of DKA&#46; As a consequence&#44; it was not possible to estimate the patient&#8217;s volemia via the inferior vena cava&#46; We consider that&#44; in contrast to other patients with severe left ventricular dysfunction&#44; in this case such a significant increase in preload caused by intensive hydration to treat DKA might have led to volume overload and acute pulmonary edema&#46; However&#44; this did not occur&#44; probably because besides DKA&#44; the patient also had L-profile HF &#40;&#8216;cold-dry&#8217;&#41;&#44;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> as shown by hypotension and hyperlactacidemia&#44; markers of hypoperfusion &#40;which may also have contributed to his altered mental state on admission&#41;&#46; L-profile HF is most often associated with excessive diuretic use&#44; and the indicated treatment is fluid replacement&#44;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> which in our opinion should be carefully monitored both clinically and by imaging studies such as are readily available in the ED&#44; like echocardiography&#44; in order to prevent complications associated with excessive restoration of volemia&#46;</p><p id="par0075" class="elsevierStylePara elsevierViewall">Berk et al&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a> report a case of a patient admitted in 2015 with hyperosmolar hyperglycemic state &#40;HHS&#41;&#44; whose TTE performed due to electrocardiographic alterations showed severe left ventricular dysfunction&#46; On the fourth day of hospitalization she underwent imaging tests for ischemia&#44; which were negative and left ventricular function was also normal&#46; The authors suggested as possible causes for this reversible dysfunction HHS&#44; SIRS and euthyroid sick syndrome&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a> Nanda et al&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a> documented a unique case of DKA-induced stress-related cardiomyopathy in a woman with type 1 diabetes&#46; They hypothesize that the rarity of this association may be due to the fact that myocytes have a decreased ability to metabolize glucose and free fatty acids in takotsubo cardiomyopathy and can preferentially change their metabolic substrate to ketones&#44; which are found in DKA&#46; Furthermore&#44; the association of DKA and stress cardiomyopathy may lead to severe acidemia&#44; with HCO<span class="elsevierStyleInf">3</span>- 4&#8239;mmol&#47;l&#44; which may be one factor in the left ventricular dysfunction reported in this case&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a></p><p id="par0080" class="elsevierStylePara elsevierViewall">Besides the role of proinflammatory cytokines and ROS in SIRS-related myocardial dysfunction&#44; changes in calcium homeostasis are also involved&#44; as calcium inflow into myocytes is reduced and release of this cation from the sarcoplasmic reticulum is inhibited&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">12</span></a></p><p id="par0085" class="elsevierStylePara elsevierViewall">The possibility cannot be excluded that the metabolic acidemia found in DKA may also have been a factor in the reversible left ventricular dysfunction observed in the present case&#46; To the best of our knowledge&#44; there have been few reports in the literature on the impact of acid-base disorders on cardiac function&#46; In a 1990 study&#44; Teplinsky et al&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a> published an experimental study of the effect of lactic acidosis on hemodynamics and left ventricular function in dogs&#46; They demonstrated that during progressive acidemia induced by continuous IV infusion of lactic acid&#44; cardiac output&#44; stroke volume&#44; and mean systemic arterial pressure fell&#44; while mean pulmonary artery pressure and right atrial pressure increased&#46; The authors concluded that lactic acidemia caused a 40&#37; reduction in stroke volume&#44; which could be attributed to depressed LV contractility&#44; characterized by a decrease in maximum dP&#47;dt&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a> Also in 1990&#44; a review of the effects of acidosis on cardiac contractility concluded that this acid-base disorder affects every step in the excitation-contraction coupling pathway&#44; including the counter-regulatory effects on Ca<span class="elsevierStyleSup">2&#43;</span> delivery to myofilaments &#40;reduced delivery by inhibition of the Ca<span class="elsevierStyleSup">2&#43;</span> current and reduced release of this cation from the sarcoplasmic reticulum&#44; as well as increased delivery by prolongation of the action potential&#41; and the responsiveness of myofilaments to Ca<span class="elsevierStyleSup">2&#43;</span>&#44; which overall is reduced&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a></p><p id="par0090" class="elsevierStylePara elsevierViewall">Another review&#44; published in 1995&#44;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a> concluded that the effect of acidemia on ventricular function depends on pH level&#58; in mild acidemia&#44; increased catecholamine release compensates for the cardiac depressant effects of acidemia&#44; with increased inotropy&#44; chronotropy&#44; cardiac output and peripheral vascular resistance&#44; while when pH is &#60;7&#46;2&#44; as in our patient&#44; H<span class="elsevierStyleSup">&#43;</span> ions have a direct cardiac depressant action that cannot be compensated by increased catecholamines&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a></p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Conclusion</span><p id="par0095" class="elsevierStylePara elsevierViewall">Myocardial dysfunction is a frequent complication associated with SIRS&#44; whether secondary to sepsis or to other acute inflammatory states such as DKA&#44; the common mechanism being high levels of proinflammatory cytokines and ROS&#46; As well as SIRS&#44; other electrolyte and acid-base disorders may have contributed to the reversible left ventricular dysfunction observed in our patient&#44; in whom acute L-profile HF was associated with DKA&#46; We consider that&#44; as the negative impact of ventricular dysfunction on the prognosis of these patients is now proven&#44; echocardiographic assessment should be performed routinely and that those with systolic or diastolic dysfunction should be scheduled for follow-up to monitor reversal of dysfunction&#44; control other risk factors and investigate other concomitant etiologies&#46;</p><p id="par0100" class="elsevierStylePara elsevierViewall">As the pathogenesis of diabetic cardiomyopathy includes oxidative stress&#44;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> the association of the latter with ventricular dysfunction in settings of acute decompensation may point the way to therapeutic studies based on inhibiting these proinflammatory processes&#44; with a view to reducing mortality in these acute settings and hopefully preventing progression to irreversible ventricular dysfunction&#46;</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Conflicts of interest</span><p id="par0105" class="elsevierStylePara elsevierViewall">The authors have no conflicts of interest to declare&#46;</p></span></span>"
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        "titulo" => "Abstract"
        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">The authors describe a case of a patient admitted to the emergency department with diabetic ketoacidosis&#46; Although there were no symptoms attributable to the cardiovascular system&#44; lab tests revealed elevated troponin I and natriuretic peptides&#44; coupled with repolarization abnormalities on the ECG&#46; The transthoracic echocardiogram &#40;TTE&#41; showed a non-dilated left ventricle with severe left ventricular systolic dysfunction due to diffuse hypokinesia&#44; and a concomitant diagnosis of profile L heart failure was proposed&#46; Etiologic investigation was negative&#44; and when a new TTE was performed seven days after the first&#44; left ventricular function was normal&#46; Although rarely considered&#44; metabolic and electrolyte disorders&#44; especially diabetic ketoacidosis&#44; can be a cause of left ventricular systolic dysfunction&#44; and should be considered in the differential diagnosis&#46; This is another way diabetes can have an impact on the cardiovascular system&#46;</p></span>"
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        "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">Os autores descrevem um caso de um doente admitido no Servi&#231;o de Urg&#234;ncia por cetoacidose diab&#233;tica&#46; Apesar de n&#227;o haver queixas do foro cardiovascular&#44; a avalia&#231;&#227;o anal&#237;tica revelou uma eleva&#231;&#227;o do n&#237;vel de troponina I &#40;TropI&#41; e de p&#233;ptidos natriur&#233;ticos &#40;proBNP&#41;&#44; associada a altera&#231;&#245;es da repolariza&#231;&#227;o no eletrocardiograma&#46; O ecocardiograma transtor&#225;cico &#40;ETT&#41; mostrou um ventr&#237;culo esquerdo n&#227;o dilatado com disfun&#231;&#227;o sist&#243;lica ventricular esquerda grave&#44; por hipocinesia difusa&#44; assumindo&#8208;se assim concomitantemente um perfil L de insufici&#234;ncia card&#237;aca &#40;IC&#41;&#46; A investiga&#231;&#227;o etiol&#243;gica foi negativa e quando um novo ETT foi realizado&#44; sete dias ap&#243;s o primeiro&#44; a fun&#231;&#227;o ventricular esquerda era normal&#46; Apesar de raramente considerados&#44; os dist&#250;rbios metab&#243;licos e hidroeletrol&#237;ticos&#44; nomeadamente a cetoacidose diab&#233;tica&#44; podem ser uma causa de disfun&#231;&#227;o VE e esta &#233; outra das formas pela qual a diabetes pode ter impacto no sistema cardiovascular&#46;</p></span>"
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        "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as&#58; Roque D&#44; Faria D&#44; Ferreira J&#44; Ferreira H&#44; Beringuilho M&#44; Magno P&#44; et al&#46;&#44; Uma causa revers&#237;vel de disfun&#231;&#227;o ventricular esquerda&#58; caso cl&#237;nico e breve revis&#227;o&#46; Rev Port Cardiol&#46; 2021&#59;40&#58;383&#8211;388&#46;</p>"
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Case report
A reversible cause of left ventricular dysfunction: Case report and brief review
Uma causa reversível de disfunção ventricular esquerda: caso clínico e breve revisão
David Roque
Corresponding author
roque_866@hotmail.com

Corresponding author.
, Daniel Faria, João Ferreira, Hilaryano Ferreira, Marco Beringuilho, Pedro Magno, Carlos Morais
Serviço de Cardiologia, Hospital Professor Doutor Fernando da Fonseca, EPE, Amadora, Portugal
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in recent years researchers have reported that even in the absence of CAD&#44; patients with diabetes have a higher prevalence of HF&#44; and that HF in these patients&#44; irrespective of its etiology&#44; carries a worse prognosis&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> It is also important to note the relatively new and as yet poorly understood entity known as diabetic cardiomyopathy&#44; in which ventricular dysfunction is caused by oxidative stress induced by hyperglycemia&#44; hyperlipidemia&#44; hypertension and inflammation resulting in abnormal gene expression and the activation of pathways leading to programmed myocardial cell death&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">The present case report aims to show that diabetes has acute as well as long-term cardiovascular effects&#44; and that associated electrolyte&#44; acid-base and hemodynamic changes can mimic the cardiovascular alterations that occur over the course of the disease&#8217;s evolution&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Case report</span><p id="par0015" class="elsevierStylePara elsevierViewall">A 46-year-old man was admitted to the emergency department &#40;ED&#41; due to uncontrollable vomiting and altered consciousness &#40;confusion&#41; lasting for two hours&#46; His personal history included type 1 diabetes&#44; diagnosed eight years previously&#44; under insulin therapy but with poor metabolic control&#44; being followed in the diabetes clinic&#44; and an unspecified psychiatric disorder&#44; previously followed in psychiatric consultations&#46; He was a current smoker &#40;70 pack-years&#41; but denied taking any drugs other than insulin therapy&#44; alcohol consumption&#44; or illegal drug use&#46;</p><p id="par0020" class="elsevierStylePara elsevierViewall">At first medical contact&#44; it was noted that the patient had ketone breath and was hypotensive &#40;non-invasive arm blood pressure measurement of 77&#47;52&#8239;mmHg&#41;&#44; tachycardic &#40;heart rate &#91;HR&#93; 102&#8239;bpm&#41;&#44; polypneic &#40;respiratory rate 30&#8239;cpm&#41;&#44; and hypothermic &#40;axillary body temperature 35&#46;8&#8239;&#176;C&#41;&#46; Capillary testing revealed unmeasurable blood glucose &#40;HIGH test result&#41; and increased ketonemia &#40;3&#59; normal &#60;1&#46;2&#41;&#46; Arterial blood gas analysis demonstrated severe metabolic acidosis &#40;pH 7&#46;1&#44; pCO<span class="elsevierStyleInf">2</span> 9&#46;2&#8239;mmHg&#44; pO<span class="elsevierStyleInf">2</span> 139&#8239;mmHg&#44; HCO<span class="elsevierStyleInf">3</span>- 2&#46;9&#8239;mmol&#47;l&#41;&#44; hyperlactacidemia &#40;lactates 9&#8239;mmol&#47;l&#41;&#44; hyperkalemia &#40;K<span class="elsevierStyleSup">&#43;</span> 7&#46;52 mEq&#47;l&#41; and hyponatremia &#40;Na<span class="elsevierStyleSup">&#43;</span> 126 mEq&#47;l&#41; considered pseudohyponatremia and when corrected for blood glucose estimated to be 500&#8239;mg&#47;dl &#40;HIGH capillary test result&#41;&#44; giving a figure of 136 mEq&#47;l&#46; A diagnosis of diabetic ketoacidosis &#40;DKA&#41; was made and therapy was begun with rapid intravenous &#40;IV&#41; insulin in continuous perfusion and IV hydration with sodium chloride 0&#46;9&#37; at 100 cc&#47;hour and external warming&#46; The decompensating factor was failure to administer insulin in the previous two days&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">The first venous blood analysis showed elevated troponin I &#40;2&#46;01&#8239;ng&#47;ml&#59; normal &#60;0&#46;02&#8239;ng&#47;ml&#41;&#44; with a peak of 3&#46;23&#8239;ng&#47;ml 12&#8239;hours after admission&#46; N-terminal pro-brain natriuretic peptide &#40;NT-proBNP&#41; was 17316&#8239;pg&#47;ml &#40;normal &#60;125&#41;&#46; The patient reported no current or previous chest pain or any symptoms of HF&#46; Physical examination showed no signs of cardiovascular disease&#59; there were no murmurs or extra heart sounds on cardiac auscultation&#44; no rales on pulmonary auscultation&#44; no enlarged organs on abdominal examination and no lower limb edema&#46; The electrocardiogram showed sinus tachycardia &#40;HR 109 bpm&#41; with ST-segment flattening in V5&#44; V6&#44; I and aVL&#46; A transthoracic echocardiogram &#40;TTE&#41; performed on the day of admission using a GE Vivid I portable ultrasound machine revealed a non-dilated and non-hypertrophied left ventricle with severe left ventricular systolic dysfunction &#40;ejection fraction &#91;EF&#93; estimated at 26&#37;&#41; due to diffuse hypokinesia&#59; no significant aortic or mitral valve disease&#59; preserved right ventricular longitudinal systolic function&#59; inferior vena cava 17&#8239;mm with preserved respiratory kinetics and pulmonary artery pressure estimated at 28&#8239;mmHg &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Figure 1</a>&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0030" class="elsevierStylePara elsevierViewall">At 48&#8239;hours of hospitalization&#44; and with his DKA resolved&#44; the patient was transferred to the cardiology ward to investigate the etiology of his left ventricular dysfunction&#46; During the investigation it transpired that he had been hospitalized about 15 months before&#44; also with a setting of diabetic ketacidosis&#46; At that time troponin I was also elevated and a rapid TTE performed in the ED demonstrated severe global left ventricular systolic dysfunction&#44; but a second TTE performed in the echocardiographic laboratory eight days after admission was normal&#46; It was assumed that the first exam had been incorrectly reported and no follow-up was scheduled&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">During the patient&#8217;s stay in the cardiology ward&#44; diagnostic cardiac catheterization revealed coronary arteries without lesions &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Figure 2</a>&#41;&#46; There was no history of HF&#44; cardiomyopathy or sudden death&#44; and the patient denied recent viral or bacterial infection and had never traveled abroad&#46; Laboratory tests were negative&#44; including for human immunodeficiency virus and hepatotropic viruses&#46; Thyroid function tests were normal&#44; as they had been throughout his follow-up in the diabetes clinic&#44; although antithyroid antibodies were not assessed&#46; Other laboratory parameters measured during hospital stay included hemoglobin 15&#8239;g&#47;dl at admission &#40;nadir 13&#8239;g&#47;dl&#41;&#44; no blood loss being documented&#59; no functional or absolute iron deficiency &#40;ferritin 326&#8239;ng&#47;ml&#41; and no folic acid or vitamin B<span class="elsevierStyleInf">12</span> deficiency &#40;5&#46;9&#8239;ng&#47;ml and 590&#8239;pg&#47;ml&#44; respectively&#41;&#59; and vitamin B<span class="elsevierStyleInf">1</span>&#44; routinely assessed in patients with HF or left ventricular dysfunction&#44; 28&#8239;ng&#47;ml &#40;normal 16&#8211;48&#41;&#46;</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0040" class="elsevierStylePara elsevierViewall">Seven days after admission&#44; a new TTE showed a non-dilated left ventricle&#44; with mild systolic dysfunction &#40;estimated EF 46&#37;&#41; and slightly reduced global longitudinal strain &#40;&#8722;16&#37;&#41; &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Figure 3</a>&#41;&#46; Cardiac magnetic resonance was proposed but the patient refused&#46; At hospital discharge he was in New York Heart Association class I&#44; with NT-proBNP 448&#8239;pg&#47;ml&#44; medicated with ramipril 2&#46;5&#8239;mg&#47;day and bisoprolol 5&#8239;mg&#47;day&#44; as well as slow-release insulin administered twice a day&#44; and was referred for cardiology and diabetes consultations&#46;</p><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0045" class="elsevierStylePara elsevierViewall">A third TTE&#44; scheduled for one week after discharge&#44; showed preserved global left ventricular systolic function &#40;EF 52&#37;&#41; and normal global longitudinal strain &#40;&#8722;20&#46;2&#37;&#41; &#40;<a class="elsevierStyleCrossRef" href="#fig0020">Figure 4</a>&#41;&#46; At eight months of follow-up&#44; the patient had not been readmitted and had no cardiovascular symptoms&#46;</p><elsevierMultimedia ident="fig0020"></elsevierMultimedia></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Discussion</span><p id="par0050" class="elsevierStylePara elsevierViewall">DKA is characterized by the triad of high blood glucose&#44; ketosis and metabolic acidemia resulting from a relative or absolute deficiency of insulin and excess of counter-regulatory hormones&#44; associated with severe electrolyte abnormalities&#46; Patients with DKA usually have mild to moderate hyperkalemia on initial assessment&#44; despite total-body potassium deficiency&#46;</p><p id="par0055" class="elsevierStylePara elsevierViewall">According to international guidelines&#44;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> our patient presented moderate to severe DKA &#40;pH 7&#46;1&#44; HCO<span class="elsevierStyleInf">3</span>- 2&#46;3 and altered mental status&#41;&#46; Thanks to rapid initiation of recommended treatment&#44; including insulin therapy and IV hydration&#44; no life-threatening complications occurred&#44; even though mortality in this entity ranges between 1&#37; and 5&#37; in different registries&#44; depending on age and comorbidities&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> Although our patient presented hyperkalemia&#44; no specific treatment was instituted for this condition&#44; in view of the knowledge that these patients in fact have a total-body K<span class="elsevierStyleSup">&#43;</span> deficiency and that beginning IV insulin therapy causes an inflow of K&#43; into cells&#44; thereby reducing kalemia&#46;</p><p id="par0060" class="elsevierStylePara elsevierViewall">In 2004 Stentz et al&#46; published a study<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> aiming to analyze the status of proinflammatory cytokines and markers of oxidative stress and cardiovascular risks associated with the known proinflammatory states of acute and chronic hyperglycemia&#44; in both DKA and nonketotic hyperglycemia&#46; They concluded that both conditions are associated with elevation of proinflammatory cytokines&#44; reactive oxygen species &#40;ROS&#41;&#44; and cardiovascular risk factors&#44; including C-reactive protein&#44; homocysteine and plasminogen activator inhibitor-1&#46; They also showed that values of these parameters returned to normal levels &#40;in the absence of obvious infection or cardiovascular pathology&#41; with insulin therapy&#44; and therefore characterize these two conditions as inflammatory diseases&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> Evidence from other studies reveals a significant and independent link between inflammation&#44; sepsis&#44; insulin resistance and cardiac dysfunction&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a> The classic outcome of this relationship is systemic inflammatory response syndrome &#40;SIRS&#41;&#44; which is found in many conditions&#44; the best-known being sepsis&#44; but also in non-infectious acute inflammatory settings such as acute pancreatitis&#44; trauma and burns&#46; It is defined by the presence of two or more of the following criteria&#58; temperature &#62;38&#8239;&#176;C or &#60;36&#8239;&#176;C&#44; HR&#8239;&#62;&#8239;90 bpm&#44; respiratory rate &#62;20&#8239;cpm or PaCO<span class="elsevierStyleInf">2</span> &#60;32&#8239;mmHg&#44; and white blood cell count &#62;12 000&#47;mm<span class="elsevierStyleSup">3</span> or &#60;4000&#47;mm<span class="elsevierStyleSup">3</span> or &#62;10&#37; immature bands&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> Our patient thus fulfilled criteria for SIRS in the setting of acute inflammation due to acute decompensation of diabetes &#40;DKA&#41;&#46;</p><p id="par0065" class="elsevierStylePara elsevierViewall">Myocardial dysfunction is a common complication in patients with SIRS due to sepsis and is associated with increased mortality&#44; which can reach 70-90&#37;&#44;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a> as well as in SIRS due to trauma or burns&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">The initial TTE in the case presented was performed urgently but after intensive hydration as part of the routine treatment of DKA&#46; As a consequence&#44; it was not possible to estimate the patient&#8217;s volemia via the inferior vena cava&#46; We consider that&#44; in contrast to other patients with severe left ventricular dysfunction&#44; in this case such a significant increase in preload caused by intensive hydration to treat DKA might have led to volume overload and acute pulmonary edema&#46; However&#44; this did not occur&#44; probably because besides DKA&#44; the patient also had L-profile HF &#40;&#8216;cold-dry&#8217;&#41;&#44;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> as shown by hypotension and hyperlactacidemia&#44; markers of hypoperfusion &#40;which may also have contributed to his altered mental state on admission&#41;&#46; L-profile HF is most often associated with excessive diuretic use&#44; and the indicated treatment is fluid replacement&#44;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a> which in our opinion should be carefully monitored both clinically and by imaging studies such as are readily available in the ED&#44; like echocardiography&#44; in order to prevent complications associated with excessive restoration of volemia&#46;</p><p id="par0075" class="elsevierStylePara elsevierViewall">Berk et al&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a> report a case of a patient admitted in 2015 with hyperosmolar hyperglycemic state &#40;HHS&#41;&#44; whose TTE performed due to electrocardiographic alterations showed severe left ventricular dysfunction&#46; On the fourth day of hospitalization she underwent imaging tests for ischemia&#44; which were negative and left ventricular function was also normal&#46; The authors suggested as possible causes for this reversible dysfunction HHS&#44; SIRS and euthyroid sick syndrome&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a> Nanda et al&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a> documented a unique case of DKA-induced stress-related cardiomyopathy in a woman with type 1 diabetes&#46; They hypothesize that the rarity of this association may be due to the fact that myocytes have a decreased ability to metabolize glucose and free fatty acids in takotsubo cardiomyopathy and can preferentially change their metabolic substrate to ketones&#44; which are found in DKA&#46; Furthermore&#44; the association of DKA and stress cardiomyopathy may lead to severe acidemia&#44; with HCO<span class="elsevierStyleInf">3</span>- 4&#8239;mmol&#47;l&#44; which may be one factor in the left ventricular dysfunction reported in this case&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a></p><p id="par0080" class="elsevierStylePara elsevierViewall">Besides the role of proinflammatory cytokines and ROS in SIRS-related myocardial dysfunction&#44; changes in calcium homeostasis are also involved&#44; as calcium inflow into myocytes is reduced and release of this cation from the sarcoplasmic reticulum is inhibited&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">12</span></a></p><p id="par0085" class="elsevierStylePara elsevierViewall">The possibility cannot be excluded that the metabolic acidemia found in DKA may also have been a factor in the reversible left ventricular dysfunction observed in the present case&#46; To the best of our knowledge&#44; there have been few reports in the literature on the impact of acid-base disorders on cardiac function&#46; In a 1990 study&#44; Teplinsky et al&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a> published an experimental study of the effect of lactic acidosis on hemodynamics and left ventricular function in dogs&#46; They demonstrated that during progressive acidemia induced by continuous IV infusion of lactic acid&#44; cardiac output&#44; stroke volume&#44; and mean systemic arterial pressure fell&#44; while mean pulmonary artery pressure and right atrial pressure increased&#46; The authors concluded that lactic acidemia caused a 40&#37; reduction in stroke volume&#44; which could be attributed to depressed LV contractility&#44; characterized by a decrease in maximum dP&#47;dt&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a> Also in 1990&#44; a review of the effects of acidosis on cardiac contractility concluded that this acid-base disorder affects every step in the excitation-contraction coupling pathway&#44; including the counter-regulatory effects on Ca<span class="elsevierStyleSup">2&#43;</span> delivery to myofilaments &#40;reduced delivery by inhibition of the Ca<span class="elsevierStyleSup">2&#43;</span> current and reduced release of this cation from the sarcoplasmic reticulum&#44; as well as increased delivery by prolongation of the action potential&#41; and the responsiveness of myofilaments to Ca<span class="elsevierStyleSup">2&#43;</span>&#44; which overall is reduced&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a></p><p id="par0090" class="elsevierStylePara elsevierViewall">Another review&#44; published in 1995&#44;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a> concluded that the effect of acidemia on ventricular function depends on pH level&#58; in mild acidemia&#44; increased catecholamine release compensates for the cardiac depressant effects of acidemia&#44; with increased inotropy&#44; chronotropy&#44; cardiac output and peripheral vascular resistance&#44; while when pH is &#60;7&#46;2&#44; as in our patient&#44; H<span class="elsevierStyleSup">&#43;</span> ions have a direct cardiac depressant action that cannot be compensated by increased catecholamines&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a></p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Conclusion</span><p id="par0095" class="elsevierStylePara elsevierViewall">Myocardial dysfunction is a frequent complication associated with SIRS&#44; whether secondary to sepsis or to other acute inflammatory states such as DKA&#44; the common mechanism being high levels of proinflammatory cytokines and ROS&#46; As well as SIRS&#44; other electrolyte and acid-base disorders may have contributed to the reversible left ventricular dysfunction observed in our patient&#44; in whom acute L-profile HF was associated with DKA&#46; We consider that&#44; as the negative impact of ventricular dysfunction on the prognosis of these patients is now proven&#44; echocardiographic assessment should be performed routinely and that those with systolic or diastolic dysfunction should be scheduled for follow-up to monitor reversal of dysfunction&#44; control other risk factors and investigate other concomitant etiologies&#46;</p><p id="par0100" class="elsevierStylePara elsevierViewall">As the pathogenesis of diabetic cardiomyopathy includes oxidative stress&#44;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> the association of the latter with ventricular dysfunction in settings of acute decompensation may point the way to therapeutic studies based on inhibiting these proinflammatory processes&#44; with a view to reducing mortality in these acute settings and hopefully preventing progression to irreversible ventricular dysfunction&#46;</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Conflicts of interest</span><p id="par0105" class="elsevierStylePara elsevierViewall">The authors have no conflicts of interest to declare&#46;</p></span></span>"
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        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">The authors describe a case of a patient admitted to the emergency department with diabetic ketoacidosis&#46; Although there were no symptoms attributable to the cardiovascular system&#44; lab tests revealed elevated troponin I and natriuretic peptides&#44; coupled with repolarization abnormalities on the ECG&#46; The transthoracic echocardiogram &#40;TTE&#41; showed a non-dilated left ventricle with severe left ventricular systolic dysfunction due to diffuse hypokinesia&#44; and a concomitant diagnosis of profile L heart failure was proposed&#46; Etiologic investigation was negative&#44; and when a new TTE was performed seven days after the first&#44; left ventricular function was normal&#46; Although rarely considered&#44; metabolic and electrolyte disorders&#44; especially diabetic ketoacidosis&#44; can be a cause of left ventricular systolic dysfunction&#44; and should be considered in the differential diagnosis&#46; This is another way diabetes can have an impact on the cardiovascular system&#46;</p></span>"
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        "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">Os autores descrevem um caso de um doente admitido no Servi&#231;o de Urg&#234;ncia por cetoacidose diab&#233;tica&#46; Apesar de n&#227;o haver queixas do foro cardiovascular&#44; a avalia&#231;&#227;o anal&#237;tica revelou uma eleva&#231;&#227;o do n&#237;vel de troponina I &#40;TropI&#41; e de p&#233;ptidos natriur&#233;ticos &#40;proBNP&#41;&#44; associada a altera&#231;&#245;es da repolariza&#231;&#227;o no eletrocardiograma&#46; O ecocardiograma transtor&#225;cico &#40;ETT&#41; mostrou um ventr&#237;culo esquerdo n&#227;o dilatado com disfun&#231;&#227;o sist&#243;lica ventricular esquerda grave&#44; por hipocinesia difusa&#44; assumindo&#8208;se assim concomitantemente um perfil L de insufici&#234;ncia card&#237;aca &#40;IC&#41;&#46; A investiga&#231;&#227;o etiol&#243;gica foi negativa e quando um novo ETT foi realizado&#44; sete dias ap&#243;s o primeiro&#44; a fun&#231;&#227;o ventricular esquerda era normal&#46; Apesar de raramente considerados&#44; os dist&#250;rbios metab&#243;licos e hidroeletrol&#237;ticos&#44; nomeadamente a cetoacidose diab&#233;tica&#44; podem ser uma causa de disfun&#231;&#227;o VE e esta &#233; outra das formas pela qual a diabetes pode ter impacto no sistema cardiovascular&#46;</p></span>"
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        "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as&#58; Roque D&#44; Faria D&#44; Ferreira J&#44; Ferreira H&#44; Beringuilho M&#44; Magno P&#44; et al&#46;&#44; Uma causa revers&#237;vel de disfun&#231;&#227;o ventricular esquerda&#58; caso cl&#237;nico e breve revis&#227;o&#46; Rev Port Cardiol&#46; 2021&#59;40&#58;383&#8211;388&#46;</p>"
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Revista Portuguesa de Cardiologia (English edition)
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