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resulting in the rapid exhaustion of the generator before the cardiologist was able to inhibit the therapies with the aid of a magnet&#46; During periods of sinus rhythm&#44; the ECG documented QRS with complete right bundle branch block&#44; PR interval at the upper normal level&#44; and corrected QT interval of 405 ms&#44; with no signs of acute ischemia &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Figure 2</a>&#41;&#46; Transthoracic echocardiography showed a severely dilated left ventricle&#44; with diffuse hypokinesia and severely impaired global systolic function&#46; Interrogation of the CRT-ICD revealed various episodes of VT in the previous 24 hours&#44; with a total of 48 appropriate shocks &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Figure 3</a>&#41;&#44; and the generator at the end of battery life&#46; Given the patient&#39;s worsening heart failure and persistence of the arrhythmic storm&#44; he was intubated and given propofol and midazolam for sedation and analgesia&#46; Laboratory tests at admission showed acute kidney injury &#40;Acute Kidney Injury Network stage 1&#41; with creatinine 1&#46;5 mg&#47;dl and urea 101 mg&#47;dl&#59; mild hypokalemia &#40;potassium 3&#46;0 mmol&#47;l&#44; normal range 3&#46;5-5&#46;1&#41;&#59; severe hypercalcemia &#40;calcium 18&#46;5 mg&#47;dl&#44; normal range 8&#46;6-10&#59; Ca<span class="elsevierStyleSup">2&#43;</span> 2&#46;46 mmol&#47;l&#44; normal range 1&#46;13-1&#46;32&#41;&#59; and slight elevation of troponin I &#40;peak 1&#46;5 mg&#47;dl&#44; cutoff &#60;0&#46;07&#41;&#46; The hypokalemia was immediately corrected&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><elsevierMultimedia ident="fig0010"></elsevierMultimedia><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">Since the patient&#39;s monomorphic VT was not associated with pain or anginal equivalents&#44; and there were no signs of acute ischemia on the baseline ECG&#44; the cause of the arrhythmia was assumed to be the presence of severe hypercalcemia&#46; With the support of internal medicine and endocrinology specialists&#44; pharmacological measures were instituted to correct hypercalcemia with pamidronate&#44; zolendronic acid&#44; furosemide and hydrocortisone&#46; However&#44; since the hypercalcemia was severe and refractory to the above treatment&#44; it was decided to begin continuous venovenous hemodiafiltration &#40;CVVHDF&#41;&#59; this resulted in progressive reduction in the frequency and duration of TV episodes&#44; which were no longer sustained and ceased completely when calcemia reached 15&#46;8 mg&#47;dl&#46; The patient was extubated and CVVHDF was discontinued after 48 hours&#44; but furosemide &#40;60 mg&#47;day&#41; was continued to maintain normocalcemia&#46; The possibility of ablation to treat the VT was discussed but was not performed since the arrhythmia did not recur after correction of hypercalcemia&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">Etiological investigation of hypercalcemia showed marked elevation of parathyroid hormone &#40;PTH&#41; &#40;1020 pg&#47;ml&#44; normal range 14-72&#41;&#44; and normal albuminemia &#40;3&#46;5 g&#47;dl&#44; normal range 3&#46;2-4&#46;9&#41;&#44; suggesting primary hyperparathyroidism &#40;PHPT&#41;&#46; Cervical ultrasound revealed a well-defined hypoechogenic homogeneous solid mass topographically slightly posterior and inferior to the left lobe of the thyroid gland suggestive of a parathyroid adenoma&#44; and scintigraphy of the parathyroid glands documented a functional lesion of the left inferior parathyroid&#46; These findings did not exclude the possibility of a malignant parathyroid tumor&#46; Left inferior parathyroidectomy was proposed to the patient&#44; who accepted&#44; and the procedure was performed without complications&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">Following parathyroidectomy the patient&#39;s calcemia and PTH levels normalized and so medical therapy for this purpose was discontinued&#46; The pathology report confirmed parathyroid adenoma&#46; The fact that there was no hypocalcemia or need for calcium therapy suggests that the hyperparathyroidism was recent or a worsening of previously less severe PHPT&#46; Baseline endocrinological assessment at admission also showed elevated levels of gastrin &#40;2130 pg&#47;ml&#44; normal range 13-115&#41;&#44; chromogranin A &#40;143&#46;5 mmol&#47;l&#44; cutoff &#60;6&#41;&#44; and urinary metanephrines and hydroxyindolacetic acid&#44; although these elevations were less marked and were absent on the second urine tests during hospital stay&#44; thereby excluding pheochromocytoma&#46; Endoscopy of the upper digestive tract revealed an ulcer in the lesser curvature of the stomach&#44; compatible with chronic gastritis&#44; and screening for <span class="elsevierStyleItalic">Helicobacter pylori</span> was positive&#46; The presence of PHPT&#44; previous history of gastric ulcer&#44; and hypergastrinemia raised the possibility of type 1 multiple endocrine neoplasia&#44; but the patient refused to undergo an octreotide scan to confirm this diagnosis&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">After 24 days of hospitalization&#44; following a favorable clinical course&#44; the patient was discharged under optimal medical therapy for heart failure&#46; He is being followed in the cardiology outpatient clinic and has had no new events to date&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Discussion</span><p id="par0040" class="elsevierStylePara elsevierViewall">Hypercalcemia is associated with cardiac rhythm disturbances&#44; most often prolongation of the PR segment and the QRS interval and hence shortening of the QT interval&#44;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">1</span></a> which is usually associated with bradycardia rather than tachycardia&#46; The clinical situation reported here is thus most unusual&#46; Only six cases of PHPT and hypercalcemia associated with ventricular arrhythmias have been described in the literature&#44; the first of which&#44; by Chaieb et al&#46;&#44;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">2</span></a> published in 1988&#44; described a case of hyperparathyroidism and ventricular bigeminy&#46; In 2000 Chang et al&#46; reported the case of a woman without structural heart disease with PHPT and spontaneous sustained monomorphic VT&#44; reproducible in electrophysiological study only following injection of calcium gluconate and terminated by verapamil&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">3</span></a> In 1993&#44; 2003 and 2004 Kearney et al&#46;&#44;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">4</span></a> Kolb et al&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">5</span></a> and Kiewiet et al&#46;&#44;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">6</span></a> respectively&#44; reported cases of polymorphic VT degenerating into ventricular fibrillation&#46; The second case reported to date of monomorphic VT was published in 2004 by Occhetta et al&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">7</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">The mechanism by which hypercalcemia can trigger ventricular arrhythmias is the subject of debate&#46; Proposed causes include early<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">4</span></a> or late<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">1</span></a> afterdepolarizations or reentry circuits secondary to shortening of the absolute refractory period&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">8</span></a> In PHPT&#44; PTH itself&#44; as well as hypercalcemia&#44; has arrhythmogenic potential&#44; which may explain the occurrence of ventricular arrhythmias with lower calcium levels than in the case reported&#46; Studies in rat hearts show that PTH has direct positive inotropic and chronotropic effects&#44; partly mediated by calcium inflow into myocardial cells&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">9</span></a> The combination of reduced conduction speed of the cardiac impulse and shortening of the refractory period thus makes reentrant mechanisms&#44; and hence ventricular arrhythmias&#44; more likely&#46; It has been suggested that the presence of heart disease may contribute to the development of arrhythmic events in patients with hypercalcemia&#44; although this relationship has yet to be confirmed&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">6</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">In the case presented&#44; the presence of alcohol- and ischemia-related dilated cardiomyopathy&#44; with transmural scar and impaired global systolic function&#44; together with the patient&#39;s failure to take his medication and hypokalemia &#40;even though mild&#41;&#44; may have contributed to his VT&#46; However&#44; PHPT and resulting hypercalcemia was the most important factor in this situation&#44; acting as the primary trigger&#44; given that the VT episodes only ceased after significant reduction in calcemia&#44; with restoration of normocalcemia and no recurrence of VT after parathyroidectomy&#46; Nevertheless&#44; the possibility cannot be excluded that high PTH levels also contributed to the patient&#39;s condition&#46;</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Conflicts of interest</span><p id="par0055" 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="spar0005" class="elsevierStyleSimplePara elsevierViewall">Hypercalcemia is a known cause of heart rhythm disorders&#44; but it is rarely associated with ventricular arrhythmias&#46; The authors present the case of a 53-year-old man with ischemic and alcoholic dilated cardiomyopathy and severely reduced ejection fraction&#44; with a cardiac resynchronization therapy-cardioverter-defibrillator &#40;ICD&#41; device&#44; who was admitted to the emergency department due to an electrical storm with multiple appropriate ICD shocks&#44; refractory to antiarrhythmic therapy&#46; Etiological investigation documented severe hypercalcemia secondary to previously undiagnosed primary hyperparathyroidism&#46; The episodes of ventricular tachycardia only ceased after serum calcium levels were reduced&#46;</p></span>"
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        "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">A hipercalcemia &#233; uma causa conhecida de perturba&#231;&#245;es do ritmo card&#237;aco&#44; contudo&#44; a sua associa&#231;&#227;o a arritmias ventriculares &#233; rara&#46; Os autores apresentam o caso cl&#237;nico de um doente de 53 anos de idade&#44; com cardiomiopatia dilatada de etiologia isqu&#233;mica e etan&#243;lica&#44; e grave compromisso da fun&#231;&#227;o sist&#243;lica global&#44; portador de sistema de ressincroniza&#231;&#227;o card&#237;aca &#40;CRT&#41; com cardioversor desfibrilhador &#40;CDI&#41;&#44; admitido no servi&#231;o de urg&#234;ncia por tempestade arr&#237;tmica&#44; com m&#250;ltiplos choques de CDI apropriados&#44; refrat&#225;ria a terap&#234;utica antiarr&#237;tmica&#46; Na investiga&#231;&#227;o etiol&#243;gica foi documentada hipercalcemia grave secund&#225;ria a hiperparatiroidismo prim&#225;rio at&#233; ent&#227;o desconhecido&#46; Somente ap&#243;s redu&#231;&#227;o da calcemia se observou cessa&#231;&#227;o dos epis&#243;dios de taquicardia ventricular&#46;</p></span>"
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        "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as&#58; Guimar&#227;es T&#44; Nobre Menezes M&#44; Cruz D&#44; do Vale S&#44; Bordalo A&#44; Veiga A&#44; et al&#46; Crise hipercalc&#233;mica e hiperparatiroidismo prim&#225;rio&#58; causa de tempestade arr&#237;tmica invulgar&#46; Rev Port Cardiol&#46; 2017&#59;36&#58;959&#46;e1&#8211;959&#46;e5&#46;</p>"
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Case report
Hypercalcemic crisis and primary hyperparathyroidism: Cause of an unusual electrical storm
Crise hipercalcémica e hiperparatiroidismo primário: causa de tempestade arrítmica invulgar
Tatiana Guimarãesa,
Corresponding author
, Miguel Nobre Menezesa, Diogo Cruzb, Sónia do Valec, Armando Bordaloa, Arminda Veigaa, Fausto J. Pintoa, Dulce Britoa
a Serviço de Cardiologia, Hospital Santa Maria, Centro Hospitalar de Lisboa Norte, Lisboa, Portugal
b Serviço de Medicina Interna, Hospital de Santa Maria, Centro Hospitalar de Lisboa Norte, Lisboa, Portugal
c Serviço de Endocrinologia, Hospital de Santa Maria, Centro Hospitalar de Lisboa Norte, Lisboa, Portugal
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he experienced an episode of monomorphic ventricular tachycardia &#40;VT&#41; with a pattern of complete right bundle branch block and superior axis prompting an ICD shock followed by chest pain and elevation of troponin I levels &#40;peak 1&#46;69 mg&#47;l&#44; cutoff &#60;0&#46;07&#41;&#46; He underwent repeat coronary angiography that showed in-stent occlusion&#44; treated by angioplasty and placement of three drug-eluting stents&#46; Among the patient&#39;s other known personal history were smoking-related chronic obstructive pulmonary disease&#44; erosive gastritis and peptic ulcer&#46; He was medicated as an outpatient with losartan&#44; bisoprolol&#44; spirolactone&#44; furosemide&#44; aspirin&#44; clopidogrel&#44; amiodarone&#44; simvastatin and pantograph&#46; He remained in New York Heart Association class II from that time&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">The patient was readmitted to our hospital one year after the previous hospitalization due to multiple ICD shocks&#44; preceded by syncope&#44; with transient recovery of consciousness following each shock&#44; beginning 24 hours previously and increasing in frequency in the hour before admission&#46; He had discontinued his medication in the previous five days due to financial difficulties&#44; since when he had complained of anorexia&#44; asthenia&#44; constipation and dizziness&#46; On admission he was conscious&#44; oriented&#44; and sweating but with no signs of peripheral hypoperfusion&#46; The electrocardiogram &#40;ECG&#41; documented monomorphic VT with complete left bundle branch block and a rate of 300 bpm &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Figure 1</a>&#41;&#46; A 300-mg bolus of amiodarone was administered followed by intravenous &#40;IV&#41; perfusion at 4 &#956;g&#47;kg&#47;min&#44; but recurrence of VT &#40;with constant morphology on telemetry&#41; was observed&#59; two boluses of IV lidocaine &#40;total 150 mg&#41; were administered but also had no effect&#46; The patient received multiple ICD shocks immediately after arrival at the hospital&#44; resulting in the rapid exhaustion of the generator before the cardiologist was able to inhibit the therapies with the aid of a magnet&#46; During periods of sinus rhythm&#44; the ECG documented QRS with complete right bundle branch block&#44; PR interval at the upper normal level&#44; and corrected QT interval of 405 ms&#44; with no signs of acute ischemia &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Figure 2</a>&#41;&#46; Transthoracic echocardiography showed a severely dilated left ventricle&#44; with diffuse hypokinesia and severely impaired global systolic function&#46; Interrogation of the CRT-ICD revealed various episodes of VT in the previous 24 hours&#44; with a total of 48 appropriate shocks &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Figure 3</a>&#41;&#44; and the generator at the end of battery life&#46; Given the patient&#39;s worsening heart failure and persistence of the arrhythmic storm&#44; he was intubated and given propofol and midazolam for sedation and analgesia&#46; Laboratory tests at admission showed acute kidney injury &#40;Acute Kidney Injury Network stage 1&#41; with creatinine 1&#46;5 mg&#47;dl and urea 101 mg&#47;dl&#59; mild hypokalemia &#40;potassium 3&#46;0 mmol&#47;l&#44; normal range 3&#46;5-5&#46;1&#41;&#59; severe hypercalcemia &#40;calcium 18&#46;5 mg&#47;dl&#44; normal range 8&#46;6-10&#59; Ca<span class="elsevierStyleSup">2&#43;</span> 2&#46;46 mmol&#47;l&#44; normal range 1&#46;13-1&#46;32&#41;&#59; and slight elevation of troponin I &#40;peak 1&#46;5 mg&#47;dl&#44; cutoff &#60;0&#46;07&#41;&#46; The hypokalemia was immediately corrected&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><elsevierMultimedia ident="fig0010"></elsevierMultimedia><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">Since the patient&#39;s monomorphic VT was not associated with pain or anginal equivalents&#44; and there were no signs of acute ischemia on the baseline ECG&#44; the cause of the arrhythmia was assumed to be the presence of severe hypercalcemia&#46; With the support of internal medicine and endocrinology specialists&#44; pharmacological measures were instituted to correct hypercalcemia with pamidronate&#44; zolendronic acid&#44; furosemide and hydrocortisone&#46; However&#44; since the hypercalcemia was severe and refractory to the above treatment&#44; it was decided to begin continuous venovenous hemodiafiltration &#40;CVVHDF&#41;&#59; this resulted in progressive reduction in the frequency and duration of TV episodes&#44; which were no longer sustained and ceased completely when calcemia reached 15&#46;8 mg&#47;dl&#46; The patient was extubated and CVVHDF was discontinued after 48 hours&#44; but furosemide &#40;60 mg&#47;day&#41; was continued to maintain normocalcemia&#46; The possibility of ablation to treat the VT was discussed but was not performed since the arrhythmia did not recur after correction of hypercalcemia&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">Etiological investigation of hypercalcemia showed marked elevation of parathyroid hormone &#40;PTH&#41; &#40;1020 pg&#47;ml&#44; normal range 14-72&#41;&#44; and normal albuminemia &#40;3&#46;5 g&#47;dl&#44; normal range 3&#46;2-4&#46;9&#41;&#44; suggesting primary hyperparathyroidism &#40;PHPT&#41;&#46; Cervical ultrasound revealed a well-defined hypoechogenic homogeneous solid mass topographically slightly posterior and inferior to the left lobe of the thyroid gland suggestive of a parathyroid adenoma&#44; and scintigraphy of the parathyroid glands documented a functional lesion of the left inferior parathyroid&#46; These findings did not exclude the possibility of a malignant parathyroid tumor&#46; Left inferior parathyroidectomy was proposed to the patient&#44; who accepted&#44; and the procedure was performed without complications&#46;</p><p id="par0030" class="elsevierStylePara elsevierViewall">Following parathyroidectomy the patient&#39;s calcemia and PTH levels normalized and so medical therapy for this purpose was discontinued&#46; The pathology report confirmed parathyroid adenoma&#46; The fact that there was no hypocalcemia or need for calcium therapy suggests that the hyperparathyroidism was recent or a worsening of previously less severe PHPT&#46; Baseline endocrinological assessment at admission also showed elevated levels of gastrin &#40;2130 pg&#47;ml&#44; normal range 13-115&#41;&#44; chromogranin A &#40;143&#46;5 mmol&#47;l&#44; cutoff &#60;6&#41;&#44; and urinary metanephrines and hydroxyindolacetic acid&#44; although these elevations were less marked and were absent on the second urine tests during hospital stay&#44; thereby excluding pheochromocytoma&#46; Endoscopy of the upper digestive tract revealed an ulcer in the lesser curvature of the stomach&#44; compatible with chronic gastritis&#44; and screening for <span class="elsevierStyleItalic">Helicobacter pylori</span> was positive&#46; The presence of PHPT&#44; previous history of gastric ulcer&#44; and hypergastrinemia raised the possibility of type 1 multiple endocrine neoplasia&#44; but the patient refused to undergo an octreotide scan to confirm this diagnosis&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">After 24 days of hospitalization&#44; following a favorable clinical course&#44; the patient was discharged under optimal medical therapy for heart failure&#46; He is being followed in the cardiology outpatient clinic and has had no new events to date&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Discussion</span><p id="par0040" class="elsevierStylePara elsevierViewall">Hypercalcemia is associated with cardiac rhythm disturbances&#44; most often prolongation of the PR segment and the QRS interval and hence shortening of the QT interval&#44;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">1</span></a> which is usually associated with bradycardia rather than tachycardia&#46; The clinical situation reported here is thus most unusual&#46; Only six cases of PHPT and hypercalcemia associated with ventricular arrhythmias have been described in the literature&#44; the first of which&#44; by Chaieb et al&#46;&#44;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">2</span></a> published in 1988&#44; described a case of hyperparathyroidism and ventricular bigeminy&#46; In 2000 Chang et al&#46; reported the case of a woman without structural heart disease with PHPT and spontaneous sustained monomorphic VT&#44; reproducible in electrophysiological study only following injection of calcium gluconate and terminated by verapamil&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">3</span></a> In 1993&#44; 2003 and 2004 Kearney et al&#46;&#44;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">4</span></a> Kolb et al&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">5</span></a> and Kiewiet et al&#46;&#44;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">6</span></a> respectively&#44; reported cases of polymorphic VT degenerating into ventricular fibrillation&#46; The second case reported to date of monomorphic VT was published in 2004 by Occhetta et al&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">7</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">The mechanism by which hypercalcemia can trigger ventricular arrhythmias is the subject of debate&#46; Proposed causes include early<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">4</span></a> or late<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">1</span></a> afterdepolarizations or reentry circuits secondary to shortening of the absolute refractory period&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">8</span></a> In PHPT&#44; PTH itself&#44; as well as hypercalcemia&#44; has arrhythmogenic potential&#44; which may explain the occurrence of ventricular arrhythmias with lower calcium levels than in the case reported&#46; Studies in rat hearts show that PTH has direct positive inotropic and chronotropic effects&#44; partly mediated by calcium inflow into myocardial cells&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">9</span></a> The combination of reduced conduction speed of the cardiac impulse and shortening of the refractory period thus makes reentrant mechanisms&#44; and hence ventricular arrhythmias&#44; more likely&#46; It has been suggested that the presence of heart disease may contribute to the development of arrhythmic events in patients with hypercalcemia&#44; although this relationship has yet to be confirmed&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">6</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">In the case presented&#44; the presence of alcohol- and ischemia-related dilated cardiomyopathy&#44; with transmural scar and impaired global systolic function&#44; together with the patient&#39;s failure to take his medication and hypokalemia &#40;even though mild&#41;&#44; may have contributed to his VT&#46; However&#44; PHPT and resulting hypercalcemia was the most important factor in this situation&#44; acting as the primary trigger&#44; given that the VT episodes only ceased after significant reduction in calcemia&#44; with restoration of normocalcemia and no recurrence of VT after parathyroidectomy&#46; Nevertheless&#44; the possibility cannot be excluded that high PTH levels also contributed to the patient&#39;s condition&#46;</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Conflicts of interest</span><p id="par0055" 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="spar0005" class="elsevierStyleSimplePara elsevierViewall">Hypercalcemia is a known cause of heart rhythm disorders&#44; but it is rarely associated with ventricular arrhythmias&#46; The authors present the case of a 53-year-old man with ischemic and alcoholic dilated cardiomyopathy and severely reduced ejection fraction&#44; with a cardiac resynchronization therapy-cardioverter-defibrillator &#40;ICD&#41; device&#44; who was admitted to the emergency department due to an electrical storm with multiple appropriate ICD shocks&#44; refractory to antiarrhythmic therapy&#46; Etiological investigation documented severe hypercalcemia secondary to previously undiagnosed primary hyperparathyroidism&#46; The episodes of ventricular tachycardia only ceased after serum calcium levels were reduced&#46;</p></span>"
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        "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">A hipercalcemia &#233; uma causa conhecida de perturba&#231;&#245;es do ritmo card&#237;aco&#44; contudo&#44; a sua associa&#231;&#227;o a arritmias ventriculares &#233; rara&#46; Os autores apresentam o caso cl&#237;nico de um doente de 53 anos de idade&#44; com cardiomiopatia dilatada de etiologia isqu&#233;mica e etan&#243;lica&#44; e grave compromisso da fun&#231;&#227;o sist&#243;lica global&#44; portador de sistema de ressincroniza&#231;&#227;o card&#237;aca &#40;CRT&#41; com cardioversor desfibrilhador &#40;CDI&#41;&#44; admitido no servi&#231;o de urg&#234;ncia por tempestade arr&#237;tmica&#44; com m&#250;ltiplos choques de CDI apropriados&#44; refrat&#225;ria a terap&#234;utica antiarr&#237;tmica&#46; Na investiga&#231;&#227;o etiol&#243;gica foi documentada hipercalcemia grave secund&#225;ria a hiperparatiroidismo prim&#225;rio at&#233; ent&#227;o desconhecido&#46; Somente ap&#243;s redu&#231;&#227;o da calcemia se observou cessa&#231;&#227;o dos epis&#243;dios de taquicardia ventricular&#46;</p></span>"
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        "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as&#58; Guimar&#227;es T&#44; Nobre Menezes M&#44; Cruz D&#44; do Vale S&#44; Bordalo A&#44; Veiga A&#44; et al&#46; Crise hipercalc&#233;mica e hiperparatiroidismo prim&#225;rio&#58; causa de tempestade arr&#237;tmica invulgar&#46; Rev Port Cardiol&#46; 2017&#59;36&#58;959&#46;e1&#8211;959&#46;e5&#46;</p>"
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          "en" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Twelve-lead electrocardiogram in sinus rhythm showing QRS with complete right bundle branch block&#44; PR interval at the upper normal limit&#44; and corrected QT of 405 ms&#46;</p>"
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                            0 => "C&#46;M&#46; Chaieb"
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                          "autores" => array:3 [
                            0 => "C&#46;J&#46; Chang"
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                      "autores" => array:1 [
                        0 => array:2 [
                          "etal" => true
                          "autores" => array:3 [
                            0 => "R&#46;M&#46; Kiewiet"
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ISSN: 21742049
Original language: English
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Idiomas
Revista Portuguesa de Cardiologia (English edition)
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