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CASE REPORT
Year : 2021  |  Volume : 20  |  Issue : 2  |  Page : 145-149  

Panhypopituitarism in acute myocardial infarction


1 Department of General Medicine, Burdwan Medical College and Hospital, Burdwan, West Bengal, India
2 Department of General Medicine, Rajendra Institute of Medical Sciences, Ranchi, Jharkhand, India
3 Department of Neuromedicine, Bangur Institute of Neurosciences, Kolkata, West Bengal, India
4 Department of Cardiology, John Ochsner Heart and Vascular Institute, New Orleans, LA, USA

Date of Submission29-Nov-2019
Date of Acceptance19-Jan-2020
Date of Web Publication30-Jun-2021

Correspondence Address:
Ritwik Ghosh
Department of General Medicine, Burdwan Medical College and Hospital, Junior Resident Hostel, BMCH, Burdwan, West Bengal
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/aam.aam_66_19

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   Abstract 


While hypopituitarism is known to be associated with increased cardiovascular morbidity and mortality, panhypopituitarism as a complication of myocardial infarction (MI) is very rare. Here, we report a case of rapidly developing empty sella syndrome with florid manifestations of panhypopituitarism after MI (due to critical stenosis in the left anterior descending artery) complicated by cardiogenic shock in a 65-year-old man. The patient was initially stabilized with conservative management of non-ST-elevated MI and cardiogenic shock, but after initial improvement, he again deteriorated with refractory shock (not adequately responding to vasopressors), seizures, hypoglycemia, hyponatremia, hyperkalemia, and metabolic acidosis. After ruling out recurrent cardiogenic shock or other causes of refractory hypotension, panhypopituitarism was diagnosed with the help of hormonal assays and imaging. With no prior evidence of hypopituitarism, we suspect that panhypopituitarism developed due to acute pituitary apoplexy secondary to initial cardiogenic shock. The patient was successfully survived by the emergency endocrine management followed by secondary coronary angioplasty.

   Abstract in French 

Résumé
Bien que l'hypopituitarisme soit associé à une augmentation de la morbidité et de la mortalité cardiovasculaires, le panhypopituitarisme en tant que complication de l'infarctus du myocarde (IM) est très rare. Ici, nous rapportons un cas de développement rapide du syndrome de la selle vide avec des manifestations florales de panhypopituitarisme après IM (en raison d'une sténose critique dans l'artère descendante antérieure gauche) compliquée par un choc cardiogénique chez un homme de 65 ans. Le patient a été initialement stabilisé avec une gestion conservatrice de l'IM non élevé ST et du choc cardiogénique, mais après une amélioration initiale, il s'est à nouveau détérioré avec un choc réfractaire (ne répondant pas adéquatement aux vasopresseurs), des convulsions, une hypoglycémie, une hyponatrémie, une hyperkaliémie et une acidose métabolique. Après avoir écarté le choc cardiogénique récurrent ou d'autres causes d'hypotension réfractaire, le panhypopituitarisme a été diagnostiqué à l'aide de tests hormonaux et d'imagerie. En l'absence de preuve antérieure d'hypopituitarisme, nous soupçonnons que le panhypopituitarisme s'est développé en raison d'une apoplexie hypophysaire aiguë secondaire au choc cardiogénique initial. Le patient a été survécu avec succès par la prise en charge endocrinienne d'urgence suivie d'une angioplastie coronaire secondaire.

Keywords: Acute myocardial infarction, empty sella, heart failure, panhypopituitarism, pituitary, pituitary apoplexy


How to cite this article:
Ghosh R, Chatterjee S, Roy D, Dubey S, Lavie CJ. Panhypopituitarism in acute myocardial infarction. Ann Afr Med 2021;20:145-9

How to cite this URL:
Ghosh R, Chatterjee S, Roy D, Dubey S, Lavie CJ. Panhypopituitarism in acute myocardial infarction. Ann Afr Med [serial online] 2021 [cited 2021 Sep 27];20:145-9. Available from: https://www.annalsafrmed.org/text.asp?2021/20/2/145/320047




   Introduction Top


The intricate relationship of the pituitary and heart is well-known. While hypopituitarism makes the patients prone to cardiovascular (CV) diseases and may present with predominant CV manifestations,[1],[2],[3],[4],[5],[6],[7],[8],[9],[10] several CV disorders are associated with perturbations of single or multiple hypothalamic–pituitary–end-organ axes either as a physiologic response[11],[12],[13],[14] or pathological consequences.[15],[16] We present a case of acute myocardial infarction (AMI) followed by left ventricular failure (LVF) and cardiogenic shock unresponsive to vasopressor therapy and complicated by panhypopituitarism and empty sella (ES).


   Case Report Top


A 65-year-old man visited the emergency department with severe central chest pain (Marburg Heart Score 4) for the past 20–24 h associated with nausea, three episodes of vomiting, progressive cooling of the extremities, and extreme fatigue. The patient had no history of coronary risk factors except dyslipidemia and was receiving rosuvastatin 5 mg and fenofibrate 67 mg once daily for the past 1 month. He did not have a history suggestive of prior endocrinological disorders. Height, weight, and body mass index were 166 cm, 56 kg, and 20.3 kg/m, 2 respectively.

On admission, the patient was dehydrated, drowsy, pale, clammy, hypothermic, and diaphoretic. In the emergency department, blood pressure was 80/46 mmHg, pulse rate was regular and 120 beats per minute, and SpO2 was 84% (room air). He had mild central cyanosis and extensive bibasilar fine crepitations. Electrocardiography showed widespread horizontal ST depression, ST elevation in aVR >1 mm, and ST elevation in aVR > V1. Cardiac troponin T kit test was strongly positive. Serum creatine phosphokinase myocardial band (CPK-MB) level was 36 ng/mL (n: <6.22). Arterial blood gas analysis was normal, and random capillary blood glucose (CBG) test revealed normoglycemia (130 mg/dl). Echocardiography revealed apical, inferoseptal, and apical-inferior wall hypokinesia with left ventricular systolic and diastolic dysfunction with ejection fraction (EF) 26%.

As there was no facility for percutaneous coronary intervention (PCI), he was treated initially with moist oxygen at 8 L/min, intravenous fluid administration, morphine, low-molecular-weight heparin (60 mg subcutaneously twice a day), aspirin (325 mg, nonenteric coated, chewable, immediately, then 150 mg/day), clopidogrel (300 mg immediately, then 75 mg/day), and rosuvastatin (40 mg/day). The patient was not thrombolysed as he was outside the window period, and beta-blocker, nitrates, and renin–angiotensin–aldosterone system inhibitors were not given because of hypotension. Left heart catheterization (LHC) was performed.

Laboratory results included mild neutrophilic leukocytosis, high plasma low-density lipoprotein cholesterol concentration (130 mg/dl, n: <100), high plasma triacylglycerol level (190 mg/dl, n: <150), normal electrolytes, normal renal and hepatic functions, and HbA1c. The plan was to shift him to the PCI-capable center after initial hemodynamic stabilization for coronary angiography (CAG) and reperfusion.

However, 10 h after admission, he complained of chest pain exacerbation, retro-orbital headache and abdominal pain with vomiting, disorientation, mental confusion, and cold intolerance. Low blood pressure (systolic: 50 mmHg) did not respond to intravenous fluid and vasopressors (dobutamine plus norepinephrine). At 36 h postadmission, he had an episode of seizure (semiology: right focal with secondary generalization). Noncontrast computed tomography (CT) brain scan revealed no abnormality. Metabolic panel revealed hyponatremia (Na: 124 mEq/L, reference range: 135–145), mild hyperkalemia (5.8 mEq/L, reference range: 3.5–5.0), mild eosinophilia (absolute eosinophil count: 0.80 thousands/mm3, n: 0.02–0.5), hypoglycemia (random CBG during seizure was 40 mg/dL, hypoglycemia was corrected rapidly with intravenous 25% dextrose infusion, thus seizure was abated and then intravenous 500 mg levetiracetam twice a day was added) and metabolic acidosis (pH: 7.28, bicarbonate: 20 mEq/L, PaCO2: 35 mmHg). Forty-eight hours after admission, systolic blood pressure remained <90 mmHg with fluid and pressure supports. Acute adrenal insufficiency was suspected, and an 8 am serum cortisol level was low (2.0 mcg/dL, n: 6.02–18.40, morning hours). Baseline 8 am Adrenocorticotropic hormone (ACTH) level was 24.4 pg/mL (n: 7.2–63.6) (the response of ACTH and cortisol to corticotropin-releasing hormone administration was almost blunted [ACTH/cortisol at 30 min and at 60 min, respectively, was 28.2/3.5 and 30.6/4.6] to set the diagnosis of secondary acute adrenal crisis). Blood cultures came back negative. Autoimmune screening was negative. Thyroid function test revealed very low free T4 (<0.023 ng/dL, normal: 0.8–2.0), free T3 (0.90 pg/mL, n: 2.1–4.4), and thyroid-stimulating hormone (TSH) (<0.004 μIU/mL, n: 0.4–4.2). Replacement with glucocorticoids (intravenous bolus hydrocortisone 200 mg immediately followed by 100 mg 6 hourly) and levothyroxine (due to unavailability of intravenous preparation of levothyroxine, 500 mcg levothyroxine was given through nasogastric tube as a bolus followed by 100 mcg/day) was started. Measurements of insulin-like growth factor (IGF-1), follicle-stimulating hormone (FSH) and luteinizing hormone (LH), and prolactin levels all were low (IGF-1: 30 ng/mL, n: 75–212; LH: 1.6 mIU/mL, n: 4–8.6; FSH: 4.0 mIU/mL, n: 4.6–12.4; prolactin: 2.0 ng/mL, n: 2.10–17.70). Serum osmolality was low (244 mOsm/Kg H2O, n: 278–298), with normal urinary osmolality, 24-h urinary Na excretion, and plasma vasopressin level. A magnetic resonance imaging (MRI) of the brain revealed partial ES with sella filled with cerebrospinal fluid, flattened, shrunk adenohypophysis, and normal neurohypophysis [Figure 1]. Screening of hypothalamic-releasing hormones showed no abnormality. Thus, the diagnosis of panhypopituitarism was confirmed.
Figure 1: Coronary angiogram showing severe (around 80%–85%) smooth tubular occlusion in left anterior descending-diagonal bifurcation (a); bifurcation stenting to left anterior descending-diagonal by culotte technique through radial approach (b); poststenting angiography showing the restoration of blood flow in the left anterior descending and diagonal (c); the drug-eluting stent can be noted in the proximal left anterior descending-diagonal during follow-up angiogram (d)

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Within 4 days, blood pressure started stabilizing, mental status improved, and hyponatremia was getting corrected. Fluid and vasopressor supports were discontinued without hemodynamic compromise. CAG showed an 80% tubular narrowing of left anterior descending (LAD)-diagonal bifurcation [Figure 2], and a drug-eluting stent was implanted. Post-PCI angiogram was normal, and the patient was symptom-free. He was discharged on the 21st day of hospitalization with aspirin (75 mg/day), clopidogrel (75 mg/day), rosuvastatin (40 mg/day), carvedilol (6.25 mg/day), ramipril (5 mg/day), controlled release nitroglycerin (5.2 mg/day), hydrocortisone (20 mg/day, in divided doses), levothyroxine (200 mcg/day), calcium (1 g/day), and Vitamin D3 (2KIU/day). Growth hormone (GH) and testosterone injectable therapies could not be initiated due to high cost and refusal by the patient.
Figure 2: Magnetic resonance imaging of the pituitary showing T2- and T1-weighted sagittal midline imaging (a and b) demonstrating pituitary fossa filled with cerebrospinal fluid and near-total compression and shrinkage of adenohypophysis, suggestive of empty sella. T1-weighted fat-sat coronal midline imaging (c) and T1-weighted fat-sat sagittal imaging with gadolinium (d) reveal infundibulum sign without any contrast enhancement

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At 3-month follow-up, he had no return of angina. Follow-up echocardiography was normal with no regional wall motion abnormality (RWMA) with EF 52%. Thyroid panel, serum cortisol, and serum electrolytes were normal. Importantly, repeat brain MRI showed further shrinkage of anterior pituitary tissue [Figure 3].
Figure 3: Follow-up (at 3 months) magnetic resonance imaging of pituitary: T2- and T1-weighted sagittal midline imaging (a and b); T2-weighted coronal midline imaging (c) and three-dimensional T1-weighted spoiled gradient recalled echo coronal imaging (d) reveal pituitary fossa completely filled with cerebrospinal fluid with complete nonvisualization of adenohypophysis, suggestive of complete empty sella

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   Discussion Top


We describe a patient with AMI due to a critical stenosing lesion in LAD-diagonal bifurcation complicated by LVF, shock, and acute panhypopituitarism. Acute decompensated cardiogenic shock was at first suspected on a backdrop of extensive AMI. However, no further deterioration of left ventricular EF or new RWMA by serial echocardiography, no recurrent rise of CPK-MB, and absence of response to vasopressors prompted us to look for other causes of shock. Acute adrenal crisis was suspected because of inappropriately low blood pressure, cold intolerance, altered mental status, spontaneous hypoglycemia, eosinophilia, lymphocytosis, hyponatremia, and hyperkalemia coupled with metabolic alkalosis. Endocrine evaluation revealed complete adenohypophyseal failure, and brain MRI showed partial ES. The exclusion of repeat MI or further deterioration of EF and effective response with hormonal supplementation suggested that acute panhypopituitarism was the reason for vasopressor-refractory shock.[17],[18]

There were several diagnostic dilemmas in our case. First, there was panhypopituitarism presenting as AMI. Panhypopituitarism may present with heart failure,[2],[6],[7],[8] cardiac tamponade,[3],[4] Takotsubo cardiomyopathy,[9] arrhythmias,[5],[19] and cardiogenic shock.[6],[20],[21] The prior diminished pituitary reserve could have persisted after a stressful AMI. Third, AMI leading to cardiogenic shock caused acute hypotension which, in turn, led to vasoconstriction, vasospasm in arteries supplying pituitary, and thus acute pituitary infarction. CT brain done 2 years earlier showed normal pituitary and sella turcica. Blood pressure, serum electrolytes, thyroid function test, and blood sugar levels were essentially normal 1 year back. The patient did not have a history of increased intracranial tension or intracranial mass lesion. He had no history of head trauma, cranial surgery, radiotherapy, meningitis, and acute blood loss. There were no protean manifestations of chronic panhypopituitarism including asthenia, weakness, anemia, dry skin, and sparse body hair. A congenital or genetic and functional defect seemed unlikely, given patient's age, previous normal growth, sexual development, and reproduction. There were also no findings suggestive of chronic pituitary insufficiency such as pericardial effusion, nonischemic cardiomyopathy, and left ventricular hypertrophy[20] which excluded the possibility of preexisting pituitary pathology. An acute and transient defect was also unlikely since the patient had previous evidence of pituitary failure and maintained that condition for as long as 6 months of follow-up requiring substitutive therapy. Thus, we believe that panhypopituitarism was acute and secondary to hypotension caused by the initial cardiogenic shock due to AMI. Interestingly, the posterior pituitary remained unaffected because of its direct arterial supply. The adenohypophysis derives its blood supply from a low-pressure portal venous system. When such vulnerable tissue is affected by hypotension, as in this case of extensive AMI, it can lead to ischemia of anterior pituitary leading to necrosis.[22] A similar case of hypopituitarism with non-ST-elevated AMI after PCI was documented by Marume et al.[23] Unlike our cases, it affected only ACTH and GH axis sparing the TSH, FSH, and LH counterparts. Moreover, in contrast to our case, MRI brain was essentially normal. Acute panhypopituitarism in a setting of AMI, lobar pneumonia, and septic shock was described by Kosari et al.[24] While pituitary hemorrhage was the reason for acute panhypopituitarism in that case, our case had ES.

Pituitary apoplexy was likely as the patient had few clinical features (headache, nausea, vomiting, and altered consciousness) suggestive of it, but visual symptoms and cranial nerve palsies were absent. MRI brain also failed to disclose classic pituitary findings either patchy central ischemic necrosis in an enlarged gland or hemorrhage in acute apoplexy.[22] ES is a frequent consequence of pituitary apoplexy from diverse causes.[22] Pituitary apoplexy rapidly progressing to ES without underlying tumor was described previously.[25] This case was peculiar because ES rapidly occurred after apoplexy with florid endocrine dysfunction.


   Conclusion Top


While CV catastrophes as the first or prominent manifestation of previously undiagnosed or untreated panhypopituitarism have been frequently reported, panhypopituitarism as a complication of AMI is exceedingly rare. Moreover, pituitary apoplexy without classical MRI findings, rapid progression to ES, and reversibility of vasopressor-refractory shock by emergency endocrine management make this case unique.

Acknowledgment

We acknowledge Prof Shlomo Melmed for his critical review of this article before submission.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

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Kang DG, Kim SE, Park MS, Kim EJ, Lee JH, Park DG, et al. Acquired long QT syndrome manifesting with torsades de pointes in a patient with panhypopituitarism due to radiotherapy. Korean Circ J 2013;43:340-2.  Back to cited text no. 19
    
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Kissell N, Mudd JO, Gelow JM, Chong LE, Yuen KC. Cardiogenic shock due to nonischemic cardiomyopathy induced by severe anterior hypopituitarism. AACE Clinical Case Rep 2015;1:e147-51.  Back to cited text no. 20
    
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Huang D, Kreitler K, Tilton S, Cavarocchi NC, Hirose H. Cardiogenic shock requiring extracorporeal membrane oxygenation support in a patient with panhypopituitarism: A Case Report. Cureus 2019;11:e4995.  Back to cited text no. 21
    
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Marume K, Arima Y, Igata M, Nishikawa T, Yamamoto E, Yamamuro M, et al. Prolonged hyponatremia due to hypopituitarism in a patient with non-ST-elevation myocardial infarction. J Cardiol Cases 2014;10:226-30.  Back to cited text no. 23
    
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