A case of hypertensive emergency, primary hypothyroidism and large pericardial effusion with early tamponade

Abstract

Thyroid hormones and the cardiovascular system are strongly intertwined with known risk of coronary disease, atrial fibrillation, and cardiomyopathy. Pericardial effusions are commonly seen in cases of severe hypothyroidism, however large to massive pericardial effusions with cardiac tamponade are exceptionally rare. We report a case of a patient presenting with hypertensive emergency and a concomitant diagnosis of primary hypothyroidism with a large pericardial effusion and early echocardiographic features of tamponade. Following pericardiocentesis, hypertension management, and thyroid replacement therapy the patient’s symptoms improved with no recurrence of pericardial effusion.

<Learning objective: Hypothyroidism is a common medical comorbidity with many clinical manifestations and cardiovascular effects including hypertension. Pericardial effusion is a known complication of hypothyroidism, however cases of massive effusion and tamponade are rare. Management of large effusions is unclear, with some patients treated with thyroid supplement and others requiring pericardiocentesis.>

Introduction

Thyroid hormones are involved with both development and function of the cardiovascular system. Major effects of thyroid hormones are mediated by triiodothyronine (T3) that increases the force of systolic contraction and diastolic relaxation as well as decreases vascular resistance. Primary hypothyroidism is characterized by decreased levels of T4 and T3 with compensatory high levels of thyroid stimulating hormone (TSH). Most common cardiovascular manifestations include diastolic hypertension and sinus bradycardia. Other manifestations include pericarditis, dyslipidemia, myxomatous valvular changes, and pericardial effusion [1]. Hypothyroidism and pericardial effusion has an incidence of 3–6% in mild cases of hypothyroidism and up to 80% in severe hypothyroidism such as myxedema coma [2]. Large to massive pericardial effusion is infrequent with rare cases of tamponade. This is the first case report to our knowledge of a hypertensive emergency and large pericardial effusion presenting as primary hypothyroidism.

Case report

A male in his late 20s presented to emergency with a one month history of worsening intermittent blurred vision and was found to have a blood pressure of 224/140 mmHg with a temperature of 36.5 °C, heart rate of 62 bpm with no evidence of cardiac or respiratory distress. There was no jugular venous distension, pulsus paradoxus, or cardiac murmurs auscultated. Neurological examination was remarkable for bitemporal hemianospia with funduscopic examination revealing significant papilledema and hypertensive retinopathy. Clinical history did not have any concerning symptoms of overt hypothyroidism and he underwent emergent neuroimaging that showed no intra-cranial pathology. He was admitted to the internal medicine service and treated as a hypertensive emergency with an IV labetolol infusion with work-up for secondary causes of hypertension.

Electrocardiogram showed normal sinus rhythm with left ventricular hypertrophy (LVH) with repolarization changes (lateral T wave inversion leads I, aVL, V5, and V6) and QTc prolongation of 495 ms. There was no QRS alternans or low voltage (Fig. 1A). Echocardiography revealed a large circumferential pericardial effusion (36 mm) with diastolic compression of the right atrium and no right ventricle diastolic compression. There was blunted respiratory variation of the mitral valve and tricuspid valve inflow suggestive of increased pericardial pressure. Left ventricular systolic function was preserved with mild concentric LVH (Fig. 2). There was no pericardial pathology identified either on trans-thoracic echocardiography or computed tomography imaging (Fig. 2, Fig. 3).

Fig. 1.

(A) Electrocardiogram of patient upon presentation [heart rate (HR) 65 bpm, QTc of 495 ms]. (B) Electrocardiogram 10 months post pericardiocentesis and thyroid replacement (HR 81 bpm, QTc of 439 ms).

Fig. 2.

Echocardiographic views in end diastole: (A) Parasternal long-axis; (B) Apical short-axis; (C) Apical four-chamber; (D) Subcostal; (E) Mitral valve inflow with respiration; (F) Parasternal long-axis with right ventricular diastolic collapse; (G) Apical four-chamber post-pericardiocentesis; (H) Parasternal long-axis post-pericardiocentesis.

Fig. 3.

Computed tomography of the chest revealing a large pericardial effusion without pericardial thickening or enhancement. (A) Non-contrast study. (B) Contrast study.

Laboratory work was remarkable for a TSH of 503.50 mIU/L (0.20–4.00 mIU/L) with a free T4 and T3 of 0.7 (10.0–25.0 pmol/L) and 1.0 pmol/L (3.5–6.5 pmol/L), respectively. Complete blood count, serum electrolytes, renal function, and liver chemistry were all within the normal limits. Ultrasound imaging of the thyroid and secondary causes of hypertension were unremarkable.

The patient was diagnosed with primary hypothyroidism and started on high-dose thyroid replacement. His blood pressure slowly improved with oral anti-hypertensive agents, however he began to develop worsening shortness of breath and repeat echocardiogram revealed early findings of cardiac tamponade (Fig. 2F–H). This prompted an echocardiography-guided pericardiocentesis with 750 cc of transudative straw-colored fluid with negative cytology and infectious cultures. He improved post pericardiocentesis and was discharged in stable condition on oral thyroid replacement therapy and anti-hypertensives.

Follow-up examination with endocrinology revealed normalization of his blood pressure without symptoms of hypothyroidism. His biochemical thyroid indices improved with a TSH 10 months post discharge of 6.28 mIU/L, normal electrocardiogram with no evidence of repeat pericardial effusion (Fig. 1B). Other etiologies of hypertension were excluded including normal renin to aldosterone ratio, metanephrines, hypothalamus pituitary axis testing for hypercortisolism, and magnetic resonance imaging and computed tomography studies to rule out sellar mass, renal artery stenosis, and reflux nephropathy, respectively. Currently it is thought that his hypertension was due to profound hypothyroidism, which has been reported as a commonly overlooked cause [3].

Discussion

The link between thyroid and the cardiovascular system has been established with the association between pericardial effusion and hypothyroidism initially called “myxedema heart” in 1918 [4]. Onset is typically insidious without significant effects on cardiac hemodynamics given the distensibility and the ability for the pericardium to adapt. The size of the pericardial effusion is related to the duration and severity of hypothryroidism [5]. Pathophysiology of pericardial fluid accumulation is thought to be due to both impairment of the lymphatic drainage system and increase capillary permeability with underlying low oncotic pressure resulting in net influx of proteins into the pericardial space [5].

Beck’s triad of hypotension, distant heart sounds, and engorgement of the jugular vein may not be seen in patients with hypothyroidism. This has been thought to be related to differences between acute tamponade and subacute tamponade that are usually related to surgical and medical etiologies respectively [6]. Rapid accumulation of fluid in the pericardial space causes sudden impairment of diastolic filling of the heart resulting in hypotension. Contrarily when pericardial fluid accumulation is slow hemodynamic adaptions occur to maintain arterial blood pressure in the face of declining cardiac output, typically mediated by the sympathetic system and increased in peripheral vascular resistance [7]. Retrospective studies have suggested that hypertensive tamponade can be present in up to 43% of cases with improvement in blood pressure post pericardiocentesis [6], [7], [8]. Contrary to the typical tachycardia, a normal heart rate may be present in hypothyroid mediated tamponade providing a clue to the etiology of the pericardial effusion [2].

Common electrocardiographic findings of tamponade include decreased voltage with electrical alternans. Sinus bradycardia, T wave flattening has been known to be associated with hypothyroidism along with QT prolongation [2], [5]. In our case the patient had a heart rate that varied between 50–70 bpm with a prolonged corrected QT interval of 495 ms in keeping with previously reported changes. The patient’s electrocardiogram overall did not meet criteria for low voltage, however the inferior limb leads were blunted. A potential combination of LVH and a large pericardial effusion may result in the lack of our patient’s typical findings associated with tamponade.

Pericardial effusion is characteristically transudative unless there is concomitant disease [2]. Echocardiographic changes of hypothyroidism include LV diastolic dysfunction with thick septa with separate E and A or inverted E/A on Doppler [2], [5]. Long-standing untreated hypothyroidism can result in increased arterial stiffness leading to concentric hypertrophy as seen with our patient [6]. M or 2D modes are the preferred investigation for diagnosis of cardiac tamponade with typical features of diastolic right atrial and right ventricular collapse, dilated inferior vena cava, and loss of respiratory variation and respiratory interventricular dependence [2], [5]. Early diastolic collapse of the right atrium and right ventricle are sensitive and specific signs that occur early and are often seen in patients with a large pericardial effusion without clinical evidence of tamponade [2].

Management is individualized from pericardiocentesis to medical management with thyroid replacement [2], [9]. In a small retrospective review, resolution of pericardial effusion after treatment with thyroid replacement occurred over a duration from 1 to 21 months [2]. Pericardiocentesis is indicated if there is evidence of tamponade and for diagnostic sampling. Currently guidelines on pericardial disease from the European Society of Cardiology do not have any specific recommendations related to hypothyroidism and cardiac tamponade [10].

Contrary to most reported cases, our patient presented with hypertension. Thyroid hormones are involved in the synthesis and regulation of adrenergic receptors with an imbalance between alpha and beta receptors leading toward increased systemic vascular resistance [3]. Moreover, hypothyroidism is associated with inappropriate anti-diuretic hormone secretion contributing to water retention leading to an increased pre-load [3]. We suspect that the combination of low oncotic pressure with hypothyroid-induced hypertension resulted in increased hydrostatic pressure leading to progressive pericardial effusion and early tamponade.

Our case reports an atypical presentation of hypertensive emergency and newly diagnosed primary hypothyroidism with a large pericardial effusion and echocardiographic features of early tamponade. Management of early tamponade is currently unclear and can involve medical management with close observation versus pericardiocentesis.

Conflicts of interest

The authors declare no conflicts of interest.