Cardiovascular Disease in Endocrine Disorders

and J. Carl Pallais1



(1)
Harvard Medical School Division of Endocrinology, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA

 




Abstract

Cardiovascular symptoms are often the first signs and symptoms of underlying endocrinopathies. This chapter reviews endocrine disorders with a focus on cardiovascular changes and presentations.


Abbreviations


ACTH

Adrenocorticotropic hormone

AF

Atrial fibrillation

AI

Adrenal insufficiency

AIT

Amiodarone-induced thyrotoxicosis

BMD

Bone mineral density

CAD

Coronary artery disease

CHF

Congestive heart failure

CMV

Cytomegalovirus

CO

Cardiac output

CV

Cardiovascular

CVD

Cardiovascular disease

DBP

Diastolic blood pressure

DTR

Deep tendon reflexes

EKG

Electrocardiogram

GH

Growth hormone

HIV

Human immunodeficiency virus

HR

Heart rate

HTN

Hypertension

IGF-1

Insulin-like growth factor – 1

IV

Intravenous

LV

Left ventricular

OGTT

Oral glucose tolerance test

PAC

Plasma aldosterone concentration

PE

Physical exam

PRA

Plasma renin activity

PTH

Parathyroid hormone

PTU

Propylthiouracil

PVR

Peripheral vascular resistance

RAI

Radioactive iodine

RAIU

Radioactive iodine uptake

SBP

Systolic blood pressure

SSKI

Supersaturated potassium iodide

SV

Stroke volume

SVR

Systemic vascular resistance

T3

Triiodothyronine

T4

Thyroxine

TB

Tuberculosis

TFT

Thyroid function tests

TSH

Thyroid stimulating hormone

TTE

Trans-thoracic echocardiography

WNL

Within normal limits



Introduction


Cardiovascular symptoms are often the first signs and symptoms of underlying endocrinopathies. This chapter reviews endocrine disorders with a focus on cardiovascular changes and presentations.


Thyroid (Table 32-1)





Table 32-1
Cardiovascular changes with thyroid disease




























CV parameter

Hyperthyroid

Hypothyroid

Systemic vascular resistance

Decreased

Increased

Heart rate

Increased

Decreased

Cardiac output

Increased

Decreased

Blood volume

Increased

Decreased


Hyperthyroidism/Thyrotoxicosis


Hyperthyroidism/Thyrotoxicosis – physiologic manifestations of excessive quantities of thyroid hormones (endogenous or exogenous) [1]



  • Signs/Symptoms:



    • General – weight loss, tremors, insomnia, heat intolerance, warm moist skin, hyperreflexia, hyperdefecation. Goiter may be present. Proptosis may occur in Graves’ disease.


    • Cardiovascular (CV) – ↑ sympathetic tone (tachycardia, palpitations, atrial fibrillation [AF]), ↑ cardiac output [CO] (from ↑ heart rate [HR], in severe cases ↑ stroke volume [SV]), ↑ inotropy, ↑ circulatory demand from hypermetabolism, ↓ peripheral vascular resistance (PVR), ↑ pulse pressure



      • Physical exam (PE) findings: dynamic precordium, systolic ejection murmur, enhanced S1, Means-Lerman scratch (systolic pleuropericardial friction rub)


      • Arrhythmia: 2–20 % of patients will have AF. Cardioversion is not indicated when thyrotoxicosis is present. 60 % revert spontaneously within 4 months after normalization of thyroid function tests (TFT). Anticoagulation is recommended in patients with AF who are at moderate risk for stroke on the basis of identified risk factors [2]. Patients with newly diagnosed AF with clearly reversible hyperthyroidism and no risk factors for thromboembolism do not warrant long-term anticoagulation.


  • Laboratory testing:



    • ↓ Thyroid stimulating hormone (TSH), ↑ thyroid hormones (free thyroxine [T4] and/or triiodothyronine [T3]); ↑ thyroid antibodies in Graves’ disease


    • Radioactive iodine uptake (RAIU)/thyroid scan – in the setting of a suppressed TSH, RAIU measures autonomous activity of the thyroid gland; thyroid scan measures the pattern of distribution of iodine trapping within the gland (homogeneous, heterogeneous, focal)


  • Causes:



    • ↑ RAIU (thyroid scan pattern): Graves’ disease (homogeneous), toxic multinodular goiter (heterogeneous), toxic adenoma (focal), TSH-secreting pituitary tumors (homogenous)


    • ↓ RAIU: Iodide-induced thyrotoxicosis, thyroiditis (autoimmune, post-viral/subacute, drug induced [amiodarone, lithium, interferon-alpha, interleukin-2, granulocyte macrophage colony-stimulating factor]), exogenous thyroid hormone ingestion, struma ovarii


  • Treatment:



    • β-blockers (preferably propranolol, atenolol, or metoprolol which also ↓ T4 to T3 conversion), methimazole, ± inorganic iodine (after methimazole) to ↓ release of preformed thyroid hormone (Wolff-Chaikoff effect), ± glucocorticoids (↓T4 to T3 conversion)


    • RAI ablation, thyroidectomy


Special Cases of Hyperthyroidism




1.

Thyroid Storm – accelerated hyperthyroidism. Precipitants usually infection, trauma, ­surgery [3].



  • Signs/Symptoms: Fever, sweating, marked tachycardia, arrhythmias, pulmonary edema, high-output congestive heart failure (CHF), tremulousness, delirium, psychosis, abdominal pain, jaundice. Can be fatal if not treated.


  • Treatment: Intensive care, propylthiouracil (PTU), super-saturated potassium iodide (SSKI) after PTU, dexamethasone. ±β-blocker depending on cardiac state

 

2.

Subclinical Hyperthyroidism – biochemical findings of low TSH with normal T4 and T3 levels



  • Increased risk for AF if TSH <0.1 mU/L (2  ×  ↑ risk over 10 years), and  ±  ↓ bone mineral density (BMD) [4]


  • Treatment impacts hemodynamic parameters (↓HR, ↓CO, ↑systemic vascular resistance [SVR], ↓ premature atrial or ventricular contractions, ↓ left ventricular [LV] mass) and improve BMD, especially in older adults [5]


  • Assessment of cause and appropriate treatment recommended for elderly, postmenopausal osteoporosis, cardiac disease (left atrial enlargement, AF, CHF, angina), and infertility

 


Hypothyroidism






  • Signs/Symptoms: Dry/coarse skin, peri-orbital puffiness, delayed relaxation phase of deep tendon reflexes (DTR), hair loss, fatigue, weight gain [6, 7]



    • CV Signs/Symptoms: ↓ CO (↓ SV & ↓HR), ↑ PVR at rest with possible diastolic hypertension (HTN), narrow pulse pressure, ↓ blood volume, ↓ circulation  →  coolness, pallor; pericardial effusion


    • Labs: ± ↑CK and LDH (skeletal muscle source), ↑ LDL


    • Electrocardiogram (EKG) changes: sinus bradycardia, prolonged PR, low voltage, non-specific ST-segment changes, flattened/inverted T-waves


    • Trans-thoracic echocardiogram (TTE): resting LV diastolic dysfunction


  • Diagnosis: Primary hypothyroidism  =  ↑ TSH, ↓ T4 & T3. Central hypothyroidism  =  low/normal TSH, ↓ T4 & T3.


  • Causes: Primary hypothyroidism is much more common than central hypothyroidism



    • Primary hypothyroidism – Hashimoto’s thyroiditis, infiltrative disease (sarcoid, hemochromatosis, etc.), thyroid resection, post-radioiodine therapy, iodine deficiency, drugs (lithium, thionamides, sulfonamides, iodine, tyrosine kinase inhibitors)


    • Thyroiditis (painless/subacute/postpartum) can cause transient hyperthyroidism followed by transient hypothyroidism


    • Central hypothyroidism – pituitary tumor, pituitary surgery, radiation therapy


  • Treatment: Thyroid hormone replacement; start at low replacement dose and slowly titrate up if coronary artery disease (CAD) suspected (thyroid hormone replacement may exacerbate angina)

Note: Hypothyroidism decreases the metabolism of many cardiac drugs. Care must be exercised when treating cardiovascular disease (CVD) in hypothyroid patients or initiating thyroid hormone replacement in these patients.


Special Cases of Hypothyroidism




1.

Myxedema coma – condition seen with severe long-standing hypothyroidism, primarily in older patients. High mortality rate [8]



  • Signs/Symptoms: Comatose state, hypothermia, bradycardia, hypotension, delayed DTR/areflexia, seizures, hypoventilation, hyponatremia, hypoglycemia


  • Risk factors: Age, exposure to cold, infection, trauma, central nervous system depressants, anesthetics


  • Diagnosis: Clinical diagnosis, delay of treatment worsens prognosis. Treatment should be initiated while awaiting thyroid function test results.


  • Treatment: Intravenous (IV) levothyroxine 500 mcg load, 100 mcg IV daily, hydrocortisone 100 mg IV q8h to cover for relative adrenal insufficiency; correction of metabolic derangements (hyponatremia, hypoglycemia), as well as respiratory failure (mechanical ventilation), and work-up for coexisting disease

 

2.

Euthyroid Sick Syndrome (Non-Thyroidal Illness Syndrome) – Abnormalities of circulating TSH, T4, and T3 levels without underlying thyroid disease. Occurs in fasting and illness [9] (Table 32-2)


Table 32-2
Stages of euthyroid sick syndrome























Stage

Severity of illness

T3 or free T3

T4 or free T4

Reverse T3

TSH

Stage 1

Mild (ex. URI)


Normal
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Jul 13, 2016 | Posted by in CARDIOLOGY | Comments Off on Cardiovascular Disease in Endocrine Disorders

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