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Signature ✍️
- Hypothyroidism, overt: ↓ thyroid hormones (T4, T3)
- Hypothyroidism, subclinical: ↑ TSH, normal FT4 (i.e. while measured thyroid hormone is “normal,” high TSH serves as a marker of ↓ intracardiac T3 availability & thyroid hormone receptor activity)
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DDx 🏳️🌈
Acute (Rare)
- (Pre)syncope (bradyarrhythmias ⊕ ↓ β1)
- Torsades (acquired long QT syndrome ⊕ PVC)
- Decompensated CHF (↓ contractility vs. pericardial effusion)
- Vasospasm → PAD mimicker
Chronic (Common)
- ↓ Exercise capacity
- Asymptomatic sinus bradycardia
- Orthostatic hypotension
- Diastolic hypertension
- Atherosclerosis → PAD
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Principles❗️
Normal Physiology ✅
- Within the heart, T3 enters cardiac myocytes & activates thyroid hormone nuclear receptors, ultimately upregulating β1 receptors (↑ contractility, ↑ HR) & enzymes necesssary for calcium flux (↑ compliance → ↑ diastolic filling)
- Peripherally, T3 stimulates endothelial NO synthase & therefore results in vascular smooth muscle vasodilation with resultant ↓ systemic vascular resistance
Pathophysiology ❌
- ↓ T3 (the bioactive thyroid hormone) results in the inverse effects of normal T3 function, as well as pericardial capillary leak (↓ lymphatic drainage)
- Notably, cardiovascular symptoms & signs in patients with hypothyroidism are uncommon & when present, often subtle
- ↑ TSH itself may also serve a pathophysiologic function via effects on cardiac myocyte resting membrane potentials & ↑ parasympathetic tone
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References 📚