A 58-year-old woman with fatigue, weight gain, and cold intolerance presents with an ECG showing sinus bradycardia (HR 48 bpm), low-voltage QRS complexes (<5 mm in limb leads), and diffusely flattened T waves. Serum TSH is 45 mIU/L and free T4 is 0.3 ng/dL. The ECG pattern marked **B** in the diagram is characteristic of overt hypothyroidism. Which of the following BEST explains the mechanism underlying the low-voltage QRS complexes seen in this patient?
A. Acute myocardial infarction with loss of viable myocardium
B. Restrictive cardiomyopathy with amyloid infiltration of the ventricular wall
C. Pericardial effusion with myxedematous infiltration of the myocardium and decreased myocardial contractility
D. Chronic obstructive pulmonary disease with right ventricular hypertrophy
Explanation
Why "Pericardial effusion with myxedematous infiltration of the myocardium and decreased myocardial contractility" is right
The classic ECG triad of overt hypothyroidism (marked B in the diagram) includes sinus bradycardia, low-voltage QRS complexes, and flattened/inverted T waves. The low-voltage QRS complexes specifically reflect TWO pathophysiologic mechanisms: (1) pericardial effusion from accumulation of myxedematous mucinous fluid around the heart, and (2) myxedematous infiltration of the myocardium itself combined with decreased myocardial contractility due to thyroid hormone deficiency. This is the hallmark of "myxedema heart disease." The low voltage dampens electrical signal transmission through the thorax, reducing QRS amplitude in all leads. This finding is reversible with levothyroxine replacement and normalization of thyroid function (Harrison's 21e, Braunwald's 12e).
Why each distractor is wrong
Acute myocardial infarction with loss of viable myocardium: While AMI can produce low-voltage complexes, it typically presents acutely with chest pain, elevated troponins, and ST-segment changes or pathologic Q waves. The clinical context here (chronic fatigue, weight gain, cold intolerance, markedly elevated TSH) is inconsistent with acute MI, and the ECG pattern is diffuse and symmetric, not localized to a coronary territory.
Chronic obstructive pulmonary disease with right ventricular hypertrophy: COPD causes right axis deviation and right ventricular hypertrophy, which typically produces tall R waves in V1–V2, not low-voltage complexes. The clinical presentation (no dyspnea, no smoking history implied) and the symmetric low voltage across all leads do not fit COPD.
Restrictive cardiomyopathy with amyloid infiltration of the ventricular wall: While restrictive cardiomyopathy can produce low-voltage QRS complexes, amyloid infiltration is a distinct pathologic process unrelated to thyroid hormone deficiency. The clinical and biochemical evidence (TSH 45, free T4 0.3) clearly points to hypothyroidism, not amyloidosis. Amyloid would not explain the bradycardia or the reversibility of ECG changes with thyroid hormone replacement.
High-YieldNEET PG
Hypothyroid ECG triad = bradycardia + low voltage + flat T waves; low voltage = pericardial effusion + myxedematous myocardial infiltration; all reverse with levothyroxine.
Harrison's 21e (Hypothyroidism); Braunwald's 12e (Cardiovascular Manifestations of Systemic Diseases); Williams Textbook of Endocrinology 14e
Practice similar questions
Sign up free to access AI-powered MCQ practice with detailed explanations and adaptive learning.
