A 47-year-old man with shortness of breath during activity and at rest for 24 hours has a history of chemotherapy with doxorubicin 4 months ago. Resting pulse was elevated during treatment and his current ejection fraction is 40% with sinus tachycardia on ECG. What is the most likely diagnosis and its pathophysiology?

A 47-year-old man with shortness of breath during activity and at rest for 24 hours has a history of chemotherapy with doxorubicin 4 months ago. Resting pulse was elevated during treatment and his current ejection fraction is 40% with sinus tachycardia on ECG. What is the most likely diagnosis and its pathophysiology?

• A. Pneumonia; infection
• B. Pulmonary embolism; venous obstruction
• C. Congestive heart failure; doxorubicin-induced dilated cardiomyopathy
• D. Arrhythmia; structural heart disease

Answer: (C)

Doxorubicin can cause dose-related injury to the heart muscle, leading to dilated cardiomyopathy and systolic heart failure. In this patient, dyspnea on exertion and at rest, a reduced ejection fraction of 40%, and sinus tachycardia align with congestive heart failure due to impaired contractility. The key mechanism is free radical–mediated damage from the anthracycline to cardiac myocytes, causing mitochondrial dysfunction, lipid peroxidation, and apoptosis. This loss of viable myocardium produces ventricular dilation and decreased the heart’s pumping ability, which often manifests months after exposure and can be dose dependent. The presentation fits a toxic cardiomyopathy from doxorubicin rather than primary pulmonary infection or a venous thromboembolism, and the rhythm abnormality on ECG is a secondary finding to the underlying pump dysfunction rather than the primary issue.

Doxorubicin can cause dose-related injury to the heart muscle, leading to dilated cardiomyopathy and systolic heart failure. In this patient, dyspnea on exertion and at rest, a reduced ejection fraction of 40%, and sinus tachycardia align with congestive heart failure due to impaired contractility. The key mechanism is free radical–mediated damage from the anthracycline to cardiac myocytes, causing mitochondrial dysfunction, lipid peroxidation, and apoptosis. This loss of viable myocardium produces ventricular dilation and decreased the heart’s pumping ability, which often manifests months after exposure and can be dose dependent. The presentation fits a toxic cardiomyopathy from doxorubicin rather than primary pulmonary infection or a venous thromboembolism, and the rhythm abnormality on ECG is a secondary finding to the underlying pump dysfunction rather than the primary issue.