Anthracycline‑induced delayed‑onset cardiac toxicity: A case report and literature review

Abstract

Anthracyclic (ANT) drugs are widely used for patients with malignant tumors and can markedly prolong the disease-free survival rate of patients. As its clinical application becomes more common, information regarding serious cardiotoxicity as a result of ANT treatment is becoming understood. However, to the best of our knowledge, delayed-onset cardiotoxicity due to ANT use has not been studied sufficiently. The present report describes a 36-year-old male patient who presented to Guiqian International General Hospital (Guiyang, China) with a complaint of dyspnea in the last 10 days. Substantially elevated B-type natriuretic peptide levels and echocardiography showing enlargement of the entire heart, of the patient suggested that severe heart failure was the cause of his symptoms. However, the cause of this potential heart failure was not apparent until the patient was questioned about his cancer treatment history. Following consultation to evaluate the assessment of end-stage heart failure, currently only anti-heart failure treatment and symptomatic treatment can be provided. The present report describes this case and reviews the existing literature to provide a basis for the diagnosis and treatment of patients with delayed-onset heart failure following ANT treatment. Case reportA 36-year-old young male patient presented to the Cardiology Department of Guiqian International General Hospital (Guiyang, China) in October 2022 due to 'difficulty breathing for >10 days. The patient felt shortness of breath after a little exercise, following which the symptoms progressively worsened, accompanied by paroxysmal nocturnal dyspnea and orthopnea. The electrocardiogram (ECG) (ECG-2306, Shanghai Optoelectronic Medical Electronic Instrument Co., Ltd) revealed 'ST-segment elevation in leads V1-V4,

Research progress in spasmodic torticollis rehabilitation treatment

“…Extracorporeal Shock Wave Therapy (ESWT) is a series of high-energy single-pulse mechanical waves, notable for high pressure, fast rise, short action period, and three-dimensional propagation, the speed of which increases with pressure. It can be divided into focused ESWT (fESWT) and radial ESWT (rESWT)[ 32 ]. Although the mechanism of ESWT in spasmodic treatment is still unclear, it may be related to the following aspects: (1) ESWT induces the production of nitric oxide, which increases neovascularization of muscles and tendons, thereby improving muscle stiffness; (2) ESWT may reduce the excitability of motor neurons by vibration stimulation of the tendons, thereby reducing muscle tone; (3) ESWT can reduce the amount of acetylcholine at the neuromuscular junction, causing nerve conduction disorders; and (4) ESWT can cause alternating biochemical reactions between metabolism and proliferation, affecting muscle fibrosis and rheological properties[ 33 ].…”