In this case, a male in his 50s presented with a worsening of rest-induced chest tightness, prompting a medical consultation. No chest symptoms were reported during exertion. The medical history included a history of smoking and ongoing treatment with medication for dyslipidemia and hypertension.

Referred to our facility for coronary arterydisease evaluation, including angina pectoris, initial assessments via restingelectrocardiogram and echocardiography revealed no abnormalities.

Coronary angiography showed no organic stenosis. Given the rest-induced chest symptoms, a coronary drug stress test was performed. A pressure wire was placed in the left anterior descending artery, and acetylcholine was administered. During low-dose acetylcholine loading, a significant reduction in peripheral coronary artery pressure was observed, prompting angiography. Severe coronary spasm in the left anterior descending and circumflex arteries confirmed coronary angina.

The integration of a pressure wire during a drug-induced coronary spasm test enables the continuous monitoring of peripheral coronary artery pressure throughout the administration of the drug. This real-time assessment is sensitive to changes that may precede the onset of chest symptoms or electrocardiographic alterations, thereby enabling the early identification of coronary spasm. Furthermore, this approach enhances catheter stability, thereby reducing the risk of catheter damage and improving the precision of drug delivery. These factors facilitate a more expedient response following diagnosis, which may mitigate the risk of hemodynamic instability, such as ventricular fibrillation.

The use of pressure wires during coronary spasm drug-induced testing allows for early recognition of coronary spasms, enabling timely intervention. Additionally, it enhances catheter stability, reduces the risk of damage during testing, and improves safety by providing precise monitoring of coronary artery pressure throughout the procedure.