Dear Sir,
We read the review article “Stable angina pectoris: a review of pathophysiology, diagnosis, and its management” 1 with interest and appreciate a review on such an important issue. We would like some suggestions to make this review more informative and evidence-based.
First, we suggest that the definition of chronic stable angina should be as mentioned in all textbooks and guidelines as “chest pain or retrosternal discomfort that may radiate to the left arm, neck, or jaw and is precipitated by physical exertion or emotional stress or other stress relieved by rest or with nitroglycerin,” 2 rather than the definition mentioned by the authors, which is a little bit confusing and does not mention rest as a relieving factor and includes pain at rest, which signifies acute coronary syndrome (ACS) rather than chronic stable angina.
Second, the review article mentions that high-sensitivity cardiac troponin concentration is a reliable predictor of obstructive coronary artery disease (CAD) in patients with suspected stable angina, but the existing evidence suggests that high-sensitivity cardiac troponin concentration is a reliable predictor of cardiac necrosis or damage to myocardium in ACS rather than obstructive CAD in patients with suspected stable angina. Evidence suggests doing troponin T or troponin I if there is a clinical suspicion of CAD instability, and if increased, management should follow the guidelines for ACSs management. 3 Once we label the patient as having chronic stable angina, it signifies obstruction in coronaries without any necrosis of myocardium, so high-sensitivity cardiac troponin concentration cannot be an indicator of only obstruction without necrosis or damage to myocardium.
Third, the review article mentions that the use of statins to achieve an optimal low-density lipoprotein cholesterol (LDL-C) level of <70 mg/dL is recommended, but the existing evidence suggests that chronic stable angina is considered at very high cardiovascular (CV) risk, so LDL-C levels of <55 mg/dL (not <70 mg/dL) or a reduction by at least 50% of LDL-C from baseline is the target with high-intensity statin therapy. In many patients, only high-intensity statin therapy is not sufficient to achieve the recommended LDL-C goals or may have side effects and intolerance, so a combination of nonstatin lipid-lowering drug therapy is required in the form of ezetimibe, bempedoic acid, or proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i). 3
ORCID
Vitull Kumar Gupta https://orcid.org/0009-0005-3146-0098
REFERENCES
ARTICLE INFO
Publication history
Published: 01 April, 2025
Copyright
Copyright © 2025; The Author(s).