Cardiac Syndrome X, or microvascular angina, is a condition characterized by angina-like symptoms, evidence of myocardial ischemia on diagnostic tests, but with angiographically normal epicardial coronary arteries.
The pathogenesis is related to an alteration in the function of the coronary microcirculation, resulting in a reduced coronary flow reserve. The main pathophysiological mechanisms involved are:
Endothelial dysfunction: Decreased nitric oxide production and impaired vasodilation.
Increased vascular tone: Hyperreactivity of the autonomic nervous system with inappropriate vasoconstriction.
Chronic inflammation: Pro-inflammatory state altering the vascular response.
Alterations in microcirculatory regulation: Reduced coronary perfusion despite normal angiography.
Epidemiology and Risk Factors
Cardiac Syndrome X predominantly affects postmenopausal women and represents an underestimated cause of angina.
It is more frequent in smokers and in individuals with other traditional cardiovascular risk factors (arterial hypertension, dyslipidemia, diabetes mellitus, metabolic syndrome)
Clinical Presentation and Diagnosis
Patients with Cardiac Syndrome X present with typical chest pain, similar to angina from coronary stenosis, but with some peculiarities:
Chronic angina, often persistent and not always related to exertion.
Poor response to nitrates, unlike angina due to coronary obstruction.
Presence of myocardial ischemia on provocative testing, but normal coronary arteries on angiography.
The most useful diagnostic tests include:
Resting ECG and stress test: Possible nonspecific ST segment changes and T wave inversion.
Myocardial scintigraphy and cardiac magnetic resonance imaging: Demonstrate reduced microvascular perfusion.
Stress echocardiography: Regional wall motion abnormalities in the absence of coronary obstruction.
Coronary angiography with coronary reactivity testing: Confirms the absence of significant epicardial coronary stenoses.
Treatment of Cardiac Syndrome X
The aim of treatment is to improve myocardial perfusion and reduce anginal symptoms.
Lifestyle modifications:
Adopting a healthy lifestyle is fundamental. A Mediterranean diet, regular physical activity, and smoking cessation improve endothelial function and reduce inflammatory status.
Pharmacological therapy:
Beta-blockers: Improve exercise tolerance and reduce myocardial oxygen consumption.
Calcium channel blockers: Vasodilation of coronary arterioles.
ACE inhibitors and sartans: Improve endothelial function.
Statins: Anti-inflammatory effect and stabilization of endothelial dysfunction.
Ranolazine and trimetazidine: Improve cardiac metabolism and reduce symptoms.
Prognosis and Complications
Although Cardiac Syndrome X is not associated with an increased risk of myocardial infarction, it can lead to a significant reduction in quality of life. Optimal therapeutic management is essential for symptom control and prevention of recurrent anginal episodes.
References
Ouldzein H, et al. Microvascular angina: the hidden part of the iceberg. J Am Coll Cardiol. 2019;74(19):2425-2438.
Taqueti VR, et al. Coronary microvascular dysfunction in women with chest pain. Circulation. 2017;135(6):518-527.
Crea F, et al. Management of microvascular angina. European Heart Journal. 2017;38(13):1024-1036.
Camici PG, et al. Microvascular dysfunction in ischemic heart disease. New England Journal of Medicine. 2015;372(10):956-967.
Shah SJ, et al. Heart failure with preserved ejection fraction and microvascular dysfunction. J Am Coll Cardiol. 2020;75(1):1-13.
O’Donoghue ML, et al. Microvascular ischemia and anti-anginal therapy. Circulation Research. 2019;124(5):622-635.
Task Force Members. ESC Guidelines for the management of chronic coronary syndromes. Eur Heart J. 2019;41(3):407-477.
Marzilli M, et al. Coronary microvascular dysfunction and cardiometabolic disorders. Nat Rev Cardiol. 2018;15(9):605-620.
Patel MR, et al. Diagnostic evaluation of chest pain and microvascular angina. J Am Coll Cardiol. 2018;71(5):538-556.
Fox K, et al. Stable angina and microvascular disease. BMJ. 2019;364:k5404.
