G A Lanza
Istituto di Cardiologia, Università Cattolica del Sacro Cuore, Largo A Gemelli, 8, 00168 Rome, Italy
All studies on patients with CSX have consistently reported an excellent clinical outcome at long-term follow up, with a total absence of major acute coronary events (that is, cardiac death or acute myocardial infarction).
The favourable prognosis of patients with CSX can be challenged by some recent data showing increased occurrence of events among patients with chest pain and normal or near normal coronary arteries who had evidence of coronary endothelial dysfunction. However, these studies included patients with characteristics (for example, with LV dysfunction or subcritical coronary artery stenoses) clearly different from those of CSX. Thus, these studies cannot be taken as a clue to a possible prognostic value of endothelial dysfunction in patients with CSX. In fact, a recent study showed no spontaneous acute coronary events at the 12-year follow up of women with CSX who also had evidence of coronary endothelial dysfunction at enrolment.
Although studies have consistently shown a good prognosis for patients with CSX, no attempts have been made to understand whether this finding may have some specific explanation. Indeed, these patients present a risk profile largely similar to that of patients with obstructive CAD, including, together with a significant prevalence of traditional cardiovascular risk factors, a higher prevalence of inflammation, insulin resistance and endothelial dysfunction.
Although studies have consistently shown a good prognosis for patients with CSX, no attempts have been made to understand whether this finding may have some specific explanation. Indeed, these patients present a risk profile largely similar to that of patients with obstructive CAD, including, together with a significant prevalence of traditional cardiovascular risk factors, a higher prevalence of inflammation, insulin resistance and endothelial dysfunction.
Thus, a challenging clinical question is whether patients with CSX may have some protective factor that, despite the evidence of coronary microvascular dysfunction, may delay the development of critical atherosclerotic lesions in large coronary vessels and prevent acute coronary events. This possibility is suggested by our data showing a reduction in platelet reactivity after stress stimuli (for example, exercise or mental stress) in patients with CSX, in contrast to patients with CAD and to normal subjects, in whom an increase and no changes in platelet reactivity, respectively, are observed. Whether these findings really imply vascular protection and whether other potential protective factors against acute thrombotic coronary events exist in patients with CSX are challenging issues that would merit investigation in future studies.
Quality of life
In contrast to the excellent prognosis, patients with CSX may have a significantly impaired quality of life. Symptoms improve over time in only about one third of patients. In 10–20% of patients, on the other hand, anginal symptoms worsen progressively during follow up, becoming more frequent and long lasting, ensuing at lower levels of exercise or even at rest and becoming less sensitive or refractory to drug treatment, thus impairing usual daily activities, which also results in high rates of absence and retirement from work. The most symptomatic patients also may often have recurrent medical visits, emergency room admissions and hospital admissions, and have repeat non-invasive diagnostic tests and coronary angiography. Thus, although prognostically benign, CSX is an individually, socially and economically relevant condition.
Although a psychological component has been suggested to be involved in patients with CSX with severe chest pain, it is not clear whether psychological disturbances have a causal role or are rather a consequence of the persistent invalidating symptoms. Some data, indeed, suggest that the prevalence of psychological disorders is similar in patients with CSX and in those with obstructive CAD, thus supporting the second hypothesis.
Heart 2007;93:159-166 (“Cardiac syndrome X: a critical overview and future perspectives”)© 2007 by BMJ Publishing Group Ltd & British Cardiovascular Society
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