The association between the severity and extension of CAD and the serum level of PCT was first evaluated by Erren et al. . The authors compared the serum PCT level in patients who were candidated electively for selective coronary angiography. They categorized their study patients, the majority of them with chronic stable angina, according to the presence or absence of CAD and peripheral artery disease, into three groups and found that the PCT level was elevated in the patients with CAD and peripheral arterial disease concomitantly by comparison with the control patients and those with CAD only. In addition, they found no correlation between the serum PCT level and the severity and extension of CAD. However, in a recent study, Kurtul and Elcik  evaluated patients candidated for selective coronary angiography because of chronic stable angina and compared the serum PCT level between the patients with low and high SYNTAX scores ( ≥ 23 vs. < 23). Their entire study population had a 50% diameter stenosis in at least one major epicardial coronary artery. In their study, patients with a history of PCI were included in the analysis, and the results showed that the PCT level was associated with a high SYNATX score.
Another possible explanation for our results is that MI by itself can lead to increased PCT levels, which – especially when PCT is measured around its plateau period – can confound the correlation between the serum level of PCT and the severity and extension of CAD. Hence, the plateau level of PCT – unlike the level measured at admission – may not be correlated with the extension and severity of CAD. The difference in the measurement times of the serum PCT level has various prognostic implications. Kelly et al.  measured the serum level of PCT in patients with ST-elevation MI and NSTEMI at discharge (median = 5 days) and found, at a median follow-up of 671 days, that PCT was an independent predictor of major adverse cardiovascular events. In a study by Kafkas et al. , the PCT level reached its baseline value on the seventh post-MI day; it, therefore, appears that the PCT level in many of their patients may have been near the baseline level. Sinning et al.  measured the serum PCT level before coronary angiography in 2131 patients, consisting of 1300 patients with stable angina and 831 with acute coronary syndrome. What is not clear in their results is the measurement times of PCT, but the authors concluded that PCT was not an independent predictor of cardiovascular mortality and events at 3.6 years’ follow-up.
It is noteworthy that the clinical profile of our study population – including age, sex, hypertension, diabetes, cigarette smoking, and a family history of CAD – is not significantly different from that in studies on the correlation between PCT and coronary atherosclerotic burden [15,17]. However, in comparison with western registries [27–30], our patients are younger by about one decade.
First and foremost among the limitations of this study is its cross-sectional design with its inherent drawbacks. This study being a single-center investigation with a small sample size can be deemed another weakness of note. In addition, our results would have been boosted had we been able to measure the PCT level serially from the admission time and onward or had we evaluated the severity and extension of CAD with other imaging modalities such as intravascular ultrasound rather than solely selective coronary angiography.
In our patients with NSTEMI, the PCT level on the second postadmission day was not statistically significantly correlated with the extension and severity of CAD assessed with the Gensini score.
This study was financially supported by Tehran University of Medical Sciences.
There are no conflicts of interest.
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