SMuRF-less CAD patients had similar coronary inflammation (PCAT attenuation -77.5 vs -78.4 HU, p=0.481) but 18-39% lower plaque burden and 2.8-fold lower odds of obstructive CAD.
Do patients without standard modifiable cardiovascular risk factors (SMuRF-less) have different levels of coronary inflammation compared to those with SMuRFs?
Patients with suspected CAD but no standard modifiable risk factors exhibit similar levels of coronary inflammation to those with risk factors, despite having less plaque burden.
Absolute Event Rate: 0% vs 0%
Abstract Background There is a growing incidence of CAD in the absence of standard modifiable cardiovascular risk factors (SMuRFs) which include hypertension, hyperlipidaemia, diabetes and smoking. This phenomenon has been termed "SMuRF-less" CAD. Identifying novel biomarkers and mechanisms for SMuRF-less CAD is crucial to uncover new therapeutic strategies. The role of inflammation in CAD has been extensively studied and was recently validated as a therapeutic target. Aims This study aimed to compare coronary inflammation in SMuRF-less patients and patients with SMuRFs using pericoronary adipose tissue (PCAT) attenuation, a novel and specific biomarker of coronary inflammation which is quantified on computed tomography coronary angiography (CTCA). Our secondary aims were to compare plaque burden and maximal coronary artery diameter stenosis between both groups. Methods We conducted a retrospective single-centre study of 309 consecutive patients who underwent clinically indicated serial CTCAs for suspected stable CAD (2010-2016). Patients with a previous known symptomatic history of CAD were excluded. We validated and subsequently used semi-automated software for PCAT attenuation measurement around the proximal right coronary artery. We assessed plaque burden, using the Segment Involvement Score (SIS) and Segment Stenosis Score (SSS). Maximal coronary artery diameter was evaluated using the Coronary Artery Disease - Reporting and Data System (CAD-RADS). Results Of 309 individuals, 83 (27%) were SMuRF-less. The median age was 57.5 years, and 51.8% of the cohort were female. Baseline demographics were similar between SMuRF-less patients and those with SMuRFs, except that patients with SMuRFs were more frequently on statins, ACEi/ARB and aspirin. Our main findings showed that SMuRF-less patients had a similar PCAT mean attenuation (HU) to patients with SMuRFs (-77.5 ± 9.5 vs. -78.4 ± 8.9 HU, p=0.481), despite having a lower plaque burden and a lower maximal coronary artery diameter stenosis. The mean SIS and SSS were 18.7% and 39.5% lower, respectively, in SMuRF-less patients compared to those with SMuRFs (SIS: 1.78 ± 2.19 vs. 2.72 ± 2.88, p =0.01; SSS: 2.22 ± 3.36 vs. 3.67 ± 4.38, p=0.004). Patients with SMuRFs had 2.8-fold higher odds of having obstructive CAD (maximal diameter stenosis 50%) compared to SMuRF-less patients (p=0.006). Conclusion In patients with suspected CAD referred for CTCA, we found that SMuRF-less individuals exhibited a similar level of coronary inflammation as those with SMuRFs, despite having a lower plaque burden and less severe maximal coronary artery stenosis. These findings might explain why SMuRF-less patients still develop CAD and subsequent cardiovascular events. Further research is needed to validate these findings. If confirmed, the therapeutic target of inflammation could be explored further in SMuRF-less patients.
Sivakumar et al. (Sat,) reported a other. SMuRF-less CAD patients had similar coronary inflammation (PCAT attenuation -77.5 vs -78.4 HU, p=0.481) but 18-39% lower plaque burden and 2.8-fold lower odds of obstructive CAD.