Abstract
Funding Acknowledgements
Type of funding sources: None.
Background
The relationship of atrial fibrillation (AF) with coronary artery disease (CAD) is well established. Atrial ischemia due to obstructive CAD has been identified as one of the key risk factors, leading to AF. However, sufficient evidence exists as to the presence of myocardial ischemia on stress imaging, even without the presence of obstructive CAD in AF patients. Slow flow and coronary tortuosity on angiogram can lead to downstream myocardial ischemia independent of CAD.
Purpose
We aimed to delineate the angiographic profiles in AF patients with attention to slow flow and tortuosity leading to ischemia in those without obstructive CAD.
Methods
The study was a nonrandomised, prospective, single-centre observational study of consecutive patients of persistent non valvular AF. Symptomatic patients despite optimal medical therapy (OMT) for 3 months were recruited and all underwent coronary angiograms (CAG). Patients with known CAD or prior history of myocardial infarction were excluded. Further angiographic analysis was done in those without obstructive CAD to determine incidence of slow flow (>27 corrected TIMI frame count) and tortuosity (presence of ≥3 fixed bends in an epicardial artery).
Results
A total of 70 patients were recruited and followed for a mean duration of 12 ± 1.4 months. The mean age of the study group was 66.07 (±11.49). Hypertension (74%) was the commonest comorbidity followed by obesity (35%) and diabetes (30%). At CAG, 32/70 (45%) had obstructive CAD, 17/70 (24%) had non obstructive (<50-70% stenosis) CAD and 21/70 (30%) had normal coronaries without atherosclerosis. Amongst patients without obstructive CAD (n = 38) slow flow was seen in 16/38 (42%) and coronary tortuosity in 11/38 (29%) patients. There ware no differences in terms of death, HF and FVR hospitalisations or stroke at follow up between the obstructive CAD vs no obstructive CAD. However in patients without obstructive CAD, hospitalisations for FVR was significantly increased in those having slow flow on CAG, 9/12 (75%) vs 7/26 (27%) in those without slow flow (p value = 0.005). The mean TIMI frame count was also significantly higher in those with FVR hospitalisations 35.3 ± 11 vs 25.8 ± 8.9 (p value = 0.005). TIMI frame count >31 had a sensitivity of 83% and a specificity of 69% for predicting hospitalisations for FVR on ROC curve(AUC = 0.71).
Conclusions
CAD is closely related to AF and majority (70%) of our patients had evidence of atherosclerotic CAD on CAG in our study. A large proportion of patients with no evidence of obstructive CAD on CAG had slow flow or coronary tortuosity. Significantly increased hospitalisation for FVR seen in the slow flow group shows its significance and may lead to newer treatment modalities in future. Further larger studies looking at these aspects on CAG may give further insight as to the nature and prognosis of these entities.
Myocardial Ischemia due to Rapid Atrial Fibrillation Revealed Using the Instantaneous Wave-Free Ratio