Objective: To investigate the possible role of repeated episodes of sudden increase in the arterial pressure in triggering a subendothelial dissection at the level of the coronary wall, as a possible pathophysiological mechanism of ANCA-type acute coronary syndromes (ACS).
Methods: The study included 54 consecutive patients with normal blood pressure values, who presented in the emergency department with ACS (unstable angi-na and non-ST elevation myocardial infarction), who underwent emergency coronary angiography and were proven to present ANCA. Optical coherence tomography (OCT) was performed in all patients. The main exclusion criterion was the presence of constant arterial hypertension above 140/90 mmHg. The study population was separated in 2 groups: gr. 1 (n=29) with repeti-tive episodes of abrupt and temporary increase in arterial pressure over 140/90 mmHg, within the last month prior to the acute event, and gr. 2 (n=25) with normal stable blood pressure and no episode of temporary rise in blood pressure.
Results: T here were no statistically significant di-fferences between the study groups in relation to the cardiovascular risk factors (diabetes: p=0.9, hypercho-lesterolemia: p=0.5, obesity: p=0.4; chronic tobacco use: p=0.09. However, patients in group 1 were signi-ficantly younger (age 44.4±8.6 vs. 53.5±7.4, p=0.005) and were more frequently females (77.1% vs, 50.2%, p=0.02). Left ventricular ejection fraction was 56.8±8.2 vs. 58.0±6.5, p=0.5. Coronary angiography revealed an abnormal non-laminar coronary flow in 79.3% of cases from group 1 (n=23) compared group 2 with 28% of ca-ses (n=7), p=0.0002. Location of this non-laminar co-ronary flow was at the level of left anterior descending artery in 21 cases (72.41%), right coronary artery in 5 cases (17.2%) and circumflex artery in 3 cases (10.3%). OCT examination found the presence of a dissection in the sub-endothelial layer in a significantly higher extent in group 1 compared to group 2 (74% vs. 30.2%, p=0.009).
Conclusions: Recurrent episodes of abrupt rise in the arterial blood pressure, especially in the young female subjects, may trigger subendothelial dissection due to de-structuration of the endothelium, which can lead to non-ST elevation ACS. The present theory could be-come an explanation for the mechanism behind ACS with ANCA, however further studies on larger popula-tions are required to validate it.