Cavitation on top of collision breaks the cover of coronary plaques and triggers acute coronary syndrome
Authors: Duong H A I , Nguyen T , Cao B I N H , Le T R A N 
Published: October 2021

Background

Coronary injuries are hypothesized to be caused by the cavitation phenomenon (explosion of air bubbles) which is seen frequently in industrial pipes. Based on hydraulics principles applied to the coronary circulation. during distal negative suctioning in diastole, if the coronary static pressure decreases below the vapor pressure (VP), bubbles will form. They explode when the coronary static pressure recovers &gt; the VP during systole. These explosions create jet waves weakening and rupturing the cover of the coronary plaques, triggering acute coronary syndrome (ACS). How could these events be observed, recorded and compared?

Methods

Coronary angiograms of patients with ACS and stable coronary artery disease (CAD) (control) were selected. The arteries were recorded at 15 frames per second and saved in the electronic health records and reviewed image by image. After the index artery was completely filled with contrast, the following images showed the blood in white moving in on a background of black contrast. The flow could be laminar, turbulent (mixing of blood in white and contrast in black), antegrade or RETROGRADE (black column traveling backward). At the same time, an artificial intelligence (AI) program was used to detect and identify the flow.

Results

There were 104 patients with ACS enrolled and 20 patients with stable CAD as control. First, in the ACS group, 84 lesions (80%) were in the end of the proximal segment of the left anterior descending artery (LAD) and mid-segment of the right coronary artery (RCA). 20 lesions (19%) were at the distal RCA. Second, during diastole, 95% of the flow were laminar. The flow became turbulent at the beginning of systole. The turbulence was caused by the COLLISION of the antegrade flow (end of diastole) and the retrograde flow (at the beginning of systole). These collisions were seen in 95% at the location of vulnerable plaques of patients with ACS. In the control patients, there were only 2 cases (10%) with collision. Third, in the 20 patients with lesions at the distal RCA, the lesions were seen to be located at the areas of recirculating flow, at the ostium of the posterior descending artery (PDA) or proximal to the origin of the PDA. The cause of turbulence was most likely due to cavitation on top of collision. The cavitation happened because of continuous steady forward flow (of the PDA) in the myocardium during systole, while at the proximal RCA the blood flew forward more slowly. (Fig.1) The DSICREPANCY of velocities at the proximal and distal RCA allowed the formation of an empty gap (bubble of air). When the flow reversed during systole, this retrograde flow slammed on the bubble which collapsed violently, injured, ruptured the cover of the plaque and started ACS.

Conclusions

Rupture of bubbles (cavitation) on top of collision was most likely the cause of injury to the cover of vulnerable plaques, triggering ACS. Understanding the mechanism will help to better manage ACS.

Funding Acknowledgement

Type of funding sources: None. Cavity formation and collisionFormation of cavitation at the PDA