Related Experiment Video
Updated: Aug 9, 2026
In Vivo Quantitative Assessment of Myocardial Structure, Function, Perfusion and Viability Using Cardiac Micro-computed Tomography
Published on: February 16, 2016
Elective percutaneous coronary intervention immediately impairs resting microvascular perfusion assessed by cardiac
Andrew J Taylor1, Nidal Al-Saadi, Hassan Abdel-Aty
1Baker Heart Research Institute, Melbourne, Australia. andrew.taylor@baker.edu.au
Insights
Percutaneous coronary intervention (PCI) impairs resting microvascular perfusion due to plaque rupture. This study shows reduced blood flow in the treated artery area after PCI, impacting coronary microcirculation.
Area of Science:
- Cardiovascular imaging
- Interventional cardiology
- Microvascular function
Background:
- Percutaneous coronary intervention (PCI) can cause plaque rupture, potentially affecting distal microvascular perfusion.
- Mechanisms include distal microvascular spasm or embolization.
- The impact of PCI on resting microvascular flow requires further evaluation.
Purpose of the Study:
- To assess the effect of PCI on resting microvascular perfusion.
- To investigate changes in myocardial blood flow post-PCI.
- To evaluate microvascular function in patients with coronary artery disease undergoing PCI.
Main Methods:
- Cardiovascular magnetic resonance imaging (CMR) was used to assess left ventricular systolic function and microvascular perfusion.
- 15 patients with stable coronary artery disease and 10 controls were scanned before and after PCI.
- Microvascular perfusion was quantified using contrast enhancement parameters (T50% max, relative upslope) and regional contrast delay.
Main Results:
- PCI led to a significant regional contrast delay in the treated artery area (0.6 +/- 0.2s post-PCI vs 0.0 +/- 0.2s pre-PCI, P < .05).
- A reduction in relative upslope indicated decreased microvascular perfusion (8.6 +/- 0.5 post-PCI vs 10.1 +/- 0.7 pre-PCI, P = .02).
- Regional systolic thickening remained unchanged post-PCI.
Conclusions:
- PCI causes impaired resting microvascular perfusion in the myocardium supplied by the treated artery.
- This impairment is likely a result of iatrogenic atherosclerotic plaque rupture during the procedure.
- Microvascular dysfunction following PCI warrants consideration in patient management.
Background:
Percutaneous coronary intervention (PCI) is known to induce atherosclerotic plaque rupture, which may affect resting distal microvascular perfusion either through distal microvascular spasm or through embolization. We evaluated the effect of PCI on resting microvascular flow.
Methods:
We performed cardiovascular magnetic resonance imaging to assess left ventricular systolic function and microvascular perfusion in 15 patients with stable coronary artery disease before and within 24 hours after PCI and in 10 control subjects without obstructive coronary artery disease on a clinical 1.5-T CMR scanner. Microvascular perfusion was evaluated at rest after injecting a bolus of gadolinium-diethylenetriamine pentaacetic acid (0.1 mmol/kg) by calculating the time to 50% maximum myocardial enhancement (T50% max), as well as the relative upslope, of the myocardial signal intensity curve. Regional perfusion and systolic thickening were evaluated using a 16-segment left ventricular model with the slice locations matched anatomically pre-PCI and post-PCI. The relative contrast delay in the region of myocardium subtended by the PCI artery was calculated by subtracting the T50% max of a remote region from the PCI region.
Results:
In subjects with coronary artery disease, PCI resulted in a regional contrast delay (mean delay 0.6 +/- 0.2 seconds post-PCI vs 0.0 +/- 0.2 seconds pre-PCI, P < .05) and a reduction in the relative upslope (8.6 +/- 0.5 post-PCI vs 10.1 +/- 0.7 pre-PCI, P = .02), consistent with reduced microvascular perfusion. This was unaccompanied by any change in regional systolic thickening (54% +/- 7% pre-PCI vs 53% +/- 5% post-PCI, P = NS).
Conclusions:
The data show PCI-induced impairment of resting microvascular perfusion in the area of myocardium subtended by the treated artery after PCI, a likely consequence of iatrogenic atherosclerotic plaque rupture.
