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Published on: March 12, 2018
Changes in Coronary Blood Flow After Acute Myocardial Infarction: Insights From a Patient Study and an Experimental
Guus A de Waard1, Maurits R Hollander1, Paul F A Teunissen1
1Department of Cardiology, ICaR-VU, VU University Medical Center, Amsterdam, the Netherlands.
Insights
Acute myocardial infarction (AMI) impairs coronary flow reserve (CFR) in both culprit and nonculprit arteries. This reduction is due to increased baseline flow and decreased hyperemic flow, impacting patient outcomes.
Area of Science:
- Cardiovascular physiology
- Interventional cardiology
- Myocardial infarction research
Background:
- Impaired coronary flow reserve (CFR) post-acute myocardial infarction (AMI) is linked to adverse outcomes.
- The specific roles of resting and hyperemic flow in reducing CFR after AMI are not well understood.
- Existing experimental AMI models may not accurately reflect clinical coronary flow dynamics.
Purpose of the Study:
- To investigate the impact of AMI on baseline and hyperemic coronary blood flow.
- To differentiate the contributions of resting and hyperemic flow to CFR reduction post-AMI.
- To compare coronary flow parameters in clinical AMI cases with an AMI porcine model.
Main Methods:
- Intracoronary Doppler flow velocity measurements in culprit and nonculprit arteries of STEMI patients (n=40) post-revascularization.
- Propensity-score matched control group (n=40) without obstructive coronary artery disease.
- Coronary flow measurements in a porcine AMI model before and after 75-minute balloon occlusion (n=11).
Main Results:
- CFR was significantly reduced in culprit arteries of patients (36% lower) and swine post-AMI.
- Both increased baseline flow and decreased hyperemic flow contributed to reduced CFR in patients and swine.
- Nonculprit arteries also showed reduced CFR post-AMI, correlating with infarct size in both models.
Conclusions:
- AMI leads to decreased CFR in both culprit and nonculprit coronary arteries.
- Elevated baseline flow and diminished hyperemic flow are key contributors to post-AMI CFR reduction.
- The observed CFR changes are attributed to post-occlusive hyperemia, myocardial damage, and compensatory mechanisms, not pre-existing microvascular dysfunction.
Objectives:
The aim of this study was to determine the effects of an acute myocardial infarction (AMI) on baseline and hyperemic flow in both culprit and nonculprit arteries.
Background:
An impaired coronary flow reserve (CFR) after AMI is related to worse outcomes. The individual contribution of resting and hyperemic flow to the reduction of CFR is unknown. Furthermore, it is unclear whether currently used experimental models of AMI resemble the clinical situation with respect to coronary flow parameters.
Methods:
Intracoronary Doppler flow velocity measurements were obtained in culprit and nonculprit arteries immediately after successfully revascularized ST-segment elevation myocardial infarction (n = 40). Stable patients without obstructive coronary artery disease served as control subjects and were selected by propensity-score matching (n = 40). Similar measurements in an AMI porcine model were taken both before and immediately after 75-min balloon occlusion of the left circumflex artery (n = 11).
Results:
In the culprit artery, CFR was 36% lower than in matched control subjects (Δ = -0.9; 1.8 ± 0.9 vs. 2.8 ± 0.7; p < 0.001) with consistent observations in swine (Δ = -0.9; 1.5 ± 0.4 vs. 2.4 ± 0.9 for after and before AMI, respectively; p = 0.04). An increased baseline and a decreased hyperemic flow contributed to the reduction in CFR in both patients (baseline flow: Δ = +5 and hyperemic flow: Δ = -7 cm/s) and swine (baseline flow: Δ = +8 and hyperemic flow: Δ = -6 cm/s). Similar changes were observed in nonculprit arteries (CFR: 2.8 ± 0.7 vs. 2.0 ± 0.7 for STEMI patients and control subjects; p < 0.001). CFR significantly correlated with infarct size as a percentage of the left ventricle in both patients (r = -0.48; p = 0.001) and swine (r = -0.61; p = 0.047).
Conclusions:
CFR in both culprit and nonculprit coronary arteries decreases after AMI with contributions from both an increased baseline flow and a decreased hyperemic flow. The decreased CFR after AMI in culprit and nonculprit vessels is not a result of pre-existing microvascular dysfunction, but represents a combination of post-occlusive hyperemia, myocardial necrosis, hemorrhagic microvascular injury, compensatory hyperkinesis, and neurohumoral vasoconstriction.
