Correlation of angiographic microvascular obstruction (no reflow phenomenon) with CMR derived microvascular obstruction: Implications and future opportunities for paradigm-shifting therapies (RF_TH_181)

Timely and complete restoration of epicardial infarct-related artery patency with primary percutaneous coronary intervention (PCI) is the preferred reperfusion strategy in patients with acute myocardial infarction (AMI). However, in a considerable number of patients myocardial perfusion remains impaired despite vessel patency, also termed “no-reflow phenomenon” in the past, which is a major obstacle for a further reduction of morbidity and mortality rates following AMI. Angiographic no-reflow most likely reflects severe microvascular obstruction and destruction. However, the exact correlation of angiographic no-reflow with cardiac magnetic resonance (CMR) derived microvascular obstruction (MVO) is currently unclear and needs further research and clarification.

Methods:

AMI patients with symptom-onset < 48h with angiographic no-reflow defined as Thrombolysis In Myocardial Infarction (TIMI) flow grade ≤2 after primary percutaneous coronary intervention (PCI) were included in this multicenter study. Primary PCI was performed by experienced interventional cardiologists according to standard clinical practice. CMR was performed within 5 days after the index event on a 1.5 Tesla CMR scanner. A standardized imaging protocol was used in all participating study centers. All images were analyzed offline in an experienced core laboratory and assessed with certified evaluation software. Regions of infarcted myocardium and MVO were delineated with semiautomated computer-aided threshold detection ( >5 standard deviations of remote myocardium in ≥10 adjacent pixels) and expressed as the percentage of LV mass (%LV). CMR derived MVO was defined as the core area of nonenhancement within the infarcted myocardium and included in the overall infarct size and quantified separately.

Results:

A total of 102 patients were included (76.7% male) with a median age of 66 years and ST-elevation myocardial infarction in 73.3% of patients. The final TIMI-flow grade after PCI was impaired in all participants – as required by the study protocol (TIMI flow 0 after PCI: 12%, TIMI flow I after PCI 21%, TIMI flow II after PCI 67%). CMR-derived MVO was detected in 85 patients (83%) with a mean size of 3g and 2.5% of the left ventricle and 8.4% of the infarct size. Almost all patients (39/41, 95%) with TIMI flow 0 and 1 had CMR derived MVO. In patients with TIMI flow 2, in 46 of 61 patients  (75%) MVO could be detected. The extent of CMR MVO was significantly larger in patients with TIMI flow 0/1 versus in patients with TIMI flow 2 (2.0 (0.3, 5.0) versus 4.0 (2.0, 12.0), p=0.025).

Conclusion:

Angiographic no-reflow reflects severe ischaemic injury affecting the microvasculature. CMR can visualize MVO and help to determine the severity of myocardial injury and microvascular destruction after PCI. Especially TIMI-flow of 0 and 1 after PCI has a very strong correlation with CMR derived MVO and therefore the term (angiographic) no-reflow should be restricted to patients with TIMI flow 0/1 after PCI and ideally replaced by angiographic MVO. As angiographic MVO has strong prognostic relevance targeting this microvascular specific injury may thus evolve as key to the discovery of novel, injury-stage-directed treatments to improve patient outcomes directly in the cath lab (e.g. with glycoprotein IIb/IIIa inhibitor or other cardioprotective strategies).