Impact of symptom-to-reperfusion-time on transmural infarct extent and left ventricular strain in patients with ST-segment elevation myocardial infarction: a 3D view on the wavefront phenomenon.

AIMS: We examined the association between the symptom-to-reperfusion-time and cardiovascular magnetic resonance (CMR)-derived global strain parameters and transmural infarct extent in ST-segment elevation myocardial infarction (STEMI) patients. METHODS AND RESULTS: The study included 108 STEMI patients who underwent successful primary percutaneous coronary intervention (PPCI). Patients were categorized according to the median symptom-to-reperfusion-time: shorter (<160 min, n = 54) and longer times (>160 min, n = 54). CMR was performed 2-7 days after PPCI and at 1 month. CMR cine imaging was performed for functional assessment and late gadolinium enhancement to evaluate transmural infarct extent. Myocardial feature-tracking was used for strain analysis. Groups were comparable in relation to incidence of LAD disease and pre- and post-PPCI thrombolysis in myocardial infarction (TIMI) flow grades. The mean transmural extent score at follow-up was lower in patients with shorter reperfusion time (P < 0.01). Both baseline and follow-up maximum transmural extent scores were smaller in patients with shorter reperfusion time (P = 0.03 for both). Patients with shorter reperfusion time had more favourable global left ventricular (LV) circumferential strain (baseline, P = 0.049; follow-up, P = 0.01) and radial strain (baseline, P = 0.047; follow-up, P < 0.01), whilst LV longitudinal strain appeared comparable for both baseline and follow-up (P > 0.05 for both). In multi-variable regression analysis including all three strain directions, baseline LV circumferential strain was independently associated with the mean transmural extent score at follow-up (ß=1.89, P < 0.001). CONCLUSION: In STEMI patients, time-to-reperfusion was significantly associated with smaller transmural extent of infarction and better LV circumferential and radial strain. Moreover, infarct transmurality and residual LV circumferential strain are closely linked.

Cardiac MRI to Visualize Myocardial Damage after ST-Segment Elevation Myocardial Infarction: A Review of Its Histologic Validation.

Cardiac MRI is a noninvasive diagnostic tool using nonionizing radiation that is widely used in patients with ST-segment elevation myocardial infarction (STEMI). Cardiac MRI depicts different prognosticating components of myocardial damage such as edema, intramyocardial hemorrhage (IMH), microvascular obstruction (MVO), and fibrosis. But how do cardiac MRI findings correlate to histologic findings? Shortly after STEMI, T2-weighted imaging and T2* mapping cardiac MRI depict, respectively, edema and IMH. The acute infarct size can be determined with late gadolinium enhancement (LGE) cardiac MRI. T2-weighted MRI should not be used for area-at-risk delineation because T2 values change dynamically over the first few days after STEMI and the severity of T2 abnormalities can be modulated with treatment. Furthermore, LGE cardiac MRI is the most accurate method to visualize MVO, which is characterized by hemorrhage, microvascular injury, and necrosis in histologic samples. In the chronic setting post-STEMI, LGE cardiac MRI is best used to detect replacement fibrosis (ie, final infarct size after injury healing). Finally, native T1 mapping has recently emerged as a contrast material-free method to measure infarct size that, however, remains inferior to LGE cardiac MRI. Especially LGE cardiac MRI-defined infarct size and the presence and extent of MVO may be used to monitor the effect of new therapeutic interventions in the treatment of reperfusion injury and infarct size reduction. © RSNA, 2021 Online supplemental material is available for this article.

Epicardial Surface Area of Infarction: A Stable Surrogate of Microvascular Obstruction in Acute Myocardial Infarction.

BACKGROUND: Microvascular obstruction (MO) is a pathophysiologic complication of acute myocardial infarction that portends poor prognosis; however, it is transient and disappears with infarct healing. Much remains unknown regarding its pathophysiology and whether there are predictors of MO that could function as stable surrogates. We tested for clinical and cardiovascular magnetic resonance predictors of MO to gain insight into its pathophysiology and to find a stable surrogate. METHODS: Three hundred two consecutive patients from 2 centers underwent cardiovascular magnetic resonance within 2 weeks of first acute myocardial infarction. Three measures of infarct morphology: infarct size, transmurality, and a new index-the epicardial surface area (EpiSA) of full-thickness infarction-were quantified on delayed-enhancement cardiovascular magnetic resonance. RESULTS: Considering all clinical characteristics, only measures of infarct morphology were independent predictors of MO. EpiSA was the strongest predictor of MO and provided incremental predictive value beyond that of infarct size and transmurality (P<0.0001). In patients with 3-month follow-up cardiovascular magnetic resonance (n=81), EpiSA extent remained stable while MO disappeared, and EpiSA was a predictor of adverse ventricular remodeling. After 20 months of follow-up, 11 died and 1 had heart transplantation. Patients with an EpiSA larger than the median value (≥6%) had worse outcome than those with less than the median value (adverse events: 6.4% versus 1.9%, P=0.045). CONCLUSIONS: The EpiSA of infarction is a novel index of infarct morphology which accurately predicts MO during the first 2 weeks of MI, but unlike MO, does not disappear with infarct healing. This index has potential as a stable surrogate of the presence of acute MO and may be useful as a predictor of adverse remodeling and outcome which is less dependent on the time window of patient assessment.

Instantaneous wave-free ratio guided multivessel revascularisation during percutaneous coronary intervention for acute myocardial infarction: study protocol of the randomised controlled iMODERN trial.

INTRODUCTION: Recent randomised clinical trials showed benefit of non-culprit lesion revascularisation in ST-elevation myocardial infarction (STEMI) patients. However, it remains unclear whether revascularisation should be performed at the index procedure or at a later stage. METHODS AND ANALYSIS: The instantaneous wave-free ratio (iFR) Guided Multivessel Revascularisation During Percutaneous Coronary Intervention for Acute Myocardial Infarction trial is a multicentre, randomised controlled prospective open-label trial with blinded evaluation of endpoints. After successful primary percutaneous coronary intervention (PCI), eligible STEMI patients with residual non-culprit lesions are randomised, to instantaneous wave-free ratio guided treatment of non-culprit lesions during the index procedure versus deferred cardiac MR-guided management within 4 days to 6 weeks. The primary endpoint of the study is the combined occurrence of all-cause death, recurrent myocardial infarction and hospitalisation for heart failure at 12 months follow-up. Clinical follow-up includes questionnaires at 3 months and outpatient visits at 6 months and 12 months after primary PCI. Furthermore, a cost-effectiveness analysis will be performed. ETHICS AND DISSEMINATION: Permission to conduct this trial has been granted by the Medical Ethical Committee of the Amsterdam University Medical Centres (loc. VUmc, ID NL60107.029.16). The primary results of this trial will be shared in a main article and subgroup analyses or spin-off studies will be shared in secondary papers. TRIAL REGISTRATION NUMBER: NCT03298659.

Temporal Changes in Coronary Hyperemic and Resting Hemodynamic Indices in Nonculprit Vessels of Patients With ST-Segment Elevation Myocardial Infarction.

Importance: Percutaneous coronary intervention (PCI) of nonculprit vessels among patients with ST-segment elevation myocardial infarction (STEMI) is associated with improved clinical outcome compared with culprit vessel-only PCI. Fractional flow reserve (FFR) and coronary flow reserve are hyperemic indices used to guide revascularization. Recently, instantaneous wave-free ratio was introduced as a nonhyperemic alternative to FFR. Whether these indices can be used in the acute setting of STEMI continues to be investigated. Objective: To assess the value of hemodynamic indices in nonculprit vessels of patients with STEMI from the index event to 1-month follow-up. Design, Setting, and Participants: This substudy of the Reducing Micro Vascular Dysfunction in Revascularized STEMI Patients by Off-target Properties of Ticagrelor (REDUCE-MVI) randomized clinical trial enrolled 98 patients with STEMI who had an angiographic intermediate stenosis in at least 1 nonculprit vessel. Patient enrollment was between May 1, 2015, and September 19, 2017. After successful primary PCI, nonculprit intracoronary hemodynamic measurements were performed and repeated at 1-month follow-up. Cardiac magnetic resonance imaging was performed from 2 to 7 days and 1 month after primary PCI. Main Outcomes and Measures: The value of nonculprit instantaneous wave-free ratio, FFR, coronary flow reserve, hyperemic index of microcirculatory resistance, and resting microcirculatory resistance from the index event to 1-month follow-up. Results: Of 73 patients with STEMI included in the final analysis, 59 (80.8%) were male, with a mean (SD) age of 60.8 (9.9) years. Instantaneous wave-free ratio (SD) did not change significantly (0.93 [0.07] vs 0.94 [0.06]; P = .12) and there was no change in resting distal pressure/aortic pressure (mean [SD], 0.94 [0.06] vs 0.95 [0.06]; P = .25) from the acute moment to 1-month follow-up. The FFR decreased (mean [SD], 0.88 [0.07] vs 0.86 [0.09]; P = .001) whereas coronary flow reserve increased (mean [SD], 2.9 [1.4] vs 4.1 [2.2]; P < .001). Hyperemic index of microcirculatory resistance decreased and resting microcirculatory resistance increased from the acute moment to follow-up. The decrease in distal pressure from rest to hyperemia was smaller at the acute moment vs follow-up (mean [SD], 10.6 [11.2] mm Hg vs 14.1 [14.2] mm Hg; P = .05). This blunted acute hyperemic response correlated with final infarct size (ρ, -0.29; P = .02). The resistive reserve ratio was lower at the acute moment vs follow-up (mean [SD], 3.4 [1.7] vs 5.0 [2.7]; P < .001). Conclusions and Relevance: In the acute setting of STEMI, nonculprit coronary flow reserve was reduced and FFR was augmented, whereas instantaneous wave-free ratio was not altered. These results may be explained by an increased hyperemic microvascular resistance and a blunted adenosine responsiveness at the acute moment that was associated with infarct size.