Intramyocardial Hemorrhage Research Articles

Abstract 4132838: Coronary Collaterals Provide Cardioprotection in Hemorrhagic ST-elevation MI (STEMI)

Introduction: Development of intramyocardial hemorrhage (IMH) in acute STEMI following reperfusion is estimated to affect 35-50% of patients. IMH is a lethal event as it contributes to larger MI size, compromised myocardial salvage, adverse left ventricular (LV) remodeling, lower LVEF, and consequential major adverse CV events post-MI. Whether coronary collateral circulation reduces the deleterious effects of IMH has not been investigated. Hypothesis: We hypothesized that coronary collaterals could reduce the extent of post-reperfusion IMH volume and offer cardioprotection to hemorrhagic MI patients. Methods: MIRON-CL (NCT05898425) recruited and studied STEMI patients (n=294) reperfused via PCI. Pre-PCI coronary angiography allowed for assessment of collateral vessels using the Rentrop grading system, from Grade 0 (no collaterals) to Grade III (complete collateral filling). Post-PCI cardiac MRI, performed 3 days later, was used to determine area affected (extent of myocardial edema) from T2 maps, extent of IMH from T2* maps and MI size from LGE as %LV. Statistical analyses were used to examine relationships between collateral grades, MI size, IMH, and area affected. Results: 124 patients were hemorrhagic and 170 were non-hemorrhagic. Patients with no collaterals (Grade 0; CL-) exhibited significantly higher IMH volumes (7.41 ± 5.33% LV) compared to those with collaterals (Grade I: 5.23 ± 3.21% LV, Grade II: 3.11 ± 2.78% LV, Grade III: 2.05 ± 1.89% LV; p<0.001). Total area affected post-PCI was larger in CL- (37.62 ± 15.32% LV) compared to CL+ (21.48 ± 13.21% LV, p<0.001). Presence of collateral circulation (Grade>0 combined; CL+) was correlated with smaller MI sizes (CL-: 38.66 ± 14.63% LV vs. CL+: 19.84 ± 13.72% LV, p<0.001) and reduced MVO volumes (CL-: 8.07 ± 6.60% LV vs. CL+: 2.17 ± 2.35% LV, p<0.001). Patients with no collaterals had a significantly higher adj. risk of IMH (OR: 5.71, 95% CI: 3.16-10.33, p<0.0001). Conclusion: Coronary collaterals reduce post-reperfusion IMH volume in STEMI patients and provide significant cardioprotection: reductions in area affected, MVO and MI size. Insight into collateral grade offers opportunities to improve risk stratification and management of revascularized STEMI patients.

The immunopathology of coronary microembolization and the underlying inflammopathophysiological mechanisms.

In coronary microembolization, inflammatory cell infiltration, patchy necrosis, and extensive intra-myocardial hemorrhage are dominant, which induce myocardial dysfunction with clinical symptoms of chronic ischemic cardiomyopathy. Microembolization can lead to obstruction of the coronary microvessels and result in the micro-infarction of the heart. The inflammation and elevated expression of the tumor necrosis factor in cardiomyocytes and the activation of extracellular ERK are involved in initiating the inflammatory response mechanism. The PI3K/Akt signaling pathway is the enriched pathway, and for controlling, inhibition of PI3K/Akt is necessary. Furthermore, the release of cytokines and the activation of inflammasomes contribute to the enhancement of vascular permeability, which results in edema within the myocardium. The immune response and inflammation represent the primary triggers in this process. The ability to control immune response and inflammation reactions may lead to the development of new therapies for microembolization.

Fractalkine Inhibition in Acute Myocardial Infarction leads to reduced intramyocardial haemorrhage

Abstract Background The fractalkine receptor CX3CR1 has been linked to the development of microvascular obstruction (MVO) in ST-elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (PPCI). Pre-clinical studies have demonstrated a reduction in infarct size, inflammation and intramyocardial haemorrhage (IMH) with inhibition of CX3CR1. Purpose The FRACTAL study is a phase IIa, pilot, randomized, 2-arm parallel group, placebo-controlled, double blinded, multi-centre trial. In addition to assessing the safety and tolerability of the fractalkine inhibitor KAND567 in STEMI patients, a subgroup exploratory analysis was performed. We investigated into the translation of MRI and blood samples characteristics between the two groups. Methods Patients with an anterior STEMI who had an occluded proximal to mid left anterior descending (LAD) artery were recruited. These patients had to present within 5 hours of the onset of their chest pain. They were subsequently randomised on a 1:1 basis to receive either KAND567 or placebo. Patients then underwent an MRI at day 3, and subsequently a comparator at 3 months. Additionally, throughout the period of their follow-up, patients would regularly undergo blood sampling to assess multiple parameters. Results Of the 71 patients recruited into the study, 29 patients in the KAND567 arm and 28 patients in the placebo arm received both MRIs. The KAND567 arm had shown a similar troponin rise at day 1 compared to placebo (4357 vs 4286). Baseline MRI demonstrated an identical infarct size between both arms. The presence and absence of IMH was then analysed defining IMH+ as presence of IMH and IMH- as IMH absence. The presence of IMH in patients showed a larger infarct size. The infarct size of IMH+ were the same between KAND567 and placebo, which was a similar finding in the IMH- arm too. However, when compared to day 90 MRI demonstrated a numerically smaller infarct size in the KAND567 group with a smaller percentage of IMH. This was consistent with a lower rate of IMH in the KAND567 arm too, when compared between the groups (35.5% vs 55.2%; p=0.15) (see table below). This seemed to be related to the smaller distribution IMH+, as the IMH+ infarcts were much larger in both arms, whilst overall infarct size in IMH subgroup were identical. Conclusion KAND567 appears to prevent the transition from IMH- to IMH+, while it doesn’t change infarct size in the respective subgroups of IMH+ or IMH-.MRI Comparator Table

Long-term prognosis after ST-elevation myocardial infarction according to the Canadian Cardiovascular Society classification of tissue injury severity in acute myocardial infarction

Abstract Background The recently proposed Canadian Cardiovascular Society (CCS) classification of acute myocardial infarction (MI) describes 4 stages of tissue injury identified by cardiac magnetic resonance imaging (CMR); 1) oedema without late gadolinium enhancement (LGE); 2) LGE without microvascular obstruction (MVO); 3) MVO; and 4) intramyocardial haemorrhage (IMH). Prior studies examining the relationship between these characteristics and outcomes are limited by variations in imaging and measurement techniques, in particular the distinction between MVO and IMH. The relationship between the proposed CCS classification of MI and outcomes has not been described. Purpose To explore the prognostic significance of the CCS classification of MI tissue injury in patients with ST-elevation MI (STEMI). Methods The British Heart Foundation MR-MI study was a prospective single-centre CMR cohort study in patients with STEMI (July 2011-November 2012). CMR was performed on a single Siemens MAGNETOM Avanto 1.5-Tesla scanner at 2 days post-STEMI. The imaging protocol included LGE and T2* mapping, allowing for the identification of infarct, MVO, and IMH. Follow-up for the occurance of major adverse cardiovascular events (MACE) (recurrent MI, ischaemic stroke and cardiovascular death) and a composite outcome of heart failure hospitalization/ICD implantation (HFH) or all-cause death was performed via electronic case note review. Results 246 patients had complete data for this analysis. Of these, 6 (2%) were CCS Stage 1, 105 (43%) were Stage 2, 33 (13%) were Stage 3, and 102 (41%) were Stage 4. Due to the low number in CCS stage 1, these patients were pooled with Stage 2 for the purposes of this analysis (CCS Stage 1/2). Average age was 58 (SD 11) years and 188 (76%) were male. With higher CCS stage, more patients were Killip class III/IV at presentation, had the LAD as culprit artery and had TIMI flow 0/1 pre-PCI. Patients with higher CCS stage had higher peak troponin-I and NT-proBNP, lower left ventricular function, higher left ventricular volumes and larger infarct size (Table). Median follow-up was 11.8 years. HFH or all-cause death occurred in 80 (33%) patients (22 HFH and 58 all-cause deaths), and MACE occurred in 63 (26%) patients (41 recurrent MI, 11 ischaemic stroke events, and 11 cardiovascular deaths). There were no significant differences in outcomes between CCS Stage 3 and CCS Stage 1/2 (Figure). Patients with CCS Stage 4 had a higher risk of HFH or all-cause death (HR 1.73, 95%CI 1.08-2.77; p=0.022) and MACE (HR 1.88, 95%CI 1.10-3.20; p=0.021) as compared with those in CCS Stage 1/2 (Figure). Conclusion The novel CCS classification of MI tissue injury identifies patients at the highest risk of adverse outcomes following STEMI. The relationship between the presence of IMH (CCS Stage 4) and adverse outcomes highlights the importance of T2* imaging in post-MI CMR protocols in order to identify this prognostically important biomarker.

Inhibition of fractalkine signalling in patients with acute myocardial infarction - First results from the FRACTAL trial

Abstract Background We have previously demonstrated a strong association between expression of the fractalkine receptor CX3CR1 on lymphocytes and microvascular obstruction (MVO) in patients undergoing primary percutaneous coronary intervention (PPCI) for ST-elevation myocardial infarction. Our pre-clinical studies also found an improvement in infarct size, inflammation and intramyocardial haemorrhage (IMH) when rats were pre-treated with the fractalkine inhibitor KAND567. Purpose FRACTAL (FRACTalkine inhibition in Acute myocardial infarction) study was a phase IIa, pilot, randomized, 2-arm parallel group, placebo-controlled, double blinded, multi-centre trial. Its primary aim was to assess the safety and tolerability of intravenous and oral administration of the fractalkine inhibitor KAND567 as well as reducing signs of reperfusion injury in STEMI patients undergoing PPCI. Methods Patients with a new diagnosis of anterior STEMI, who had index chest pain within 5 hours and angiographic occlusion of the LAD, were randomised on a 1:1 basis to receive either KAND567 or placebo over a period of 72 hours. All patients then underwent a baseline MRI scan at 3 days with a follow-up scan at 3 months, paralleled by longitudinal deep immuno­phenotyping over 9 time points. Results A total of 71 patients were enrolled into the study with 64 (90.1%) being male patients. The mean age of patients was 59.2 years. 37 patients received KAND567, whilst 34 received placebo over 72-hour period. Throughout the 3-month follow-up period, 23 (62%) patients from the KAND567 arm as compared to 24 (71%) patients in the placebo arm had reported adverse events. There was no statistical difference in serious adverse events (SAEs) between both arms with 9 documented in the placebo arm and 12 in the KAND567 arm. Safety bloods also demonstrated no significant differences between the two groups across all time points. There was a higher incidence of left ventricular (LV) thrombus in the placebo arm as compared to the KAND567 arm (17.6% vs. 2.7%; p=0.049). Additionally, the study also demonstrated a lower occurrence of IMH in the KAND567 arm compared to the placebo arm (35.5% vs. 55.2%; p=0.19). Deep immunephenotyping suggested clear target engagement in the KAND567 arm in natural killer cells as well as in cytotoxic T-lymphocytes. Conclusion This first in-man study demonstrates that inhibition of the fractalkine pathway in STEMI patients appears safe and well-tolerated, while demonstrating a promising potential in preventing LV thrombus and IMH. The results suggest a new mechanism and class of drug to target reperfusion injury, clearly warranting a larger phase III study.LV thrombus and IMH

TCT-4 Rationale and Design of the IMODERN STOP-IMH Randomized Trial: The Safety of Ticagrelor Monotherapy After Primary Percutaneous Coronary Intervention for ST-Segment Elevation Myocardial Infarction and the Effect on Intramyocardial Hemorrhage

TCT-4 Rationale and Design of the IMODERN STOP-IMH Randomized Trial: The Safety of Ticagrelor Monotherapy After Primary Percutaneous Coronary Intervention for ST-Segment Elevation Myocardial Infarction and the Effect on Intramyocardial Hemorrhage

Association of Circulating PCSK9 With Ischemia-Reperfusion Injury in Acute ST-Elevation Myocardial Infarction.

Beyond therapeutic implications, PCSK9 (proprotein convertase subtilisin/kexin 9) has emerged as a promising cardiovascular biomarker. The exact role of PCSK9 in the setting of acute ST-elevation myocardial infarction (STEMI) is incompletely understood. We aimed to investigate the association of PCSK9 with ischemia-reperfusion injury, visualized by cardiac magnetic resonance imaging, in patients with STEMI revascularized by primary percutaneous coronary intervention (PCI). In this prespecified substudy from the prospective MARINA-STEMI (NCT04113356) registry, we included 205 patients with STEMI. PCSK9 concentrations were measured from venous blood samples by an immunoassay 24 and 48 hours after PCI. The primary end point was defined as presence of intramyocardial hemorrhage according to cardiac magnetic resonance T2* mapping. Secondary imaging end points were the presence of microvascular obstruction (MVO) and infarct size. The clinical end point was the occurrence of major adverse cardiac events. We observed a significant increase in PCSK9 levels from 24 to 48 hours (268-304 ng/mL; P<0.001) after PCI. PCSK9 24 hours after PCI did not show any relation to intramyocardial hemorrhage, MVO, and infarct size (all P>0.05). PCSK9 concentrations 48 hours post-STEMI were higher in patients with intramyocardial hemorrhage (333 versus 287 ng/mL; P=0.004), MVO (320 versus 292 ng/mL; P=0.020), and large infarct size (323 versus 296 ng/mL; P=0.013). Furthermore, patients with increased PCSK9 levels >361 ng/mL at 48 hours were more likely to experience major adverse cardiac events (15% versus 8%; P=0.002) during a median follow-up of 12 months. In patients with STEMI, a significant increase in PCSK9 was observed from 24 to 48 hours after PCI. While PCSK9 levels after 24 hours were not related to myocardial or microvascular injury, PCSK9 after 48 hours was significantly associated with intramyocardial hemorrhage, MVO, and infarct size as well as worse subsequent clinical outcomes. URL: https://www.clinicaltrials.gov; Unique identifier; NCT04113356.

Deciphering the Enigma of Intramyocardial Hemorrhage Following Reperfusion Therapy in Acute ST-Segment Elevation Myocardial Infarction: A Comprehensive Exploration from Mechanisms to Therapeutic Strategies.

Acute ST-segment elevation myocardial infarction (STEMI) is a formidable challenge in cardiovascular medicine, demanding advanced reperfusion strategies such as emergency percutaneous coronary intervention. While successful revascularization is pivotal, the persistent "no-reflow" phenomenon remains a clinical hurdle, often intertwined with microvascular dysfunction. Within this intricate scenario, the emergence of intramyocardial hemorrhage (IMH) has garnered attention as a significant contributor. This review offers a detailed exploration of the multifaceted relationship between IMH and the "no-reflow" phenomenon, delving into the mechanisms governing IMH occurrence, state-of-the-art diagnostic modalities, predictive factors, clinical implications, and the evolving landscape of preventive and therapeutic strategies. The nuanced examination aims to deepen our comprehension of IMH, providing a foundation for the identification of innovative therapeutic avenues and enhanced clinical outcomes for STEMI patients.

Left ventricular ejection fraction and white blood cell count are the two independent risk factors for predicting intramyocardial hemorrhage in patients with ST-segment elevation myocardial infarction after reperfusion.

Left ventricular ejection fraction and white blood cell count are the two independent risk factors for predicting intramyocardial hemorrhage in patients with ST-segment elevation myocardial infarction after reperfusion.

The role of microvascular obstruction and intramyocardial hemorrhage in reperfusion injury to the heart

Microvascular obstruction (MVO) of coronary arteries promotes an increase in mortality and major adverse cardiac events in patients with acute myocardial infarction (AMI) and percutaneous coronary intervention (PCI). Intramyocardial hemorrhage (IMH) is observed in 41–50 % of patients with ST-segment elevation myocardial infarction and PCI and is accompanied by inflammation. There is evidence that microthrombi are not involved in the development of MVO, which is associated with infarct size, the duration of ischemia, and myocardial edema. However, there is no conclusive evidence that the latter plays an important role in the development of MVO. There is evidence that platelets, inflammation, Ca2+ overload, neuropeptide Y, and endothelin-1 could be involved in the pathogenesis of MVO. The role of endothelial cell dysfunction in MVO formation in patients with AMI and PCI remains under question. It is unclear whether nitric oxide production is decreased in patients with MVO. It was obtained only indirect evidence on the involvement of inflammation in the development of MVO. The role of reactive oxygen species, necroptosis and pyroptosis in the pathogenesis of MVO is also not studied. The participation of thromboxane A2, vasopressin, and prostacyclin in the formation of MVO is unknown. It was not obtained conclusive evidence on the involvement of coronary artery spasm in the development of MVO. Dual antiplatelet therapy improves the efficacy of PCI in prevention of MVO. It is unknown whether epinephrine or L-type Ca2+-channel blockers improves coronary blood flow in patients with MVO.

A nomogram model for predicting intramyocardial hemorrhage post-PCI based on SYNTAX score and clinical features

ObjectiveThe aim of this study is to develop a nomogram model for predicting the occurrence of intramyocardial hemorrhage (IMH) in patients with Acute Myocardial Infarction (AMI) following Percutaneous Coronary Intervention (PCI). The model is constructed utilizing clinical data and the SYNTAX Score (SS), and its predictive value is thoroughly evaluated.MethodsA retrospective study was conducted, including 216 patients with AMI who underwent Cardiac Magnetic Resonance (CMR) within a week post-PCI. Clinical data were collected for all patients, and their SS were calculated based on coronary angiography results. Based on the presence or absence of IMH as indicated by CMR, patients were categorized into two groups: the IMH group (109 patients) and the non-IMH group (107 patients). The patients were randomly divided in a 7:3 ratio into a training set (151 patients) and a validation set (65 patients). A nomogram model was constructed using univariate and multivariate logistic regression analyses. The predictive capability of the model was assessed using Receiver Operating Characteristic (ROC) curve analysis, comparing the predictive value based on the area under the ROC curve (AUC).ResultsIn the training set, IMH post-PCI was observed in 78 AMI patients on CMR, while 73 did not show IMH. Variables with a significance level of P < 0.05 were screened using univariate logistic regression analysis. Twelve indicators were selected for multivariate logistic regression analysis: heart rate, diastolic blood pressure, ST segment elevation on electrocardiogram, culprit vessel, symptom onset to reperfusion time, C-reactive protein, aspartate aminotransferase, lactate dehydrogenase, creatine kinase, creatine kinase-MB, high-sensitivity troponin T (HS-TnT), and SYNTAX Score. Based on multivariate logistic regression results, two independent predictive factors were identified: HS-TnT (Odds Ratio [OR] = 1.61, 95% Confidence Interval [CI]: 1.21–2.25, P = 0.003) and SS (OR = 2.54, 95% CI: 1.42–4.90, P = 0.003). Consequently, a nomogram model was constructed based on these findings. The AUC of the nomogram model in the training set was 0.893 (95% CI: 0.840–0.946), and in the validation set, it was 0.910 (95% CI: 0.823–0.970). Good consistency and accuracy of the model were demonstrated by calibration and decision curve analysis.ConclusionThe nomogram model, constructed utilizing HS-TnT and SS, demonstrates accurate predictive capability for the risk of IMH post-PCI in patients with AMI. This model offers significant guidance and theoretical support for the clinical diagnosis and treatment of these patients.

The Role of Microvascular Obstruction and Intra-Myocardial Hemorrhage in Reperfusion Cardiac Injury. Analysis of Clinical Data.

Microvascular obstruction (MVO) of coronary arteries promotes an increase in mortality and major adverse cardiac events in patients with acute myocardial infarction (AMI) and percutaneous coronary intervention (PCI). Intramyocardial hemorrhage (IMH) is observed in 41-50% of patients with ST-segment elevation myocardial infarction and PCI. The occurrence of IMH is accompanied by inflammation. There is evidence that microthrombi are not involved in the development of MVO. The appearance of MVO is associated with infarct size, the duration of ischemia of the heart, and myocardial edema. However, there is no conclusive evidence that myocardial edema plays an important role in the development of MVO. There is evidence that platelets, inflammation, overload, neuropeptide Y, and endothelin-1 could be involved in the pathogenesis of MVO. The role of endothelial cell damage in MVO formation remains unclear in patients with AMI and PCI. It is unclear whether nitric oxide production is reduced in patients with MVO. Only indirect evidence on the involvement of inflammation in the development of MVO has been obtained. The role of reactive oxygen species (ROS) in the pathogenesis of MVO is not studied. The role of necroptosis and pyroptosis in the pathogenesis of MVO in patients with AMI and PCI is also not studied. The significance of the balance of thromboxane A2, vasopressin, angiotensin II, and prostacyclin in the formation of MVO is currently unknown. Conclusive evidence regarding the role of coronary artery spasm in the development of MVhasn't been established. Correlation analysis of the neuropeptide Y, endothelin-1 levels and the MVO size in patients with AMI and PCI has not previously been performed. It is unclear whether epinephrine aggravates reperfusion necrosis of cardiomyocytes. Dual antiplatelet therapy improves the efficacy of PCI in prevention of MVO. It is unknown whether epinephrine or L-type channel blockers result in the long-term improvement of coronary blood flow in patients with MVO.

A novel intracoronary hypothermia device reduces myocardial reperfusion injury in pigs.

Hypothermia therapy has been suggested to attenuate myocardial necrosis; however, the clinical implementation as a valid therapeutic strategy has failed, and new approaches are needed to translate into clinical applications. This study aimed to assess the feasibility, safety, and efficacy of a novel selective intracoronary hypothermia (SICH) device in mitigating myocardial reperfusion injury. This study comprised two phases. The first phase of the SICH was performed in a normal porcine model for 30 minutes ( n = 5) to evaluate its feasibility. The second phase was conducted in a porcine myocardial infarction (MI) model of myocardial ischemia/reperfusion which was performed by balloon occlusion of the left anterior descending coronary artery for 60 minutes and maintained for 42 days. Pigs in the hypothermia group ( n = 8) received hypothermia intervention onset reperfusion for 30 minutes and controls ( n = 8) received no intervention. All animals were followed for 42 days. Cardiac magnetic resonance analysis (five and 42 days post-MI) and a series of biomarkers/histological studies were performed. The average time to lower temperatures to a steady state was 4.8 ± 0.8 s. SICH had no impact on blood pressure or heart rate and was safely performed without complications by using a 3.9 F catheter. Interleukin-6 (IL-6), tumor necrosis factor-α, C-reactive protein (CRP), and brain natriuretic peptide (BNP) were lower at 60 min post perfusion in pigs that underwent SICH as compared with the control group. On day 5 post MI/R, edema, intramyocardial hemorrhage, and microvascular obstruction were reduced in the hypothermia group. On day 42 post MI/R, the infarct size, IL-6, CRP, BNP, and matrix metalloproteinase-9 were reduced, and the ejection fraction was improved in pigs that underwent SICH. The SICH device safely and effectively reduced the infarct size and improved heart function in a pig model of MI/R. These beneficial effects indicate the clinical potential of SICH for treatment of myocardial reperfusion injury.

Impact of Bivalirudin on Ischemia/Reperfusion Injury in Patients with Reperfused STEMI Assessed by Cardiac Magnetic Resonance.

Thrombin is an important ischemia/reperfusion injury (IRI) mediator in patients with ST-elevation myocardial infarction (STEMI). This study examines the use of bivalirudin, a direct thrombin inhibitor, in reducing IRI in STEMI patients. STEMI patients (n = 21) were treated with bivalirudin and compared to 21 patients treated with unfractionated heparin (UFH) from the EARLY Assessment of Myocardial Tissue Characteristics by CMR in STEMI (EARLY-MYO-CMR) registry (NCT03768453). Infarct size (IS) and left ventricular ejection fraction (LVEF) were comparable between the two groups at follow up. During the first cardiac magnetic resonance (CMR) scan within the first week after percutaneous coronary intervention (PCI), all patients in both the bivalirudin and UFH groups exhibited myocardial edema. However, the myocardium edema volume was significantly less in the bivalirudin group (p < 0.05). At the one-month follow-up, a smaller proportion of patients in the bivalirudin group than in the UFH group exhibited myocardial edema (4.7% vs. 33.3%, p < 0.05). At the three-month follow-up, myocardial edema had completely resolved in the bivalirudin group, while it persisted in two patients in the UFH group. The incidence and volume of microvascular obstruction (MVO) were significantly lower in the bivalirudin group during the acute phase. Additionally, the incidence of intramyocardial hemorrhage (IMH) was significantly lower in the bivalirudin group during both the acute and follow up (p < 0.05). These findings were corroborated by T2 and T1 mapping results. The study concluded that the use of bivalirudin for anticoagulation is associated with attenuated IRI in STEMI patients who receive primary PCI.

Culprit Lesion Vessel Size and Risk of Reperfusion Injury in ST-Segment Elevation Myocardial Infarction: A Cardiac Magnetic Resonance Imaging Study.

Microvascular obstruction (MVO) and intramyocardial hemorrhage (IMH) are well-established imaging biomarkers of failed myocardial tissue reperfusion in patients with ST-segment elevation-myocardial infarction treated with percutaneous coronary intervention. MVO and IMH are associated with an increased risk of adverse outcome independent of infarct size, but whether the size of the culprit lesion vessel plays a role in the occurrence and severity of reperfusion injury is currently unknown. This study aimed to evaluate the association between culprit lesion vessel size and the occurrence and severity of reperfusion injury as determined by cardiac magnetic resonance imaging. Patients (n=516) with first-time ST-segment-elevation myocardial infarction underwent evaluation with cardiac magnetic resonance at 4 (3-5) days after infarction. MVO was assessed with late gadolinium enhancement imaging and IMH with T2* mapping. Vessel dimensions were determined using catheter-based reference. Median culprit lesion vessel size was 3.1 (2.7-3.6) mm. MVO and IMH were found in 299 (58%) and 182 (35%) patients. Culprit lesion vessel size was associated with body surface area, diabetes, total ischemic time, postinterventional thrombolysis in myocardial infarction flow, and infarct size. There was no association between vessel size and MVO or IMH in univariable and multivariable analysis (P>0.05). These findings were consistent across patient subgroups with left anterior descending artery and non-left anterior descending artery infarctions and those with thrombolysis in myocardial infarction 3 flow post-percutaneous coronary intervention. Comprehensive characterization of myocardial tissue reperfusion injury by cardiac magnetic resonance revealed no association between culprit lesion vessel size and the occurrence of MVO and IMH in patients treated with primary percutaneous coronary intervention for ST-segment-elevation myocardial infarction.

Cardiac magnetic resonance imaging detection of intramyocardial hemorrhage in patients with ST-elevated myocardial infarction: comparison between susceptibility-weighted imaging and T1/T2 mapping techniques.

Susceptibility-weighted imaging (SWI) and T1/T2 mapping can be used to detect reperfusion intramyocardial hemorrhage (IMH) in ST-segment elevation myocardial infarction (STEMI) patients. However, the sensitivity and accuracy of the SWI and T1/T2 mapping sequences were not systematically compared. The study aimed to evaluate image quality and diagnostic performance of SWI in patients with IMH, compared with T1/T2 mapping. A prospective study was conducted on consecutive acute STEMI patients who were recruited from January to July 2022. Within 2-6 days after reperfusion treatment, all patients underwent a 3T cardiac magnetic resonance (CMR) examination, including T2-weighted short-tau inversion recovery (T2W-STIR), T1/T2 mapping, and SWI. A total of 36 patients [age, 56.50±17.25 years; males, 83.33% (30/36)] were enrolled. The relative infarct-remote myocardium signal intensity ratio (SIinfarct-remote) and contrast-to-noise ratio (CNR) were calculated for each patient on T1/T2 mapping and SWI, and the difference between relative signal intensity-to-noise ratio (rSNR) in the IMH (rSNRIMH) was measured for IMH patients on T1/T2 mapping and SWI. SIinfarct-remote, CNR, and rSNRIMH were compared among the three sequences. Receiver operating characteristic (ROC) analyses were used to evaluate the diagnostic performance of three sequences by SIinfarct-remote and visual assessment. A total of 26 (72.22%) patients had IMH. Quantitatively, the SIinfarct-remote of three sequences had excellent diagnostic performance for detecting IMH [SWI area under the curve (AUC) =1.000, 95% confidence interval (CI): 1.000-1.000 vs. T1 mapping AUC =0.954, 95% CI: 0.885-1.000 vs. T2 mapping AUC =0.985, 95% CI: 0.955-1.000; SWI vs. T1 mapping, P=0.300; SWI vs. T2 mapping, P=0.188; T1 mapping vs. T2 mapping, P=0.302). Qualitatively, three sequences had similar performance on detecting IMH (SWI AUC =0.895, 95% CI: 0.784-1.000; T1 mapping AUC =0.835, 95% CI: 0.711-0.958; and T2 mapping AUC =0.855, 95% CI: 0.735-0.974; SWI vs. T1 mapping, P=0.172; SWI vs. T2 mapping, P=0.317; T1 mapping vs. T2 mapping, P=0.710). The rSNRIMH was highest in T1 mapping, followed by T2 mapping and SWI, but SWI had the highest CNR. SWI, as well as T1/T2 mapping, is a feasible and accurate approach for clinical diagnosis of IMH with excellent performance.

Long-Term Prognostic Value of Infarct Transmurality Determined by Contrast-Enhanced Cardiac Magnetic Resonance after ST-Segment Elevation Myocardial Infarction.

The long-term prognostic significance of maximal infarct transmurality evaluated by contrast-enhanced cardiac magnetic resonance (CE-CMR) in ST-segment elevation myocardial infarction (STEMI) patients has yet to be determined. This study aimed to see if maximal infarct transmurality has any additional long-term prognostic value over other CE-CMR predictors in STEMI patients, such as microvascular obstruction (MVO) and intramyocardial hemorrhage (IMH). The study included 112 consecutive patients who underwent CE-CMR after STEMI to assess established parameters of myocardial injury as well as the maximal infarct transmurality. The primary clinical endpoint was the occurrence of major adverse cardiac events (MACE), which included all-cause death, non-fatal reinfarction, and new heart failure hospitalization. The MACE occurred in 10 patients over a median follow-up of 7.9 years (IQR, 5.8 to 9.2 years) (2 deaths, 3 nonfatal MI, and 5 heart failure hospitalization). Patients with MACE had significantly higher rates of transmural extent of infarction, infarct size >5.4 percent, MVO, and IMH compared to patients without MACE. In stepwise multivariable Cox regression analysis, the transmural extent of infarction defined as 75 percent or more of infarct transmurality was an independent predictor of the MACE after correction for MVO and IMH (hazard ratio 8.7, 95% confidence intervals [CIs] 1.1-71; p=0.043). In revascularized STEMI patients, post-infarction CE-CMR-based maximal infarct transmurality is an independent long-term prognosticator. Adding maximal infarct transmurality to CE-CMR parameters like MVO and IMH could thus identify patients at high risk of long-term adverse outcomes in STEMI.

Kiosk 4R-TB-04 - Relationship Between Left Ventricular Blood Flow Kinetic Energy with Intramyocardial Hemorrhage in Patients with Acute St-segment-elevation

Kiosk 4R-TB-04 - Relationship Between Left Ventricular Blood Flow Kinetic Energy with Intramyocardial Hemorrhage in Patients with Acute St-segment-elevation

Characterization of quantitative susceptibility mapping in the left ventricular myocardium

Myocardial quantitative susceptibility mapping (QSM) may offer better specificity to iron than conventional T2* imaging in the assessment of cardiac diseases, including intra-myocardial hemorrhage. However, the precision and repeatability of cardiac QSM have not yet been characterized. The aim of this study is to characterize these key metrics in a healthy volunteer cohort and show the feasibility of the method in patients. Free breathing respiratory-navigated multi-echo 3D gradient echo images were acquired, from which QSM maps were reconstructed using the Morphology Enhanced Dipole Inversion toolbox. This technique was first evaluated in a susceptibility phantom containing tubes with known concentrations of gadolinium. In vivo characterization of myocardial QSM was then performed in a cohort of 10 healthy volunteers where each subject was scanned twice. Mean segment susceptibility, precision (standard deviation of voxel magnetic susceptibilities within one segment), and repeatability (absolute difference in segment mean susceptibility between repeats) of QSM were calculated for each American Heart Association (AHA) myocardial segment. Finally, the feasibility of the method was shown in 10 patients, including four with hemorrhagic infarcts. The phantom experiment showed a strong linear relationship between measured and predicted susceptibility shifts (R2 >0.99). For the healthy volunteer cohort, AHA segment analysis showed the mean segment susceptibility was 0.00±0.02ppm, the mean precision was 0.05±0.04ppm, and the mean repeatability was 0.02±0.02ppm. Cardiac QSM was successfully performed in all patients. Focal iron deposits were successfully visualized in the patients with hemorrhagic myocardial infarctions. The precision and repeatability of cardiac QSM were successfully characterized in phantom and in vivo experiments. The feasibility of the technique was also successfully demonstrated in patients. While challenges still remain, further clinical evaluation of the technique is now warranted. This work does not report on a health care intervention.

Kiosk 8R-TC-09 - T2* Mapping of Intramyocardial Hemorrhage: Mitigating the Effects of Off-resonant Conditions in Phantoms and Explanted Heart Tissue

Kiosk 8R-TC-09 - T2* Mapping of Intramyocardial Hemorrhage: Mitigating the Effects of Off-resonant Conditions in Phantoms and Explanted Heart Tissue