The role of nutritional additives in prevention: dietary supplementation with Spirulina reduces myocardial damage and improves cardiac function post-myocardial infarction in swine

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
P Sutelman ◽  
G Vilahur ◽  
L Casani ◽  
L Badimon
Keyword(s):  
Myocardial Infarction ◽  
Weight Loss ◽  
Weight Gain ◽  
Infarct Size ◽  
Myocardial Damage ◽  
Dietary Supplementation ◽  
Cholesterol Concentration ◽  
Funding Source ◽  
Cardiac Damage ◽  
Anti Inflammatory

Abstract Introduction The outcome of acute ST-elevation myocardial infarction depends, to a large extent, on the size of the infarct. Myocardial damage due to infarction involves several pathogenic mechanisms among which excessive generation of reactive oxygen species and an exacerbated inflammatory reaction play a critical role. Spirulina is a dietary supplement made from blue-green algae (Arthrospira platensis) used to manage weight loss and metabolic syndrome disorders. In addition, Spirulina has experimentally shown to exert anti-oxidant and anti-inflammatory properties because its composition rich in antioxidants, polyunsaturated fatty acids, essential amino-acids, and minerals. Purpose The purpose of the present study was to investigate whether dietary supplementation with Spirulina may serve as a cardioprotective agent by attenuating cardiac damage and ventricular dysfunction due to myocardial infarction in a highly translatable animal model. Methods Pigs (n=10) were fed a normocholesterolemic diet supplemented with Spirulina (1 gr/animal/bid; n=5) or placebo (n=5) for 10 days and then they were subjected to myocardial infarction by means of 1.5h balloon occlusion of the mid left anterior descending coronary artery. Thereafter animals were reperfused for 2.5h and then sacrificed. Infarct size was assessed by TTC staining and ischemic and non-ischemic myocardial tissue was obtained for molecular analysis of cardioprotective kinases, anti-apoptotic- and anti-inflammatory- related markers. Biochemical analyses (lipid levels, kidney and liver parameters) and weight gain were monitored throughout the study. Results Supplementation with Spirulina led to an absolute significant reduction in infarct size of 10±1% of the left ventricle (LV) as compared to control animals (p<0.05). At a functional level, all animals displayed comparable LV ejection fraction (LVEF) prior-MI induction (control: 64.5±2.6%; Spirulina: 61.5±2.6%). However, after 2.5h of reperfusion control animals showed a worsening of 18.2±2.0% LVEF whereas it was only of 7.2±2.5% in Spirulina-administered pigs (60% relative improvement vs. controls; p<0.05). At a molecular level, Spirulina administered animals showed higher expression of PI3K, Bcl-2, and Cox-2 and reduced content of MCP-1 in the jeopardized myocardium. Supplementation with Spirulina for 10 days markedly reduced total- cholesterol by 25% (p<0.04), LDL- cholesterol by 47% (p<0.05), enhanced HDL-cholesterol concentration by 79% (p<0.03) and limited weight gain (p<0.05) as compared to controls. Kidney and liver enzymes were found to be within the physiological range. Conclusion Supplementation with Spirulina, beyond its proven benefits in weight loss and lipid profile, exerts cardioprotection by inducing myocardial survival kinases, and triggering cytoprotective and anti-inflammatory mechanisms, thereby limiting cardiac damage and improving ventricular contractility post-MI. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Ministerio de Ciencia Innovacion y Universidades / Instituto de Salud Carlos III

scholarly journals C-reactive protein increases myocardial damage after STEMI

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
C.D Garlichs ◽  
W Ries ◽  
J Torzewski ◽  
C Pfluecke ◽  
F Heigl ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Plasma Levels ◽  
Circumferential Strain ◽  
Myocardial Damage ◽  
Study Endpoint ◽  
Funding Source ◽  
Infarction Size ◽  
Myocardial Infarction Size

Abstract Background The CAMI-1 study dealt with the depletion of CRP by apheresis in patients with acute myocardial infarction (AMI). CRP, the prototype human acute phase protein, has been known as a marker of poor prognosis in AMI and independently predicts 30-day mortality. Methods 66 STEMI patients were enrolled in the study following complete coronary revascularization (2–12 h after the onset of symptoms). 32 patients received CRP apheresis, whereas 34 patients treated by standard protocols served as controls. CRP apheresis started 24±12 h and 48±12 h after onset of symptoms. In case of a rapid increase in CRP plasma levels following the 2nd session, a 3rd session was carried out another 24 h later. A specific CRP adsorber removed up to 79% of the original CRP. In each apheresis session, 6000 ml of plasma was treated via peripheral venous access. Primary study endpoint was myocardial infarction size as determined by Cardiac Magnetic Resonance Imaging (CMR) 2–9 days after STEMI. Results Aphereses sessions were well tolerated with no relevant side effects. Peak CRP plasma levels after STEMI ranged from 9 to 279 mg/l. The expected peak CRP level after AMI can be calculated precisely with 2–3 CRP quantifications during the first 24 h after the onset of symptoms. The regression coefficient for this analysis is 0.91. This mathematical step allows for the comparison of the CRP-apheresis group and the controls on the basis of their individual CRP peak levels. The statistical evaluation shows that the CRP concentration is significantly associated with the damage (infarct size, LVEF, circumferential strain) in the controls. This association was lost in the aphereses patients: they performed significantly better at all endpoints (infarct size, LVEF, circumferential strain) than the controls. The CRP apheresis significantly reduced myocardial damage. To our surprise, two apheresis patients had an infarct size of 0%. Conclusions For the first time we find an unequivocal association between myocardial infarct size and the CRP concentration. This is in some respects a surprise, since the basic assumption in AMI is that the vascular occlusion leads to primary damage and the reperfusion to secondary damage, which would not have led one to expect such a clear dose-response relationship as that observed here. In addition, our results show a significant beneficial effect of CRP apheresis on myocardial infarction size and wall motion. Selective CRP apheresis is now being further evaluated as a therapeutic approach in the treatment of acute myocardial infarction in a registry (CAMI registry). Funding Acknowledgement Type of funding source: Private company. Main funding source(s): Pentracor GmbH

Implication of anti-angiogenic VEGF-A165b in angiogenesis and systolic function after reperfused myocardial infarction

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
V Marcos Garces ◽  
C Rios-Navarro ◽  
L Hueso ◽  
A Diaz ◽  
C Bonanad ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Adjuvant Therapy ◽  
Ejection Fraction ◽  
Infarct Size ◽  
Systolic Function ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Funding Source ◽  
Coronary Reperfusion ◽  
Ventricular Ejection Fraction

Abstract Background Angiogenesis participates in re-establishing microcirculation after myocardial infarction (MI). Purpose In this study, we aim to further understand the role of the anti-angiogenic isoform vascular endothelial growth factor (VEGF)-A165b after MI and explore its potential as a co-adjuvant therapy to coronary reperfusion. Methods Two mice MI models were formed: 1) permanent coronary ligation (non-reperfused MI), 2) transient 45-min coronary occlusion followed by reperfusion (reperfused MI); in both models, animals underwent echocardiography before euthanasia at day 21 after MI induction. Serum and myocardial VEGF-A165b levels were determined. In both experimental MI models, functional and structural implication of VEGF-A165b blockade was assessed. In a cohort of 104 ST-segment elevation MI patients, circulating VEGF-A165b levels were correlated with cardiovascular magnetic resonance-derived left ventricular ejection fraction at 6-months and with the occurrence of adverse events (death, heart failure and/or re-infarction). Results In both models, circulating and myocardial VEGF-A165b presence was increased 21 days after MI induction. Serum VEGF-A165b levels inversely correlated with systolic function evaluated by echocardiography. VEGF-A165b blockage increased capillary density, reduced infarct size, and enhanced left ventricular function in reperfused, but not in non-reperfused MI experiments. In patients, higher VEGF-A165b levels correlated with depressed ejection fraction and worse outcomes. Conclusions In experimental and clinical studies, higher serum VEGF-A165b levels associates with a worse systolic function. Its blockage enhances neoangiogenesis, reduces infarct size, and increases ejection fraction in reperfused, but not in non-reperfused MI experiments. Therefore, VEGF-A165b neutralization represents a potential co-adjuvant therapy to coronary reperfusion. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): This study was funded by “Instituto de Salud Carlos III” and “Fondos Europeos de Desarrollo Regional FEDER” (Exp. PIE15/00013, PI17/01836, PI18/00209 and CIBERCV16/11/00486).

2230Results from the CAMI1 Study: selective CRP apheresis as a new treatment option in acute myocardial infarction

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
C Garlichs ◽  
J Torzewski ◽  
A Sheriff ◽  
C Pfluecke ◽  
H Darius ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Plasma Levels ◽  
Myocardial Damage ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Study Endpoint ◽  
Infarction Size ◽  
Myocardial Infarction Size

Abstract Background Inflammation is increasingly recognized as an important pathogenic feature in cardiovascular disease. In patients with STEMI, C-reactive protein (CRP), the prototype human acute phase protein, is a marker of poor prognosis and independently predicts 30-day mortality. In STEMI, CRP may indeed be intimately involved in myocardial damage by activating the complement system in the ischemic tissue. In animal experiments, CRP removal after STEMI reduces infarct size and results in a significantly better left ventricular ejection fraction (LVEF). Recently, in the multi-center matched-control pilot study on CRP apheresis in Acute Myocardial Infarction (CAMI1), a newly designed CRP adsorber has been demonstrated to efficiently and selectively lower CRP plasma levels in humans. Here, we present preliminary data of the ongoing trial. Methods Up to the present day, 67 STEMI patients were enrolled in the study following complete coronary revascularization. 32 patients received CRP apheresis, whereas 35 patients treated by standard protocols served as controls. CRP apheresis started 24±12 h and 48±12 h after onset of symptoms. In case of a rapid increase in CRP plasma levels following the 2nd session, a 3rd session was carried out another 24 h later. In each apheresis session, 6000 ml plasma was treated via peripheral venous access. Primary study endpoint was myocardial infarction size as determined by Cardiac Magnetic Resonance Imaging (MRI) 5±3 days after STEMI. Results Apheresis sessions were well tolerated with no relevant side effects. Peak CRP plasma levels after STEMI ranged from 12 mg/l to 279 mg/l. The peak CRP level after AMI can be calculated precisely with at 2–3 CRP quantifications during the first 24 h after the onset of symptoms. The regression coefficient for this analysis is 0.95. This mathematical step allows for the comparison of the CRP-apheresis group and the controls on the basis of their individual CRP peak levels. The statistical evaluation shows that the apheresis patients no longer correlate with the control with regard to the endpoints infarct size, LVEF, longitudinal strain and circumferential strain. They perform significantly better at all endpoints. The CRP apheresis reduced the development of myocardial damage. Conclusions Here, an unequivocal association between infarct size and CRP is demonstrated for the first time. CRP apheresis following STEMI is feasible and safe. Our preliminary results in a small cohort show a significant beneficial effect of CRP apheresis on myocardial infarction size and wall motion. Selective CRP apheresis may emerge as a new therapeutic approach in the treatment of acute myocardial infarction.

scholarly journals Rituximab in patients with acute ST-elevation myocardial infarction (RITA-MI)

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
T.X Zhao ◽  
M Aetesam-Ur-Rahman ◽  
A Sage ◽  
Y Lu ◽  
S Victor ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
B Cells ◽  
Infarct Size ◽  
B Cell ◽  
Cardiac Biomarkers ◽  
Lymphoid Tissues ◽  
Funding Source ◽  
Inflammatory Monocytes ◽  
St Elevation

Abstract Background In pre-clinical models of acute myocardial infarction (MI), mature B cells selectively mobilise inflammatory monocytes into the heart, leading to increased infarct size and deterioration of myocardial function. Anti-CD20 antibody-mediated depletion of B cells limited infarct size and improved cardiac function. Rituximab is a monoclonal antibody targeted against human B cells and has been used in the treatment of autoimmune diseases and cancers. However, its use in cardiovascular disease is untested and is currently contraindicated. Purpose We assessed the safety, feasibility and pharmacodynamic effect of rituximab given acutely to patients with ST-elevation MI (STEMI). Method RITA-MI was a prospective, open-label, dose-escalation, single-arm, phase 1/2a clinical trial, which tested rituximab administered as a single intravenous dose in patients with STEMI within 48 hours of symptom onset. Four escalating doses (200, 500, 700 and 1000mg) were used with 6 patients in each group. Follow-up was performed during initial inpatient stay; on days 6 and 14; and at 3 and 6 months. The primary endpoint was safety, whilst secondary endpoints were changes in B cells and their subsets, immune cell subsets, and cardiac and inflammatory biomarkers. [NCT:03072199] Results Overall, rituximab was well tolerated across all doses with the most common adverse event being gastrointestinal disturbance. This was due to the concomitant oral secondary prevention medication started after a STEMI. Five severe adverse events were reported, none of which were assessed as being related. Rituximab caused a mean 96.3% (95% CI 93.8–98.8%) depletion of B cell within 30 mins of the infusion starting across all dose groups. At 6 hours a rebound in B cells was seen in the 200, 500 and 700mg doses, likely related to the emigration of B cells from secondary lymphoid tissues. Maximal B cell depletion was seen at day 6, which was lower than baseline for all doses (p<0.001) (figure 1). B cell repopulation at 6months was dose-dependent. In addition, there was modulation of returning B cell subsets characterised by increased transitional B cells (figure 1C). Immunoglobulin (IgG, IgM and IgA) levels were not affected during follow-up. Rituximab also caused an acute and transient decrease in lymphocytes (both CD4+ and CD8+ T cells) and monocytes, whilst transiently increasing neutrophils at the 6-hour timepoint. Cardiac biomarkers showed a decrease in CRP and BNP. Clinical echocardiogram showed an increase in ejection fraction at follow up (mean increase in EF of 7.8% (95% CI 3.11–12.6)). Conclusion Rituximab appears safe and feasible when given in acute STEMIs. We have shown for the first time that depletion of B cells within 30mins of starting rituximab which demonstrates the biological plausibility of our treatment paradigm. Additional new insight into the mechanism of action of rituximab was found. This has led directly to the setting up of a phase 2b trial. Funding Acknowledgement Type of funding source: Public grant(s) – EU funding. Main funding source(s): European Union Research Council

scholarly journals Impact of Morphine Treatment on Infarct Size and Reperfusion Injury in Acute Reperfused ST-Elevation Myocardial Infarction

2020 ◽  
Vol 9 (3) ◽  
pp. 735 ◽  
Author(s):  
Ingo Eitel ◽  
Juan Wang ◽  
Thomas Stiermaier ◽  
Georg Fuernau ◽  
Hans-Josef Feistritzer ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Infarct Size ◽  
Reperfusion Injury ◽  
Microvascular Obstruction ◽  
Myocardial Damage ◽  
St Elevation Myocardial Infarction ◽  
Current Evidence ◽  
Morphine Administration ◽  
Intravenous Morphine ◽  
St Elevation

Current evidence regarding the effect of intravenous morphine administration on reperfusion injury and/or cardioprotection in patients with myocardial infarction is conflicting. The aim of this study was to evaluate the impact of morphine administration, on infarct size and reperfusion injury assessed by cardiac magnetic resonance imaging (CMR) in a large multicenter ST-elevation myocardial infarction (STEMI) population. In total, 734 STEMI patients reperfused by primary percutaneous coronary intervention <12 h after symptom onset underwent CMR imaging at eight centers for assessment of myocardial damage. Intravenous morphine administration was recorded in all patients. CMR was completed within one week after infarction using a standardized protocol. The clinical endpoint of the study was the occurrence of major adverse cardiac events (MACE) within 12 months after infarction. Intravenous morphine was administered in 61.8% (n = 454) of all patients. There were no differences in infarct size (17%LV, interquartile range [IQR] 8–25%LV versus 16%LV, IQR 8–26%LV, p = 0.67) and microvascular obstruction (p = 0.92) in patients with versus without morphine administration. In the subgroup of patients with early reperfusion within 120 min and reduced flow of the infarcted vessel (TIMI-flow ≤2 before PCI) morphine administration resulted in significantly smaller infarcts (12%LV, IQR 12–19 versus 19%LV, IQR 10–29, p = 0.035) and reduced microvascular obstruction (p = 0.003). Morphine administration had no effect on hard clinical endpoints (log-rank test p = 0.74) and was not an independent predictor of clinical outcome in Cox regression analysis. In our large multicenter CMR study, morphine administration did not have a negative effect on myocardial damage or clinical prognosis in acute reperfused STEMI. In patients, presenting early ( ≤120 min) morphine may have a cardioprotective effect as reflected by smaller infarcts; but this finding has to be assessed in further well-designed clinical studies

Abstract 16142: Grad 3-Ischemia (QRS Complex Distortion) as a Predictor of Myocardial Damage as Assessed by Cardiac Magnetic Resonance Imaging and Clinical Prognosis in Patients With ST-Elevation Myocardial Infarction

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Karl-Philipp Rommel ◽  
Hadil Badarnih ◽  
Steffen Desch ◽  
Matthias Gutberlet ◽  
Gerhard Schuler ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Infarct Size ◽  
Cox Regression ◽  
Myocardial Damage ◽  
St Elevation Myocardial Infarction ◽  
Myocardial Salvage ◽  
Qrs Complex ◽  
Clinical Prognosis ◽  
Cox Regression Analysis ◽  
St Elevation

Introduction: Predicting the extent of myocardial damage on early electrocardiographic (ECG) findings could be helpful for improved risk stratification in patients with acute reperfused ST-elevation myocardial infarction (STEMI). Distortion in the terminal portion of the QRS complex (so called grade 3 ischemia, G3I) has been associated with adverse outcomes in STEMI patients. The correlation of G3I with infarct size and microvascular injury is not well defined. Objective: To studied the relation of G3I with myocardial damage as assessed by CMR and the association of G3I with adverse clinical outcomes in a STEMI population treated by primary percutaneous coronary intervention (PCI). Methods: We analyzed the ECGs of 572 consecutive STEMI patients regarding the presence or absence of G3I. G3I was defined as: 1) complete loss of S waves in 2 adjacent leads with typical Rs configuration (i.e. V1-V3), or 2) ST-J point to R wave amplitude ratio >0.5 in other leads with qR configuration. CMR was performed within 1 week after infarction for comprehensive assessment of myocardial damage using a standardised protocol. The primary clinical end-point was major adverse cardiac events (MACE) defined as death, reinfaction and readmission for congestive heart failure within 12 months after the index event. Results: G3I was present in 186 (32%) patients. The presence of G3I was associated with larger infarct size (18.3%LV [10.4 to 27.6] versus 16.5%LV (8.2 to 23.5), p=0.01), late microvascular obstruction (0.4%LV [0 to 2.7] versus 0%LV [0 to 1.5], p= 0.05, presence of intramyocardial hemorrhage (41 versus 32%, p=0.04) and less myocardial salvage (47 [28 to 64] versus 53 (35 to 68), p=0.01). G3I was associated with a significant higher incidence of MACE (p=0.01) and was identified as an independent predictor of MACE in Cox regression analysis (Hazard ratio 2.19 [1.10 to 4.38], p=0.03). Conclusions: This largest study to date correlating G3I on the admission ECG with CMR markers of myocardial damage demonstrates that G3I is significantly associated with infarct size, myocardial salvage and reperfusion injury in a STEMI population reperfused by primary PCI. Moreover, G3I was independently associated with MACE.

5234KAND567, the first selective small molecule CX3CR1 antagonist in clinical development, mediates anti-inflammatory cardioprotective effects in rodent models of atherosclerosis and myocardial infarction

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
S Abdelmoaty ◽  
H Arthur ◽  
I Spyridopoulos ◽  
M Wagberg ◽  
R Fritsche Danielson ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiovascular Disease ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Small Molecule ◽  
Atherosclerotic Plaque ◽  
Vehicle Group ◽  
Potential Candidate ◽  
Rodent Models ◽  
Anti Inflammatory

Abstract Background Fractalkine is a chemokine that mediates recruitment and extravasation of CX3CR1-expressing subsets of leukocytes and monocytes and has been implicated in the inflammation-driven pathology of cardiovascular disease. More specifically, fractalkine signaling has been proposed to contribute to increased infarct size and enhanced atherosclerotic plaque vulnerability in patients and experimental models. Blocking fractalkine/CX3CR1 signaling is suggested as a promising anti-inflammatory strategy for the treatment of both acute and chronic cardiovascular disease. KAND567 is a small molecule, selective, non-competitive, allosteric antagonist of the fractalkine receptor CX3CR1, that is under preparation for a clinical phase IIa study in AMI patients. Purpose To explore the therapeutic effects of the short and long term administration of KAND567 in experimental rodent models of acute myocardial infarction and atherosclerosis, respectively. Methods Myocardial infarction was induced in Wistar rats (N=6–8 per group) by ligation of the left anterior descending (LAD) coronary artery for 30 minutes followed by 2 h of reperfusion. The drug or vehicle infusion started either 5 min before or 30 min after start of reperfusion and continued during the remainder of the experiment. Hearts were collected and subjected to triphenyl tetrazolium chlorine (TTC) staining and the infarction area/area at risk of the left ventricle was determined by planimetry and compared against vehicle group. Atherosclerosis-prone LDL-receptor deficient mice on a high-cholesterol diet, (N=15–25 per group) were treated with KAND567 for 15–23 weeks. Atherosclerotic plaque development in the thoracic arch was determined by ultrasound imaging and histology. Immunohistochemistry was used to follow changes in the cellular composition in the atherosclerotic lesions. Results In the acute myocardial infarction study, the infusion of KAND567 before the start of reperfusion significantly reduced infarcted/risk area (by up to 50%) as compared to the vehicle group. However, the infusion had no effect on the infarct size when administration was initiated 30 min after start of reperfusion. In the atherogenesis study, oral treatment with KAND567 significantly reduced vascular macrophage infiltration by 50% and reduced intima media thickness. Furthermore, reduced plaque volume and a more stable plaque phenotype was noted following treatment with KAND567. KAND567 experimental results Conclusion Specific inhibition of fractalkine-driven inflammation by KAND567 provides cardioprotective, anti-atherosclerotic and plaque stabilizing effects via mechanisms related to immune cell infiltration, in rodent models. Further studies should be initiated to test if KAND567 is a potential candidate drug, targeting the excessive inflammatory injury associated with ischemia/reperfusion in myocardial infarction and providing plaque stabilization by reducing inflammatory risk for recurrent coronary events.

scholarly journals Hyperglycemia, inflammatory response and infarct size in obstructive acute myocardial infarction and MINOCA

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Pasquale Paolisso ◽  
Alberto Foà ◽  
Luca Bergamaschi ◽  
Francesco Donati ◽  
Michele Fabrizio ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Inflammatory Markers ◽  
Myocardial Damage ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Lymphocyte Ratio ◽  
Glucose Levels ◽  
Admission Glucose

Abstract Background Hyperglycemia has been associated with increased inflammatory indexes and larger infarct sizes in patients with obstructive acute myocardial infarction (obs-AMI). In contrast, no studies have explored these correlations in non-obstructive acute myocardial infarction (MINOCA). We investigated the relationship between hyperglycemia, inflammation and infarct size in a cohort of AMI patients that included MINOCA. Methods Patients with AMI undergoing coronary angiography between 2016 and 2020 were enrolled. The following inflammatory markers were evaluated: C-reactive protein, neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR) and neutrophil-to-platelet ratio (NPR). Myocardial infarct size was measured by peak high sensitivity troponin I (Hs-TnI) levels, left-ventricular-end-diastolic-volume (LVEDV) and left ventricular ejection fraction (LVEF). Results The final study population consisted of 2450 patients with obs-AMI and 239 with MINOCA. Hyperglycemia was more prevalent among obs-AMI cases. In all hyperglycemic patients—obs-AMI and MINOCA—NLR, NPR, and LPR were markedly altered. Hyperglycemic obs-AMI subjects exhibited a higher Hs-TnI (p < 0.001), a larger LVEDV (p = 0.003) and a lower LVEF (p < 0.001) compared to normoglycemic ones. Conversely, MINOCA patients showed a trivial myocardial damage, irrespective of admission glucose levels. Conclusions Our data confirm the association of hyperglycemic obs-AMI with elevated inflammatory markers and larger infarct sizes. MINOCA patients exhibited modest myocardial damage, regardless of admission glucose levels.

scholarly journals Influence of myocardial damage on serum procalcitonin in ST-elevation myocardial infarction

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M Reindl ◽  
C Tiller ◽  
M Holzknecht ◽  
I Lechner ◽  
B Henninger ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Injury ◽  
Release Kinetics ◽  
Myocardial Damage ◽  
High Sensitivity ◽  
St Elevation Myocardial Infarction ◽  
Funding Source ◽  
St Elevation ◽  
Hs Crp ◽  
Cmr Imaging

Abstract Background Myocardial tissue injury due to acute ST-elevation myocardial infarction (STEMI) initiates an inflammatory response with a release of systemic inflammatory biomarkers including C-reactive protein (CRP) and white blood cell count (WBCc), which, however, hampers the usefulness of these routine biomarkers to identify concomitant infections. The clinical role of Procalcitonin (PCT), a promising marker of bacterial infections, to detect concomitant infections in acute STEMI is unknown, mainly because it is unclear whether myocardial injury per se induces a systemic PCT release. Purpose To investigate release kinetics of serum PCT in the acute setting of STEMI and possible associations with myocardial injury markers as comprehensively assessed by cardiac magnetic resonance (CMR) imaging. Methods In this prospective observational study, we included 141 STEMI patients treated with primary percutaneous coronary intervention (PCI). Concentrations of PCT, high-sensitivity CRP (hs-CRP), WBCc and high-sensitivity cardiac troponin T (hs-cTnT) were measured serially at day 1 and day 2 after infarction. CMR imaging to assess infarct size (IS), extent of microvascular injury (MVI) and occurrence of intramyocardial haemorrhage (IMH) was performed within the first week following STEMI. Results Median concentrations of PCT were 0.07μg/l at both time points. In 140 patients (99%), both PCT values were within the normal range (≤0.5μg/l). Whereas hs-CRP, WBCc, and hs-TnT were significantly correlated with CMR markers of myocardial damage, PCT did not show significant correlations (all p&gt;0.10) with IS (PCT24h: r=0.07; PCT48h: r=0.13) or MVI (PCT24h: r=−0.03; PCT48h: r=0.09). Furthermore, PCT failed to discriminate between large and small IS or MVI or between presence and absence of IMH (AUC values:0.46–0.55). Conclusions In the acute phase after PCI for STEMI, circulating PCT remained unaffected by the extent of myocardial and microvascular tissue damage as visualized by CMR imaging. These data highlight the clinical potential of PCT to identify concomitant infections and to guide antibiotic treatments in STEMI patients. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Austrian Science Fund, Tiroler Wissenschaftsförderung

scholarly journals Hyperglycemia, Inflammatory Response and Infarct Size in Obstructive Acute Myocardial Infarction and MINOCA

2020 ◽  
Author(s):  
Pasquale Paolisso ◽  
Alberto Foà ◽  
Luca Bergamaschi ◽  
Francesco Donati ◽  
Michele Fabrizio ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Inflammatory Markers ◽  
Myocardial Damage ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Myocardial Infarct Size ◽  
Ventricular Ejection Fraction ◽  
Lymphocyte Ratio

Hyperglycemia has been associated with increased inflammatory indexes and larger infarct sizes in patients with obstructive acute myocardial infarction (obs-AMI). In contrast, no studies have explored these correlations in non-obstructive acute myocardial infarction (MINOCA). We investigated the relationship between hyperglycemia, inflammation and infarct size in a cohort of AMI patients that included MINOCA. Patients with AMI undergoing coronary angiography between 2016 and 2020 were enrolled. The following inflammatory markers were evaluated: C-reactive protein, neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR) and neutrophil-to-platelet ratio (NPR). Myocardial infarct size was measured by peak high sensitivity troponin I (Hs-TnI) levels, left-ventricular-end-diastolic-volume (LVEDV) and left ventricular ejection fraction (LVEF). The final study population consisted of 2450 patients with obs-AMI and 239 with MINOCA. Hyperglycemia was more prevalent among obs-AMI cases. In all hyperglycemic patients - obs-AMI and MINOCA - NLR, NPR, and LPR were markedly altered. Hyperglycemic obs-AMI subjects exhibited a higher Hs-TnI, a larger LVEDV and a lower LVEF compared to normoglycemic ones. Conversely, MINOCA patients showed similar myocardial damage, irrespective of glycemia. Our data confirm the association of hyperglycemic obs-AMI with elevated inflammatory markers and larger infarct sizes. MINOCA patients exhibited modest myocardial damage, regardless of admission glucose levels.

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