scholarly journals Quantitative evaluation of coronary artery occlusion by 3D coronary volume reconstruction in a large animal model of acute myocardial infarction

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
V D Bruno ◽  
E Sammut ◽  
A Gall ◽  
D Baz-Lopez ◽  
R Ascione ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Troponin I ◽  
Segment Length ◽  
Youden Index ◽  
P Value ◽  
Large Animal ◽  
Closed Chest ◽  
Scar Size

Abstract Background Large animal models of acute myocardial infarction (MI) offer an important platform to test novel therapies. Consistency of infarct size between animals is critical to ensure an accurate assessment of therapies against control. However, anatomical variation challenges the ability to achieve a consistent infarct size and care must be taken to respect the principles of the 3Rs through minimisation of interventional fatalities. Purpose To standardise the approach of a closed chest model of balloon occlusion-facilitated MI. Novel 3-dimensional quantitative coronary angiography (3DQCA) software has been used retrospectively to identify a correlation between coronary volume occlusion and the extension of the myocardial scar. Methods Twenty-four Yorkshire pigs (mean weight 63.1±3 kg) underwent a closed chest MI model via percutaneous occlusion of the mid portion of the left anterior descending artery (LAD) for 60 minutes. The evaluation of the myocardial damage was obtained via cardiac magnetic resonance imaging (CMR) between 24 and 48 hours after the MI model (Acute) and at 4–5 weeks after MI (Chronic). Troponin I was also measured at multiple timepoints. 3DQCA reconstruction (QAngio XA 3D, Medis medical imaging systems NL) was generated from 2 angiographic projections with segmental analysis of all 3 major epicardial vessels including lumen volume, reference diameters, and segment length. The occlusive volume and vessel length was identified through co-registration of balloon position. Results At the short term timepoint, a significant correlation was found between the LAD volume occluded and the scar size as percentage of the LV mass (Spearman correlation 0.72, p value <0.01, Fig. 1). Using Youden index analysis we identified a cut-off point of 32.8% of the LAD volume to determine a scar volume >20% (Fig. 2). At chronic phase the correlation between these two variables was not significant, although there was a trend towards significance (p value = 0.06, Cor = 0.54). No significant correlation was found with serum Troponin I. Conclusions There is a significant correlation between the LAD volume occluded and the overall scar size in the acute phase and at least 32.8% of the LAD volume should be occluded to determine a scar volume >20% of the entire LV. This indicates that a prospective measure of occluded LAD volume might minimise the intra-experimental variability in studies aiming to reduce infarct size and acute myocardial injury. FUNDunding Acknowledgement Type of funding sources: Other. Main funding source(s): This research work was supported by grants awarded to Professor Ascione: the British Heart Foundation (BHF) (BHF IG/14/2/30991, BHF RM/13/2/30158), and the Medical Research Council (MRC) (MRC MR/L012723/1).

scholarly journals Gender-Related Differences of Cardiac Troponin-I Levels in Patients with Acute Myocardial Infarction at Time of Acute Chest Pain

2021 ◽  
pp. 199-205
Author(s):  
Mahir Abdulkadhum Khudhair Alzughaibi ◽  
Ammar Waheeb Obeiad ◽  
Nassar Abdalaema Abdalhadi Mera ◽  
Mohammed Sadeq Hamzah Al-Ruwaiee
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Chest Pain ◽  
Troponin I ◽  
Statistical Significance ◽  
Acute Chest Pain ◽  
Blood Analysis ◽  
P Value ◽  
Cross Sectional ◽  
Time Of Admission

Background: Cardiac Troponins-I (CTNI) are myoregulatory polypeptides that control the actin-myosin interface, considered specific to cardiomyocytes. Age and sex variances in the extent of CTNI levels have arisen a recent debatable emphasis. Existing revisions do not display a reliable clinical power of sex-specific CTNI 99th centiles, which actually might mirror procedural aspects. Nevertheless, from a biochemical viewpoint, the trends of sex-specific CTNI 99th centiles seem sensible for the ruling-in of acute myocardial infarction AMI. Vulnerable females may be missed when applying the male sex-specific threshold. This study aimed to determine whether gender differences in CTNI exist in patients with AMI presented with chest pain. Methodology: The study was a cross-sectional, single-center, included 236-patients with AMI diagnosis by cardiologists at Merjan teaching hospital during the period from April to July 2020 from patients attending the hospital for cardiac consultation complaining of acute chest pain suggestive of AMI. Blood analysis had initiated at the time of admission included serum creatinine, blood urea, R/FBS, WBCs, PCV, and serum CTNI. A p-value below 0.05 specifies statistical significance. All statistical bioanalyses had performed by IBM-SPSS, version-25 for Windows. Results: The mean age of participants was 67.5 years, the men were dominant 76.2%. The incidence of DM and hypertension were significantly high and 24.5% of the patients were current smokers. Biochemical serum analysis revealed mean creatinine, urea, sugar, and STI values were 79.8±4.2 mmol/l, 15.9±1.7 mmol/l, 10.9±0.9 mmol/l, and 7.9±0.6 ng/ml separately. Both hypertension and smoking were significantly (p-0.001) more among males compared to the females, which is not the case for the prevalence of DM. The males were heavier significantly than females (p-0.001). Almost, there was no impact of gender on most of the other study variables other than serum TNI levels, which were significantly higher among the males (p-0.001). Conclusion: In patients with AMI presented with acute chest pain, the routine of CTNI in the diagnosis of AMI is based on the patient's gender. The application of gender-dependent cutoff levels for CTNI analyses appears to be highly suggested.

Abstract 2832: Which Cardiac Marker is Most Useful to Predict Final Infarct Size and Cardiac Function Following Primary Percutaneous Coronary Intervention For Acute Myocardial Infarction?

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Stanley Chia ◽  
O. Christopher Raffel ◽  
Faisal Merchant ◽  
Frans J Wackers ◽  
Fred Senatore ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Troponin I ◽  
Troponin T ◽  
Coronary Intervention ◽  
Left Ventricular ◽  
Cardiac Biomarkers ◽  
Primary Pci ◽  
Percutaneous Coronary

Background: Assessment of cardiac biomarker release has been traditionally used to estimate the size of myocardial damage after acute myocardial infarction (AMI). However, the significance of cardiac biomarkers in the setting of primary percutaneous coronary intervention (PCI) has not been systematically studied in a large patient cohort. We evaluated the usefulness of serial and single time-point measures of various cardiac biomarkers (creatine kinase (CK), CK-MB, troponin T and I) in predicting infarct size and left ventricular ejection fraction (LVEF) after primary PCI. Methods: EVOLVE (Evaluation of MCC-135 for Left Ventricular Salvage in AMI) was a randomized double-blind, placebo-controlled trial comparing the efficacy of intracellular calcium modulator as an adjunct to primary PCI in patients with first large AMI. Levels of cardiac biomarkers (CK, CK-MB mass, troponin T and I) were determined in 375 patients at baseline before PCI and 2, 4, 12, 24, 48 and 72 hours thereafter. Single photon emission computed tomography imaging was performed to measure infarct size and LVEF on day 5. Results: Area under curve and peak concentrations of all cardiac markers: CK, CK-MB mass, troponin T and troponin I were significantly correlated with myocardial infarct size and LVEF determined on day 5 (Spearman correlation, all P< 0.001; Table ). Troponin I, however provided the best predictor and a single measure at 72 hr was a strong indicator of both infarct size and LVEF. Using receiver operator characteristics curve, troponin I cutoff value of >55 pg/mL at 72 hr has 90% sensitivity and 70% specificity for detection of large infarct size≥10% ( c =0.88; P< 0.001). Conclusions: Plasma levels of CK, CK-MB, troponin T and troponin I remain useful predictors of infarct size and cardiac function in the era of primary PCI for AMI. A single measurement of circulating troponin I at 72 hours can provide an effective and convenient indicator of infarct size and LVEF in clinical practice. Correlation of cardiac biomarkers with Day 5 SPECT determined infarct size and LVEF

Abstract 18996: Impact of Infarct Size on Left Ventricular Diastolic Function Following Acute Myocardial Infarction

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Andrew Lin ◽  
Christopher Kwan ◽  
Kristyan Guppy-Coles ◽  
Joanne Sippel ◽  
John Atherton ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Diastolic Dysfunction ◽  
Diastolic Function ◽  
Troponin I ◽  
Left Ventricular Diastolic Function ◽  
Left Ventricular ◽  
Ventricular Diastolic Function ◽  
St Elevation

Introduction: Severe left ventricular diastolic dysfunction is associated with worse prognosis after acute myocardial infarction (MI). Twenty percent of patients have a restrictive filling pattern (RFP) following MI, and this is associated with a fourfold increase in mortality. The determinants of diastolic function in this setting are not well defined. Aim: We sought to determine the correlation between enzymatic infarct size and RFP in patients with a first ever MI. We hypothesized that a larger infarct size would result in greater impairment of left ventricular diastolic function. Methods: Data analysis was performed on consecutive patients admitted with first ever non-ST elevation MI (NSTEMI) or ST-elevation MI (STEMI) to a single large tertiary referral hospital from January 2013 to December 2014. All patients underwent coronary angiography during the index admission. Infarct size was determined by peak troponin I. Doppler transmitral flow pattern was obtained from the initial transthoracic echocardiogram performed within 48 hours of admission. RFP was defined as: E/A ratio >2.0 and/or E-wave deceleration time <160ms (American Society of Echocardiography Guidelines 2009). Results: Data were available on 645 consecutive patients who underwent coronary angiography for MI. We excluded 160 patients with a previous MI. Of the remaining 485 patients (mean age 62±13 years; mean left ventricular ejection fraction (LVEF) 53±12%), there were 338 NSTEMIs (70%) and 147 STEMIs (30%). PCI was performed in 360 (74%) patients (single vessel (82%), ≥2 vessels (18%)); coronary artery bypass surgery in 58 (13%); and medical management in 67 (13%). Sixty-nine patients (14.4%) had RFP; 52% of these had a LVEF ≥45%. Peak troponin I levels were higher in the RFP group (31.8±30.9μg/L vs 16.8±25.2μg/L, p=<0.001). On multivariate analysis, infarct size by peak troponin I (OR 1.02, 95%CI 1.00-1.03, p=0.026) and low LVEF (OR 0.95, 95%CI 0.91-0.99, p=0.015) were the only independent predictors of RFP. Conclusion: Infarct size was a major determinant of diastolic dysfunction following first ever MI. Whilst LV systolic dysfunction was strongly associated with impaired diastolic function, 52% of patients with severe diastolic dysfunction had relatively preserved LVEF.

scholarly journals Study of Hs Troponin I & uric acid in patients of myocardial infarction

2022 ◽  
Vol 8 (4) ◽  
pp. 281-284
Author(s):  
Farah Ahsan ◽  
Manas Talukdar ◽  
Naeem Qureshi ◽  
Sumera Samreen ◽  
Sonali Kukreti
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Uric Acid ◽  
Troponin I ◽  
Prognostic Indicator ◽  
P Value ◽  
Serum Samples ◽  
Male And Female ◽  
Cardiac Emergency

We aimed to provide Correlation of Hs Troponin I & Uric Acid in patients of Myocardial Infarction.: 100 patients who came to cardiac emergency in Shri Mahant Indresh Hospital. Serum samples taken for Hs Troponin I and Uric Acid for patients of Myocardial Infarction and run on VITROS 5600/7600 which is based on dry chemistry. : With 100 patients of more than 40 years of age 61 were males & 39 were females. For both males & females age mean & SD was 59.8±10.77.In our study we took 100 random patients coming to cardiac emergency out of which 50 patients had raised trop I and 45 patients had raised uric acid levels. Out of those 50 patients with raised HS Trop I 25 patients had raised values for uric acid. For Hs Trop I males – 21.88±48.8 & females 1676±57.58. For uric acid for males-6.545±3.75 & for females- 6.315±1.86.Therefore Hs Trop I & uric acid were both significant when compared with age T value was 2.7001 and P value was 0.0075. Whereas when compared with sex that is male and female to both Hs Trop I and uric acid then Hs Trop I was more significant with P value 0.0001.Uric acid is an economical marker that is readily, quickly and reliably obtainable & can be one of the predictable prognostic indicator in acute Myocardial Infarction.

Impact of Chronic Antiplatelet Therapy on Infarct Size and Bleeding in Patients With Acute Myocardial Infarction

2018 ◽  
Vol 23 (5) ◽  
pp. 407-413
Author(s):  
Jeness Campodonico ◽  
Nicola Cosentino ◽  
Valentina Milazzo ◽  
Mara Rubino ◽  
Monica De Metrio ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Antiplatelet Therapy ◽  
Troponin I ◽  
Bleeding Risk ◽  
St Segment Elevation ◽  
Segment Elevation Myocardial Infarction ◽  
St Segment ◽  
Increased Risk

Background: Patients hospitalized with acute myocardial infarction (AMI) are often on prior single antiplatelet therapy (SAPT) or a dual antiplatelet therapy (DAPT). Whether chronic SAPT or DAPT is beneficial or associated with an increased risk in AMI is still controversial. Methods and Results: We prospectively enrolled 1718 consecutive patients with AMI (798 ST-segment elevation myocardial infarction and 920 non-ST-segment elevation myocardial infarction) who were divided according to their chronic APT (no APT, SAPT, or DAPT). The study primary end point was the infarct size, as estimated by troponin I peak. Incidence of major bleeding was also evaluated. Five hundred thirty-six (31%) patients were on chronic SAPT and 215 (13%) on DAPT. A graded increase in Global Registry of Acute Coronary Events (GRACE) and Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with Early implementation of the ACC/AHA guidelines (CRUSADE) risk scores was found going from patients without APT to those with DAPT, while a progressive smaller troponin I peak was observed with the increasing number of chronic antiplatelet agents (11.2 [interquartile range: 2-45] ng/mL, 6.6 [1-33] ng/mL, and 4.1 [1-24] ng/mL; P < .001 for trend). This result was maintained after adjustment for baseline ischemic risk profile (GRACE score) and other major confounders ( P < .001). The incidence of bleeding was higher in patients on chronic APT than in those without APT (5.2% vs 2.4%; P = .002). However, when the bleeding risk was adjusted for the CRUSADE risk score, chronic SAPT (odds ratio [OR]: 1.40, 95% confidence interval [CI]: 0.77-2.53) and DAPT (OR: 0.70, 95% CI: 0.29-1.70) were not associated with an increased bleeding risk. Conclusion: In patients with AMI, chronic APT is associated with higher baseline ischemic and bleeding risks. Despite this and unexpectedly, they have a smaller infarct size and similar adjusted bleeding risk.

scholarly journals Targeting Mitochondrial Fission Using Mdivi-1 in A Clinically Relevant Large Animal Model of Acute Myocardial Infarction: A Pilot Study

2019 ◽  
Vol 20 (16) ◽  
pp. 3972 ◽  
Author(s):  
Sang-Bing Ong ◽  
Xiu-Yi Kwek ◽  
Khairunnisa Katwadi ◽  
Sauri Hernandez-Resendiz ◽  
Gustavo Crespo-Avilan ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Pilot Study ◽  
Mitochondrial Fission ◽  
Vehicle Control ◽  
Left Ventricular ◽  
Mitochondrial Morphology ◽  
Large Animal ◽  
Myocardial Infarct Size ◽  
Closed Chest

Background: New treatments are needed to reduce myocardial infarct size (MI) and prevent heart failure (HF) following acute myocardial infarction (AMI), which are the leading causes of death and disability worldwide. Studies in rodent AMI models showed that genetic and pharmacological inhibition of mitochondrial fission, induced by acute ischemia and reperfusion, reduced MI size. Whether targeting mitochondrial fission at the onset of reperfusion is also cardioprotective in a clinically-relevant large animal AMI model remains to be determined. Methods: Adult pigs (30–40 kg) were subjected to closed-chest 90-min left anterior descending artery ischemia followed by 72 h of reperfusion and were randomized to receive an intracoronary bolus of either mdivi-1 (1.2 mg/kg, a small molecule inhibitor of the mitochondrial fission protein, Drp1) or vehicle control, 10-min prior to reperfusion. The left ventricular (LV) size and function were both assessed by transthoracic echocardiography prior to AMI and after 72 h of reperfusion. MI size and the area-at-risk (AAR) were determined using dual staining with Tetrazolium and Evans blue. Heart samples were collected for histological determination of fibrosis and for electron microscopic analysis of mitochondrial morphology. Results: A total of 14 pigs underwent the treatment protocols (eight control and six mdivi-1). Administration of mdivi-1 immediately prior to the onset of reperfusion did not reduce MI size (MI size as % of AAR: Control 49.2 ± 8.6 vs. mdivi-1 50.5 ± 11.4; p = 0.815) or preserve LV systolic function (LV ejection fraction %: Control 67.5 ± 0.4 vs. mdivi-1 59.6 ± 0.6; p = 0.420), when compared to vehicle control. Similarly, there were no differences in mitochondrial morphology or myocardial fibrosis between mdivi-1 and vehicle control groups. Conclusion: Our pilot study has shown that treatment with mdivi-1 (1.2 mg/kg) at the onset of reperfusion did not reduce MI size or preserve LV function in the clinically-relevant closed-chest pig AMI model. A larger study, testing different doses of mdivi-1 or using a more specific Drp1 inhibitor are required to confirm these findings.

Preinfarction Angina and Improved Reperfusion of the Infarct-related Artery

1999 ◽  
Vol 82 (S 01) ◽  
pp. 68-72 ◽  
Author(s):  
Alessandro Sciahbasi ◽  
Eugenia De Marco ◽  
Attilio Maseri ◽  
Felicita Andreotti
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Ischemic Preconditioning ◽  
Early Reperfusion ◽  
Vast Number ◽  
Beneficial Effects ◽  
Infarct Related Artery ◽  
Cardioprotective Effects ◽  
Collateral Vessels

SummaryPreinfarction angina and early reperfusion of the infarct-related artery are major determinants of reduced infarct-size in patients with acute myocardial infarction. The beneficial effects of preinfarction angina on infarct size have been attributed to the development of collateral vessels and/or to post-ischemic myocardial protection. However, recently, a relation has been found between prodromal angina, faster coronary recanalization, and smaller infarcts in patients treated with rt-PA: those with preinfarction angina showed earlier reperfusion (p = 0.006) and a 50% reduction of CKMB-estimated infarct-size (p = 0.009) compared to patients without preinfarction angina. This intriguing observation is consistent with a subsequent observation of higher coronary recanalization rates following thrombolysis in patients with prodromal preinfarction angina compared to patients without antecedent angina. Recent findings in dogs show an enhanced spontaneous lysis of plateletrich coronary thrombi with ischemic preconditioning, which is prevented by adenosine blockade, suggesting an antithrom-botic effect of ischemic metabolites. Understanding the mechanisms responsible for earlier and enhanced coronary recanalization in patients with preinfarction angina may open the way to new reperfusion strategies.A vast number of studies, globally involving ≈17,000 patients with acute myocardial infarction, have unequivocally shown that an infarction preceded by angina evolves into a smaller area of necrosis compared to an infarct not preceded by angina (Table 1) (1). So far, preinfarction angina has been thought to have cardioprotective effects mainly through two mechanisms: collateral perfusion of the infarctzone (2-4), and ischemic preconditioning of the myocardium (5-7). Here we discuss a further mechanism of protection represented by improved reperfusion of the infarct-related artery.

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