P4436Impaired myocardial healing in patients with diabetes after ST-Elevation Myocardial Infarction

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Wamil ◽  
A Borlotti ◽  
A Banerjee ◽  
L Gaughran ◽  
G L De Maria ◽  
...  

Abstract Background Diabetes mellitus (DM) significantly increases mortality following myocardial infarction (MI). The underlying mechanism explaining this adverse prognosis is not completely understood. Purpose This study sought to investigate the characteristics of myocardial healing after MI in DM patients. Methods 62 recruited ST-elevation myocardial infarction (STEMI) patients (21 with DM and 41 controls) underwent acute (1–3 days post-STEMI) and 6 months (6M) follow-up cardiac magnetic resonance scans (CMR). Control cases were matched for the peak troponin levels and area at risk on the acute CMR scans. Blood samples were obtained 6, 24, 48 hours and 6 months after STEMI. Results Despite similar severity of the initial ischaemic injury, DM patients had lower myocardial salvage index (MSI) and as a result larger final infarct size at 6 months. Further segment-based analysis of the acute CMR scans showed significantly prolonged T1-mapping values in all segments including non-ischaemic myocardium in DM patients and poorer recovery of the late gadolinium enhancement (LGE) of the infarcted segments in that group. Additionally, DM patients had higher monocyte counts 24 hours post-MI (1.2±0.4x109/μl DM vs 0.88±0.3 x109/μl control, p=0.001). We found that HbA1C correlated with monocyte count measured 24 hours after STEMI (r=0.577, p=0.006, n=21). HbA1C also predicted myocardial salvage index (MSI) at 6M post STEMI in the DM patients (r=0.891, p=0.017, n=13). Conclusions DM patients presenting with STEMI have increased peripheral blood monocytosis and larger final infarct size compared with STEMI patients without DM. Poorly controlled DM predisposes to adverse cardiac remodelling after STEMI. Acknowledgement/Funding OHSRC Research Grant, National Institute for Health Research (NIHR), British Heart Foundation Centre of Excellence Oxford

Heart ◽  
2011 ◽  
Vol 97 (6) ◽  
pp. 460-465 ◽  
Author(s):  
G. O. Andersen ◽  
E. C. Knudsen ◽  
P. Aukrust ◽  
A. Yndestad ◽  
E. Oie ◽  
...  

Author(s):  
Asmaa Ramadan Abd El Naby ◽  
Magdy Mohamed Elmasry ◽  
Mai M. Abd Elmoneim Salama ◽  
Mohamed El Sayed El Setiha ◽  
Raghda Ghonimy Elsheikh

Objectives: The aim of this work was assessment of myocardial salvage using various magnetic resonance imaging techniques immediately after primary percutaneous coronary intervention of ST elevation myocardial infarction patients and at midterm follow up. Methods: The current study was conducted on 30 patients referred to Aswan heart center or Cardiology department, Tanta University hospital with a diagnosis of ST elevation myocardial infarction during the period from august2017 to December 2017. All patients were subjected to history taking ,clinical assessment ,12 lead ECG, Laboratory biomarkers including cardiac enzyme biomarkers, complete blood count, liver function test, renal function test and lipid profile primary then primary percutaneous coronary intervention was done then cardiac magnetic resonance imaging within 3 days and after 3 months including the following sequences: Steady-state free precession, T2 weighted triple inversion recovery sequence and Early and late gadolinium enhancement to measure the area at risk and myocardial salvage index. Results: Myocardial salvage index was found to improve with improving thrombolysis in myocardial infarction (TIMI) flow post intervention (p value=0.004), also the presence of microvascular obstruction (p value =0.034) and intramyocardial hemorrhage (p value=0.014) had a negative impact on myocardial salvage index. Peak cardiac enzyme biomarkers (troponin p value=0.001,CK p value=0.005,CKMB p value=0.002) were also associated with increased area at risk however did not affect the myocardial salvage index. Conclusion: Proper management of the occluded coronary artery is a corner stone in improving myocardial salvage index which can be properly assessed with cardiac MRI.


Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Karl-Philipp Rommel ◽  
Hadil Badarnih ◽  
Steffen Desch ◽  
Matthias Gutberlet ◽  
Gerhard Schuler ◽  
...  

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.


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Ingo Eitel ◽  
Sebastian Reinstadler ◽  
Charlotte Eitel ◽  
Georg Fuernau ◽  
Suazanne de Waha ◽  
...  

Introduction: There is evidence suggesting a positive effect of cigarette smoking on myocardial tissue reperfusion and clinical outcomes in patients with myocardial infarction (“smoker’s paradox”). Hypothesis/Aim: We aimed to evaluate the relationship of smoking status with cardiac magnetic resonance (CMR)-determined myocardial salvage and damage as well as clinical outcome in patients undergoing primary percutaneous coronary intervention (PPCI) for ST-elevation myocardial infarction (STEMI). Methods: This multicenter study included 727 consecutive STEMI patients reperfused within 12 hours after symptom onset. CMR imaging parameters (area-at-risk [AAR], infarct size [IS], myocardial salvage index [MSI], and microvascular obstruction [MVO]) were compared according to admission smoking status. Major adverse cardiac events (MACE) rates at 12 months after infarction were compared between groups. Results: In our study cohort 339 (46.6%) patients were current smokers. There was no difference in the extent of AAR (35[24-47] vs. 37[27-49] %LV, p=0.10), IS (16[8-25] vs. 17[10-26] %LV, p=0.21), MSI (53[29-70] vs. 52[34-71], p=0.47) or MVO (0[0-1.7] vs. 0[0-1.6] %LV, p=0.91) between smokers and non-smokers. Smokers had lower MACE (3.8% vs. 8.2%, p=0.01) and mortality (0.9% vs. 3.9%, p=0.01) rates. However, after adjustment for differences in baseline risk factors, smoking was no longer associated with MACE (HR=0.72, 95% CI 0.37 to 1.41, p=0.34) or mortality (HR=0.49, 95% CI 0.14 to 1.76, p=0.27). Conclusion: Smoking is not associated with PPCI efficacy (myocardial salvage) or irreversible myocardial damage in patients with acute STEMI. The lower MACE and mortality rates of smokers were entirely explained by differences in baseline risk characteristics, thus challenging the existence of a “smoker’s paradox”.


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