scholarly journals Prognostic implications of left ventricular torsion by feature-tracking cardiac magnetic resonance in patients with ST-elevation myocardial infarction

2021 ◽  
Vol 22 (Supplement_2) ◽  
Author(s):  
LAI Wei ◽  
HENG Ge ◽  
JUN Pu

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): the National Key Research and Development Program of China OnBehalf Renji Hospital Affiliated to Medical College of Shanghai Jiaotong University Background  The prognostic implications of left ventricular (LV) torsion on the long-term prognosis of patients with acute ST-elevation myocardial infarction (STEMI) is not clear. Methods  We analyzed Cardiac Magnetic Resonance (CMR) images and followed up 420 first STEMI patients from the EARLY Assessment of MYOcardial Tissue Characteristics by CMR in STEMI (EARLY-MYO-CMR) registry (NCT03768453). These patients received timely primary percutaneous coronary intervention (PCI) within 12h and CMR examination within 1 week (median,5 days; range, 2-7 days) after infarction. Besides, CMR images of 40 normal people were enrolled as the control group. LV torsion, torsion rate and other conventional CMR indexes were measured. Ultrasound cardiogram examinations were performed in the acute phase and 1 year post-STEMI to assess LV remodeling (≥ 20% increase in LV end-diastolic volume). Primary end point was composite major adverse cardiac and cerebrovascular events (MACCEs) including cardiovascular death, re-infarction, re-hospitalization for heart failure and stroke. Secondary end points were the formation of LV aneurysm/thrombus in hospital as well as LV remodeling at 1 year post-STEMI. Results During follow-up (median: 52 months, inter-quartile range: 29–78 months), 80 patients developed MACCEs. Compared with normal people, patients with STEMI had more decreased LV torsion (P < 0.001) and torsion rate (P = 0.033). Patients who experienced MACCEs had more impaired LV torsion (P < 0.001) and torsion rate (P < 0.001) than those who didn’t. LV torsion ≤ 0.876 deg/cm in the acute phase of STEMI was an independent predictive factor of MACCE (P = 0.001) and LV remodeling (P = 0.001). Patients with impaired LV torsion were more likely to experience MACCEs (P < 0.001). The impairment of LV torsion was also associated with the higher incidence of LV aneurysm (P < 0.001) and thrombus (P = 0.006). The addition of LV torsion to a risk model comprising LV ejection fraction (LVEF), infarct size (IS), and microvascular obstruction (MVO) led to a net reclassification improvement (continuous NRI 0.499 [95% CI, 0.261–0.737]; P < 0.001). Hypertension (P = 0.047), tobacco use (P = 0.005), worse TIMI flow post-PCI (P < 0.001), more extensive IS (P < 0.001) / MVO size (P = 0.002) were associated with the impairment of LV torsion. Conclusions Compared with normal people, patients with STEMI had more decreased LV torsion and torsion rate. LV torsion ≤ 0.876 deg/cm in the acute phase was an independent predictive factor of MACCE and LV remodeling. The addition of LV torsion to a risk model comprising LVEF, LV-IS and LV-MVO significantly improved risk stratification of patients with STEMI .

2021 ◽  
Vol 22 (Supplement_2) ◽  
Author(s):  
LAI Wei ◽  
HENG Ge ◽  
JUN Pu

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): the National Key Research and Development Program of China OnBehalf Renji Hospital Affiliated to Medical College of Shanghai Jiaotong University Background:The prognostic value of Peak Early Diastolic Strain Rate (PEDSR) measured by Cardiac Magnetic Resonance (CMR) in ST-Elevation Myocardial Infarction (STEMI) is not clear. Methods:420 first-STEMI patients from the EARLY Assessment of MYOcardial Tissue Characteristics by CMR in STEMI (EARLY-MYO-CMR) registry (NCT03768453) and 40 normal people were enrolled and followed up. The patients received timely percutaneous coronary intervention (PCI) within 12h and CMR within 1 week (median,5 days; range, 2-7 days) after infarction. LV circumferential, radial, longitudinal PEDSR and other routine CMR parameters were measured. Clinical end point was a composite major adverse cardiovascular events (MACEs) including cardiovascular death, re-infarction and re-hospitalization for heart failure. Results:During follow-up (median: 52 months, inter-quartile range: 29–78 months), 73 (17.4%) patients experienced a MACE event. Compared with normal people, STEMI patients had lower PEDSR (circumf. PEDSR 0.77 vs. 1.27%/s, P < 0.001). Patients who developed MACEs also had lower PEDSR than patients who didn’t (circumf. PEDSR 0.64 vs. 0.78%/s, P < 0.001). Circumf. PEDSR can significantly predict MACEs with an AUC of 0.659 (95%CI 0.587-0.731, P < 0.001) which is not inferior to LVEF (0.659 vs. 0.651, P = 0.843), LVIS (0.659 vs. 0.661, P = 0.678) and LVMVO (0.659 vs. 0.666, P = 0.600). Circumf. PEDSR ≤ 0.665%/s is the independent predictive factor of MACEs in clinical (HR 2.099 [95%CI 1.273-3.461], P = 0.004) and CMR models (HR 1.795 [95%CI 1.065-3.026], P = 0.028). In Kaplan-Meier curve, patients with impaired PEDSR are more likely to experience MACEs (P < 0.001). When subdivided by LVEF, PEDSR still makes a significant difference to MACEs in patients with LVEF > 50.28% (P = 0.003) but not in reduced LVEF patients (P = 0.204). PEDSR is also incremental to LVEF (Continuous NRI 0.515 [95%CI 0.268-0.763], P < 0.001), LVIS (Continuous NRI 0.576 [95%CI 0.330-0.822], P < 0.001), and LVMVO (Continuous NRI 0.576 [95%CI 0.330-0.822], P < 0.001). Finally, worse TIMI flow post-PCI (HR 3.353 [95%CI 1.603-7.016], P = 0.001) and LVEF (HR 0.920 [95%CI 0.900, 0.940], P < 0.001) are the risk factors for PEDSR impairment. Conclusions:CMR-derived PEDSR can significantly predict MACEs with the discriminative power not inferior to LVEF, LVIS and LVMVO. Circumf. PEDSR ≤ 0.665%/s is an independent predictive factor of MACEs and is incremental in the prognostic risk stratification of STEMI.


Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Rhondalyn C McLean ◽  
Glenn A Hirsch ◽  
Gary Gerstenblith ◽  
Steven P Schulman

Background: Prior studies demonstrate an association between specific β-adrenergic receptor polymorphisms and clinical outcomes in patients with chronic heart failure and following an acute coronary syndrome. The mechanism may relate to an effect on left ventricular (LV) remodeling. We hypothesized that β-adrenergic receptor polymorphisms predict LV remodeling after acute ST elevation myocardial infarction (STEMI). Methods: We assessed the presence of β-1 and β-2 adrenergic receptor polymorphisms in 122 patients after their first STEMI enrolled in a single-center randomized, double-blind placebo controlled trial of L-arginine vs. placebo, 91% of whom received successful early reperfusion therapy. All patients were treated with a beta-1 receptor antagonist and underwent baseline (mean 5.9 days following STEMI) and 6-month LV volume evaluation using gated blood pool imaging. Univariate and multivariate linear and logistic regressions were used to assess the relationships between the polymorphisms, β1 Arg389Gly, β1 Ser49Gly, β2 Gly16Arg and β2 Gly27Glu and the six-month changes in LV volumes. The top quintiles of LV end-systolic (ESV) and end-diastolic (EDV) 6-month volume increases and LV ejection fraction decrease were compared to the lower quintiles in the logistic regression analyses. Results: The polymorphisms β1 Arg389Gly, β1 Ser49Gly, β2 Gly16Arg were not associated LV remodeling. However, the 25% of patients homozygous for the β2 Glu27 variant were 5.2 times more likely to have an increase in 6-month ESV than those who had the Gln27 variant (OR 5.2, 95%CI 1.4 –19.0). Multiple linear regression analyses demonstrated that absolute ESV at six months was 19 ml greater (p = 0.02) and EDV was 21 ml greater (p = 0.01) in post STEMI patients with the β2 Glu27 polymorphism compared to the wild type or heterozygous patients. Conclusions: Increased LV volumes post-STEMI are associated with an increased risk of heart failure and death. The common β2 receptor polymorphism, Glu27Glu, is associated with increased odds of adverse LV remodeling in patients treated with a beta-one receptor antagonist. Whether treatment with a non-specific β-adrenergic receptor blocker guided by this genetic polymorphism ameliorates the effect requires further study.


2021 ◽  
Vol 22 (Supplement_1) ◽  
Author(s):  
AI Scarlatescu ◽  
S Onciul ◽  
A Pascal ◽  
I Petre ◽  
D Zamfir ◽  
...  

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – EU funding. Main funding source(s): This work was supported by CREDO Project - ID: 49182, financed through the SOP IEC -A2-0.2.2.1-2013-1 cofinanced by the ERDF - I agree that this information can be anonymised and then used for statistical purposes only Background Left ventricular (LV) remodeling after ST elevation myocardial infarction (STEMI) plays an important role in predicting the outcome of this patient group. It is also useful in assessing the benefit of revascularization. Its identification is also of clinical importance in order to set up preventive strategies for patients with adverse remodeling Purpose To find an echocardiographic predictor of LV adverse remodeling following STEMI. Materials and methods In this prospective study we included 52 consecutive patients, aged between 35-70,  with STEMI treated by primary PCI. We performed conventional 2D transthoracic echocardiography for patients. In addition to conventional parameters we also measured LV global longitudinal strain (GLS) and LV mechanical dispersion using 2D speckle tracking imaging. For morphological and functional analysis of LV we used 3D echocardiography (volumes, LVEF). LV remodeling (LVR) was defined as an increase of over 15% of the LV end diastolic volume (LVEDV) at 6 months follow up. Results We found significant differences in time (baseline and 6 month follow up) between LVEF (43,08 vs 47,91, p = 0.034), LVEDV (105,95 vs 113,21, p = 0.000), LV GLS (-12.61 vs - 14,58, p = 0.01), and mechanical dispersion (61,68 vs 56,11, p = 0.00) in all patients. LV remodeling at 6 months (15% increase in LVEDV) was observed in 30 % of the included patients. At 6 months after STEMI we observed a significant difference between the two groups (remodeling vs no remodeling) regarding 3D LVEF (42.28 %vs 50.30%,p = 0.009), LVEDV (131 ml vs 109 ml, p = 0.05), GLS (-11.15 vs -16.02, p = 0.00) and LV mechanical dispersion (69.02 vs 50.54, p = 0.00). Patients with LV remodeling at 6 months after STEMI had lower LVEF, worse LV GLS and higher LV mechanical dispersion at baseline. Using ROC curve analysis we identified two cut off values, one of -11.55 for baseline LV GLS (Sb 78%, Sp 81%, AUC 0.852, CI 95%, p = 0.00) and another one of 63.7 for LV baseline mechanical dispersion (Sb 71,4%, Sp 66 %, AUC 0.762, p 0.005) to discriminate between patients with or without LV adverse remodeling at 6 months. Using linear regression analysis, we demonstrated that GLS (p = 0.00) and LV mechanical dispersion (p = 0.016) are able to predict LV remodeling in time. We also found a negative correlation between peak CK-MB levels at baseline LVEF at 6 months. Regression analysis showed that CK-MB levels at baseline could predict LVEF at 6 months (p = 0.008) Conclusion Baseline LV mechanical dispersion and LV GLS can predict LV adverse remodeling at 6 months after STEMI. These parameters could be used at baseline in order to predict worse outcome in STEMI patients. Further larger scale studies are needed to validate these findings.


Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Kiyotake Ishikawa ◽  
Jaume Aguero ◽  
Kenneth Fish ◽  
Lauren Leonardson ◽  
Roger J Hajjar

Background: Hypertension (HT) increases cardiac afterload and is one of the risk factors of poor prognosis after myocardial infarction (MI). However, there is little information on how HT impacts the healing processes during sub-acute phase MI. We investigated the role of an increased afterload on left ventricular (LV) performance and remodeling shortly after MI. Methods: Anterior MIs were created in 15 Yorkshire pigs via percutaneous access. To mimic HT condition, 7 pigs (Banding, n=7) underwent surgical banding of the ascending aorta 10 days after the MI, and were compared to the remaining pigs (Control, n=8). LV remodeling and function were assessed one month after MI using 3-D echocardiography and invasive hemodynamic measurements. Results: Echocardiographic assessment at day 10 revealed no significant differences in LV ejection fraction (EF) or LV volumes. One month after MI, aortic banding increased the systemic vascular resistance index, but was not statistically significant (1658±282 dyn/s/cm5/m 2 vs 1153±658 dyn/s/cm5/m 2 , P=0.08). Banding group presented with significantly impaired LVEF (Figure, P=0.002), larger end systolic volume (Figure, P=0.045), lower cardiac index (3.1±0.9 L/min/m 2 vs 4.4±0.6 L/min/m 2 , P=0.01), and elevated LV end diastolic pressure (22.4±5.0 mmHg vs 14.4±7.5 mmHg: P=0.04, Banding vs Control, respectively). Reduced EF was associated with remote myocardial dysfunction and histological analysis revealed increased interstitial fibrosis in this area. Conclusion: Increased afterload in sub-acute phase of MI induces more severely impaired cardiac function and LV remodeling, and was associated with worse heart failure status.


2016 ◽  
Vol 6 (2) ◽  
pp. 143-149 ◽  
Author(s):  
Yacov Shacham ◽  
Amir Gal-Oz ◽  
Jeremy Ben-Shoshan ◽  
Gad Keren ◽  
Yaron Arbel

Background: Only limited data is present regarding the incidence and prognostic implications of acute kidney injury (AKI) in ST elevation myocardial infarction (STEMI) patients with preserved left ventricular (LV) function in the primary percutaneous coronary intervention (PCI) era. Methods: We conducted a retrospective study of 842 consecutive STEMI patients with preserved LV function (ejection fraction ≥50%, assessed by echocardiography) who underwent primary PCI between January 2008 and January 2015. AKI was defined as an increase of ≥0.3 mg/dl in serum creatinine within 48 h following admission. Patients were assessed for all-cause mortality up to 5 years. Results: Fifty-two patients (6.2%) developed AKI. Patients with AKI were older, had impaired baseline renal function, and presented more often with heart failure throughout their hospitalization. Patients with AKI had a higher 5-year all-cause mortality (13.4 vs. 2.4%, p < 0.001). Compared to patients with no AKI, the adjusted hazard ratio for all-cause mortality was 2.64 (95% CI 1.25-5.56, p = 0.01). Conclusions: Among STEMI patients with preserved LV function undergoing primary PCI, AKI is associated with a higher long-term mortality.


Cardiology ◽  
2017 ◽  
Vol 138 (2) ◽  
pp. 91-96 ◽  
Author(s):  
Sam C. Latet ◽  
Paul L. Van Herck ◽  
Marc J. Claeys ◽  
Amaryllis H. Van Craenenbroeck ◽  
Steven E. Haine ◽  
...  

Background: MicroRNA are noncoding RNA that have a significant role in both inflammatory and cardiovascular diseases. Aims: We aimed to assess whether the inflammation-related microRNA-155 is associated with the development of adverse left ventricular (LV) remodeling following ST elevation myocardial infarction (STEMI). Methods: Peripheral blood samples were collected in the inflammatory (day 2), proliferative (day 5), and maturation phases (6 months) after STEMI (n = 20). Granulocytes, monocytes, and lymphocytes were enumerated with flow cytometry. The changes in LV volumes were assessed with 3-D echocardiography on day 1 and after 6 months. Adverse remodeling was defined as a >20% increase in end-diastolic volume. Healthy subjects were recruited as controls. Results: MicroRNA-155 measured on day 5 correlated positively with the relative change in end-diastolic volume (ρ = 0.490, p = 0.028). MicroRNA-155 (day 5) was significantly higher in patients with compared to patients without adverse LV remodeling. The expression level was similar in healthy subjects (n = 8) and in patients with LV remodeling. There was a positive correlation between microRNA-155 and the amount of monocytes (day 5, ρ = 0.463, p = 0.046). Conclusion: Impaired downregulation of microRNA-155 during the second phase of the post- STEMI inflammatory response is a determinant of the development of adverse LV remodeling.


2021 ◽  
Author(s):  
Ramime Ozel ◽  
Pelin Karaca Ozer ◽  
Nail Guven Serbest ◽  
Adem Atıcı ◽  
Imran Onur ◽  
...  

Abstract BackgroundMitral regurgitation may develop due to left ventricular (LV) remodeling within 3 months following acute myocardial infarction (AMI) and is called ischemic mitral regurgitation (IMR). Ischemic preconditioning (IPC) has been reported as the most important mechanism of the association between prior angina and the favorable outcome. The aim of this study was to investigate the effect of prior angina on the development and severity of IMR at 3rd month in patients with ST elevation MI (STEMI).MethodsFourty five (45) patients admitted with STEMI and at least mild IMR, revascularized by PCI were enrolled. According to presence of prior angina within 72 hours before STEMI, patients were then divided into two groups as angina (+) (n:26; 58%) and angina (-) (n:19; 42%). All patients underwent 2D transthoracic echocardiography at 1st, 3rd days and 3rd month. IMR was evaluated by proximal isovelocity surface area (PISA) method: PISA radius (PISA-r), effective regurgitant orifice area (EROA), regurgitant volume (Rvol). LV ejection fraction (EF %) was calculated by Simpson’s method. High sensitive troponin T (hs-TnT), creatine phosphokinase myocardial band (CK-MB) and N-terminal pro-brain natriuretic peptid (NTpro-BNP) levels were compared between two groups.ResultsAlthough PISA-r, EROA and Rvol were similar in both groups at 1st and 3rd days, all were significantly decreased (p=0.012, p=0.007, p=0.011, respectively) and EF was significantly increased (p< 0.001) in angina (+) group at 3rd month. NTpro-BNP and hs-TnT levels at 1st day and 3rd month were similar, however CK-MB level at 3rd month was found to be significantly lower in the angina (+) group (p=0.034).ConclusionAt the end of the 3rd month, it was observed that the severity of IMR evaluated by PISA method was decreased and EF increased significantly in patients who defined angina within 72 hours prior to STEMI, suggesting a relation with IPC.


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