scholarly journals Association of Dephosphorylated-Uncarboxylated Matrix Gla Protein and Risk of Major Bleeding in Patients Presenting with Acute Myocardial Infarction

Life ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 733
Author(s):  
Admira Bilalic ◽  
Tina Ticinovic Kurir ◽  
Josip A. Borovac ◽  
Marko Kumric ◽  
Daniela Supe-Domic ◽  
...  

The “Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with Early implementation of the ACC/AHA guidelines” (CRUSADE) score emerged as a predictor of major bleeding in patients presenting with the acute coronary syndrome. On the other hand, previous studies established the association of dephosphorylated-uncarboxylated Matrix Gla protein (dp-ucMGP) and vitamin K, as well as their subsequent impact on coagulation cascade and bleeding tendency. Therefore, in the present study, we explored if dp-ucMGP plasma levels were associated with CRUSADE bleeding score. In this cross-sectional study, physical examination and clinical data, including plasma dp-ucMGP levels, were obtained from 80 consecutive patients with acute myocardial infarction (AMI). A significant positive correlation was found between CRUSADE bleeding score and both dp-ucMGP plasma levels (r = 0.442, p < 0.001) and risk score of in-hospital mortality (r = 0.520, p < 0.001), respectively. In comparing the three risk groups of risk for in-hospital bleeding, the high/very high-risk group had significantly higher dp-ucMGP levels from both very low/low group (1277 vs. 794 pmol/L, p < 0.001) and the moderate group (1277 vs. 941 pmol/L, p = 0.047). Overall, since higher dp-ucMGP levels were associated with elevated CRUSADE score and prolonged hemostasis parameters, this may suggest that there is a biological link between dp-ucMGP plasma levels and the risk of bleeding in patients who present with AMI.

2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
R King ◽  
D Giedrimiene

Abstract Funding Acknowledgements Type of funding sources: None. Background The management of patients with multiple comorbidities represents a significant burden on healthcare each year. Despite requiring regular medical care to treat chronic conditions, a large number of these patients may not receive proper care. Significant disparities have been identified in patients with multiple comorbidities and those who experience acute coronary syndrome or acute myocardial infarction (AMI). Only limited data exists to identify the impact of comorbidities and utilization of primary care physician (PCP) services on the development of adverse outcomes, such as AMI. Purpose The primary objective was to analyze how PCP services utilization can be associated with comorbidities in patients who experienced an AMI. Methods This study was based on retrospective data analysis which included 250 patients admitted to the Hartford Hospital Emergency Department (ED) for an AMI. Out of these, 27 patients were excluded due to missing documentation. Collected data included age, gender, medications and recorded comorbidities, such as hypertension, hyperlipidemia, diabetes mellitus (DM), chronic kidney disease (CKD) and previous arrhythmia. Each patient was assessed regarding utilization of PCP services. Statistical analysis was performed in order to identify differences between patients with documented PCP services and those without by using the Chi-square test. Results The records allowed for identification of documented PCP services for 172 out of 223 (77.1%) patients. The most common comorbidities were hypertension and hyperlipidemia: in 165 (74.0%) and 157 (70.4%) cases respectively. The most frequent comorbidity was hypertension: 137 out of 172 (79.7%) in pts with PCP vs 28 out of 51 (54.9%) without PCP, and significantly more often in patients with PCP, p&lt; 0.001. Hyperlipidemia was the second most frequent comorbidity: in 130 out of 172 (75.6%) vs 27 out of 51 (52.9%) accordingly, and also significantly more often (p&lt; 0.002) in patients with PCP services. The number of comorbidities ranged from 0-5, including 32 (14.3%) patients without comorbidities: 16 (9.3%) with a PCP and 16 (31.4%) without PCP services. The majority of patients - 108 (48.5% of 223), had 2-3 documented comorbidities: 89 (51.8%) had two and 19 (34.6%) had three. The remaining 40 (17.9%) patients had 4-5 comorbidities: 37 (21.5%) of them with a PCP and 3 (10.3%) without, with a significant difference (p &lt; 0.001) found for patients with a higher number of comorbidities who utilized PCP services. Conclusions Our study shows that the majority of patients who presented with an AMI had one or more comorbidities. Furthermore, patients who did not utilize PCP services had fewer identified comorbidities. This suggests that there may be a significant number of patients who experienced AMI with undiagnosed comorbidities due to not having access to PCP services.


2021 ◽  
Vol 8 ◽  
Author(s):  
Junyu Pei ◽  
Xiaopu Wang ◽  
Pengfei Chen ◽  
Keyang Zheng ◽  
Xinqun Hu

Background: Women had worse outcomes after acute myocardial infarction (AMI), and physiologically, women had lower hemoglobin values. We examined whether there were sex-related differences in the relationship between hemoglobin levels and adverse outcomes in patients with acute myocardial infarction.Method: We conducted a post-hoc analysis of data from the Acute Coronary Syndrome Quality Improvement in Kerala (ACS-QUIK) Study. We explored the relationship between baseline hemoglobin level and 30-days adverse outcomes by logistic regression model, generalized additive model (GAM) and two-piecewise linear regression model. We used multiple imputation, based on five replications and a chained equation approach method in the R multiple imputation procedure, to account for missing data. The primary outcome were 30-day major adverse cardiovascular events (MACEs) defined as death, reinfarction, stroke, and major bleeding. The secondary outcomes were 30-day major bleeding, 30-day stroke and 30-day cardiovascular death (CVD death).Results: Twenty thousand, five hundred fifty-nine patients with AMI were included in our analysis. Baseline hemoglobin level was associated with major bleeding [OR: 0.74, 95%CI (0.60, 0.92) P &lt; 0.01], CVD death [OR: 0.94, 95%CI (0.90, 0.99) P &lt; 0.01], and MACEs [OR: 0.95, 95%CI (0.92, 0.99) P &lt; 0.01]. There was no significant relationship between baseline hemoglobin level and stroke incidence in both men [OR: 1.02, 95%CI (0.90, 1.14) P = 0.77] and women [OR: 1.15, 95%CI (0.96, 1.37) P = 0.18]. Baseline hemoglobin level was associated with major bleeding [OR: 0.71, 95%CI (0.58, 0.85) P &lt; 0.01] in male patients, however we did not find the same relationship in female patients [OR: 0.89, 95%CI (0.56, 1.41) P = 0.61]. GAM and two-piecewise linear regression model showed the relationships of hemoglobin level with major bleeding, CVD death, and MACEs were non-linear (non-linear P &lt; 0.05), and the threshold value were 13, 14.8, and 14.3 g/dL for MACEs and CVD death, respectively.Conclusion: Baseline hemoglobin level was one of the independent predictors of prognosis in South Asia patients with acute myocardial infarction. Moreover, its impact on prognosis was largely different depending on the patients' sex.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
V Novosadov ◽  
T N Vlasik ◽  
M Y A Ruda ◽  
D V Pevsner ◽  
I N Rybalkin ◽  
...  

Abstract Background Takotsubo cardiomyopathy (TTC) is an acute, life-threatening condition which is typically induced by stress and manifested by chest pain and ECG changes. The TTC prevalence among patients (pts) with acute coronary syndrome is 1.7–2.2%. The mortality rate from TTC is up to 8%. TTC is clinically indistinguishable from acute myocardial infarction (AIM). Differential diagnosis of TTC and AIM remains an unresolved problem. Recent studies have shown the differences in profiles of plasma microRNAs inTTC and AIM. Purpose To evaluate the possibility of differentiating TTC and AIM using a PCR-based semi-quantitative analysis of mRNAs, the plasma levels of which had been shown to be increased in patients with AIM (miR-1, miR-208a, miR-133a, miR-499a) and TTC (miR-16, miR-26a). Methods Plasma from 38 pts was used: 13 pts with confirmed TTC (12 women, 1 man), 25 pts with AIM (9w, 16m). For 10 pts with AIM, blood was collected twice: at 6 and 24 hours after the heart attack. The control arm comprised 40 healthy people from the same age group (12w, 28m). Plasma was obtained using the Cell-Free DNA blood collection tubes. Nucleic acids were separated using a modified Boom method. A semi-quantitative assessment of the mRNA levels was performed using dCq method with stem-loop qRT-PCR. Normalization for spiked synthetic cel-miR-39 and endogenous miR-23a was performed. Control of hemolysis was performed by measuring the ratio of miR-451 (specific for RBCs) and miR-23a (absent from RBCs). The statistical significance of differences between mRNA levels was assessed using Mann–Whitney test. Results No significant differences in the levels of miR-16, miR-26a and miR-208a in TTC group and control group have been found. Pts with AIM significantly differed from pts with TTC (p=0.0038 and 0.0002, respectively) and control pts (p=3.1x10–9 and 2,66x10–10) with the increased levels of cardiac-specific miR-1 and miR-133a. As compared to plasma levels at 6 hours after the heart attack, at 24-hour point the levels of these mRNAs were markedly reduced in 9 of 10 pts (mean reduction was 22.3-fold for miR-133a and 7.5-fold for miR-1). The correlation between changes in the levels of these mRNAs was high (Spearman correlation coefficient=0.89). Significant differences in plasma levels of miR-133a between pts with AIM and TTC were maintained even if blood was collected after 24 hours (p=0.007). For miR-16 and miR-26a, no significant differences between pts with AIM and TTC were found. The results of analysis of these mRNAs are affected to a substantial degree by the residual hemolysis due to their high content in blood cells. Conclusions It was shown that measuring the plasma levels of mRNAs miR-1 and miR-133a allows to distinguish TTC from AIM by excluding the diagnosis of TTC. The differential diagnosis is possible only within several hours after acute clinical symptoms and requires proper normalization and full compliance with the technical specifications.


2019 ◽  
Vol 10 (4) ◽  
pp. 3204-3208
Author(s):  
Castelino Renita Edwin ◽  
Jitha Thankachan ◽  
Lisa Mathew Adackapara ◽  
Aneena Suresh

Use of intravenous heparin in Acute coronary syndrome possess a major risk of bleeding to patients. However, the estimation of risk using bleeding scores in Indian settings is yet to be established. These case series assess the risk of major bleeding associated with the use of Antithrombotic agents in patients with acute coronary syndrome using CRUSADE (Can Rapid risk stratification of Unstable angina patients Suppress ADverse outcomes with Early implementation of the ACC/AHA guidelines) bleeding score. Relevant patient data was collected from hospital records and patients were followed up till discharge. All the four cases reported showed the risk of in-hospital bleeding with anti-thrombotic agents evident as two cases of hematuria, one case of gum bleeding and one case of hemorrhagic stools. All the patient presented with chest pain to the hospital; following a diagnosis of the acute coronary syndrome, they were prescribed with antiplatelets and anticoagulants. This accompanied a bleeding event which was categorized using CRUSADE bleeding risk score. In-hospital major bleeding imposes a burden on the patient's quality of life. Use of CRUSADE bleeding score helps to predict the severity of risk in a less expensive, non-invasive manner. Further, large scale studies will pave the way for using CRUSADE as an efficient bleeding predictor score.


Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 5013-5013
Author(s):  
Jens Posma ◽  
Rene van Oerle ◽  
Diane Fens ◽  
Jose govers Riemslag ◽  
Julia Mueller ◽  
...  

Abstract Background: Acute coronary syndrome (ACS), the main contributor to myocardial infarction, is a thrombotic complication of atherosclerosis. Growing evidence supports a role for the intrinsic coagulation cascade in various thrombotic diseases. To gain more inside in the contribution of the intrinsic coagulation cascade in an ACS, we developed novel, ELISA-based assays for the quantification of Kallikrein, activated factor XII (FXIIa), FXIa, FXa, FIXa, and thrombin in complex with a physiological inhibitor. Methods: During this prospective cohort study, blood from patients with a first ACS (n=61) was collected upon admission (before heparin injection(t=0), and after 1(t=1) and 6 (t=2) months. Plasma levels of Kallikrein-C1inhibitor (K-C1inh), FXIIa-C1inh, FXIa-C1inh, FXIa-α1 anti trypsin, FXIa-antithrombin (AT), FIXa-AT, FXa-AT, and thrombin-AT(TAT) were measured using newly developed ELISA's and compared to apparently healthy controls (n=60). Methods were validated according to the EP5-protocol for within- and -between run variability. Results: The inter coefficients of variability for K-C1inh is 11.9%, FXIa-α1-AT 14.4%, FXIa-AT 13.7%, FIXa-AT 4.9%, FXa-AT 2.6% and TAT 8.6 %. Levels of FXIa-α1-AT, FXI- ΑΤ, FIXa-AT and TAT were all significantly elevated in plasma from ACS patients at time of the acute event compared to healthy control: FXIa-α1 anti trypsin respectively 202.8 (IQR 156.6 - 283.4) vs 29.0 pM (IQR 0.00 - 101.0); FXIa-AT levels were respectively 35.9 pM (IQR 23.9 - 43.4) vs 28.0 pM (IQR 23.3 - 34.0); FIXa-AT respectively 102.0pM (IQR 87.4 - 123.0) vs 90.5 pM (IQR 83.2 - 104.3); TAT respectively 5.59 (IQR 3.91 - 9.85) vs 2.26 pM (IQR 1.78 - 2.71)(Fig1). Plasma levels of FXIa-α1-AT, FXIa-AT FIXa-AT, and TAT decreased during follow up. Additionally, FXIa-α1-AT, FXIa-AT FIXa-AT, and TAT were higher in patients with ST-elevated myocardial infarction (STEMI) compared to subjects with non-STEMI or angina pectoris. Conclusion: Elisa based profiling of the coagulation proteases provide a highly sensitive and reproducible method used to distinguish the different activation states of single proteases in the coagulation cascade. With these novel assays we show that FXIa-α1-AT, FXIa-AT FIXa-AT, and TAT are significantly elevated in patients with ACS. Additionally, patients with STEMI have a more pronounced hypercoagulable state than non-STEMI and angina pectoris patients. Figure 1. Figure 1. Disclosures No relevant conflicts of interest to declare.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Roxana Mehran ◽  
George D Dangas ◽  
Helen Parise ◽  
Giulio Guagliumi ◽  
Bernard Witzenbichler ◽  
...  

Background: Inflammation plays a crucial role in atherosclerosis. Previous studies have suggested an association between elevated white blood cell (WBC) and adverse outcomes in patients with ST-elevation acute myocardial infarction (STEMI). We sought to determine the relationship between admission WBC count and mortality in patients with STEMI in the HORIZONS-AMI trial. Methods: HORIZONS-AMI enrolled 3602 patients with STEMI undergoing primary PCI. We compared rates of 30-day major adverse cardiac events (MACE: death, reinfarction, target vessel revascularization for ischemia, or stroke), non-CABG major bleeding, and net adverse clinical events (NACE: MACE or major bleeding) in patients with baseline WBC count >12,000 cells/mm 3 vs ≤12,000 cells/mm 3 . Results: Of the 3497 patients with baseline WBC data, 2206 (63.1%) had a WBC count of ≤12,000 and 1291 (38.9%) had a WBC of >12,000 (median 10,800 mm 3 , mean 11,700 mm 3 ). Patients with WBC ≤12,000 were older, had more hypertension, hyperlipidemia, diabetes, prior MI, and prior CABG. Compared to patients with WBC ≤12,000, those with WBC >12,000 had significantly higher rates of 30-day adverse outcomes (Table ). By multivariate analyses, WBC >12,000 was an independent predictor of 30-day mortality (HR [95% CI] = 2.51 [1.61–3.91], p30.001), MACE (1.82 [1.36, 2.44], p<0.0001), and major bleeding (1.52 [1.16 –1.99], p=0.003). Conclusions: In patients presenting with STEMI undergoing primary PCI, an elevated WBC count identifies a high risk cohort with significantly higher mortality, MACE and major bleeding at 30-days. These results further support the pivotal role of inflammation in ACS/AMI.


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