Importance of EuroSCORE-II in the Development of Acute Ischemic Heart Failure After Acute Anterior ST Elevation Myocardial Infarction

2016 ◽  
Vol 19 (2) ◽  
pp. 65-71
Author(s):  
İlker Gül ◽  
Mustafa Zungur ◽  
Ahmet Çağrı Aykan ◽  
Aysel İslamlı ◽  
Bekir Serhat Yıldız ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Ischemic Heart ◽  
St Elevation Myocardial Infarction ◽  
Ischemic Heart Failure ◽  
St Elevation

scholarly journals ACE Inhibition Modulates Myeloid Hematopoiesis after Acute Myocardial Infarction and Reduces Cardiac and Vascular Inflammation in Ischemic Heart Failure

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 396
Author(s):  
Wolf-Stephan Rudi ◽  
Michael Molitor ◽  
Venkata Garlapati ◽  
Stefanie Finger ◽  
Johannes Wild ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Bone Marrow ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Vascular Inflammation ◽  
Ace Inhibition ◽  
Left Ventricular ◽  
Ischemic Heart ◽  
Ischemic Heart Failure

Aims: Angiotensin-converting-enzyme inhibitors (ACE inhibitors) are a cornerstone of drug therapy after myocardial infarction (MI) and improve left ventricular function and survival. We aimed to elucidate the impact of early treatment with the ACE inhibitor ramipril on the hematopoietic response after MI, as well as on the chronic systemic and vascular inflammation. Methods and Results: In a mouse model of MI, induced by permanent ligation of the left anterior descending artery, immediate initiation of treatment with ramipril (10 mg/k/d via drinking water) reduced cardiac inflammation and the number of circulating inflammatory monocytes, whereas left ventricular function was not altered significantly, respectively. This effect was accompanied by enhanced retention of hematopoietic stem cells, Lin−Sca1−c-Kit+CD34+CD16/32+ granulocyte–macrophage progenitors (GMP) and Lin−Sca1−c-Kit+CD150−CD48− multipotent progenitors (MPP) in the bone marrow, with an upregulation of the niche factors Angiopoetin 1 and Kitl at 7 d post MI. Long-term ACE inhibition for 28 d limited vascular inflammation, particularly the infiltration of Ly6Chigh monocytes/macrophages, and reduced superoxide formation, resulting in improved endothelial function in mice with ischemic heart failure. Conclusion: ACE inhibition modulates the myeloid inflammatory response after MI due to the retention of myeloid precursor cells in their bone marrow reservoir. This results in a reduction in cardiac and vascular inflammation with improvement in survival after MI.

scholarly journals Association of Interleukin 8 and Myocardial Recovery in Patients with ST-Elevation Myocardial Infarction Complicated by Acute Heart Failure

PLoS ONE ◽  
2014 ◽  
Vol 9 (11) ◽  
pp. e112359 ◽  
Author(s):  
Trygve Husebye ◽  
Jan Eritsland ◽  
Harald Arnesen ◽  
Reidar Bjørnerheim ◽  
Arild Mangschau ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Heart Failure ◽  
Interleukin 8 ◽  
St Elevation Myocardial Infarction ◽  
Myocardial Recovery ◽  
St Elevation

scholarly journals The risk of admission acute heart failure in ST-elevation myocardial infarction patients and air pollution with PM2.5

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
A Sinkovic ◽  
M Krasevec ◽  
D Suran ◽  
M Marinsek ◽  
A Markota
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Air Pollution ◽  
Acute Heart Failure ◽  
St Elevation Myocardial Infarction ◽  
Vascular Events ◽  
Limit Values ◽  
Predictive Role ◽  
St Elevation

Abstract Introduction Air pollution, in particular exposure to particulate matter fine particles of less than 2.5 microns in diameter (PM2.5), increases the risk of cardiovascular events. Short-term exposure (hours to few days prior) to increased PM2.5 levels even may help trigger ST-elevation myocardial infarction (STEMI) and heart failure exacerbation in susceptible individuals. The risk of vascular events is increased even in exposures below the current European air quality limit values (mean annual levels for PM2.5 less than 10μg/m3, 24-hour mean level less than 25μg/m3). Purpose To evaluate predictive role of PM2.5 levels ≥20 μg/m3 one day prior to hospital admission for the risk of admission acute heart failure (AAHF) in STEMI patients. Methods In 290 STEMI patients (100 women, 190 men, mean age 65.5±12.9 years), treated by primary percutaneous coronary intervention (PPCI) in 2018, we retrospectively registered the AAHF, defined as classes II-IV by Killip Kimbal classification. Additionally, we registered admission clinical data, potentially contributing to AAHF in STEMI patients such as gender, age ≥65 years, prior resuscitation, admission cTnI ≥5 μg/L (normal levels up to 0.045 μg/L), comorbidities, time to PPCI, and mean daily levels of PM2.5 ≥20 μg/m3 one day before admission. Mean daily, freely available, levels of PM2.5 were measured and registered by Chemical analytic laboratory of Environmental agency of Republic Slovenia. We evaluated the predictive role of admission data for admission AHF in STEMI patients. Results AAHF was observed in 34.5% of STEMI patients with the mean daily PM2.5 level 15.7±10.9 μg/m3 on the day before admission. PPCI was performed in 92.1% of all STEMI patients, in AAHF in 87.1% and in non-AAHF patients in 94.7% (p=0.037). AAHF in comparison to non-AAHF was associated significantly with female gender (50.5% vs 25.9%, p<0.001), age over 65 years (71.3% vs 45%, p<0.001), prior diabetes (33.7% vs 14.8%, p<0.001), left bundle branch block (LBBB) (10.9% vs 0.5%, <0.001), admission cTnI ≥5 μg/L (46.7% vs 25.9%, p<0.001) and mean daily levels of PM2.5 ≥20 μg/m3 one day before admission (31.7% vs 19%, p=0.020), but nonsignificantly with arterial hypertension, prior myocardial infarction, anterior STEMI and time to PPCI. Logistic regression demonstrated that significant independent predictors of AAHF were age over 65 years (OR 3.349, 95% CI 1.787 to 6.277, p<0.001), prior diabetes (OR 2.934, 95% CI 1.478 to 5.821, p=0.002), admission LBBB (OR 10.526, 95% CI 1.181 to 93.787, p=0.03), prior resuscitation (OR 3.221, 95% CI 1.336 to 7.761, p=0.009), admission cTnI ≥5μg/l (OR 2.984, 95% CI 1.618 to 5.502, p<0.001) and mean daily levels of PM2.5 ≥20 μg/m3 (OR 2.096, 95% CI 1.045 to 4.218, p=0.038) one day before admission. Conclusion Mean daily levels of PM2.5 ≥20μg/m3 one day before admission were among significant independent predictors of AAHF in STEMI patients. FUNDunding Acknowledgement Type of funding sources: None.

scholarly journals Culprit vessel: impact on short-term and long-term prognosis in patients with ST-elevation myocardial infarction

Open Heart ◽  
2018 ◽  
Vol 5 (2) ◽  
pp. e000852 ◽  
Author(s):  
Artin Entezarjou ◽  
Moman Aladdin Mohammad ◽  
Pontus Andell ◽  
Sasha Koul
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
High Risk ◽  
Left Ventricular ◽  
St Elevation Myocardial Infarction ◽  
Clinical Event ◽  
Left Ventricular Ejection ◽  
Increased Risk ◽  
St Elevation ◽  
The Impact

BackgroundST-elevation myocardial infarction (STEMI) occurs as a result of rupture of an atherosclerotic plaque in the coronary arteries. Limited data exist regarding the impact of culprit coronary vessel on hard clinical event rates. This study investigated the impact of culprit vessel on outcomes after primary percutaneous coronary intervention (PCI) of STEMI.MethodsA total of 29 832 previously cardiac healthy patients who underwent primary PCI between 2003 and 2014 were prospectively included from the Swedish Coronary Angiography and Angioplasty Registry and the Registry of Information and Knowledge about Swedish Heart Intensive care Admissions. Patients were stratified into three groups based on culprit vessel (right coronary artery (RCA), left anterior descending artery (LAD) and left circumflex artery (LCx)). The primary outcome was 1-year mortality. The secondary outcomes included 30-day and 5-year mortality, as well as heart failure, stroke, bleeding and myocardial reinfarction at 30 days, 1 year and 5 years. Univariable and multivariable analyses were done using Cox regression models.ResultsOne-year analyses revealed that LAD infarctions had the highest increased risk of death, heart failure and stroke compared with RCA infarctions, which had the lowest risk. Sensitivity analyses revealed that reduced left ventricular ejection fraction on discharge partially explained this increased relative risk in mortality. Furthermore, landmark analyses revealed that culprit vessel had no significant influence on 1-year mortality if a patient survived 30 days after myocardial infarction. Subgroup analyses revealed female sex and multivessel disease (MVD) as significant high-risk groups with respect to 1-year mortality.ConclusionsLAD and LCx infarctions had a relatively higher adjusted mortality rate compared with RCA infarctions, with LAD infarctions in particular being associated with an increased risk of heart failure, stroke and death. Culprit vessel had limited influence on mortality after 1 month. High-risk patient groups include LAD infarctions in women or with concomitant MVD.

Abstract P155: Etiology And Complications Associated With High-output Heart Failure; A National Readmission Database Study.

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Mohammed M Uddin ◽  
Tarec Micho Ulbeh ◽  
Tanveer Mir ◽  
Joseph Sebastian ◽  
Qasim Jehangir ◽  
...  
Keyword(s):  
United States ◽  
Myocardial Infarction ◽  
Heart Failure ◽  
Myeloproliferative Disorders ◽  
The United States ◽  
Primary Diagnosis ◽  
St Elevation Myocardial Infarction ◽  
High Output Heart Failure ◽  
St Elevation ◽  
High Output

Background: The literature on the etiologies and complications of high-output heart failure (HOHF) is limited. Objective: To study the causes and complications related to HOHF in the United States (US). Methods: Data from the national readmissions database (NRD) sample that constitutes 49.1% of the stratified sample of all hospitals in the United States, representing more than 95% of the national population were analyzed for hospitalizations with primary diagnosis of HOHF for the years 2017-2018. Etiology associated with HOHF were extracted using ICD-10 codes. Results: A total of 2,107 index hospitalizations (mean age 62.2 ± 19.1) with primary diagnosis of HOHF were recorded in the NRD for the years 2017-2018. The most common causes of HOHF include sepsis 204 (9.7%), leukemia 53 (2.5%), arteriovenous fistula 13 (0.6%), liver cirrhosis 155 (7.4%), Hyperthyroidism 133 (6.3%), thalassemia 23 (1.14%), sickle cell disease 71 (3.35%), morbid obesity 188 (8.95%), COPD 406 (19.3%), myeloproliferative disorders 166 (7.87%). Among the HOHF group, major complications include acute ischemic stroke (42 or 2%), acute kidney injury (593 or 28.1%), hypertensive emergency (74 or 3.5%), atrial fibrillation (409 or 19.4%), ventricular tachycardia/fibrillation (77 or 3.7%), and conduction block (81 or 3.8%) and ST-Elevation myocardial infarction (11 or 0.5%). A total of 83 (3.9%) patients had died during the inpatient hospitalization. Out of the remaining 2,024 patients, a significant portion (62 or 3.1%) required readmission within 30 days. Conclusion: HOHF is an under-reported cardiovascular complication associated with non-cardiovascular disorders. HOHF is associated with significant 30-day readmissions and mortality rates. Proper management of the underlying etiology can prevent the development of HOHF and associated complications. Keywords: cirrhosis; hemodynamics; obesity, leukemia, myeloproliferative disorders, ST-Elevation myocardial infarction (STEMI).

scholarly journals Role of P2X purinergic receptors in the rescue of ischemic heart failure

2008 ◽  
Vol 295 (3) ◽  
pp. H1191-H1197 ◽  
Author(s):  
Dmitry Sonin ◽  
Si-Yuan Zhou ◽  
Chunxia Cronin ◽  
Tatiana Sonina ◽  
Jeffrey Wu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Infarct Size ◽  
Purinergic Receptors ◽  
P2x Receptors ◽  
Left Ventricular ◽  
Ischemic Heart ◽  
Post Myocardial Infarction ◽  
Ischemic Heart Failure

Evidence is accumulating to support the presence of P2X purinergic receptors in the heart. However, the biological role of this receptor remains to be defined. The objectives here were to determine the role of cardiac P2X receptors in modulating the progression of post-myocardial infarction ischemic heart failure and to investigate the underlying mechanism. The P2X4 receptor (P2X4R) is an important subunit of native cardiac P2X receptors, and the cardiac-specific transgenic overexpression of P2X4R (Tg) was developed as a model. Left anterior descending artery ligation resulted in similar infarct size between Tg and wild-type (WT) mice ( P > 0.1). However, Tg mice showed an enhanced cardiac contractile performance at 7 days, 1 mo, and 2 mo after infarction and an increased survival at 1 and 2 mo after infarction ( P < 0.01). The enhanced intact heart function was manifested by a greater global left ventricular developed pressure and rate of contraction of left ventricular pressure in vitro and by a significantly increased fractional shortening and systolic thickening in the noninfarcted region in vivo ( P < 0.05). The salutary effects on the ischemic heart failure phenotype were seen in both sexes and were not the result of any difference in infarct size in Tg versus WT hearts. An enhanced contractile function of the noninfarcted area in the Tg heart was likely an important rescuing mechanism. The cardiac P2X receptor is a novel target to treat post-myocardial infarction ischemic heart failure.

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