P5011Impact of guideline-recommended medical therapy at discharge on long-term mortality in patients with or without left ventricular dysfunction after primary PCI for STEMI

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Radomirovic ◽  
D Milasinovic ◽  
Z Mehmedbegovic ◽  
D Jelic ◽  
V Zobenica ◽  
...  

Abstract Background Clinical practice guidelines provide class I recommendation for the use of angiotensin-converting enzyme inhibitors (ACE-I) and beta-blockers in patients with prior myocardial infarction and left ventricular (LV) dysfunction, whereas their use in patients without LV dysfunction is considered to be a class IIa recommendation. Purpose Our aim was to comparatively assess the impact of ACE-I and/or beta-blockers on 3-year mortality in patients with or without impaired left ventricular (LV) function undergoing primary percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI). Methods The analysis included 4425 patients admitted for primary PCI during 2009–2015 from a prospective, electronic registry of a high-volume tertiary center, who survived initial hospitalization, and for whom information on LV function and discharge medication were available. Patients were stratified according to LV systolic dysfunction, defined as LVEF <40%. Unadjusted and adjusted Cox regression models were created to investigate the impact of beta-blocker and/or ACE-I therapy on 3-year mortality. Results 22.9% (n=1013) had LV dysfunction, 23.0% (n=1017) received either an ACE-I or a beta-blocker and 72.2% received both medications at discharge (n=3197). The concurrent use of both ACE-I and beta-blockers was not different in LVEF≥40% vs. LVEF<40% (72.4% vs. 71.7%, p=0.43). The use of at least one of the guideline-recommended medications was associated with a significantly lower 3-year mortality in both patients with LVEF≥40% (18.7% if neither was used, 11.2% if either a beta-blocker or an ACE-I were used and 9.4% if both were used, p=0.001), and LVEF<40% (55.4% if neither was used, 32.5% if either a beta-blocker or an ACE-I were used and 22.9% if both were used, p<0.001) (Figure). After adjusting for significant mortality predictors including older age, diabetes, hypertension, renal failure, previous stroke, Killip class ≥2 and non-culprit chronic total occlusion (CTO), the concurrent use of both a beta-blocker and an ACE-I remained independently associated with lower 3-year mortality in both patients with LVEF<40% (HR 0.30, p<0.001) and LVEF≥40% (HR=0.41, p=0.001). The use of a single agent was independently associated with lower mortality in patients with LVEF<40% (HR 0.45, p=0.002), but not in patients with LVEF≥40% (HR 0.61, p=0.07). Conclusions Guideline-recommended use of both a beta-blocker and an ACE-I in post-MI patients was associated with a lower 3-year mortality regardless of the LV function, whereas using only one of the two agents was associated with improved prognosis only in patients with LV dysfunction, but not in patients without LV impairment.

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A Pavlovic ◽  
D.G Milasinovic ◽  
Z Mehmedbegovic ◽  
D Jelic ◽  
S Zaharijev ◽  
...  

Abstract Background Atrial fibrillation (AF) and impaired left ventricular (LV) function have both been separately associated with increased risk of mortality following primary percutaneous coronary intervention (PCI) in patients with ST-elevation myocardial infarction (STEMI). Purpose Our aim was to comparatively evaluate the impact of LV dysfunction and AF on the risk of mortality in primary PCI-treated patients. Methods This analysis included 8561 patients admitted for primary PCI during 2009–2019, from a prospectively kept, electronic registry of a high-volume tertiary center, from whom echocardiographic parameters were available. LV dysfunction was defined as EF&lt;40%. Adjusted Cox regression models were used to assess 30-day and 1-year mortality hazard. Results AF was present in 3.2% (n=273), whereas 37% had LV dysfunction (n=3189). Crude mortality rates were increased in the presence of either AF or LV dysfunction, and were the highest in the group of patients having both AF and impaired LV function, at 30 days (1.8% in no AF and no LV dysfunction vs. 5.4% if AF only vs. 7.0% if EF&lt;40% only vs. 14.9% if AF and LV dysfunction concurrently present, p&lt;0.001) and at 3 years (10.5% if no AF and no LV dysfunction vs. 35.8% if AF only vs. 28.5% if EF&lt;40% only vs. 60.3% if AF and LV dysfunction both present, p&lt;0.001). After multivariable adjustment for other significant mortality predictors, including age, previous stroke, MI, diabetes, hyperlipidemia, anemia and Killip≥2, LV dysfunction alone and in combination with AF was an independent predictor of mortality at both 30 days (HR=2.2 and HR=2.5, respectively, p&lt;0.001 for both) and at 3 years (HR=1.9 and HR=2.9, respectively, p&lt;0.001 for both). However, presence of AF alone, in the absence of an impaired LV function, was not independently associated with mortality at 30 days (HR 1.34, CI 95% 0.58–3.1, p=0.48), but rather at 3 years (HR 1.74, CI 95% 1.91–2.54, p=0.004). Conclusion Atrial fibrillation is associated with long-term mortality in STEMI patients undergoing primary PCI, irrespective of the LV function. Conversely, short-term prognostic relevance of atrial fibrillation in STEMI is dependent on the presence of LV dysfunction. Kaplan Meier curve_AF_LV dysfunction Funding Acknowledgement Type of funding source: None


Open Heart ◽  
2021 ◽  
Vol 8 (2) ◽  
pp. e001614
Author(s):  
Mohammad R Ostovaneh ◽  
Raj R Makkar ◽  
Bharath Ambale-Venkatesh ◽  
Deborah Ascheim ◽  
Tarun Chakravarty ◽  
...  

BackgroundMost cell therapy trials failed to show an improvement in global left ventricular (LV) function measures after myocardial infarction (MI). Myocardial segments are heterogeneously impacted by MI. Global LV function indices are not able to detect the small treatment effects on segmental myocardial function which may have prognostic implications for cardiac events. We aimed to test the efficacy of allogeneic cardiosphere-derived cells (CDCs) for improving regional myocardial function and contractility.MethodsIn this exploratory analysis of a randomised clinical trial, 142 patients with post-MI with LVEF <45% and 15% or greater LV scar size were randomised in 2:1 ratio to receive intracoronary infusion of allogenic CDCs or placebo, respectively. Change in segmental myocardial circumferential strain (Ecc) by MRI from baseline to 6 months was compared between CDCs and placebo groups.ResultsIn total, 124 patients completed the 6-month follow-up (mean (SD) age 54.3 (10.8) and 108 (87.1%) men). Segmental Ecc improvement was significantly greater in patients receiving CDC (−0.5% (4.0)) compared with placebo (0.2% (3.7), p=0.05). The greatest benefit for improvement in segmental Ecc was observed in segments containing scar tissue (change in segmental Ecc of −0.7% (3.5) in patients receiving CDC vs 0.04% (3.7) in the placebo group, p=0.04).ConclusionsIn patients with post-MI LV dysfunction, CDC administration resulted in improved segmental myocardial function. Our findings highlight the importance of segmental myocardial function indices as an endpoint in future clinical trials of patients with post-MI.Trial registration numberNCT01458405.


2006 ◽  
Vol 291 (1) ◽  
pp. R155-R162 ◽  
Author(s):  
Stephanie A. Dean ◽  
Junhui Tan ◽  
Roselyn White ◽  
Edward R. O’Brien ◽  
Frans H. H. Leenen

The present study tested the hypothesis that 17β-estradiol (E2) inhibits increases in angiotensin-converting enzyme (ACE) and ANG II type 1 receptor (AT1R) in the brain and heart after myocardial infarction (MI) and, thereby, inhibits development of left ventricular (LV) dysfunction after MI. Age-matched female Wistar rats were treated as follows: 1) no surgery (ovary intact), 2) ovariectomy + subcutaneous vehicle treatment (OVX + Veh), or 3) OVX + subcutaneous administration of a high dose of E2 (OVX + high-E2). After 2 wk, rats were randomly assigned to coronary artery ligation (MI) and sham operation groups and studied after 3 wk. E2 status did not affect LV function in sham rats. At 2–3 wk after MI, impairment of LV function was similar across MI groups, as measured by echocardiography and direct LV catheterization. LV ACE mRNA abundance and activity were increased severalfold in all MI groups compared with respective sham animals and to similar levels across MI groups. In most brain nuclei, ACE and AT1R densities increased after MI. Unexpectedly, compared with the respective sham groups the relative increase was clearest (20–40%) in OVX + high-E2 MI rats, somewhat less (10–15%) in ovary-intact MI rats, and least (<10–15%) in OVX + Veh MI rats. However, because in the sham group brain ACE and AT1R densities increased in the OVX + Veh rats and decreased in the OVX + high-E2 rats compared with the ovary-intact rats, actual ACE and AT1R densities in most brain nuclei were modestly higher (<20%) in OVX + Veh MI rats than in the other two MI groups. Thus E2 does not inhibit upregulation of ACE in the LV after MI and amplifies the percent increases in ACE and AT1R densities in brain nuclei after MI, despite E2-induced downregulation in sham rats. Consistent with these minor variations in the tissue renin-angiotensin system, during the initial post-MI phase, E2 appears not to enhance or hinder the development of LV dysfunction.


Cardiology ◽  
2015 ◽  
Vol 130 (2) ◽  
pp. 82-86
Author(s):  
H.M. Gunes ◽  
G.B. Guler ◽  
E. Guler ◽  
G.G. Demir ◽  
S. Hatipoglu ◽  
...  

Objective: Osteopontin (OPN), a sialoprotein present within atherosclerotic lesions, especially in calcified plaques, is linked to the progression of coronary artery disease and heart failure. We assessed the impact of valve surgery on serum OPN and left ventricular (LV) function in patients with mitral regurgitation (MR). Methods: Thirty-two patients with severe MR scheduled for surgery were included in the study. Echocardiography markers were assessed preoperatively and at 3 months following the surgery and matched with the serum OPN levels. Results: Valve surgery was associated with a reduction of the ejection fraction (EF) from 55.2 ± 6.3 to 48.8 ± 7.1% after surgery, p < 0.001. Following surgery, the OPN level was significantly higher than preoperatively (mean 245, range 36-2,284 ng/ml vs. 76, 6-486 ng/ml, p = 0.007). Preoperative OPN exhibited a slight negative correlation with the EF (r = -0.35, p = 0.04), and a moderate correlation with vena contracta (r = -0.38, p = 0.02). There were no other meaningful correlations between conventional echocardiographic parameters and OPN. Conclusion: Following valve surgery due to severe MR, patients exhibited a decrease in EF and an increase in OPN levels. The assessment of preoperative OPN failed to strongly predict probable LV dysfunction.


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Yanti Octavia ◽  
Elza D van Deel ◽  
Monique de Waard ◽  
Martine de Boer ◽  
Dirk J Duncker

Introduction: The cardiovascular benefits of exercise training (EX) are widely appreciated. Previously we found that the cardiac effects of EX critically depend on the underlying cause of heart disease. Hypothesis: The underlying etiology determines how EX affects the endothelial nitric oxide (NO) synthase (eNOS)-mediated balance between NO and superoxide (O2-). Methods: Mice were subjected to sham surgery, myocardial infarction (MI) or transverse aortic constriction (TAC), and subsequently exposed to 8 weeks of voluntary wheel running or sedentary housing. Left ventricular (LV) function was assessed by echocardiography and hemodynamic measurements; fibrosis by Picro-sirius Red staining; peroxynitrite (ONOO-) and O2- production by luminol- and lucigenin-enhanced chemiluminescence respectively, with or without the NOS inhibitor L-NAME; eNOS uncoupling and eNOS S-glutathionylation by western blot and coimmunoprecipitation, respectively; cardiac NO by the Griess reaction. Results: EX ameliorated LV dysfunction and fibrosis in MI but not TAC (Table 1). Strikingly, O2- generation was blunted by EX in MI, but exacerbated by EX in TAC, which was largely NOS-dependent. Accordingly, eNOS uncoupling and eNOS S-glutathionylation were corrected by EX in MI but aggravated in TAC mice. In parallel, ONOO- levels was attenuated by EX in MI but aggravated by EX in TAC. Cardiac NO levels were reduced in MI and TAC and normalized by EX in MI. Conclusions: The contrasting effects of EX in MI vs TAC can be explained by the highly divergent effects of EX on eNOS regulation, resulting in blunted vs aggravated oxidative stress by EX in MI vs TAC.


2008 ◽  
Vol 389 (6) ◽  
Author(s):  
Matthias Koch ◽  
Klaus Bonaventura ◽  
Frank Spillmann ◽  
Andreas Dendorfer ◽  
Heinz-Peter Schultheiss ◽  
...  

Abstract Bradykinin (BK) coronary outflow and left ventricular (LV) performance of kininogen-deficient Brown Norway Katholiek (BNK) rats and Brown Norway Hannover (BNH) controls were investigated. We analyzed whether the angiotensin-converting enzyme (ACE) inhibitor ramipril is able to attenuate LV dysfunction after induction of myocardial infarction (MI) in this animal model. Ex vivo, the basal BK content in the coronary outflow of buffer-perfused, isolated hearts was measured by specific radioimmunoassay. In vivo, left ventricular pressure (LVP), the maximal rate of LVP increase, LV end-diastolic pressure, the maximal rate of LVP decrease and heart rate were determined using a tip catheter 3 weeks after induction of MI. Compared to BNK rats, basal BK outflow was increased 30-fold in controls (p<0.01). In vivo, we found no significant differences between sham-ligated BNK and BNH rats in basal LV function. After MI, the impairment of LV function was significantly worse in BNK rats when compared to BNH rats. ACE inhibition significantly attenuated this LV dysfunction in both groups, when compared to untreated animals. Reduced basal BK level resulting from kininogen deficiency has no effect on basal LV function, but remains to be a risk factor for the ischemic heart. However, ACE inhibition is sufficient to improve LV function despite kininogen deficiency.


2019 ◽  
Author(s):  
Shuning Zhang ◽  
Xin Deng ◽  
Wenlong Yang ◽  
Liping Xia ◽  
Kang Yao ◽  
...  

Abstract Background: To detect the impact of loss of main diagonal branch (D) flow on cardiac function and clinical outcomes in patients with anterior ST-segment elevation myocardial infarction (STEMI).Methods: Patients with anterior STEMI undergoing primary percutaneous coronary intervention (PCI)at our clinic between October 2015 and October 2018were reviewed. Anterior STEMI due to left anterior descending artery (LAD) occlusion with or without loss of the main D flow (TIMI grade 0-1 or 2-3) was enrolled in the analysis. The short- and long-term incidence of major adverse cardiac events (MACEs, a composite of all-cause death, target vessel revascularization and reinfarction) and left ventricular ejection fraction (LVEF) were analyzed.Results: A total of 392 patients (mean age of 63.9years) with anterior STEMI treated with primary PCI was enrolled in the study. They were divided into two groups, loss (TIMI grade 0-1, n=69) and no loss (TIMI grade2-3, n=323) of D flow, before primary PCI. Compared with the group without loss of D flow, the group with loss of D flow showed a lower LVEF post PCI (41.0% vs. 48.8%, p=0.003). Meanwhile, loss of D flow resulted in the higher in-hospital, one-month, and 18-month incidence of MACEs, especially in all-cause mortality (all p<0.05). Landmark analysis further indicated that the significant differences in 18-month outcomes between the two groups mainly resulted from the differences during the hospitalization. In addition, multivariate Cox proportional hazards analysis found that D flow loss before primary PCI was independent factor predicting short- and long-term outcomes in patients with anterior STEMI.Conclusion: Loss of the main D flow in anterior STEMI patients was independently associated with the higher in-hospital incidences of MACEs and all-cause death as well as the lower LVEF.


2019 ◽  
Vol 8 (3) ◽  
pp. e000676 ◽  
Author(s):  
Paul Forsyth ◽  
Lynsey Moir ◽  
Iain Speirits ◽  
Steve McGlynn ◽  
Margaret Ryan ◽  
...  

Glasgow city has the highest cardiovascular disease (CVD) mortality rate in the UK. Patients with left ventricular systolic dysfunction after acute myocardial infarction represent a ‘high-risk’ cohort for adverse CVD outcomes. The optimisation of secondary prevention medication in this group is often suboptimal. Our aim was to improve the use and target dosing of ACE inhibitors (ACEI), angiotensin II receptor blockers (ARBs) and beta-blockers in such patients, through pharmacist-led clinics and cardiology multidisciplinary team collaboration. Retrospective audits characterised baseline care. Prospective pharmacist-led clinics were piloted and rolled out across seven hospitals and primary care localities over four Plan–Do–Study–Act cycles. ‘Hub’ and ‘spoke’ clinics utilised independent prescribing pharmacists with different levels of cardiology experience. Pharmacists were trained through a bespoke training programme—‘Teach and Treat’. Consultant cardiologists provided senior support and governance. Patients attending prospective pharmacist-led clinics were more likely to be prescribed an ACEI (or ARB) and beta-blocker (n=856/885 (97%) vs n=233/255 (91%), p<0.001 and n=813/885 (92%) vs n=224/255 (88%), p=0.048, respectively) and be on target dose of ACEI (or ARB) and beta-blocker (n=585/885 (66%) vs n=64/255 (25%), p<0.001 and n=218/885 (25%) vs n=17/255 (7%), p<0.001, respectively) compared with baseline. The mean dose of ACEI (or ARB) and beta-blocker was also higher (79% vs 48% of target dose, p<0.001% and 48% vs 33% of target dose, p<0.001, respectively) compared with baseline. Use of secondary prevention medication was significantly improved by pharmacist and cardiology collaboration. These improvements were sustained across a 4-year period, supported by a novel approach called ‘Teach and Treat’ which linked training to defined clinical service delivery. Further work is needed to assess the impact of the programme on long-term CVD outcomes.


Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Monique C de Waard ◽  
Dirk J Duncker

Introduction: Regular physical activity in patients with established coronary heart disease not only reduces the incidence of cardiac events, but also reduces the risk of all-cause mortality. Recently, we showed in mice that exercise training (EX) started immediately after myocardial infarction (MI) ameliorates left ventricular (LV) dysfunction. Here we tested the hypothesis that additional exercise training prior to an acute MI, i.e. a higher level of physical fitness at the time of MI, is associated with improved survival and attenuated LV dysfunction after MI. Methods and Results: MI was induced by permanent coronary ligation in 128 C57Bl/6 mice and subsequently followed by 8 weeks of voluntary wheel running (MI-EX) or sedentary housing (MI). In a third group, voluntary wheel running was started two weeks before induction of MI (EX-MI-EX). Sham operated mice served as controls. EX after MI had no effect on survival, infarct size, LV hypertrophy or dilation (Table ). However, EX improved LV function, reflected in enhanced LV fractional shortening (FS), rate of rise in LV pressure at 30 mmHg (LVdP/dt P30 ), and decreased pulmonary congestion and right ventricular weight (RVW). When EX was started prior to MI, post-MI survival nearly doubled and mice ran an average post-MI distance of ~7km/d compared to ~5km/d in MI-EX mice. Infarct cross-sectional area was larger, which was principally due to an increased infarct thickness (0.15±0.02mm EX-MI-EX vs 0.11±0.01mm MI; P =0.06). Surprisingly, however, LV hypertrophy and dysfunction were aggravated in the EX-MI-EX group compared to MI-EX. Conclusion: In line with our hypothesis, EX started prior to MI improved survival. However, contrary to our hypothesis, the improved survival was associated with a deterioration of LV dysfunction. The latter may have been the result of survival and hence inclusion of mice with the most severe LV dysfunction.


Author(s):  
Nabila Soufi Taleb Bendiab ◽  
Souhila Ouabdesselam ◽  
Latefa Henaoui ◽  
Marilucy Lopez-Sublet ◽  
Jean-Jacques Monsuez ◽  
...  

Background: Although the combination of high blood pressure (HBP) and type 2 diabetes (T2DM) increases the risk of left ventricular (LV) dysfunction, the impact of T2DM on LV geometry and subclinical dysfunction in hypertensive patients and normal ejection fraction (EF) has been infrequently evaluated. Methods: Hypertensive patients with or without T2DM underwent cardiac echocardiography coupled with LV global longitudinal strain (GLS) assessment. Results: Among 200 patients with HBP (mean age 61.7 ± 9.7 years) and EF > 55%, 93 had associated T2DM. Patients with T2DM had a higher body mass index (29.9 ± 5.1 kg/m2 vs. 29.3 ± 4.7 kg/m2, p = 0.025), higher BP levels (158 ± 23/95 ± 13 vs. 142 ± 33/87 ± 12 mmHg, p = 0.003), a higher LV mass index (115.8 ± 32.4 vs. 112.0 ± 24.7 g/m2, p = 0.004), and higher relative wall thickness (0.51 ± 0.16 vs. 0.46 ± 0.12, p = 0.0001). They had more frequently concentric remodeling (20.4% vs. 16.8%, p < 0.001), concentric hypertrophy (53.7% vs. 48.6%, p < 0.001), elevated filling pressures (25.8 vs. 12.1%, p = 0.0001), indexed left atrial volumes greater than 28 mL/m2 (17.2 vs. 11.2%, p = 0.001), and a reduced GLS less than −18% (74.2 vs. 47.7%, p < 0.0001). After adjustment for BP and BMI, T2DM remains an independent determinant factor for GLS decline (OR = 2.26, 95% CI 1.11–4.61, p = 0.023). Conclusions: Left ventricular geometry and subclinical LV function as assessed with GLS are more impaired in hypertensive patients with than without T2DM. Preventive approaches to control BMI and risk of T2DM in hypertensive patients should be emphasized.


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