Postinfarction Left Ventricular Ejection Fraction Research Articles

CCN family member 1 (CCN1) is an early marker of infarct size and left ventricular dysfunction in STEMI patients

Background and aimsCCN family member 1 (CCN1) has recently been proposed as a novel biomarker of myocardial injury, improving prediction of 30-day and one-year mortality following acute coronary syndromes. Among ST-elevation myocardial infarction (STEMI) patients, we evaluated the utility of CCN1 measured immediately before primary percutaneous coronary intervention (PPCI) as a predictor of two earlier endpoints: final myocardial infarct size and post-infarction left ventricular ejection fraction (LVEF). Furthermore, we evaluated the impact of CCN1 on the discriminatory power of the CADILLAC score. MethodsSTEMI patients were obtained from the SPUM-ACS cohort. Serum CCN1 was measured prior to PPCI. Linear regression assessed the association between CCN1, peak creatinine kinase (CK), and post-infarction LVEF. Cox models assessed an association between CCN1 and 30-day all-cause mortality. ResultsCCN1 was measured in 989 patients with a median value of 706.2 ng/l (IQR 434.3–1319.6). A significant correlation between CCN1, myocardial infarct size (peak CK) and LVEF was observed in univariate and multivariate analysis (both p < 0.001). Even among patients with normal classical cardiac biomarker levels at the time of PPCI, CCN1 correlated significantly with final infarct size. CCN1 significantly improved prediction of 30-day all-cause mortality by the CADILLAC score (C-index 0.864, likelihood-ratio chi-square test statistic 6.331, p = 0.012; IDI 0.026, p= 0.050). ConclusionsCompared with classical cardiac biomarkers, CCN1 is potentially the earliest predictor of final myocardial infarct size and post-infarction LVEF. CCN1 improved the discriminatory capacity of the CADILLAC score suggesting a potential role in the very-early risk stratification of STEMI patients.

Effect of COVID-19 on acute treatment of ST-segment elevation and Non-ST-segment elevation acute coronary syndrome in northwestern Switzerland.

BackgroundTo investigate the effect of the corona virus disease 2019 (COVID-19) pandemic on the acute treatment of patients with ST-segment elevation (STEMI) and Non-ST-segment elevation acute coronary syndrome (NSTE-ACS).MethodsWe retrospectively identified patients presenting to the emergency department (ED) with suspected ACS. We evaluated the number of percutaneous coronary interventions (PCIs) for STEMI, NSTE-ACS, and elective PCI cases. In STEMI patients, we assessed the time from chest pain onset (cpo) to ED presentation, post-infarction left ventricular ejection fraction (LVEF), and time from ED presentation to PCI. We directly compared cases from two time intervals: January/February 2020 versus March/April 2020 (defined as 2 months before and after the COVID-19 outbreak). In a secondary analysis, we directly compared cases from March/April 2020 with patients from the same time interval in 2019.ResultsFrom January to April 2020, 765 patients presented with acute chest pain to the ED. A dramatic reduction of ED presentations after compared to before the COVID-19 outbreak (31% relative reduction) was observed. Overall, 398 PCIs were performed, 220/398 PCIs (55.3%) before versus 178/398 PCIs (44.7%) after the outbreak. While numbers for NSTE-ACS and elective interventions declined by 21% and 31%, respectively, the number of STEMI cases remained stable. Time from cpo to ED presentation, post-infarction LVEF, and median door-to-balloon time remained unchanged.ConclusionsIn contrast to previous reports, our findings do not confirm the dramatic drop in STEMI cases and interventions in northwestern Switzerland as observed in other regions and hospitals around the world.

Coronary perivascular epicardial adipose tissue and major adverse cardiovascular events after ST segment-elevation myocardial infarction

Background and aimsPerivascular epicardial adipose tissue (pEAT) plays a key role in the progression of atherosclerosis, plaque rupture, and thrombosis. However, the relationship between pEAT and prognosis after revascularization of ST-segment elevation myocardial infarction (STEMI) is unknown. This study aimed to investigate the relationship between pEAT thickness and prognosis after STEMI. MethodsWe studied 180 STEMI patients (mean age 59.4 ± 13.3 years, 78.9% male) who underwent cardiac magnetic resonance (CMR) imaging within 1 week of prompt infarct-related artery revascularization and 52 age/sex/body mass index-matched controls (mean age 59.9 ± 13.5 years, 78.9% male). pEAT thickness indexed to body surface area at five locations, infarct size, left ventricular ejection fraction (LVEF), and coronary microvascular obstruction (MVO) were evaluated by CMR. Associations between pEAT index and 1-year composite major adverse cardiovascular events (MACE), infarct size, LVEF, and MVO were analyzed. ResultsMean pEAT indices were significantly higher in STEMI patients than controls. In STEMI patients, higher pEAT indices at the superior and inferior interventricular groove (SIVG and IIVG, respectively) were significantly associated with larger infarct size, higher prevalence of MVO, and inversely correlated with post-infarct LVEF. SIVG pEAT index was an independent predictor of composite MACE in post-STEMI patients with an odds ratio of 2.26 (95% confidence interval 1.63–3.13; p < 0.0001) after adjustment for age, sex, LVEF, and 2.71 (95% confidence interval 1.93–3.80; p < 0.0001) after adjustment for age, sex, previous myocardial infarction, diabetes mellitus, and renal function. ConclusionsSTEMI patients have significantly higher pEAT indices than controls. SIVG pEAT index independently predicts composite MACE in revascularized STEMI patients, underscoring the potentially prognostic value of this variable.

Detailed analysis of bone marrow from patients with ischemic heart disease and left ventricular dysfunction: BM CD34, CD11b, and clonogenic capacity as biomarkers for clinical outcomes.

Bone marrow (BM) cell therapy for ischemic heart disease (IHD) has shown mixed results. Before the full potency of BM cell therapy can be realized, it is essential to understand the BM niche after acute myocardial infarction (AMI). To study the BM composition in patients with IHD and severe left ventricular (LV) dysfunction. BM from 280 patients with IHD and LV dysfunction were analyzed for cell subsets by flow cytometry and colony assays. BM CD34(+) cell percentage was decreased 7 days after AMI (mean of 1.9% versus 2.3%-2.7% in other cohorts; P<0.05). BM-derived endothelial colonies were significantly decreased (P<0.05). Increased BM CD11b(+) cells associated with worse LV ejection fraction (LVEF) after AMI (P<0.05). Increased BM CD34(+) percentage associated with greater improvement in LVEF (+9.9% versus +2.3%; P=0.03, for patients with AMI and +6.6% versus -0.02%; P=0.021 for patients with chronic IHD). In addition, decreased BM CD34(+) percentage in patients with chronic IHD correlated with decrement in LVEF (-2.9% versus +0.7%; P=0.0355). In this study, we show a heterogeneous mixture of BM cell subsets, decreased endothelial colony capacity, a CD34+ cell nadir 7 days after AMI, a negative correlation between CD11b percentage and postinfarct LVEF, and positive correlation of CD34 percentage with change in LVEF after cell therapy. These results serve as a possible basis for the small clinical improvement seen in autologous BM cell therapy trials and support selection of potent cell subsets and reversal of comorbid BM impairment. http://www.clinicaltrials.gov. Unique identifiers: NCT00684021, NCT00684060, and NCT00824005.

Impact of the Prehospital Activation Strategy in Patients With ST-Elevation Myocardial Infarction Undergoing Primary Percutaneous Revascularization

The strategy of prehospital activation by the emergency medical system (EMS) in patients with ST-elevation myocardial infarction (STEMI) has been poorly adopted among the US hospitals that currently offer 24/7 primary percutaneous coronary intervention. In this study, we report a single center experience after the implementation of this strategy. From 2008 to 2011, we identified a total 188 STEMI patients (age 65 ± 15 years) presenting via EMS for primary percutaneous coronary intervention. Of these, 112 (59.6%) underwent prehospital activation (EMS group), whereas the remaining 76 (40.4%) underwent emergency department activation [emergency department (ED) group]. Baseline demographic characteristics were similar between both groups. The overall median door-to-balloon (DTB) time was 49 ± 14 minutes. Patients undergoing prehospital activation had on average significantly lower overall DTB times (EMS 44 ± 11 minutes vs. ED 57 ± 15 minutes; P < 0.001). Concordantly, DTB times <60 minutes were much more commonly achieved with this strategy (EMS 95.5% vs. ED 64.5%; P < 0.001). Fallouts beyond the recommended 90-minute DTB time were seen among ED patients only. No difference in in-hospital death (EMS 5.4% vs. ED 6.6%; P = 0.75) or cumulative 30-day mortality (EMS 6.3% vs. ED 7.9%; P = 0.68) was observed between both groups. However, on average, EMS patients had higher postinfarct left ventricular ejection fraction (EMS 48 ± 9.5% vs. ED 39 ± 14.6%; P = 0.004). Differences in DTB time and left ventricular ejection fraction remained significant after adjusting for differences in baseline characteristics. In conclusion, the prehospital activation strategy is largely effective and should be systematically adopted in the treatment scheme of STEMI patients to lower mechanical reperfusion times and reduce the potential for untoward clinical outcomes.

Intracoronary infusion of bone marrow-derived mononuclear cells contributes to longstanding improvements of left ventricular performance and remodelling after acute myocardial infarction: A meta-analysis

Conflicting results exist now on the sustained effects of intracoronary bone marrow-derived mononuclear cells (BMMNCs) infusion in patients with acute myocardial infarction (AMI). Systematical literature search of PubMed, ISI Web of Science, and Cochrane databases was conducted. We included the randomised controlled trials with at least 12-month follow-up data for AMI patients receiving primary percutaneous coronary intervention in addition to intracoronary BMMNCs transfer or not (the control). Summary statistics were calculated using random-effects models. A total of 10 trials with 757 patients were available for analysis. The pooled statistics showed intracoronary administration of BMMNCs significantly improved post-infarction left ventricular ejection fraction (weight mean differences [WMD]=4.04%, 95% confidence intervals [CI], 3.01-5.07%; p<0.01), and attenuated the enlargement of left ventricular end-diastolic volume (WMD=-6.13 ml, 95%CI, -10.56 ml to -1.69 ml; p=0.007) as well as infarct size (WMD=-2.47%, 95%CI, -3.79% to -1.15%; p=0.0002). However, for the major adverse clinical events (MACEs), there appeared to be neutral results (between-group differences of p>0.10). Intracoronary BMMNCs infusion leads to longstanding and moderate improvements of post-infarction left ventricular performance as well as remodelling. Meanwhile, the procedure did not increase the risk of MACEs.

Impact of ischemic time on post-infarction left ventricular function in ST-elevation myocardial infarction treated with primary percutaneous coronary intervention

BackgroundMyocardial necrosis is a time-dependent event. Nevertheless, clinical studies on association between ischemic time and left ventricle function showed inconsistent findings. Aim of current study is to evaluate the association between ischemic time and the post-infarction left ventricular function in ST-elevation myocardial infarction treated with primary PCI. MethodsIn 2529 patients treated with primary PCI, left ventricular ejection fraction (LVEF) was measured before discharge (median day 4) by radionuclide ventriculography or by echocardiography if patients had atrial fibrillation. Ischemic time was calculated from symptom onset to first balloon inflation. ResultsThe correlation between ischemic time as continuous variable and LVEF was significant but weak (P=0.002, r=−0.062). The LVEF of patients in ischemic time intervals of >6, >3–6, and ≤3h was 45.1±11.7%, 44.6±11.9%, and 43.2±12.2%, respectively (P=0.029). Adjusted odds ratio of the ischemic time intervals for LVEF<40% was 1.14 (95% CI 1.00–1.30). TIMI flow 0 before and TIMI flow 3 after PCI were related with both longer ischemic time and low LVEF. ConclusionIschemic time was associated with post infarction LVEF in patients treated with primary PCI, although this association was weak. Initial TIMI flow and post-PCI TIMI flow played important role in impact of the ischemic time on the LVEF.

The 30-Year Outcome for Patients After Myocardial Infarction Due to Coronary Artery Lesions Caused By Kawasaki Disease

This study determined the long-term outcome for patients after myocardial infarction (MI) due to Kawasaki disease (KD). Retrospective analysis was performed for 60 patients who had experienced MI between 1976 and 2007. Their ages at the initial MI ranged from 3 months to 33 years (median, 2 years). The maximum follow-up period after the initial MI was 33 years (median, 16 years). Coronary angiography, left ventriculography, and radioisotope myocardial perfusion imaging (MPI) had been performed for 56 patients more than 2 months after MI when all were in stable condition. The survival rate and ventricular tachycardia (VT)-free survival rate were calculated after the initial MI by the Kaplan-Meier method. Both sustained and nonsustained VT were included. Furthermore, the Cox proportional hazards model was used to analyze which factors influenced the post-MI outcome and which influenced the appearance of VT. The 30-year survival rate was 62.7% (95% confidence interval [CI], 44.6-77.9%), and the 25-year VT-free survival rate after MI was 28.5% (95% CI 15.4-46.5%). The postinfarction left ventricular ejection fraction (LVEF) was related to the outcome in this population (hazard ratio 0.86; 95% CI 0.75-0.95; P = 0.002), whereas the development of VT was related to the post-LVEF and to perfusion abnormalities in MPI (P = 0.0002). The 30-year survival rate after MI was poor for the patients with a low LVEF. With aging, the existence of nonviable myocardium in the infarct area can induce fatal ventricular arrhythmia more than 10 years after the original MI.

Three-Year Experience of Primary Percutaneous Coronary Intervention for Acute ST-Segment Elevation Myocardial Infarction in a Hospital without On-site Cardiac Surgery

Introduction: Primary percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI) in hospitals without on-site cardiac surgery capability, despite receiving only a class IIb recommendation in the ACC/AHA practice guidelines, can be per-formed effectively and safely. We reviewed the first 3 years of our experience. Materials and Methods: This is a retrospective single centre review of all patients receiving primary PCI for STEMI between 2003 and 2005. Demographic, procedural and outcome data were analysed. Results: There were 259 patients who underwent primary PCI. The mean age was 55.3 ± 12.3 years. Median door-to-balloon time was 97.5 minutes and 45.2% and 52.9% had anterior and inferior STEMI, respectively. The majority of patients presented with Killip class I (87.6%); however, 5.8% were in Killip class IV. Single vessel disease was found in 47.1%. Angiographic PCI success (defined as residual stenosis &lt;50% with TIMI 3 flow) was achieved in 89.1%. Usage of stents, distal protection and aspiration devices were 97.2%, 27.8% and 34.1 %, respectively; 9.3% required intra-aortic balloon pump insertion. No patients required transfer for emergency coronary bypass surgery as a result of PCI complications. Post-PCI ST resolution &gt;50% was achieved in 80.6%. The mean post-infarct left ventricular ejection fraction was 44.1%. In-hospital, 30-day, 6-month and 1-year mortality rates were 2%, 2.8%, 4.0% and 4.8%, respectively. Clini-cally driven target lesion revascularisation rate was 2.8% at 1 year. Conclusions: Our results are comparable to those from on-site surgical centres. This supports the feasibility and safety of primary PCI in cardiac centres without on-site cardiac surgery. Key words: Emergency, PCI, STEMI, Transfer

Symptom-to-door time in ST segment elevation myocardial infarction: Overemphasized or overlooked? Results from the AMI-McGill study

Ischemic time is a major determinant of infarct size in ST segment elevation myocardial infarction (STEMI). Emphasis is placed on reducing the door-to-reperfusion therapy time component, whereas the symptom-to-door time is often overlooked. To correlate the symptom-to-door time with left ventricular ejection fraction (LVEF) in patients with STEMI. Acute Myocardial Infarction (AMI)-McGill was a cohort study of consecutive patients with STEMI who presented to three adult university hospitals. Multivariate linear regression was performed to correlate the symptom-to-door time with postinfarction LVEF adjusted for reperfusion method, prior myocardial infarction and components of the Thrombolysis In Myocardial Infarction (TIMI) risk score. There were 188 patients, with a mean age of 66 years. On arrival to hospital, 23% of patients were in Killip class II to IV and 87% received reperfusion therapy (20% fibrinolytic therapy and 67% primary percutaneous coronary intervention). The median symptom-to-door time was 120 min (first quartile: 60 min, third quartile: 290 min) and the median door-to-reperfusion therapy time was 93 min (first quartile: 54 min, third quartile: 155 min). Three variables were independently correlated with LVEF in the study's regression model: symptom-to-door time (beta: -0.66, 95% CI -1.18 to -0.14; P=0.01), Killip class II to IV on arrival (beta: -6.43, 95% CI -11.87 to -0.99; P=0.02) and anterior territory of the infarction (beta: -5.86, 95% CI -10.55 to -1.18; P=0.02). Symptom-to-door time was negatively correlated with postinfarction LVEF in patients with STEMI. Strategies to shorten this delay, such as educating high-risk patients about the symptoms of AMI, should be considered.

The effect of granulocyte colony stimulating factor on regional and global myocardial function in the porcine infarct model

Background Stem cell therapy has been shown to attenuate the reduction of left ventricular function following myocardial infarction. Most studies have utilized either a direct injection or intra-coronary infusion of cells, but cytokine mobilization of stem cells in the murine model of acute myocardial infarction has been reported to induce similar improvement in cardiac function. Methods An antero-apical infarction was induced in swine by balloon occlusion, followed by the daily administration of granulocyte colony stimulating factor (G-CSF) or placebo for 5 days. We used left ventricular angiograms and 2D echocardiograms to assess global function, and 3D echocardiograms to assess regional function prior to infarction, immediately following infarction, and at 8 weeks. Histologic evaluation was performed after sacrifice at 8 weeks. Results There was no significant difference in early or late post-infarction left ventricular ejection fraction or in myocardial histology between the two groups. Following G-CSF therapy, however, 3D echocardiography demonstrated that the regional ejection fractions of the infarcted segments showed a 50.3% improvement in the G-CSF pigs compared to a 7.4% deterioration in the untreated pigs ( p = 0.005). Conclusions Global left ventricular ejection fraction remained unchanged, and there is no histologic evidence for infarct attenuation following G-CSF infusion in the porcine infarct–reperfusion model. There was recovery of regional function in the infarcted segment in the G-CSF pigs. These data suggest that bone marrow mobilization in larger species has limited potential as a therapy designed to replace infarcted myocardium or to improve overall cardiac function, although further studies are needed to examine regional effect in the infarct area.

Dyslipidemias Have a Detrimental Effect on Left Ventricular Systolic Function in Patients With a First Acute Myocardial Infarction

Several large-scale clinical trials have shown that lipid-lowering interventions are associated with reduced coronary events and mortality. However, whether dyslipidemias have a detrimental effect on the evolution of myocardial infarction (MI) is still unknown. To examine whether dyslipidemias can aggravate myocardial vulnerability following MI, 165 patients with a first MI were studied. All patients underwent measurements of serum lipid profiles 1 week and 3 months after MI, a radionuclide ventriculographic study, and a coronary angiographic study. The patients were divided into 3 groups according to their 3-month serum cholesterol levels (group 1, <200 mg/dl; group 2, 200 to 240 mg/dl; group 3, >240 mg/dl). Groups 1, 2, and 3 consisted of 66, 59, and 40 patients, respectively. Group 3 had a higher Gensini score than groups 1 and 2, although this was not statistically significant (p = 0.13). The postinfarct left ventricular ejection fraction (LVEF) was highest in group 1 (53 ± 13%), at mid level in group 2 (43 ± 14%), and lowest in group 3 (35 ± 11%) (p <0.0001). A significant negative correlation between 3-month low-density lipoprotein (LDL) cholesterol (r = −0.55, p <0.0001) and the postinfarct LVEF was found. The product of peak creatine kinase (CK MAX) and time to CK MAX (p = 0.001), and patency of the infarct-related artery (p = 0.009), rather than variables of coronary atherosclerosis, were also independent predictors of the postinfarct LVEF. Increases in 1-week LDL cholesterol and decreases in 1-week high-density lipoprotein cholesterol were associated with a higher CK MAX and a lower patency rate of the infarct-related artery, respectively. This study revealed that dyslipidemias per se, especially LDL cholesterol, had a detrimental effect on the postinfarct LVEF; this effect might be independent of the atherogenic properties of dyslipidemias.

Clinical characteristics of nonfatal myocardial infarction among individuals on prophylactic low-dose aspirin therapy.

The influence of prophylactic low-dose aspirin on the clinical characteristics of subsequent nonfatal myocardial infarction was examined in the Physicians' Health Study, a randomized, double-blind placebo-controlled trial of alternate-day aspirin (325 mg) among 22,071 US male physicians. During 60.2 months of follow-up, 342 incident cases of nonfatal myocardial infarction were confirmed (95.2% of all reports): 129 on aspirin and 213 on placebo (p less than 0.00001). Despite this statistically extreme reduction in occurrence of a first nonfatal infarction attributable to aspirin, there were no significant differences in the size, location, electrocardiographic features, or postinfarction left ventricular ejection fraction between the aspirin and placebo groups. Furthermore, among those undergoing angiography, there were no differences in the distribution or number of coronary vessels obstructed. These data indicate that chronic platelet inhibition with alternate-day aspirin therapy reduces the risk of a first myocardial infarction but does not appear to have a significant effect on the clinical characteristics of events that are survived. This finding may result from a direct effect of aspirin or from an aspirin-induced shift in infarction severity. Regardless of mechanism, these clinical observations suggest that treatment decisions for acute infarction patients should be made independently of a history of aspirin use.

Prognostic significance of left ventricular ejection fraction after acute myocardial infarction. A bedside radionuclide study.

The prognostic significance of left ventricular ejection fraction measurements obtained at the bedside was assessed in 171 patients as soon as possible after acute myocardial infarction. Ejection fraction was measured with a radionuclide first pass portable probe method within a mean of 24 hours of the onset of major symptoms. The results were related prospectively to the subsequent incidence of ventricular fibrillation in hospital, and to hospital and postdischarge deaths in a mean follow up period of 15 (range 9-21) months. All eight episodes of primary ventricular fibrillation, all 12 deaths due to pump failure in hospital, and also 12 out of 13 postdischarge deaths occurred in that minority of 81 patients whose initial postinfarction left ventricular ejection fraction was less than 0.35. Multivariate correlation with clinical, enzymatic, and electrocardiographic indicators of myocardial infarction showed that the prognostic significance of these indicators could largely be explained by their association with low left ventricular ejection fractions. Left ventricular ejection fraction measured within the initial 24 hours after acute myocardial infarction predicts prognosis throughout the subsequent year.