Post Infarction Research Articles

196 A Significant Proportion of Post-infarct VT is Unrelated to Acute Myocardial Scar

Ventricular tachycardia (VT) is a leading cause of sudden cardiac death post ST elevation myocardial infarction (STEMI). Guidelines dictate evaluating ejection fraction 40 days post coronary re-vascularisation for risk stratification. VT in chronic ischaemic cardiomyopathy is almost exclusively from myocardial scar related re-entry, however VT immediately post STEMI is not as well understood. We retrospectively studied 46 patients who presented to Westmead Hospital with STEMI (2014-2019), a left ventricular ejection fraction (LVEF) <40%, and inducible VT on electrophysiology study (EPS). 12-lead ECGs of the induced VTs were comprehensively analysed and compared to scar location determined by regional wall abnormality on gated heart pool scan (GHPS). These were plotted on a 17-segment model of the LV. The study included 46 patients (male =37, female =9) with an average age 60.6 (33-80). The mean time from STEMI to EPS was 12.0 days (4-36), and average LVEF was 30.2%. The average VT cycle length and extra stimuli required were 221.8 and 3.2 respectively. Of the 50 VTs analysed, 18 (36%) did not match the GHPS determined scar site. Of these, 7 (39%) were within 1 segment of scar-border, 2 (11%) were within 2 segments. 9 (50%) were deemed completely remote. 32 (64%) VTs arose from within the scar-border. Whilst acute ischaemic scar related re-entry may still explain the majority of inducible VT post STEMI, a significant proportion may be due to remote automaticity, which may be a target for acute catheter ablation.

Value of Brain Computed Tomographic Angiography to Predict Post Thrombectomy Final Infarct Size and Clinical Outcome in Acute Ischemic Stroke.

Aims:This study aims to analyze the predictor in preoperative brain computed tomographic angiography (CTA) for final infarct and outcome in postendovascular thrombectomy patient.Subjects and Methods:52 patients were retrospectively reviewed. The Alberta Stroke Program Early Computed Tomography Score (ASPECTS) comparison between preoperative noncontrast computed tomography (NCCT) and 24-h NCCT as well as preoperative CTA source image (CTA-SI) and 24-h NCCT were performed. Factors associated with increased ASPECTS and clinical outcome were evaluated.Results:Preoperative NCCT ASPECTS = 24-h NCCT in 23%. Whereas, 46% showed preoperative CTA-SI ASPECTS = 24-h NCCT. Moreover, 40.4% showed 24-h NCCT ASPECTS > preoperative CTA-SI (increased ASPECTS). The two significant factors associated with increased ASPECTS are thrombolysis in cerebral infarct score 2b/3 (P = 0.02) and good collateral status (P = 0.02). Finally, good clinical outcome was associated with age <60 (P = 0.04), preoperative CTA-SI ASPECTS >5 (P = 0.01), good collaterals status (P = 0.02), and increased ASPECTS (P = 0.05).Conclusions:Preoperative brain CTA provided the necessary factors that are associated with good clinical outcomes, which are CTA-SI ASPECTS > 5, good collateral status, and increased ASPECTS.

EXTRACORPOREAL MEMBRANE OXYGENATION AS A BRIDGE FOR DELAYED CLOSURE OF VENTRICULAR SEPTAL RUPTURE

SESSION TITLE: Wednesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/23/2019 09:45 AM - 10:45 AM INTRODUCTION: Ventricular septal rupture (VSR) is a rare complication of myocardial infarction often seen three to five days after an acute myocardial infarction. Presentation typically includes hypotension and cardiogenic shock with resultant multi-organ failure, biventricular failure and new murmur. While delayed repair is associated with decreased mortality, there is no consensus on appropriate timing. The use of Extracorporeal Membrane oxygenation (ECMO) provides hemodynamic stabilization thus allowing for delayed repair. We report a case of 59 yo female who presented with post myocardial infarction VSR and was stabilized on ECMO for 13 days for delayed repair. CASE PRESENTATION: A 59 yo female with medical history of osteoarthritis and tobacco abuse was transferred to our facility for substernal chest pressure and anterior STEMI after presenting to an outlying facility with complaints of hematuria, nausea and vomiting. She received treatment with therapeutic lovenox, aspirin, atorvastatin and Plavix en route to our facility. Labs were significant for troponin of 2.2 peaking at 11.485, lactic acid 7.4, creatinine of 2.3, leukocytosis of 27 and hyponatremia with sodium of 124, ALT 1006, AST 2628. Transthoracic echocardiogram showed a ventricular septal rupture (VSR). Emergent cardiac catherization showed severe two vessel disease with 100% stenosis of the mid LAD and 90% stenosis of the mid R coronary artery with a 90% stenosis of the mid R posterior descending artery. Given the severity of her coronary artery disease and cardiogenic shock, an intraortic balloon pump was placed for hemodynamic support. Emergent surgical repair of the ventricular septal rupture was decided against due to her severe morbidity and high risk of mortality. VA ECMO was initiated, resulting in normalization of her lactate, renal function and transaminases. Her clinical course was complicated by bleeding gastric ulcers and an ischemic LLE requiring below the knee guillotine amputation. She was transfused per protocol and multiple endoscopic interventions failed to control her gastrointestinal bleeding. Coronary artery bypass graft and ventricular septal repair surgery was delayed due to her new complications. Her family decided to pursue comfort care with her worsening GI bleed and need for hip disarticulation stemming from her worsening limb ischemia. DISCUSSION: VSR is a rare complication of myocardial infarction with a 1-2% incidence in patients presenting with an acute myocardial infarction. Delaying repair which allows for adequate healing of the infarct and subsequent strengthening and scarring of the tissue for suture anchoring and is associated with a 20% mortality rate as compared to 50% mortality rate in immediate repair. CONCLUSIONS: ECMO should be offered to select patients with post myocardial infarction VSR to improve surgical outcomes. Reference #1: Serpytis P; Karvelyte N; Serpytis R; Kalinauskas G; Rucinskas K; Samalavicius R; Ivaska J; Glaveckaite S; Berukstis E; Tubaro M; Alpert JS; Laucevičius A Post-infarction ventricular septal defect: risk factors and early outcomes. Hellenic J Cardiol. 2015; 56(1):66-71 DISCLOSURES: No relevant relationships by Eugene Quaye, source=Web Response

Endothelial function, systemic inflammation and cardiac hemodynamics in different age patients with post infarction chronic heart failure.

Endothelial function, systemic inflammation and cardiac hemodynamics in different age patients with post infarction chronic heart failure.

P778Valsartan reduces level of soluble ST2 and left ventricle remodeling in patients with dual chamber pacemaker

Abstract Introduction Permanent right ventricle pacing leads to left ventricle remodeling, its systolic dysfunction and symptomatic heart failure in the long run. Valsartan is well known for its preventive anti-remodeling function in the post infarction heart remodeling. Objectives To assess the effect of valsartan on left ventricle remodeling in patients with second and third degree atrioventricular block with first-time implantation of dual chamber pacemaker. Methods This was a randomized, double-blind, placebo controlled single center study. One hundred eligible patients were assigned in a 1:1:1 fashion to receive placebo, valsartan 80mg or 160mg once daily, respectively. Echocardiographic assessment of left ventricle geometry, its systolic and diastolic function was performed at baseline and at twelve months. One patient from placebo group suffered stroke. We present the baseline date for 100 enrolled patients and follow-up data for 88 patients who have completed the study. Data in valsartan arms are pooled in one group. Concentration of soluble ST2 was measured in duplicates with Aspect Reader (Critical Diagnostics). Results Results are presented in table. Data are presented as mean and standard deviation. Table 1 Placebo (n=28) Valsartan (n=60) ANOVA Baseline 12 mths Baseline 12 mths sST2, ng/mL 36.0±16.0 39.4±15.3 35.1±15.2 19.9±6.5 0.01 LVEF, % 60±8 55±9 60±8 58±8 0.01 LVEDD, mm 48±5 50±4 48±6 49±5 NS LVESD, mm 29±4 32±5 29±5 31±4 NS LVEDV, mL 79±12 84±13 80±12 81±13 NS LVESV, mL 32±5 38±7 31±5 34±6 0.01 E/A 0.94±0.12 0.92±0.13 0.94±0.15 0.95±0.15 NS DecT, ms 211±38 226±43 223±45 218±37 0.01 IVRT, ms 98±14 108±17 101±17 99±18 0.01 Conclusion Valsartan has protective effect of left ventricle remodeling and function. It may be useful in prevention of pacing induced heart failure. Decrease in soluble ST2 concentration may help explain the alternative mechanism for protective role of valsartan. (NCT01805804)

Longitudinal Outcomes After Surgical Repair of Postinfarction Ventricular Septal Defect in the Medicare Population

Patients undergoing post infarction ventricular septal defect repair are at high risk for early morbidity and mortality, but little is known about subsequent clinical events. This study uses short-term clinical data from The Society of Thoracic Surgeons National Database linked with Medicare data to examine longer term outcomes in these patients. This was a retrospective review of The Society of Thoracic Surgeons National Database to link with Medicare data all adults (≥65 years) who underwent ventricular septal defect repair after a myocardial infarction between 2008 and 2012. The primary outcome was 1-year mortality. Risk factors for 1-year survival were modeled using a multivariable Cox regression. Five hundred thirty-seven patients were identified using The Society of Thoracic Surgeons database and Medicare linkage. Median age was 74 years, and 277 patients (52%) were men. One hundred ninety-two patients (36%) were supported preoperatively with an intraaortic balloon pump. Surgical status was emergent or salvage in 138 (26%), and 158 patients (29%) died within 30 days and 207 (39%) within 1 year. Among patients who survived to hospital discharge, 44% were discharged to a facility and 172 (32%) experienced at least 1 all-cause readmission within 1 year. Unadjusted 1-year mortality rates were 13% for elective patients and 69% for emergency status (P < .01). On multivariable analysis emergency/salvage status, older age, and concomitant coronary artery bypass grafting were independently associated with worse 1-year survival. These data suggest the greatest mortality risk in this patient population occurs in the first 30 days. Emergency or salvage status strongly predicts 1-year mortality. Optimizing physiologic derangements before operative repair may be considered when possible in this subgroup of patients.

CORRELATION BETWEEN SERUM LEVEL GALECTIN-3 AND EARLY REMODELLING INDICATOR OF LEFT VENTRICLE IN PATIENT WITH ACUTE MYOCARDIAL INFARCTION DURING PRE-PERCUTANEOUS CORONARY INTERVENTION

Background: Coronary heart disease (CHD) is a leading cause of death worldwide. Acute coronary syndrome (ACS) is a spectrum of CHD. Left ventricle remodelling is one of the complication with the bad outcome either short-term or long term. Early remodelling process (within 0-72 hours) post infarction can be assessed by circulating biomarker (Galectin-3), echocardiography, coronary angiography, and clinically.&#x0D; Objective: The aim of study is to know the correlation between serum level of Galectin-3 and early remodelling indicator in patient with acute myocardial infarction during pre-percutaneous coronary intervention. The parameters are LVEDV, LVEF, diastolic function component, TIMI flow, MBG, and presence of acute heart failure.&#x0D; Materials and Methods: This cross sectional study was conducted in Sanglah General Hospital during March-May 2018. A 62 sample was determined consecutively.&#x0D; Results: Bivariate analysis with Spearman correlation shows Galectin-3 correlated with LVEDV (r = 0,808; p= 0,000), E/e’ average (r = 0,297; p = 0,019), E/A ratio (r = 0,261; p= 0,041), and MBG (QuBE) (r = 0,647; p = 0,000). No correlation was found between Galectin-3 and LVEF Teich (r = -0,213; p= 0,097), LVEF Biplane (r = -0,226; p = 0,077), LAVI (r = 0,301; p = 0,170), e’septal (r = -0,079; p = 0,539), e’lateral (r = -0,092; p = 0,476), and TR Vmax (r=0,068; p=0,600). Chi square analysis shows no association between Galectin-3 and diastolic dysfunction left ventricle (OR= 1,032, p= 0,966, CI95%= 0,239-4,462), TIMI flow (OR= 1,032, p= 0,966, CI95%= 0,239-4,462), MBG score (OR= 0,264, p= 0,197, CI95%= 0,031-2,259), and acute heart failure (OR=0,577, p= 0,476, CI95%= 0,127-2,617). Multivariat analysis with multiple linear regression shows an increase in Galectin-3 has been proven associated independently with LVEDV, LAVI, E/e’ average, and E/A ratio. Multiple logistic regression shows Galectin-3 has not been proven independently with diastolic dysfunction, TIMI flow, MBG score, and acute heart failure. LVEDV is the best outcome that can be explained as its value influenced by constant, BMI, and Galectin-3 (R2 = 0,509).&#x0D; Conclusion: Galectin-3 correlated with LVEDV, average E/e’, E/A ratio, and MBG (QuBE). There is an independent association between Galectin-3 and LVEDV, LAVI, average E/e, and E/A ratio. Early remodelling process within 0-72 hours post infarction was happened pre-PCI. Anti-remodelling (including anti failure) during early phase is strongly recommended in order to prevent worse outcome in short and long term.&#x0D; Keywords: Galectin-3, early remodelling left ventricle, acute myocardial infarction, percutaneous coronary intervention.

Abstract 404: Deterministic Paracrine Repair of Injured Myocardium using Microfluidic Cocooning of Heart Explant-Derived Cells

Previous work has shown that cocooning heart explant-derived cells (EDCs) within protective nanoporous gel capsules before intra-myocardial injection increases the retention of transplanted cells and the paracrine production of nanoparticles to improve post infarct cardiac function. In this study, we investigated the influence of cocoon size and intracapsular cell number on cell-treatment outcomes using a newly developed microfluidic-based (MF) cellular cocooning platform. Methods/Results: Traditional vortex-based encapsulation (Vx) inherently provides cocoons of varying diameters (30-100 μm; 68±5 μm). By altering the flow pressure ratios and the nozzle diameters within the MF chip, we encapsulated human EDCs within small (51±1 μm, MF50) and large (90±1 μm, MF90) diameter nanoporous gel cocoons for comparison with standard Vx-defined capsules (71±1 μm, MF70). MF cocooning mirrored the expected Poisson distribution with smaller cocoons having a greater proportion of single cells while larger diameter cocoons contained greater proportions of multicellular aggregates. Immunodeficient mice underwent left coronary artery ligation 1 week before randomization to echocardiographic guided intra-myocardial injection of EDCs (suspended or variable diameter cocoons) or vehicle. Increasing cocoon diameter stimulated progressive salutary effects on post-infarct function (ejection fraction), scar burden and newly generated peri-infarct blood vessels (isolectin B4+) and cardiomyocytes (BrdU+/TNT+) 4 weeks after treatment. Bioluminescent imaging of luciferase tagged cells revealed increasing cocoon diameter reduced the rate of cell clearance from injured tissues. Disrupting cell-cell contact within the capsules (using a custom antibody cocktail to block E/P-selectin and N-cadherin) reduced the amount and profile of pro-healing cytokines + nanoparticles delivered to injured myocardium. Conclusions: Increasing cocoon diameter and cell occupancy within protective nanoporous gel cocoons boosts paracrine-mediated repair of damaged myocardium by slowing clearance of cells from injured tissues and the number of cytokines + nanoparticles secreted by micro-encapsulated cells.

RETRACTED: Rheumatoid arthritis (RA) and cardiovascular disease.

Abstract Patients with rheumatoid arthritis (RA) suffer cardiovascular events 1.5-2 fold than the general population, and cardiovascular (CV) events are leading cause of death in patients with RA. It is known that patients with RA have endothelial dysfunction, related with impaired function of endothelial progenitor cells (EPCs). The mechanistic pathways leading to endothelial function are complicated, but understanding these mechanisms may open new frontiers of management and therapies to patients suffering from atherosclerosis. Inflammation is a key factor in atherosclerosis, including endothelial function, plaque stabilization and post infarct remodeling; thus, inhibition of TNF-α may affect the inflammatory burden and plaque vulnerability leading to less cardiovascular events and myocardial infarctions. An aggressive management of inflammation may lead to a significant improvement in the clinical cardiovascular outcome of patients with RA. The clinical evidence that showed a reduced risk of CV events following treatment with anti-inflammatory agents may suggest a new approach to treat atherosclerosis, i.e., inhibition of inflammation using biological medications that were primarily aimed to treat the high scale inflammation of RA and other autoimmune-inflammatory diseases, but may be useful also to prevent progression of atherosclerosis.

Rheumatoid arthritis (RA) and cardiovascular disease.

Patients with rheumatoid arthritis (RA) suffer cardiovascular events 1.5-2 fold than the general population, and cardiovascular (CV) events are leading cause of death in patients with RA. It is known that patients with RA have endothelial dysfunction, related with impaired function of endothelial progenitor cells (EPCs). The mechanistic pathways leading to endothelial function are complicated, but understanding these mechanisms may open new frontiers of management and therapies to patients suffering from atherosclerosis. Inflammation is a key factor in atherosclerosis, including endothelial function, plaque stabilization and post infarct remodeling; thus, inhibition of TNF-α may affect the inflammatory burden and plaque vulnerability leading to less cardiovascular events and myocardial infarctions. An aggressive management of inflammation may lead to a significant improvement in the clinical cardiovascular outcome of patients with RA. The clinical evidence that showed a reduced risk of CV events following treatment with anti-inflammatory agents may suggest a new approach to treat atherosclerosis, i.e., inhibition of inflammation using biological medications that were primarily aimed to treat the high scale inflammation of RA and other autoimmune-inflammatory diseases, but may be useful also to prevent progression of atherosclerosis.

Early thrombolysis is associated with decreased operative mortality in postinfarction ventricular septal rupture

BackgroundPost myocardial infarction ventricular septal rupture (PMI-VSR) is a dreaded mechanical complication of acute coronary syndromes. Given that surgical mortality approaches 50%, it is pragmatic that the risk factors for mortality and outcomes after surgical correction of PMI- VSR are carefully scrutinized. MethodsWe performed a single-center, retrospective cohort study of 35 patients presenting for surgical closure of post myocardial infarction ventricular septal rupture over six years. We reviewed patient characteristics, clinical, echocardiographic, angiographic and perioperative risk factors which may affect mortality after surgical repair of PMIVSR and 30 day and one year mortality rates of these patients. Univariate and multivariate logistic and cox proportional hazard regression analysis was used to identify predictors of operative and overall mortality. Long term survival was presented with Kaplan-Meier Survival Curve. ResultsSixteen patients (46%) were in cardiogenic shock. Concomitant coronary artery bypass grafting (CABG) was done in 22 patients (63%) but did not influence survival. Preoperative thrombolysis was done in 12 patients (34%) out of which 10 (53%) survived Operative mortality was 46% and one-year mortality was 49%. Multivariate analysis identified preoperative thrombolysis: Hazards ratio, 0.12; 95% CI, 0.02-0.61; p value of 0.01, as significant independent predictor of survival in PMIVSR cohort. ConclusionsPreoperative thrombolysis is associated with decreased odds of operative and overall mortality after surgical repair in PMIVSR patients.

Monocyte-platelet aggregates affect local inflammation in patients with acute myocardial infarction

The local inflammatory response following acute myocardial infarction (AMI) is increasingly being recognized as a central factor determining infarct healing. Myocardial inflammation can be visualized in patients using fasting 18F-FDG PET/MRI. Although this novel biosignal correlates with long-term functional outcome, the corresponding cellular substrate is not well understood. Here we present a retrospective analysis of 29 patients with AMI who underwent revascularization, suggesting a connection between post infarction myocardial fasting 18F-FDG uptake, monocyte platelet aggregates (MPA), and P2Y12 inhibition. In detail, patients with high MPA percentages of CD14highCD16+ and CD14lowCD16+ monocytes had significantly higher local 18F-FDG uptake (SUVmean) in the infarcted myocardium than patients with low MPA (p < 0.05). Furthermore, there was an association of high MPA percentage in all monocyte subpopulations with deteriorating ΔLV-EF after 6 months (p < 0.01), which was confirmed in an extended analysis with additional 29 patients without PET/MRI data available. In this analysis, administration of Ticagrelor was associated with lower MPA percentage of CD14high monocyte subpopulations than Clopidogrel (p < 0.01) or Prasugrel (p < 0.05).Taken together, the findings from this analysis suggest that platelet aggregability may affect monocyte extravasation into the infarcted myocardium and influence long-term functional outcome. P2Y12 inhibition may intervene in this pathophysiologic process. Prospective studies are needed to further examine this important relationship.

Long-term outcome of catheter ablation in post-infarction recurrent ventricular tachycardia

Objectives. Severe LV dysfunction and advanced age are associated with VT recurrence after catheter ablation in patients with post-infarction drug-refractory VT. We present retrospective analysis of long-term outcome after single and repeat VT ablation procedures in patients with ischemic heart disease. Design. Patients with recurrent VT post infarction who underwent catheter ablation between 2006 and 2017 in Isala Heart Centre were retrospectively analyzed. Univariate and multivariate analysis were used to identify predictors of arrhythmia recurrence post ablation. Patients were allocated to subgroups based on LVEF: severe (<30%), moderate (30–40%) and mild LV dysfunction (41–51%) and analyzed with log rank test. Results. A total of 144 patients were included. Two years VT free survival after a single procedure was 56.6% with median follow-up 46 [17–78] months. Recurrence of VT postablation wash high among patients with an old anteroseptal MI and LVEF < 30% with multiple morphologies of inducible VTs, indicating an extensive and complex substrate. Patients who underwent repeat ablations (27.1%) had significant more often LV aneurysms (20.5% vs. 7.6%, p = .03) and electrical storms (38.5% vs. 21.9%, p = .04). VT free survival was higher in patients with LVEF 41–51% compared to LVEF < 30% (71.4% vs. 47.8%, p = .01). In multivariate analysis, LVEF < 30% (vs 41–51%) was an independent predictor of arrhythmia recurrence (HR = 2.16, CI 1.15–4.06, p = .02). Conclusions. In patients with ischemic VT, success rate of ablation was highest among patients with preserved LV function and recurrent VT and ES was highest among patients with severe LV dysfunction after single and multiple ablation procedures.

Influence of Body Mass Index on Recurrence of Ventricular Arrhythmia, Mortality in Defibrillator Recipients With Ischaemic Cardiomyopathy

Obesity is associated with increased risk of cardiovascular disease. There is little known, however, about the influence of body mass index (BMI) on spontaneously occurring ventricular arrhythmias in patients with ischaemic heart disease. We sought to examine the effect of BMI on the ventricular arrhythmia (VA) recurrence and mortality in defibrillator recipients with ischaemic cardiomyopathy. Consecutive patients (n = 123) with ischaemic cardiomyopathy (left ventricular ejection fraction (LVEF) ≤ 40%) and a primary or secondary prevention defibrillator were included. Patients were classified according to their BMI as being normal (18.5-24.99, n = 54/ 43.9%), overweight (2 -29.99, n = 43/ 35%) or obese (>30, n = 26/20.3%). The primary combined endpoint of VA recurrence and mortality occurred in 36%, 5.4% and 11.5% of patients with normal, overweight and obese BMI (p = 0.001). When adjusting for risk factors such as ejection fraction, age and triple vessel disease, on multivariable analysis, normal BMI remained a significant predictor for the primary outcome (Hazard Ratio, Normal vs Overweight = 7.1, 95% CI 1.8-25, p = 0.002: Hazard Ratio, Normal vs Obese = 5.5, 95% CI 1.11-25, p = 0.033). There was a non-significant trend towards reduced survival in patients with normal weight in comparison to overweight and obese patients (p = 0.08). In defibrillator recipients with ischaemic cardiomyopathy, BMI appears to be a significant predictor for the combined primary outcome of spontaneously occurring ventricular arrhythmias and mortality. Normal BMI, compared to overweight and obese patients had worse outcomes, suggesting the presence of the obesity paradox in ventricular arrhythmogenesis late post infarction.

EFFECT OF MYOCARDIAL INFARCTION ON SPLEEN AND KIDNEY OF ISOPRENALINE-INDUCED MYOCARDIAL INJURY RAT MODEL

Myocardial infarction (MI)-associated inflammation is crucial for post-infarct healing. However, unregulated inflammation may lead to unnecessary systemic inflammation, and affect other organs. This study investigated the effects of MI on spleen and kidneys over early time-points (2 and 7 days) in isoprenaline-induced MI rat model. MI was evident by elevated levels of cardiac injury marker, troponin T, and lactate dehydrogenase (LDH). MI rats showed significant upregulation of myeloperoxidase (MPO) activity at day-2 post infarct while kidney MPO activity remained unaffected. Kidney function test revealed only slightly increased plasma urea at day-2 post MI with no changes in plasma creatine at both time-points. Histological observation on the spleen showed disorganization of spleen structure at day-2 post MI while the kidney structures were preserved at both time-points. In conclusion, although MI-associated damages in the spleen were seen at day-2 post infarct, it had no impact on the kidney structures at both time-points.

Risk factors of post traumatic cerebral infarction after craniotomy for severe traumatic brain injury

Objective To investigate the risk factors associated with post traumatic cerebral infarction (PTCI) after craniotomy hematoma evacuation for severe traumatic brain injury (sTBI) so as to provide clinical reference for the early prevention of postoperative PTCI. Methods A retrospective case control study was conducted to analyze the clinical data of 558 sTBI patients who received craniotomy hematoma evacuation admitted to Changsha Hospital of Traditional Chinese Medicine from October 2006 to June 2016. There were 340 males and 218 females, aged 15-71 years, with an average of 47.8 years. Among them, 75 patients were at the age of less than 30 years, 315 were at 30-50 years, and 168 were above 50 years. According to the Glasgow coma score (GCS), there were 127 patients with 3-4 points, 124 with 5-6 points, and 307 with 7-8 points. The patients were divided into PTCI group (51 patients) and non-PTCI group (507 patients). The related indicators of the two groups of patients after admission were collected, including gender, age, injury cause, GCS, skull base fracture, traumatic subarachnoid hemorrhage (tSAH), cerebral hernia, hypotension, the time from injury to craniotomy, and whether decompressive craniectomy was performed. Univariate analysis was first performed for these factors, followed by multivariate logistic regression analysis. Results There were no significant differences in gender, age, injury cause, skull base fracture, and decompressive craniectomy between PTCI group and control group (P>0.05). In the PTCI group, there were 29 patients with GCS of 3-4 points, 17 with 5-6 points, and five with 7-8 points; there were 48 patients with tSAH, 37 patients with cerebral hernia, and 18 patients with hypotension. In terms of the time from injury to craniotomy, it took 12 hours in four. In the non-PTCI group, there were 98 patients with GCS of 3-4 points, 107 with 5-6 points, and 302 with 7-8 points. There were 34 patients with tSAH, 117 with cerebral hernia, and 35 with hypotension. In terms of the time from injury to craniotomy, it took 12 hours in 15. The differences between the two groups were statistically significant (P<0.05). Multivariate logistic regression analysis indicated that GCS of 3-6 points, tSAH, cerebral hernia, time from injury to craniotomy, and hypotension were significantly associated with PTCI after operation for sTBI (P<0.01). Conclusions GCS of 3-6 points, tSAH, cerebral hernia, duration from injury to craniotomy, and hypotension time >3 hours are the high risk factors of PTCI in sTBI patients after craniotomy. For patients with these high risk factors, craniotomy should be performed in time, and the perioperative blood pressure and intracranial pressure stability should be maintained so as to relieve vasospasm. Key words: Brain injuries; Decompressive craniectomy; Cerebral infarction; Hypotension

Day-to-day glycemic variability and the incidence of complications due to myocardial infarctions in the first 72 hours post infarction in patients with diabetes mellitus

Day-to-day glycemic variability and the incidence of complications due to myocardial infarctions in the first 72 hours post infarction in patients with diabetes mellitus

The role of perioperative cardiorespiratory support in post infarction ventricular septal rupture-related cardiogenic shock

Current guidelines recommend emergency surgical correction in patients with post infarction ventricular septal rupture (PIVSR), but patients with multiorgan failure are commonly managed conservatively because of high surgical risk. We assessed characteristics and outcomes of operated PIVSR patients with or without the use of short-term ventricular assist devices (ST-VADs). We also assessed the impact of a ST-VAD on the performance of surgery. We retrospectively analysed all consecutive patients with PIVSR between January 2004 and May 2017. Baseline clinical characteristics, use of ST-VAD and performance of surgery during admission were assessed. The main outcome measured was in-hospital mortality. A total of 28 patients were included. Mean age was 69.2 years. Most patients (20/28, 71.4%) underwent surgical repair. ST-VADs were used in 11/28 patients (39.3%). This percentage progressively increased across the study period, from 22.2% (2/9) in 2004-2011 to 58.3% (7/12) in 2015-2017 (p=0.091). Patients undergoing ST-VAD use had poorer INTERMACS status, higher values of creatinine, lactate and alanine aminotransferase and lower left ventricular ejection fraction as compared with operated patients without support. In-hospital mortality did not differ according to the use of ST-VADs in operated patients (27.3% without ST-VAD vs. 22.2% with ST-VAD, p=0.604). All five patients undergoing early preoperative venoarterial extracorporeal membrane oxygenator support and delayed surgery survived at hospital discharge. ST-VAD use increased in patients with PIVSR. Despite a higher risk profile in operated patients undergoing ST-VAD use, mortality was not significantly different in these patients. Early preoperative venoarterial extracorporeal membrane oxygenation should be considered for very high risk PIVSR patients.

A cost-utility analysis of decompressive hemicraniectomy versus medical treatment in the management of space-occupying brain oedema post middle cerebral artery infarction.

Data from randomly controlled trials have indicated that a decompressive hemicraniectomy is more clinically effective than medical treatment in the management of space-occupying brain oedema post middle cerebral artery infarction. This economic evaluation compares the impact of the two options in the UK. No recent study has conducted an economic evaluation on this topic for the UK. A cost-utility analysis over a time period of 1year was used, measuring benefits in terms of quality adjusted life years (QALYs) and costs in pound sterling, discounted to 2015 prices. The evaluation was from the perspective of the National Health Service, the largest healthcare provider in the UK. The cost-utility analysis found an incremental cost effectiveness of £116595.10 for every QALY gained if patients were offered a decompressive hemicraniectomy compared to the best medical treatment. This is above the National Institute for Health and Care Excellence (NICE) 'cost-effective' threshold of £20000-£30000 per QALY, but lower mortality rates associated with the surgical alternative raises ethical considerations for healthcare providers in the UK.

Abstract 17122: Cardioprotection With Proangiogenic Nanomaterials Formulated With CHIR99021 and FGF1

Introduction: We aimed at to investigate whether activation of both FGF1 and Wnt1 synergistically enhances angiogenesis and render the cardioprotection in hearts with post infarction LV remodeling. Materials and methods: CHIR99021 (a Wnt1 activator) and FGF1 were encapsulated into poly lactic-co-glycolic acid nanoparticles (CHIR99021/FGF1-NPs). Ischemic heart models were generated in C57BL/6 mice or Yorkshire swine by ligation of the left anterior descending coronary. The mice were randomly divided into 6 groups: Myocardial infarction (MI) Only (n=11), MI with nanoparticles (CHIR99021 or/and FGF1 loaded) injection (n=12, each), MI with non-loaded nanoparticles injection (n=11) and Sham group (n=10). The swine were divided into 3 groups: ischemic reperfusion injury (IRI) (n=4), IRI with CHIR99021/FGF-NPs injection (n=4) and Sham group (n=4). Left ventricle function 4 week after surgery were evaluated by Echocardiography. Cell proliferation was assessed via immunostaining in ischemic hearts and in cultivated human umbilical vein endothelial cells (HUVECs) and Human vascular smooth muscle cells (HVSMCs) using the following markers: Ki67, Brdu, PH3, and Aurora B. Apoptosis was determined with TUNEL staining. Cardiac fibrosis was evaluated via Sirius red and Fast green staining (mice) and magnetic resonance imaging (swine). Results: CHIR99021/FGF1-NPs treatment attenuated fibrosis and preserved heart contractile function in mice and swine models of postinfarction LV remodeling. The proportion of cells that expressed cell cycle markers (Ki67; BrdU; Aurora B and PH3) was significantly greater in CHIR99021+FGF1 treatment group than CHIR99021, FGF1 and PBS treatment group. The proportion of apoptotic cells was significantly smaller in CHIR99021+FGF1 treatment group than in groups of control, VEGF, CHIR99021, or FGF1 treatment alone. Conclusions: CHIR99021 and FGF synergistically activate cell cycle and reduce apoptosis, which accompanied by a significant improvement of cardiac function.