Time Of Acute Myocardial Infarction Research Articles

The relationship between apnoea hypopnoea index and Gensini score in patients with acute myocardial infarction undergoing emergency primary percutaneous coronary intervention.

Sleep apnoea hypopnoea syndrome (SAHS) is characterised by repetitive nocturnal hypoxemia and has a high prevalence among patients with acute myocardial infarction (AMI). But there are few studies on patients with AMI undergoing emergency primary percutaneous coronary intervention (pPCI). In this study, we want to find the prevalence of SAHS among patients with AMI undergoing emergency pPCI and determine whether SAHS would worsen the condition among these people, and especially affect the damage degree of the coronary artery. Over four months, 95 patients admitted for the first time for AMI were observed. All of them had emergency primary PCIs. A total of 86 patients accepted the sleep study and were divided into four groups according to the apnoea hypopnoea index (AHI): SAHS was diagnosed when AHI ≥5/h and was defined as mild for AHI ≥5/h and <15/h, moderate for AHI ≥15/h and <30/h, and severe for AHI ≥30/h. On the contrary, the patients whose AHI <5/h were Non-SAHS. And the characteristics of the patients among these four groups were compared. According to the time of chest pain onset, the number of the patients between SAHS and non-SAHS, and patients' AHI during three intervals of one day were measured and compared; Makers including the sensitivity of serum troponin T (hs-TnT), creatine kinase isoenzyme MB (CK-MB), left ventricular ejection fraction (LVEF), pro-brain-type natriuretic peptide (pro-BNP), Gensini score and collateral vessels between the SAHS and non-SAHS were compared. And the relationships between the AHI of these patients and the markers were analysed. Of the 86 patients studied, 65 had SAHS, representing a SAHS prevalence of 75.58% among patients with AMI undergoing emergency pPCI. There were significant differences in average ages, smoking and arrhythmia (P<0.05) between these four groups. There was no significant difference between AMI patients with or without SAHS regarding the day-night pattern. But there showed significant differences between SAHS and non-SAHS in Gensini score (P<0.05) and pro-BNP (P<0.05). Also, there were positive correlations between AHI and Gensini score (r=0.490, P<0.05) and pro-BNP (r=0.338, P<0.05). Among patients with AMI undergoing emergency pPCI, there is a high prevalence of SAHS. There are also positive correlations between AHI and Gensini score, and pro-BNP. Therefore, guided by the results, should we conduct a routine screening to those patients normally and could we relieve the damage to the coronary artery by curing the SAHS?

Early Anti-inflammatory and Pro-angiogenic Myocardial Effects of Intravenous Serelaxin Infusion for 72 H in an Experimental Rat Model of Acute Myocardial Infarction

Sprague Dawley rats were subjected to acute myocardial infarction (AMI) by permanent ligation of the left anterior descending coronary artery. At the time of AMI, a subcutaneous mini-osmotic pump was implanted and animals were randomized into three groups, according to the intravenous therapy received during the first 72h: placebo-treated (saline), serelaxin10-treated (SRLX10=10μg/kg/day), or serelaxin30-treated (SRLX30=30μg/kg/day). Treatment with SRLX30 reduced the expression of inflammatory cytokines and chemokines, as well as the infiltration of macrophages, and increased the expression of pro-angiogenic markers and vessel density in the infarcted myocardium after 7days. SRLX30 did not reduce early myocardial fibrosis but reduced myocardial levels of sST2 and galectin-3. No significant effects were observed with SRLX10 treatment. A significant correlation was observed between plasma levels of serelaxin and effect measures. The results suggest serelaxin has a protective effect in early processes of cardiac remodeling after AMI.

Circulating irisin levels are lower in patients with either stable coronary artery disease (CAD) or myocardial infarction (MI) versus healthy controls, whereas follistatin and activin A levels are higher and can discriminate MI from CAD with similar to CK-MB accuracy

BackgroundSeveral myokines are produced by cardiac muscle. We investigated changes in myokine levels at the time of acute myocardial infarction (MI) and following reperfusion in relation to controls. MethodsPatients with MI (MI Group, n=31) treated with percutaneous coronary intervention (PCI) were compared to patients with stable coronary artery disease (CAD) subjected to scheduled PCI (CAD Group, n=40) and controls with symptoms mimicking CAD without stenosis in angiography (Control Group, n=43). The number and degree of stenosis were recorded. Irisin, follistatin, follistatin-like 3, activin A and B, ALT, AST, CK and CK-MB were measured at baseline and 6 or 24h after the intervention. ResultsMI and CAD patients had lower irisin than controls (p<0.001). MI patients had higher follistatin, activin A, CK, CK-MB and AST than CAD patients and controls (all p≤0.001). None of the myokines changed following reperfusion. Circulating irisin was associated with the degree of stenosis in all patients (p=0.05). Irisin was not inferior to CK-MB in predicting MI while folistatin and activin A could discriminate MI from CAD patients with similar to CK-MB accuracy. None of these myokines was altered following PCI in contrast to CK-MB. ConclusionsIrisin levels are lower in MI and CAD implying that their production may depend on myocadial blood supply. Follistatin and activin A are higher in MI than in CAD suggesting increased release due to myocardial necrosis. They can predict MI with accuracy similar to CK-MB and their role in the diagnosis of MI remains to be confirmed by prospective large clinical studies.

The Unraveling of the Matryoshka Doll.

Significant advances have been made in the field of cardiac regenerative medicine. Investigations into the mechanism of action have identified multiple strategies of the delivery of biologics that are both cell and cell free that yield quantitatively equivalent results. Here in, we present a viewpoint of the successive layers within the cell that can be exploited to prevent or treat cardiac dysfunction . In the beginning, it was supposed to be simple, transplant noncommitted bone marrow–derived stem cells to the myocardium, where they would migrate into the infarct zone and differentiate into cardiac myocytes, replacing the lost contractile function of the heart and limiting the risk of heart failure.1 Soon, it became evident that circulating stem cells were being signaled to home to the site of myocardial injury; whether those stem cells were exogenously infused or endogenously released from the bone marrow. These early findings led to a bifurcation of the field where clinicians performed trials trying to prevent or restore cardiac function in patients with ischemic heart disease,2 and bench scientists focused on distinct cell types and mechanisms of action.3 Sixteen years later, stem cell therapy is no closer to standard of care, but we have learned a great deal. Although our successes have been limited,4 our understanding of the physiology and biology has grown immensely: 1. First and foremost, we understand that adult stem cell therapy seems to be safe. Unlike the arrhythmias we observed with skeletal myoblasts, we have not seen adverse electric, mechanical, or oncogenic effects of adult stem cells. 2. The concept of stem cell transplantation at the time of acute myocardial infarction is not as easy as we had first thought as stem cell preparation seems to have significant consequences on whether the therapy will work4 or not.5 3. We have …

SERUM PROLIDASE ACTIVITY IN STABLE CORONARY ARTERY DISEASE AND ACUTE MYOCARDIAL INFARCTION

Background: Collagen is a major determinant of atherosclerotic plaque stability and prolidase is a rate-limiting enzyme in the breakdown and formation of collagen. We sought to determine prolidase activity at the time of acute myocardial infarction (MI) as compared to quiescent state and to patients

Right ventricular function measured by TAPSE in obese subjects at the time of acute myocardial infarction and 2 year outcomes

IntroductionObesity is associated with significantly better outcome after acute myocardial infarction (AMI), a phenomenon known as ‘obesity paradox’. Tricuspid annular plane systolic excursion (TAPSE) is an echocardiographic measurement of right ventricular (RV) function and has prognostic implications at the time of AMI. MethodsWe examined the difference in RV function among patients admitted with AMI according to obesity status. In a single center cohort analysis of 105 patients admitted between 2010 and 2011 with the diagnosis of AMI. Demographic, anthropometric data and cardiovascular risk factors were prospectively collected. All subjects had echocardiogram within 48h of AMI diagnosis for TAPSE calculations. Subjects were divided into two groups based on their obesity status. ResultsObese subjects had better RV function compared to non-obese, TAPSE: 19±6.6 vs. 16±4.9mm; p 0.02 at the time of AMI. There was no significant difference in TAPSE between OSA and non-OSA subjects, 19±6.3 vs. 17±6.2mm; p 0.21. After 2years of follow up, patients with obesity and better RV function were less likely to develop new onset heart failure (HF) with OR 0.30 (95% CI 0.09–0.93; p 0.03) and OR 0.31 (95% CI 0.11–0.76; p 0.007) respectively. ConclusionObese patients had better RV function measured by TAPSE at the time AMI when compared non-obese patients. Patients with better RV function at the time of AMI were less likely to develop new-onset HF and there was a trend in the obese group to less likely develop new-onset HF after 2year follow up.

Effects of Low-Dose Recombinant Human Brain Natriuretic Peptide on Anterior Myocardial Infarction Complicated by Cardiogenic Shock.

Introduction The mortality due to cardiogenic shock complicating acute myocardial infarction (AMI) is high even in patients with early revascularization. Infusion of low dose recombinant human brain natriuretic peptide (rhBNP) at the time of AMI is well tolerated and could improve cardiac function.Objective The objective of this study was to evaluate the hemodynamic effects of rhBNP in AMI patients revascularized by emergency percutaneous coronary intervention (PCI) who developed cardiogenic shock.Methods A total of 48 patients with acute ST segment elevation myocardial infarction (STEMI) complicated by cardiogenic shock and whose hemodynamic status was improved following emergency PCI were enrolled. Patients were randomly assigned to rhBNP (n=25) and control (n=23) groups. In addition to standard therapy, study group individuals received rhBNP by continuous infusion at 0.005 µg kg−1 min−1 for 72 hours.Results Baseline characteristics, medications, and peak of cardiac troponin I (cTnI) were similar between both groups. rhBNP treatment resulted in consistently improved pulmonary capillary wedge pressure (PCWP) compared to the control group. Respectively, 7 and 9 patients died in experimental and control groups. No drug-related serious adverse events occurred in either group.Conclusion When added to standard care in stable patients with cardiogenic shock complicating anterior STEMI, low dose rhBNP improves PCWP and is well tolerated.

Platelet Count and Mean Platelet Volume at the Time of and After Acute Myocardial Infarction

Platelet count has been shown to be lower and mean platelet volume (MPV) to be higher in acute myocardial infarction (MI). However, it is not known whether these changes persist post-MI or if these measures are able to distinguish between acute thrombotic and non-thrombotic MI. Platelet count and MPV were measured in 80 subjects with acute MI (thrombotic and non-thrombotic) and stable coronary artery disease (CAD) at cardiac catheterization (acute phase) and at >3-month follow-up (quiescent phase). Subjects were stratified using stringent clinical, biochemical, histological, and angiographic criteria. Outcome measures were compared between groups by analysis of variance. Forty-seven subjects met criteria for acute MI with clearly defined thrombotic (n = 22) and non-thrombotic (n = 12) subsets. Fourteen subjects met criteria for stable CAD. No significant difference was observed in platelet count between subjects with acute MI and stable CAD at the acute or quiescent phase. MPV was higher in acute MI (9.18 ± 1.21) compared to stable CAD (8.13 ± 0.66; P = 0.003) at the acute phase but not at the quiescent phase (8.48 ± 0.58 vs 8.94 ± 1.42; P = 0.19). No difference in platelet count or MPV was detected between thrombotic and non-thrombotic subsets at acute or quiescent phases. The power to detect differences in these measures between thrombotic and non-thrombotic subsets was 58%. Higher MPV at the time of acute MI is not observed by 3 months post-MI (quiescent phase). Platelet count and MPV do not differ in subjects with thrombotic versus non-thrombotic MI. Further investigation is warranted to evaluate the utility of these measures in the diagnosis of acute MI.

T1 High glucose and myocardial ischaemia/reperfusion injury: the role of the sodium/glucose transporter, SGLT1

Background Hyperglycaemia, frequently found at the time of acute myocardial infarction, is associated with excess cardiovascular mortality. The sodium-glucose transporter SGLT1 is present in mammalian myocardium, but its role in acute ischaemia/reperfusion injury is currently unknown. We hypothesise high glucose at reperfusion increases infarct size following injurious ischaemia and this excess injury can be ameliorated by inhibition of SGLT1. Methods and results Langendorff-perfused Sprague-Dawley rat (SDR) heart were subjected to 35 min regional ischaemia and 60min variable glucose (3.5–22 mmol/L) reperfusion, with osmolality controlled by reciprocal dose mannitol. Reperfusion High Glucose (RHG) significantly dose-dependently increased infarct size (45 to 65%, p Discussion and conclusion We demonstrate for the first time that high glucose at reperfusion exacerbates myocardial injury following lethal myocardial ischaemia that can be ameliorated by inhibition of SGLT, which appears not directly targeted at cardiomyocytes, but rather non-myocyte myocardial cell populations. These data therefore provide the first data for a novel repurposing of SGLT inhibitors in non-diabetic patients presenting with acute coronary syndromes complicated by hyperglycaemia, and provides a tantalising insight into the mechanisms of hyperglycaemic-driven excess cardiovascular mortality.

Editor's Choice-Sex differences in young patients with acute myocardial infarction: A VIRGO study analysis.

Young women with acute myocardial infarction (AMI) have a higher risk of adverse outcomes than men. However, it is unclear how young women with AMI are different from young men across a spectrum of characteristics. We sought to compare young women and men at the time of AMI on six domains of demographic and clinical factors in order to determine whether they have distinct profiles. Using data from Variation in Recovery: Role of Gender on Outcomes of Young AMI Patients (VIRGO), a prospective cohort study of women and men aged ⩽55 years hospitalized for AMI ( n = 3501) in the United States and Spain, we evaluated sex differences in demographics, healthcare access, cardiovascular risk and psychosocial factors, symptoms and pre-hospital delay, clinical presentation, and hospital management for AMI. The study sample included 2349 (67%) women and 1152 (33%) men with a mean age of 47 years. Young women with AMI had higher rates of cardiovascular risk factors and comorbidities than men, including diabetes, congestive heart failure, chronic obstructive pulmonary disease, renal failure, and morbid obesity. They also exhibited higher levels of depression and stress, poorer physical and mental health status, and lower quality of life at baseline. Women had more delays in presentation and presented with higher clinical risk scores on average than men; however, men presented with higher levels of cardiac biomarkers and more classic electrocardiogram findings. Women were less likely to undergo revascularization procedures during hospitalization, and women with ST segment elevation myocardial infarction were less likely to receive timely primary reperfusion. Young women with AMI represent a distinct, higher-risk population that is different from young men.

Enhancement of Gap Junction Function During Acute Myocardial Infarction Modifies Healing and Reduces Late Ventricular Arrhythmia Susceptibility.

ObjectivesThe purpose of this study was to investigate the effects of enhancing gap junction (GJ) coupling during acute myocardial infarction (MI) on the healed infarct scar morphology and late post-MI arrhythmia susceptibility.BackgroundIncreased heterogeneity of myocardial scarring after MI is associated with greater arrhythmia susceptibility. We hypothesized that short-term enhancement of GJ coupling during acute MI can produce more homogeneous infarct scars, reducing late susceptibility to post-MI arrhythmias.MethodsFollowing arrhythmic characterization of a rat 4-week post-MI model (n = 24), another 27 Sprague-Dawley rats were randomized to receive rotigaptide to enhance GJ coupling (n = 13) or to saline control (n = 14) by osmotic minipump immediately prior to and for the first 7 days following surgically induced MI. At 4 weeks post-MI, hearts were explanted for ex vivo programmed electrical stimulation (PES) and optical mapping. Heterogeneity of infarct border zone (IBZ) scarring was quantified by histomorphometry.ResultsDespite no detectable differences in infarct size at 4 weeks post-MI, rotigaptide-treated hearts had reduced arrhythmia susceptibility during PES (inducibility score for rotigaptide: 2.4 ± 0.8; for control: 5.0 ± 0.6; p = 0.02) and less heterogeneous IBZ scarring (dispersion of IBZ complexity score: rotigaptide: 1.1 ± 0.1; control: 1.4 ± 0.1; p = 0.04), associated with an improvement in IBZ conduction velocity (rotigaptide: 43.1 ± 3.4 cm/s; control: 34.8 ± 2.0 cm/s; p = 0.04).ConclusionsEnhancement of GJ coupling for only 7 days at the time of acute MI produced more homogeneous IBZ scarring and reduced arrhythmia susceptibility at 4 weeks post-MI. Short-term GJ modulation at the time of MI may represent a novel treatment strategy to modify the healed infarct scar morphology and reduce late post-MI arrhythmic risk.

Abstract TMP9: Hospitals' Performance on Timely Reperfusion in Stroke and Myocardial Infarction is not Correlated

Introduction: Timely reperfusion is performed less optimally in acute ischemic stroke (AIS) than in acute myocardial infarction (AMI). The degree to which hospital performance is correlated on emergent AMI and AIS care is unknown. Hypothesis: There would be a positive correlation between hospital performance on door-to-balloon time (D2B) for AMI and door-to-needle time (DTN) for AIS; and hospital performance on D2B would predict DTN even after controlling for patient and hospital differences. Methods: Prospective study of all hospitals participating in both Get With The Guidelines (GWTG)-Stroke and -Coronary Artery Disease from 2006-09 and treating ≥10 patients. We compared hospital-level DTN and D2B before and after risk adjustment using Spearman’s rank correlation coefficients and hierarchical linear regression modeling. We also correlated hospitals’ DTN and D2B data from 2013-14 using GWTG (DTN) and Hospital Compare (D2B). Results: There were 43 hospitals contributing data (1976 AIS and 59,823 AMI patients). Hospitals’ DTN times for AIS did not correlate with their D2B times for AMI (median DTN 85 min [IQR 77-99] vs. median D2B 72 min [IQR 62-81]; ρ=-0.09; p=0.55). There was no correlation between hospitals’ proportion of eligible patients treated within target time windows for AIS and AMI (median DTN&lt;60 minutes: 21% [IQR 11-30]; median D2B&lt;90 minutes: 68% [IQR 62-79]; ρ=-0.14; p=0.36). The lack of correlation between hospitals’ DTN and D2B times persisted after risk adjustment. From 2013-14, hospitals’ DTN performance in GWTG was not correlated with D2B performance in Hospital Compare (N=546 hospitals; see figure). Conclusions: We found no correlation between hospitals’ observed or risk-adjusted DTN and D2B times. Opportunities exist to improve hospitals’ performance of time-critical care processes for AIS and AMI in a coordinated rather than condition-specific manner.

Excess weight and life expectancy after acute myocardial infarction: The obesity paradox reexamined

An "obesity paradox" has been described in patients with acute myocardial infarction (AMI), whereby obese and overweight patients have a lower risk of short-term mortality after AMI than normal-weight patients. However, the long-term association of obesity with mortality after AMI remains unknown. We used data from the Cooperative Cardiovascular Project, a prospective medical record study of Medicare beneficiaries hospitalized with AMI with 17 years of follow-up (N = 124,981), to evaluate the association of higher body mass index (BMI) with short- and long-term survival after AMI. Cox proportional hazards models were used to estimate life expectancy after AMI and the years of potential life lost or gained attributable to excess weight. Approximately 41.5% of patients were classified as normal weight; 38.7%, as overweight; 14.3%, as obese; and 5.5%, as morbidly obese. Normal-weight patients had the highest crude mortality at all follow-up time points, whereas obese patients had the lowest. Adjustment for patient and treatment characteristics reduced this difference, but the survival benefit persisted in overweight and obese patients at all time points. Morbidly obese and normal-weight patients had a comparable risk of death at 17 years. Life expectancy estimates were generally lowest for morbidly obese patients and highest for overweight patients. Differences in life expectancy between BMI groups were most pronounced in younger patients. After adjustment, overweight and obesity were associated with greater life years at all ages; however, morbid obesity was only associated with better survival in patients ≥75 years of age at the time of AMI. Overweight and obesity are associated with improved short- and long-term survival after AMI, which results in moderate gains in life expectancy relative to normal-weight patients. These findings suggest that higher BMI confers a protective advantage over the entire remaining lifespan in older patients with AMI.

Abstract 15117: Undiagnosed Diabetes at the Time of Acute Myocardial Infarction is Frequent and Associated With Poor Cardiovascular Outcomes

Introduction: Diabetes mellitus (DM) is associated with poor cardiovascular disease (CVD) outcomes, especially in the setting of acute myocardial infarction (AMI). As both a first diagnosis (dx) of DM and missed dx of incident DM also may be associated with poor outcomes; we sought to determine their frequency and related CVD impact in patients presenting with AMI. Hypothesis: Many individuals with AMI have undiagnosed DM based on standard criteria, which leads to poor MACE outcomes. Methods: Patients (pts) presenting with AMI between 2002 and 2013 were studied (n=5719). Criteria-defined (CD)-DM was a fasting glucose (FG) ≥126 mg/dL, a random glucose (RG) ≥200, or a hemoglobin A1c ≥6.5%. DM groups were: 1) history (hx) of DM (n=1941, 34%), 2) no hx of DM, with CD-DM undiagnosed at AMI (n=500, 9%), 3) no hx of DM, with CD-DM diagnosed (dx) at hospitalization (n=207, 4%), and 4) no hx of DM and no CD-DM (n=3071, 53%). MACE (all-cause death, MI, stroke, heart failure hospitalization) was determined at 1 year post discharge. Results: Univariate comparisons are shown in the Table. After adjusting for covariables in a multivariate logistic regression using subjects with no hx of DM as the referent, hx of DM (OR=1.6; 95% CI: 1.3, 2.0; p&lt;0.0001) and CD-DM without dx at AMI (OR=1.5; 95% CI: 1.3, 1.7; p&lt;0.0001) were associated with greater risk of MACE. The difference between those with CD-DM with dx at AMI and those with no DM was not significant (OR=1.3; 95% CI: 0.9, 1.7; p=.15). Conclusions: The prevalence of DM is high in those presenting with AMI. Recognition of undiagnosed DM in the setting of CD-DM remains poor. Furthermore, MACE outcomes are 1.5 times higher with CD-DM undiagnosed than without DM, whereas outcomes are moderated if CD-DM is recognized at the time of AMI. Protocols for more aggressive identification of incident DM should be instituted and may importantly impact clinical outcomes for pts with previously undiagnosed DM.

Thyroxine in acute myocardial infarction (ThyrAMI) - levothyroxine in subclinical hypothyroidism post-acute myocardial infarction: study protocol for a randomised controlled trial.

BackgroundCardiac disease is the most common cause of morbidity and mortality in the United Kingdom. Even minor changes in thyroid hormone concentration may impact adversely on the cardiovascular system. Subclinical hypothyroidism (SCH) after admission for an acute cardiac problem has been associated with an increase in cardiac mortality and overall death. We have designed protocols for a prospective observational study to assess the association of thyroid function at the time of acute myocardial infarction (AMI) with cardiovascular outcomes, and a double-blinded randomised placebo-controlled trial of levothyroxine to evaluate its effect on LV function and vascular health.Methods/DesignThyrAMI 1: This will be a prospective longitudinal observational study of patients with AMI that will be followed for 24 months to study the association between thyroid status at the time of AMI (within 24 hours of diagnosis) with vascular outcomes.ThyrAMI 2: This will be a prospective double-blinded randomised placebo-controlled trial of levothyroxine of 12 months duration in patients with AMI and SCH.Setting: Patients will be recruited from five hospitals in the North East of England.Participants: One hundred patients with thyroid function tests within the subclinical hypothyroid range upon admission with an AMI and no previous history of thyroid disease.Intervention: Levothyroxine will be administered at a starting dose of 25 mcg once daily, which will be increased at intervals if needed to maintain a TSH level between 0.4 to 2.5 mU/L, versus a placebo.Randomisation: Participants will be randomized with a computerised randomisation algorithm, stratified by type of MI (NSTEMI versus STEMI), in a 1:1 ratio to levothyroxine therapy or placebo (as container or bottle numbers), starting within 21 (+/− 7) days of AMI.Blinding: Assignment to either the LT4 or placebo arm will be double-blinded.Outcomes: The outcome will be the effect of levothyroxine on ventricular function, endothelial function and blood coagulability and rheology.DiscussionThere is evidence to suggest that treatment of SCH can improve cardiovascular parameters. Therefore, ThyrAMI 1 and ThyrAMI 2 will be the first trials investigating SCH in AMI to give a better insight into whether thyroid hormone levels are a key target for improving cardiovascular outcomes.Trial registrationISRCTN number: ISRCTN52505169. Date of registration: 09/01/2015

Association between obesity and severity of coronary artery disease at the time of acute myocardial infarction: Another piece of the puzzle in the “obesity paradox”

Association between obesity and severity of coronary artery disease at the time of acute myocardial infarction: Another piece of the puzzle in the “obesity paradox”

Association of lifestyle-related factors with circadian onset patterns of acute myocardial infarction: a prospective observational study in Japan

ObjectiveThe onset of acute myocardial infarction (AMI) shows characteristic circadian variations involving a definite morning peak and a less-defined night-time peak. However, the factors influencing the circadian patterns of AMI...

Natural Disasters and Myocardial Infarction: The Six Years After Hurricane Katrina

ObjectiveTo determine the prolonged effect of Hurricane Katrina on the incidence and timing of acute myocardial infarction (AMI) in the city of New Orleans. Patients and MethodsOur study population consisted of 1476 patients with AMI before (August 29, 1999, to August 28, 2005) and after (February 14, 2006, to February 13, 2012) Hurricane Katrina at Tulane University Health Sciences Center to determine post-Katrina alterations in the occurrence and timing of AMI. ResultsCompared with pre-Katrina values, there was a more than 3-fold increase in the percentage of admissions for AMI during the 6 years after Hurricane Katrina (P<.001). The percentage of admissions for AMI after Hurricane Katrina increased significantly on nights (P<.001) and weekends (P<.001) and decreased significantly on mornings (P<.001), Mondays (P<.001), and weekdays (P<.001). Patients with AMI after Hurricane Katrina also had significantly higher rates of psychiatric comorbidities (P=.01), smoking (P<.001), lack of health insurance (P<.05), and unemployment (P<.001). ConclusionThese results indicate that the effect of natural disasters on the occurrence of AMI may persist for at least a 6-year period and may be related to various factors including population shifts, alterations in the health care system, and the effects of chronic stress and associated behaviors.

Alteration of nerve growth factor in dorsal root ganglia at early time of acute myocardial infarction and the role of spinal nerve afferents

Nerve growth factor (NGF) plays important roles in transmission of nociception, neural innervation and survival in sympathetic and sensory neurons. Evidence indicates that NGF may sensitize the sensory and sympathetic reaction upon noxious stimulation. Understanding of the alterations of NGF in the sensory neurons during acute myocardial infarction and the underlying mechanism may promote clinical prognosis of the pathology. The aim of the study was to investigate the changes of NGF in the sensory neurons innervating the heart at early time after myocardial infarction and potential role of afferent nerve signals in modulation of NGF. The myocardial infarction was induced by ligation of the left anterior descending branch of coronary artery in anesthetized rats. The expressions of NGF and its coding mRNA in the sensory neurons in the dorsal root ganglia of upper thoracic segments (1–5), with and without prior blockade of the spinal nerves, were examined using immunohistochemical assay, enzyme-linked immunosorbent assay and real-time quantitative reverse transcription polymerase chain reaction assay. It was found that the immunoreactive material for NGF was significantly increased in the ganglia (P<0.05) at 60min of myocardial infarction, without change in NGF mRNA before and after the time. Blockade of the spinal nerves obviously inhibited the expression of NGF (P<0.05) and the coding mRNA (P<0.01). The results may indicate that the spinal nerve afferents are important in sustaining and up-regulating the expression of NGF in the sensory neurons innervating the heart in acute myocardial infarction.

Esmolol activates endogenous neurokinin activity inhibiting infarction-induced arrhythmias in rats: Novel mechanisms of anti-arrhythmia

Endogenous neurokinin and adrenergic mechanisms might co-participate in the pathology of acute myocardial infarction (MI). This study sought to investigate the role of endogenous neurokinin and its relationship with β1-adrenergic mechanism in the infarction induced arrhythmias.In 60min of MI in rats, the contents of substance P (SP), a native agonist of neurokinin 1 receptor (NK1-R), norepinephrine (NE), NK1-R and β1-adrenergic receptor in the myocardium at risk of ischemia were examined and the ventricular arrhythmias were analyzed. The effects of pretreatment with D-SP (152ng/kg), a specific antagonist of NK1-R, esmolol (10mg/kg), a specific blocker of β1-adrenergic receptor, and a combination of the two blockers were studied. The results showed that the overlaps of up-regulation of NE, SP and the increase of ventricular arrhythmias were observed. D-SP exacerbated the episodes and duration of VT & VF by 54% and 104%, respectively (all P<0.05). Esmolol inhibited the morbidity rate, the episodes and the duration of VT & VF by 66%, 92% and 95%, respectively. Surprisingly, esmolol significantly attenuated the arrhythmogenic effect of D-SP throughout the MI, beyond the time span of esmolol action, during which a significant up-regulation of the NK1-R (by 19%, P<0.05) was detected.In conclusion, the findings of this study may indicate an anti-arrhythmic effect of endogenous neurokinin mechanism, through the activation of which, via up-regulation of NK1 receptor, esmolol may exert its anti-arrhythmic action at the early time of acute myocardial infarction.