scholarly journals Colchicine to Prevent Sympathetic Denervation after an Acute Myocardial Infarction: The COLD-MI Trial Protocol

Medicina ◽  
2021 ◽  
Vol 57 (10) ◽  
pp. 1047
Author(s):  
Fabien Huet ◽  
Quentin Delbaere ◽  
Sylvain Aguilhon ◽  
Valentin Dupasquier ◽  
Delphine Delseny ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Single Photon ◽  
Ischemia Reperfusion ◽  
Photon Emission ◽  
Border Zone ◽  
Sympathetic Denervation ◽  
First Episode ◽  
Emission Computed Tomography

Inflammatory processes are deeply involved in ischemia-reperfusion injuries (IRI) and ventricular remodelling (VR) after a ST-segment elevation myocardial infarction (STEMI). They are associated with clinical adverse events (heart failure and cardiovascular death) adding damage to the myocardium after reperfusion. Moreover, acute myocardial infarction (AMI) induces a local sympathetic denervation leading to electrical instability and arrythmia. Colchicine, a well-known alkaloid with direct anti-inflammatory effects, was shown to reduce the myocardial necrosis size and limit the VR. In a recent proof of concept study, colchicine appears to prevent sympathetic denervation in a mice model of ischemia/reperfusion, but not in the necrosis or in the border zone areas. The Colchicine to Prevent Sympathetic Denervation after an AMI study (COLD-MI) is an ongoing, confirmative, prospective, monocentre, randomized, open-label trial. The COLD-MI trial aims to evaluate the intensity of sympathetic denervation after AMI and its potential modulation due to low dose colchicine. Sympathetic denervation will be noninvasively evaluated using single-photon emission computed tomography (SPECT). After a first episode of STEMI (Initial TIMI flow ≤1) and primary percutaneous coronary intervention (PPCI), patients will be randomized (n = 56) in a 1:1 ratio to either receive colchicine or not for 30 days. The primary end point will be the percentage of myocardial denervation measured by 123I-metaiodobenzylguanidine (123I-MIBG) SPECT at a 6-month follow-up. The main secondary end points will be basic ECG parameters (QRS duration, corrected QT) and HRV parameters from a 24 hour-recording Holter at 1- and 6-months follow-up. Results from this study will contribute to a better understanding of the cardioprotective effect of colchicine after AMI. The present study describes the rationale, design, and methods of the trial.

scholarly journals INTEGRATION OF COMPLEMENTARY BIOMARKERS IN PATIENTS WITH FIRST EPISODE PSYCHOSIS: RESEARCH PROTOCOL OF A PROSPECTIVE FOLLOW UP STUDY

2019 ◽  
Author(s):  
Petra ◽  
Martina Rojnic Kuzman ◽  
Porin Makaric ◽  
Dina Bosnjak Kuharic ◽  
Ivana Kekin ◽  
...  
Keyword(s):  
Genome Wide Association Study ◽  
Single Photon ◽  
Single Gene ◽  
Photon Emission ◽  
Blood Perfusion ◽  
First Episode ◽  
Emission Computed Tomography ◽  
Healthy Controls ◽  
Post Mortem

In this project, we recruited a sample of 150 patients with first episode of psychosis with schizophrenia features (FEP) and 100 healthy controls. We assessed the differences between these two groups, as well as the changes between the acute phase of illness and subsequent remission among patients over 18-month longitudinal follow-up. The assessments were divided into four work packages (WP): WP1- psychopathological status, neurocognitive functioning and emotional recognition; WP2- stress response measured by saliva cortisol during a stress paradigm; cerebral blood perfusion in the resting state (with single photon emission computed tomography (SPECT) and during activation paradigm (with Transcranial Ultrasonography Doppler (TCD); WP3-post mortem analysis in histologically prepared human cortical tissue of post mortem samples of subjects with schizophrenia in the region that synaptic alteration was suggested by WP1 and WP2; WP4- pharmacogenetic analysis (single gene polymorphisms and genome wide association study (GWAS). We expect that the analysis of these data will identify a set of markers that differentiate healthy controls from patients with FEP, and serve as an additional diagnostic tool in the first episode of psychosis, and prediction tool which can be then used to help tailoring individualized treatment options. In this paper, we describe the project protocol including aims and methods and provide a brief description of planned post mortem studies and pharmacogenetic analysis.

Abstract 170: Inflammation Imaging in the Primate Heart Using 111 In-Labeled Anti-Tenascin-C Antibody

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Michiaki Hiroe ◽  
Naohide Ageyama ◽  
Yasuhiro Yasutomi ◽  
Hiroyuki Kurosawa ◽  
Ousuke Fujimoto ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Single Photon ◽  
Photon Emission ◽  
Border Zone ◽  
Myocardial Inflammation ◽  
Emission Computed Tomography ◽  
Myocardial Uptake ◽  
Dual Isotope ◽  
Tenascin C ◽  
Active Inflammation

Myocardial inflammation after myocardial infarction and myocarditis may cause cardiac remodeling, leading to congestive heart failure and arrhythmias. Tenascin-C (TNC), an extracellular matrix glycoprotein, is not normally expressed but specifically expressed associated with active inflammation. The aim of this study was to explore the myocardial expression of TNC after myocardial infarction in Macaca fascicularis (crab-eating monkey) using 111 In-labeled anti-TNC antibody ( 111 In-TNC-Fab’). The left coronary artery was permanently ligated in two monkies and 4 days later, we performed dual-isotope single-photon emission computed tomography imaging (SPECT) of 111 In-TNC-Fab’ and 99m Tc methoxy- isobutyl isonitrile (MIBI), and compared with those of an age-matched control. Then, dual autoradiography was compared with histology and immunostaining for TNC of the heart. Dual-isotope SPECT demonstrated the regional myocardial uptake of 111 In-TNC-Fab’ in the areas of decreased uptake of MIBI. On autoradiography, the radioactivities were observed in the border zone between the infarcted and the noninfarcted area of MI hearts. The hot spots corresponded with the positively immunostained areas. In contrast, no radioactivites of 111 In-TNC-Fab’ were detected in the control. These data clearly indicated that, using 111 In-TNC-Fab’, we can visualize the inflammatory lesions followed by myocardial infarction of the primate.

Abstract 836: Impact of Hypoadiponectinemia on Left Ventricular Remodeling after Primary Coronary Intervention for Acute Myocardial Infarction

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Yukio Arita
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Ventricular Remodeling ◽  
Ischemia Reperfusion ◽  
Photon Emission ◽  
Coronary Intervention ◽  
Left Ventricular ◽  
Volume Index ◽  
Emission Computed Tomography ◽  
Lv Remodeling

Left ventricular (LV) remodeling after acute myocardial infarction (AMI) is a precursor of the development of overt heart failure and is an important predictor of mortality. Adiponectin (AN) is an adipose-derived plasma protein that has the cardio-protective role against ischemia-reperfusion injury. Altered activity of matrix metalloproteinase (MMP) family has been implicated in the development of LV remodeling after myocardial infarction. Serum AN levels affect MMPs and tissue inhibitor of MMP (TIMP) levels, and attenuate adverse LV remodeling after AMI. In 88 consecutive patients with AMI successfully treated with primary percutaneous coronary intervention (PCI), serum levels of AN, MMP-2, MMP-9, and TIMP-1 were measured on admission, at day 7, and at 6 months after the onset. LV end-diastolic volume index (EDVI) and ejection fraction (EF) were assessed with 99m− Tc-tetrofosmin quantitative gated single-photon emission computed tomography within 10 days (early) and six months (chronic) after the onset. Serum AN and MMP-2 levels were decreased and serum MMP-9 and TIMP-1 levels were increased at day 7 compared to those at the onset and 6 months. Chronic/early EDVI ratio was negatively correlated with log AN at day 7 (r= −0.265, p=0.013), log AN at 6 months (r= −0.335, p=0.008), log MMP-2 at day 7 (r= −0.229, p=0.042), and positively correlated with log MMP-9 at day 7 (r= 0.237, p=0.037), log TIMP-1 on admission (r=0.277, p=0.0408). Chronic EF was positively correlated with log AN at day 7 (r=0.225, p=0.0374) and negatively correlated with log TIMP-1 at day 7 (r= −0.281, p=0.0133). Multiple logistic regression analyses revealed that chronic/early EDVI ratio independently correlated with log AN (r= −0.249, p=0.034) at day 7, although Log AN correlated positively log MMP-2, and negatively with log MMP-9 both at day 7 and 6 months. Measurement of AN at subacute phase can predict adverse cardiac remodeling in patients with AMI successfully treated with PCI.

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