Myocardial Infarction
Best match
All
Pubmeds
(163K+)
Pubmed
Journal: Clinical chemistry
November/29/2015
Abstract
BACKGROUND
The limit of detection (LoD) is the minimal amount of a substance that can be consistently detected. In the diagnosis of acute myocardial infarction (AMI) many patients present with troponin concentrations below the LoD of contemporary sensitive cardiac troponin I (cs-cTnI) assays. These censored values below the LoD influence the diagnostic performance of these assays compared to highly sensitive cTnI (hs-cTnI) assays. Therefore we assessed the impact of a new approach for interpolation of the left-censored data of a cs-cTnI assay in the evaluation of patients with suspected AMI.
METHODS
Our posthoc analysis used a real world cohort of 1818 patients with suspected MI. Data on cs-cTnI was available in 1786 patients. As a comparator the hs-cTnI version of the assay was used. To reconstruct quantities below the LoD of the cs-cTnI assay, a gamma regression approach incorporating the GRACE (Global Registry of Acute Coronary Events) score variables was used.
RESULTS
Censoring of cs-cTnI data below the LoD yielded weaker diagnostic information [area under the curve (AUC), 0.781; 95% CI, 0.731-0.831] regarding AMI compared to the hs-cTnI assay (AUC, 0.949; CI, 0.936-0.961). Use of our model to estimate cs-cTnI values below the LoD showed an AUC improvement to 0.921 (CI, 0.902-0.940). The cs-cTnI LoD concentration had a negative predictive value (NPV) of 0.950. An estimated concentration that was to be undercut by 25% of patients presenting with suspected AMI was associated with an improvement of the NPV to 0.979.
CONCLUSIONS
Estimation of values below the LoD of a cs-cTnI assay with this new approach improves the diagnostic performance in evaluation of patients with suspected AMI.
Pubmed
Journal: American heart journal
February/14/2004
Authors
Pubmed
Journal: Bulletins et memoires de la Societe medicale des hopitaux de Paris
April/30/2003
Authors
Pubmed
Journal: Autonomic neuroscience : basic & clinical
April/28/2014
Abstract
BACKGROUND
The aim of this study was to investigate the effects of chronic treatment with carvedilol in blood pressure (BPV) and heart rate (HRV) variability of rats with myocardial infarction (MI).
METHODS
MI was produced in male rats by ligature of anterior interventricular branch of left coronary artery. Control rats were submitted to a sham surgery (SO). MI and SO rats were randomized to receive for 30 days placebo (Plac 0.5% metilcelulose) or carvedilol (Carv, 2mg/Kg body weight/day, drinking water): SO-Plac (N = 10), SO-Carv (N = 10), MI-Plac (N = 12), MI-Carv (N = 13). Blood pressure (BP) was directly recorded in the awake animals and BPV was determined, in time (variance, mmhg(2)) and frequency domains by the autoregressive method. Statistical significance was set in P<0.05. Data are median and interquartile range.
RESULTS
No significant changes in HRV was observed in MI rats, while BPV showed significant decreasing of blood pressure variance (SO-Plac = 42.08 (39.21) mmHg(2) vs. MI-Plac = 21.67 (12.58) mmHg(2), P<0.05), reversed by the Carv treatment (MI-Plac = 21.67 (12.58) vs. MI-Carv = 38.64 (29.25), P<0.05). In the frequency domain analyses, MI reduced absolute and normalized LF component (LF (mmHg(2)): SO-Plac = 8.98 (14.84) vs. MI-Plac = 2.08 (4.84), P<0.05; LF(nu): SO-Plac = 79.48 (45.03) nu vs. MI-Plac = 24.25 (40.67) nu, P<0.05) and increased the normalized HF component of the BPV (SO-Plac = 20.51 (39.18) vs. MI-Plac = 60.51 (39.73). Carv treatment significantly attenuated the LF component fall.
CONCLUSIONS
Chronic treatment with carvedilol restored the variance of BPV altered by the MI.
Pubmed
Journal: Asian cardiovascular & thoracic annals
September/18/2016
Abstract
Coronary artery aneurysms are life-threatening conditions that are quite uncommon in adults. They are observed in 1.1% to 4.9% of patients undergoing coronary angiography. They are usually located in the right coronary artery, may sometimes be thrombosed or rupture, and occasionally reach an enormous size leading to compressive symptoms. We report a case of thrombosed left circumflex artery aneurysm presenting with myocardial infarction. The thrombosed aneurysm, which could not be clearly demonstrated by coronary angiography, was definitively diagnosed by coronary computed tomography angiography. No operation was planned owing to total thrombosis of the aneurysm.
Pubmed
Journal: Cardiovascular drugs and therapy
September/21/2016
Abstract
Numerous interventions have been shown to limit myocardial infarct size in animal models; however, most of these interventions have failed to have a significant effect in clinical trials. One potential explanation for the lack of efficacy in the clinical setting is that in bench models, a single intervention is studied without the background of other interventions or modalities. This is in contrast to the clinical setting in which new medications are added to the "standard of care" treatment that by now includes a growing number of medications. Drug-drug interaction may lead to alteration, dampening, augmenting or masking the effects of the intended intervention. We use the well described model of statin-induced myocardial protection to demonstrate potential interactions with agents which are commonly concomitantly used in patients with stable coronary artery disease and/or acute coronary syndromes. These interactions could potentially explain the reduced efficacy of statins in the clinical trials compared to the animal models. In particular, caffeine and aspirin could attenuate the infarct size limiting effects of statins; morphine could delay the onset of protection or mask the protective effect in patients with ST elevation myocardial infarction, whereas other anti-platelet agents (dipyridamole, cilostazol and ticagrelor) may augment (or mask) the effect due to their favorable effects on adenosine cell reuptake and intracellular cAMP levels. We recommend that after characterizing the effects of new modalities in single intervention bench research, studies should be repeated in the background of standard-of-care medications to assure that the magnitude of the effect is not altered before proceeding with clinical trials.
Pubmed
Journal: Ukrainskii biokhimicheskii zhurnal (1978)
September/14/1997
Pubmed
Journal: Cardiovascular drugs and therapy
July/1/1997
Abstract
Abnormally high levels of some hemostatic variables are often associated with the occurrence of the major ischemic complications of atherosclerosis, myocardial infarction, and stroke. Intervention studies have shown that prolonged treatment with antiplatelet drugs significantly reduces the recurrence of coronary and cerebral ischemic episodes. The association of the ischemic event with the hemostatic abnormality has often been just descriptive. Although suggestive, the link between the abnormality and the development and progression of atherosclerosis is only circumstantial. Finally, no information is available on the presence of one or more abnormal variables in subjects who did or did not experience a recurrence of thrombosis with treatment. To strengthen the clinical relevance of these hemostatic variables and to maximize the effectiveness of antithrombotic strategies, these indices should be taken into account in studies evaluating nonpharmacological and pharmacological interventions against arterial thrombosis. We believe that a task force on this subject would serve a useful purpose. The task force should develop and publicize within the cardiological community guidelines for (a) defining the size of the problem, (b) identifying the variables to measure, (c) standardizing detection and monitoring techniques, and (d) suggesting appropriate strategies of prevention and treatment.
Pubmed
Journal: Archives des maladies du coeur et des vaisseaux
August/20/1997
Abstract
The authors report the case of a woman admitted to hospital for minor trauma of the left hip and who presented major ST segment elevation on the second day suggesting an acute anterior wall myocardial infarction at the same time as a cerebrovascular accident. Complementary investigations and follow-up excluded the diagnosis of myocardial infarction with normalisation of the ECG on the 5th day. ECG changes during cerebrovascular accidents may be very variable ranging from extrasystoles to ST elevation mimicking myocardial infarction. They carry a poor prognosis with an increased risk of sudden death necessitating continuous ECG monitoring until the ECG reverts to normal. The cardiac involvement is not ischaemic but due to disease of the insular cortex of the brain which induces myocytolysis (centered around the intra-cardiac nerve endings) due to the sudden liberation of catecholamines. These lesions may be treated by propranolol or phentolamine.
Pubmed
Journal: Kardiologia polska
January/11/2004
Pubmed
Journal: Casopis lekaru ceskych
January/7/2004
Abstract
Acute coronary syndromes (ACS) are caused by neoinclusive thrombosis of the coronary artery. Arterial atherothrombosis usually results from a cracked atheroma plate and includes platelet and plasmatic component of coagulation. The aim of pharmacological treatment is to influence activated platelets and plasma procoagulant activity. Several clinical studies have demonstrated the benefits of antithrombotic treatment by acetylsalicylic acid, clopidogrel and by blockers of platelet receptors IIb/IIIa. In ACS anticoagulant therapy the non-fractionated heparin are replace ed by low-molecular heparins. The new standard in ACS therapy should become a combination of the acetylsalicylic acid, enoxaparine and clopidogrel. Blockers of platelet receptors IIb/IIIa should be given namely to patients indicated for the early invasive treatment.
Pubmed
Journal: Biochemical and biophysical research communications
August/31/1994
Abstract
Infarcted areas of rabbit myocardium show relatively higher inducible nitric oxide synthase activity, measured by the conversion of L-[14C]arginine to L-[14C]citrulline. The principal finding in this study is that dexamethasone (2 mg/kg) prevents the induction of inducible nitric oxide synthase in heart muscle when given before, or even 3 hr after coronary artery ligation. Additionally cyclic GMP levels remain unchanged following treatment with dexamethasone. It is possible that the enhanced production of nitric oxide by inducible nitric oxide synthase accounts, at least in part, for the depression of myocardial contractility seen in myocardial infarction and in other clinical conditions.
Pubmed
Journal: Zentralblatt fur allgemeine Pathologie u. pathologische Anatomie
April/30/2003
Authors
Pubmed
Journal: Medical hypotheses
December/7/2015
Abstract
Remote ischaemic preconditioning is emerging as a promising clinical technique which can afford immediate protection against coronary ischaemia. The mechanisms which mediate the signal transduction from remote organ to the heart are still unclear. The role of ATP sensitive potassium channels in ischaemic preconditioning has been established. It is known that the red blood cell (RBC) acts as a mediator of local autoregulation in adjusting oxygen supply to demand by sensing hypoxia and releasing ATP locally to achieve vasodilatation in the adjacent vascular beds. Our hypothesis links these two known mechanisms. Remote ischaemic preconditioning and local RBC autoregulation might share a common mechanism using the ATP sensitive potassium channels. Therefore, we hypothesize that the signal transduction by RBC might be partly responsible for this protection against ischaemia.
Pubmed
Journal: Wiener klinische Wochenschrift
April/24/2016
Abstract
OBJECTIVE
Systems of care to treat acute ST-elevation myocardial infarction (STEMI) have been developed world wide in the past decade. Their effectiveness can only be proven by including and analyzing outcome data of consecutive patients in registries, which is not the case in the majority of STEMI networks. This study investigates 1-year mortality in STEMI patients in Vienna included over a 14 months time interval. The Vienna STEMI network is organized by a specific rotational system and offers both, primary percutaneous intervention (PPCI) and thrombolytic therapy (TT) as reperfusion strategies according to the recent guidelines.
METHODS
At the time of investigation, the Vienna STEMI network consisted of the Viennese Ambulance Systems and five high-volume interventional cardiology departments. This network has been organized in order to increase the number of STEMI patients admitted for PPCI and to offer the fastest available reperfusion strategy, in the majority PPCI but in selected patients also TT (STEMI of short duration, mainly anterior wall MI and mainly patients younger than 75 years), followed by rescue PCI in non-responders and elective angiography with/without PCI in responders to TT during the index hospital stay.
RESULTS
One-year all-cause mortality rates in the Vienna STEMI network by use of the fastest available reperfusion strategy were 13.4% in patients who received reperfusion therapy after 2 h of symptom onset and 7.4% in patients treated within 2 h; (p = 0.017). Whereas PPCI and TT demonstrated a nonsignificant difference in 1-year mortality rates when initiated within 2 h of symptom onset (10.0% vs 5.7%; p = 0.59), PPCI was more effective in acute STEMI of > 2 h duration as compared to TT but this difference did not reach statistical significance (12.1% vs 18.2%; p = 0.07).
CONCLUSIONS
The reassuring long-term results of the Viennese STEMI network are another example of a specific regional system of care to offer timely diagnosis, transfer and reperfusion in patients with STEMI. In contrast to other metropolitan areas where TT has almost completely abandoned, we still use pharmacological reperfusion as a backup in case of expected and unacceptable time delays for PPCI in order to reduce myocardial damage especially in patients with larger infarctions of short duration with a low risk of bleeding complications.
Pubmed
Journal: The Medical journal of Australia
February/6/1969
Pubmed
Journal: Chest
December/13/1973
Pubmed
Journal: Hoppe-Seyler's Zeitschrift fur physiologische Chemie
March/9/1975
Pubmed
Journal: Deutsche medizinische Wochenschrift (1946)
August/29/1974
Pubmed
Journal: Journal of cardiothoracic and vascular anesthesia
January/2/2003
Pubmed
Journal: Journal of thrombosis and haemostasis : JTH
September/21/2005
Authors
Pubmed
Journal: Stem cell research
March/24/2016
Abstract
Circulating endothelial progenitor cells (EPCs) provide revascularisation for cardiovascular disease and the expansion of these cells opens up the possibility of their use as a cell therapy. Herein we show that interleukin-3 (IL3) strongly expands a population of human non-adherent endothelial forming cells (EXnaEFCs) with low immunogenicity as well as pro-angiogenic capabilities in vivo, making their therapeutic utilisation a realistic option. Non-adherent CD133(+) EFCs isolated from human umbilical cord blood and cultured under different conditions were maximally expanded by day 12 in the presence of IL3 at which time a 350-fold increase in cell number was obtained. Cell surface marker phenotyping confirmed expression of the hematopoietic progenitor cell markers CD133, CD117 and CD34, vascular cell markers VEGFR2 and CD31, dim expression of CD45 and absence of myeloid markers CD14 and CD11b. Functional experiments revealed that EXnaEFCs exhibited classical properties of endothelial cells (ECs), namely binding of Ulex europaeus lectin, up-take of acetylated-low density lipoprotein and contribution to EC tube formation in vitro. These EXnaEFCs demonstrated a pro-angiogenic phenotype within two independent in vivo rodent models. Firstly, a Matrigel plug assay showed increased vascularisation in mice. Secondly, a rat model of acute myocardial infarction demonstrated reduced heart damage as determined by lower levels of serum creatinine and a modest increase in heart functionality. Taken together, these studies show IL3 as a potent growth factor for human CD133(+) cell expansion with clear pro-angiogenic properties (in vitro and in vivo) and thus may provide clinical utility for humans in the future.
Pubmed
Journal: Circulation research
February/8/2015
Pubmed
Journal: Minerva medica
April/30/2003
load more...