Relevant bibliographies by topics / Myocardial infarction

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Myocardial infarction'

Author: Grafiati
Published: 4 June 2021
Last updated: 29 July 2024

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Journal articles on the topic "Myocardial infarction"

1

Strömbäck, Ulrica, Åsa Engström, Robert Lundqvist, Dan Lundblad, and Irene Vikman. "The second myocardial infarction: Is there any difference in symptoms and prehospital delay compared to the first myocardial infarction?" European Journal of Cardiovascular Nursing 17, no. 7 (May 11, 2018): 652–59. http://dx.doi.org/10.1177/1474515118777391.

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Background: Knowledge is limited concerning the type of symptoms and the time from onset of symptoms to first medical contact at first and second myocardial infarction in the same patient. Aim: This study aimed to describe the type of symptoms and the time from onset of symptoms to first medical contact in first and second myocardial infarctions in men and women affected by two myocardial infarctions. Furthermore, the aim was to identify factors associated with prehospital delays ≥2 h at second myocardial infarction. Methods: A retrospective cohort study with 820 patients aged 31–74 years with a first and a second myocardial infarction from 1986 through 2009 registered in the Northern Sweden MONICA registry. Results: The most common symptoms reported among patients affected by two myocardial infarctions are typical symptoms at both myocardial infarction events. Significantly more women reported atypical symptoms at the second myocardial infarction compared to the first. Ten per cent of the men did not report the same type of symptoms at the first and second myocardial infarctions; the corresponding figure for women was 16.2%. The time from onset of symptoms to first medical contact was shorter at the second myocardial infarction compared to the first myocardial infarction. Patients with prehospital delay ≥2 h at the first myocardial infarction were more likely to have a prehospital delay ≥2 h at the second myocardial infarction. Conclusions: Symptoms of second myocardial infarctions are not necessarily the same as those of first myocardial infarctions. A patient’s behaviour at the first myocardial infarction could predict how he or she would behave at a second myocardial infarction.
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Ristic-Andjelkov, Andjelka, Branislav Baskot, Milorad Damjanovic, and Sasa Rafajlovski. "Ischemic preconditioning." Vojnosanitetski pregled 62, no. 1 (2005): 73–77. http://dx.doi.org/10.2298/vsp0501073r.

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Background. Ischemic preconditioning is a phenomenon during which myocardium, subjected to brief episodes of ischemia followed by reperfusion, tolerates better the subsequent, more prolonged episode of this ischemia, thus reducing the infarction size substantially. Case report. Two patients with acute left anterior descendent artery occlusion received fibrinolytic therapy (alteplase) within 6 hours of the onset of chest pain, but developed myocardial infarctions of different sizes. The first patient, without the history of preinfarction angina, developed large anterior infarct, because there was no time either for ischemic preconditioning or for the coronary collateral vessels development. In the second patient, with 4-day history of preinfarction angina, the more favorable outcome was seen he developed smaller apical necrosis, with the great degree of myocardial viability in the infarct-related area. Conclusion. Ischemic preconditioning in patients with acute myocardal infarction results in the reduction of mortality, infarction size, as well as in the frequency of malignant arrhythmias.
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Jenkins, Crystal P., Diana M. Cardona, Jennifer N. Bowers, Bahram R. Oliai, Robert W. Allan, and Sigurd J. Normann. "The Utility of C4d, C9, and Troponin T Immunohistochemistry in Acute Myocardial Infarction." Archives of Pathology & Laboratory Medicine 134, no. 2 (February 1, 2010): 256–63. http://dx.doi.org/10.5858/134.2.256.

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Abstract Context.—Full activation and involvement of the complement pathway follows acute myocardial infarction. Complement fragment C4d is a stable, covalently bound marker of complement activation. Troponin T is specific for cardiomyocytes. Objectives.—To determine the specificity of C4d, C9, and troponin T immunoreactivity in necrotic myocytes and to establish whether they can be used to delineate acute myocardial infarction. Design.—Twenty-six autopsy cases with a total of 54 myocardium areas of infarction were reviewed retrospectively. Immunohistochemistry for C4d, C9, and troponin T was used on paraffin sections of formalin-fixed tissue. Controls consisted of 5 cases without evidence of infarction, and histologically normal myocardium functioned as an internal control. Results.—C4d and C9 antibodies reacted strongly and diffusely with necrotic myocytes in all samples of infarctions for up to 2 days (19 of 19; 100%). Adjacent histologically normal myocytes were nonreactive, resulting in a clear delineation between damaged and viable myocardium. Reactivity declined with increased duration and was absent in scars. Troponin T showed loss of staining in preinflammatory lesions (8 of 13; 62%); however, nonspecific patchy loss of staining was present in negative controls and in viable myocardium. Immunostains provided new diagnoses in 2 cases, including evidence of reinfarction and a newly diagnosed acute myocardial infarction. Conclusions.—C4d and C9 have comparable reactivity and specificity for necrotic myocytes. C4d and C9 staining of necrotic myocytes is apparent before the influx of inflammatory cells, demonstrating utility in early myocardial infarction. Patchy loss of Troponin T in some cases of histologically normal myocardium limited its usefulness as a sole marker of infarction.
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Kurhaluk, Natalia, Krzysztof Tota, Małgorzata Dubik-Tota, and Halyna Tkachenko. "LEVEL OF ALDEHYDIC AND KETONIC DERIVATIVES OF OXIDATIVELY MODIFIED PROTEINS IN THE BLOOD OF MEN AND WOMEN WITH MYOCARDIAL INFARCTIONS AND HYPOTHYROIDISM." Biota. Human. Technology, no. 2 (December 29, 2022): 79–91. http://dx.doi.org/10.58407/bht.2.22.6.

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Oxidative stress and excessive reactive oxygen species production play considerable roles in infarction-induced injury impairing cardiac functions, as well as thyroid diseases. Purpose: assessment of the oxidative stress markers, including oxidation of proteins [concentrations of aldehydic and ketonic derivatives of oxidatively modified proteins (OMB)] in the blood of individuals with hypothyroidism and/or myocardial infarction living in the Central Pomerania. Methodology. The level of oxidative stress markers was assessed among 225 individuals, i.e. 132 males (58.67%) and 93 females (41.33%) aged 35-71 years residing in Central Pomerania. In the obtained plasma, an assessment of levels of aldehydic and ketonic derivatives of oxidatively modified protein analyses was carried out. Scientific novelty. The highest level of aldehydic and ketonic derivatives of oxidatively modified proteins was found in the group of males with myocardium infarctions and hypothyroidism compared to other groups. In females, an increase in aldehydic and ketonic derivatives was observed in the group with myocardial infarctions and in the group with hypothyroidism compared to the control group, while a decrease in aldehydic and ketonic derivatives was observed in subjects with myocardial infarction compared to individuals both with myocardial infarctions and hypothyroidism. In males, an increase in aldehydic and ketonic derivatives in both groups with myocardial infarctions and with hypothyroidism compared to the control group was observed, while in relation to the individuals with myocardial infarctions and hypothyroidism there was a decrease in aldehydic and ketonic derivatives in the group with myocardial infarctions and a decrease in ketonic derivatives in individuals with hypothyroidism. In addition, a decrease in the level of ketonic derivatives in the males with myocardial infarction and hypothyroidism compared to the group of females was observed. Conclusions. In the course of myocardial infarction, gender affects the level of the aldehydic derivatives of oxidative modification of proteins. Among individuals with hypothyroidism, the increase of ketonic derivatives of oxidatively modified proteins is also affected by sex. Analysis of oxidative stress markers depending on the sex may provide a biochemical basis for epidemiological differences in susceptibility to disease between sexes and suggest different strategies for risk assessment, diagnosis, and treatment specifically targeted at groups of males and females of different ages.
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Gosselin, H., X. Qi, and J. L. Rouleau. "Correlation between cardiac remodelling, function, and myocardial contractility in rat hearts 5 weeks after myocardial infarction." Canadian Journal of Physiology and Pharmacology 76, no. 1 (January 1, 1998): 53–62. http://dx.doi.org/10.1139/y97-175.

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Early after infarction, ventricular dysfunction occurs as a result of loss of myocardial tissue. Although papillary muscle studies suggest that reduced myocardial contractility contributes to this ventricular dysfunction, in vivo studies indicate that at rest, cardiac output is normal or near normal, suggesting that contractility of the remaining viable myocardium of the ventricular wall is preserved. However, this has never been verified. To explore this further, 100 rats with various-sized myocardial infarctions had ventricular function assessed by Langendorff preparation or by isolated papillary muscle studies 5 weeks after infarction. Morphologic studies were also done. Rats with large infarctions (54%) had marked ventricular dilatation (dilatation index from 0.23 to 0.75, p << 0.01) and papillary muscle dysfunction (total tension from 6.7 to 3.2 g/mm2, p << 0.01) but only moderate left ventricular dysfunction (maximum developed tension from 206 to 151 mmHg (1 mmHg = 133.3 Pa), p << 0.01), a decrease less than one would expect with an infarct size of 54%. The contractility of the remaining viable myocardium of the ventricle was also moderately depressed (peak systolic midwall stress 91 to 60 mmHg, p << 0.01). Rats with moderate infarctions (32%) had less marked but still moderate ventricular dilatation (dilatation index 0.37, p << 0.001) and moderate papillary muscle dysfunction (total tension 4.2 g/mm2, p << 0.01). However, their decrease in ventricular function was only mild (maximum developed pressure 178 mmHg, p << 0.01) and less than one would expect with an infarct size of 32%. The remaining viable myocardium of the ventricular wall appeared to have normal contractility (peak systolic midwall stress = 86 mmHg, ns). We conclude that in this postinfarction model, in large myocardial infarctions, a loss of contractility of the remaining viable myocardium of the ventricular wall occurs as early as 5 weeks after infarction and that papillary muscle studies slightly overestimate the degree of ventricular dysfunction. In moderate infarctions, the remaining viable myocardium of the ventricular wall has preserved contractility while papillary muscle function is depressed. In this relatively early postinfarction phase, ventricular remodelling appears to help maintain left ventricular function in both moderate and large infarctions. Key words: postinfarction, contractility, ventricular function, ventricular remodelling.
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Hirsch, Alan T., John A. Opsahl, Mary M. Lunzer, and Stephen A. Katz. "Active renin and angiotensinogen in cardiac interstitial fluid after myocardial infarction." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 6 (June 1, 1999): H1818—H1826. http://dx.doi.org/10.1152/ajpheart.1999.276.6.h1818.

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The renin-angiotensin system promotes cardiac hypertrophy after myocardial infarction. The purpose of this study was to measure renin and angiotensinogen in plasma and myocardium 10 days after myocardial infarction. Infarction involving 45 ± 4% of left ventricular circumference with accompanying hypertrophy was induced in rats ( n = 14). Plasma and myocardial renin were increased after infarction compared with sham controls ( n = 8) (27.4 ± 3.2 vs. 7.5 ± 1.8 ng ANG I ⋅ ml plasma ⋅ h−1, P < 0.0002; and 8.8 ± 1.6 vs. 2.5 ± 0.1 ng ANG I ⋅ g myocardium−1 ⋅ h−1, P < 0.008, respectively). After infarction, myocardial renin was correlated with infarct size ( r = 0.62, P < 0.02) and plasma renin ( r = 0.55, P < 0.04). Plasma angiotensinogen decreased in infarct animals, but myocardial angiotensinogen was not different from shams (1.1 ± 0.08 vs. 2.03 ± 0.06 nM/ml plasma, P < 0.002; and 0.081 ± 0.008 vs. 0.070 ± 0.004 nM/g myocardium, respectively). In conclusion, myocardial renin increased after infarction in proportion to plasma renin and infarct size, and myocardial angiotensinogen was maintained after infarction despite decreased plasma angiotensinogen and increased levels of myocardial renin.
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Nilsson, S., G. Wikström, A. Ericsson, M. Wikström, A. Waldenström, and A. Hemmingsson. "MR Imaging of Gadolinium-DTPA-BMA-Enhanced Reperfused and Nonreperfused Porcine Myocardial Infarction." Acta Radiologica 36, no. 4-6 (July 1995): 633–40. http://dx.doi.org/10.1177/028418519503600465.

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To investigate whether Gd-DTPA-BMA-enhanced MR imaging permits differentiation between reperfused and nonreperfused myocardial infarction, myocardial infarction was induced in 12 domestic pigs. In 6 pigs, Gd-DTPA-BMA, 0.3 mmol/kg b.w. was administered i.v. 60 min after the occlusion. In 6 other pigs, the infarctions were reperfused 80 min after the occlusion, followed by injection of Gd-DTPA-BMA after 20 min of reperfusion. Radiolabeled microspheres were used to confirm zero-flow during the occlusion period and reperfusion in the infarcted myocardium. All pigs were killed 20 min after injection of contrast medium, and the hearts were excised and imaged with MR. The Gd concentration was measured in infarcted and nonischemic myocardium by ICPAES. In the reperfused hearts, the infarctions were strongly highlighted, corresponding to a 5-fold higher Gd concentration in infarcted vis-à-vis nonischemic myocardium. In the hearts subjected to occlusion without reperfusion, there was only a rim of enhancement in the peripheral part of the infarctions.
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Nudrat Fatima. "Enhanced Myocardial Infarction Prediction Using Machine Learning Algorithms and Gender-Specific Insights." Journal of Electrical Systems 20, no. 7s (May 4, 2024): 973–88. http://dx.doi.org/10.52783/jes.3478.

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A serious medical condition called myocardial infarction (MI), sometimes referred to as a "heart attack," is caused by disruptions in the blood supply to the myocardium. This research examines the efficacy of machine learning (ML) algorithms in forecasting myocardial infarction (MI) using a dataset of 350 records. The study identifies key risk factors for predicting myocardial infarction (MI), such as elevated cholesterol levels, diabetes, advanced age, overall health status, mental well-being, obesity, physical activity, smoking habits, hypertension, and depression. Significantly, gender does not manifest as a predictor of myocardial infarction (MI) when employing various classification methods. The research achieves high accuracy rates of 89.32%, 87.53%, 81.29%, and 76.59% using different machine learning algorithms, including Deep Belief Network (DBN), C4.5, Random Forest (RF), and Bayesian Network (BN), respectively. Algorithm-specific rule sets identify correlations, with the C4.5 algorithm revealing interesting connections between smoking habits and protection against myocardial infarction (MI). Performance metrics like accuracy, precision, sensitivity, and specificity attest to the effectiveness of the proposed technique. The results demonstrate the superior performance of the DBN algorithm, surpassing other algorithms in terms of accuracy (89.32%), precision (84.04%), sensitivity (86.63%), and specificity (82.45%). This paper provides crucial insights into predictive modeling for myocardial infarction (MI), highlighting the importance of various risk factors and advanced machine learning (ML) algorithms. The results offer clinicians and researchers a strong foundation for comprehending and potentially averting myocardial infarction, relying on personalized patient profiles. This paper has the potential to significantly contribute to the field by applying ensemble classifiers and machine learning models to forecast gender-specific myocardial infarctions. As a result, diagnostic precision and patient outcomes could be revolutionized.
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Alemu, Rahel, Eileen E. Fuller, John F. Harper, and Mark Feldman. "Influence of Smoking on the Location of Acute Myocardial Infarctions." ISRN Cardiology 2011 (April 17, 2011): 1–3. http://dx.doi.org/10.5402/2011/174358.

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Objective. To determine whether there is an association between smoking and the location of acute myocardial infarctions. Methods. Using a cohort from our hospital and published cohorts from Ireland, Uruguay, and Israel, we calculated odds of having an inferior wall as opposed to an anterior wall acute myocardial infarction among smokers and nonsmokers. Results. In our cohort, there was a higher proportion of smokers than nonsmokers in patients with inferior acute myocardial infarctions than in patients with anterior infarctions. This difference was also present in each of the other cohorts. Odds ratios for an inferior versus an anterior acute myocardial infarction among smokers ranged from 1.15 to 2.00 (median odds ratio, 1.32). When the cohorts were combined (), the pooled odds ratio for an inferior as opposed to an anterior acute myocardial infarction among smokers was 1.38 ( confidence interval, 1.20 to 1.58) (). Conclusions. Cigarette smoking increases the risk of inferior wall acute myocardial infarction more than the risk of anterior wall infarction. Smoking thus appears to adversely affect the right coronary arterial circulation to a greater extent than the left coronary arterial circulation by a mechanism not yet understood.
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Nilsson, Stefan, Mats Wikström, Anders Ericsson, Gerhard Wikström, Anders Waldenström, Audun Øksendal, and Anders Hemmingsson. "MR Imaging of Double-Contrast Enhanced Porcine Myocardial Infarction." Acta Radiologica 36, no. 4-6 (July 1995): 346–52. http://dx.doi.org/10.1177/028418519503600404.

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MR imaging was performed to investigate whether Gd-DTPA-BMA-induced contrast enhancement of myocardial infarction is counteracted by Dy-DTPA-BMA. Myocardial infarction was induced in 5 pigs. Microdialysate probes were inserted in ischemic and nonischemic myocardium. Gd-DTPA-BMA (0.3 mmol/kg b.w.) and Dy-DTPA-BMA (1.0 mmol/kg b.w.) were administered i.v. 4 hours post occlusion. The microdialysate was collected every 10 min and measured for Gd and Dy using inductively coupled plasma atomic emission spectrometry. The pigs were sacrificed 2 hours after administration of contrast media. The concentration of both contrast agents was 3 times higher in infarcted myocardium than in nonischemic myocardium. The infarctions displayed high signal intensity in spin-echo sequences ex vivo. This lack of detectable susceptibility effects from Dy may be caused by loss of cell membrane integrity in infarcted tissue as shown by our microdialysate and biopsy data.
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Dissertations / Theses on the topic "Myocardial infarction"

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Elhdere, Souada Ahmed. "Illness cognitions in myocardial infarction." Thesis, University of Surrey, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.548363.

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Williams, John. "Marker proteins in myocardial infarction." Thesis, University of Ulster, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.359319.

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Ruparelia, Neil. "Monocytes in acute myocardial infarction." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:02ad6ebd-a8c2-4cb6-a1f7-0cdf8cec59ed.

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Acute myocardial infarction (AMI) results in the activation of the innate immune system with monocytes playing critical roles in both the initial inflammation following myocardial ischaemia and subsequent recovery. Monocytes are a heterogeneous cell population and observations from experimental models demonstrate that immediately following myocardial injury, classical inflammatory monocytes, which are highly phagocytic, are recruited to ischaemic myocardium from the bone marrow and spleen and peak at 48 hours. This is followed by the recruitment of non-classical monocytes that are involved in repair and healing, peaking at day 5. The monocyte response in humans following AMI is currently poorly understood. Due to their central role in the pathogenesis of AMI, monocytes are attractive both as potential biomarkers to inform of extent of myocardial injury (and recovery) and also as therapeutic targets with the specific targeting of monocytes in experimental models resulting in reduced infarction size and improved LV remodelling. However, in spite of these promising results and our greater understanding of the pathogenesis of AMI, no immune-modulating therapeutic has been translated into routine clinical practice. We therefore hypothesized that characterisation of the monocyte response to AMI by flow cytometry and gene expression profiling in both experimental models and humans would give novel insights into underlying biological processes and function (both locally in the myocardium and systemically), identify novel therapeutic targets, enable their use as cellular biomarkers of disease, and test conservation between species validating the experimental model for future investigation. Classical inflammatory monocytes were found to significantly increase in the peripheral blood 48 hours following AMI in both mice and humans, with the magnitude of the monocyte response correlating with the extent of myocardial injury in both species. Gene expression profiling of peripheral circulating monocytes following AMI identified a number of candidate genes, biological pathways and upstream regulators that were conserved between species and that could represent novel therapeutic targets. Furthermore, in an experimental model of AMI, leukocytes appeared to have effects beyond the ischaemic myocardium, with leukocyte recruitment in remote myocardium and in kidneys associated with elevated inflammatory markers and endothelial activation.
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Buchanan, Lynne M. "Psychophysiological recovery after acute myocardial infarction /." Thesis, Connect to this title online; UW restricted, 1989. http://hdl.handle.net/1773/7244.

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Dawson, Lynn Gail. "Coping behaviours in myocardial infarction rehabilitation." Thesis, University of British Columbia, 1986. http://hdl.handle.net/2429/25722.

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This study was designed to discover the coping behaviours used by patients six to twelve months following a myocardial infarction (MI). The conceptualization of coping behaviours was based on the UBC Model for Nursing which directed the researcher to examine coping behaviours used to meet the patients' basic human needs. The specific research question was, "What new or already established coping behaviours have patients utilized after an MI in an attempt to satisfy their basic human needs?" Seven participants who had experienced an MI six to twelve months previously, were recruited from cardiologists. Data were collected from the participants during interviews using semi-structured open-ended questioning technique. Data were coded and analyzed using the constant comparative method developed by Glaser and Strauss. Three themes that emerged from the data were: 1) coping behaviours related to risk reduction, 2) coping behaviours related to returning to normal, 3) coping behaviours related to reaching a new normal. The findings supported the need for lifestyle changes involving the use of existing coping behaviours and/or the development of new coping behaviours to meet subjects' basic human needs. Certain unmet basic human needs were identified following an MI which required the development of new coping behaviours to meet them. Nurses are in a unique position to assist MI patients in developing coping behaviours to meet their basic human needs. The descriptions and explanations of coping behaviours identified in this study may serve as a useful guide for nurses to help patients deal with changes in their lives and develop necessary coping behaviours to meet their basic human needs.
Applied Science, Faculty of
Nursing, School of
Graduate
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Dulku, Amarjit. "Causal attributions, worry and myocardial infarction." Thesis, University of Leicester, 2002. http://hdl.handle.net/2381/31333.

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Although previous research has pointed to worry as one of the highest causal attributions reported by MI patients, no studies have primarily investigated the concept of worry in this cohort. This study aimed to determine the prevalence of pathological worry in MI patients who reported worry as a causal factor to their MI (Experimental group), compared to MI patients that did not implicate worry as a causal attribute (Control group). A central hypothesis to this study was that higher pathological worry would be found in the Experimental group, and would be significantly associated with meta-worry (worry about worry), rather than health worry. The design was cross-sectional, and consisted of administering self-report questionnaires to a total of 34 post-MI patients (n=17 in each group). The questionnaire measured: pathological worry, meta-worry, anxiety, depression, and thought control strategies. Participants in the Experimental group were found to be significantly younger than the Control group, and a higher proportion were employed. The main results indicated that no differences were found between the two groups in terms of worries relating to their health. However, pathological worry, meta-worry, social worry, anxiety and the use of thought control strategies were significantly higher in the Experimental group, compared with the Control group. Interestingly, none of the participants (N=34) reported symptoms of depression at a clinical level. Further analysis revealed that pathological worry significant correlated with meta-worry and the thought control strategy known as 'Punishment'. In conclusion MI patients who rated worry highly as causal to their MI were also found to be more pathologically worried after their MI than participants who implicated physical factors as causal attributes. However, this pathological worry was not related to worry about health, but was regarded as a coping response that is best understood from a metacognitive model of a generalised anxiety disorder.
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Stuckey, Daniel James. "Stem cell therapy for myocardial infarction." Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.442996.

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Volmink, James Andrew. "The Oxford Myocardial Infarction Incidence Study." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.389026.

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de, Waha Suzanne, Ingo Eitel, Steffen Desch, Georg Fuernau, Philipp Lurz, Thomas Stiermaier, Stephan Blazek, Gerhard Schuler, and Holger Thiele. "Prognosis after ST-elevation myocardial infarction." Universitätsbibliothek Leipzig, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-148644.

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Background: This study aimed to evaluate the incremental prognostic value of infarct size, microvascular obstruction (MO), myocardial salvage index (MSI), and left ventricular ejection fraction (LV-EFCMR) assessed by cardiac magnetic resonance imaging (CMR) in comparison to traditional outcome markers in patients with ST-elevation myocardial infarction (STEMI) reperfused by primary percutaneous intervention (PCI). Methods: STEMI patients reperfused by primary PCI (n = 278) within 12 hours after symptom onset underwent CMR three days after the index event (interquartile range [IQR] two to four). Infarct size and MO were measured 15 minutes after gadolinium injection. T2-weighted and contrast-enhanced CMR were used to calculate MSI. In addition, traditional outcome markers such as ST-segment resolution, pre- and post-PCI Thrombolysis In Myocardial Infarction (TIMI)-flow, maximum level of creatine kinase-MB, TIMI-risk score, and left ventricular ejection fraction assessed by echocardiography were determined in all patients. Clinical follow-up was conducted after 19 months (IQR 10 to 27). The primary endpoint was defined as a composite of death, myocardial reinfarction, and congestive heart failure (MACE). Results: In multivariable Cox regression analysis, adjusting for all traditional outcome parameters significantly associated with the primary endpoint in univariable analysis, MSI was identified as an independent predictor for the occurrence of MACE (Hazard ratio 0.94, 95% CI 0.92 to 0.96, P <0.001). Further, C-statistics comparing a model including only traditional outcome markers to a model including CMR parameters on top of traditional outcome markers revealed an incremental prognostic value of CMR parameters (0.74 versus 0.94, P <0.001). Conclusions: CMR parameters such as infarct size, MO, MSI, and LV-EFCMR add incremental prognostic value above traditional outcome markers alone in acute reperfused STEMI.
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Chew, Eng Wooi. "Ventricular late potentials in myocardial infarction." Thesis, Queen's University Belfast, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334467.

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Books on the topic "Myocardial infarction"

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J, Gersh Bernard, and Rahimtoola Shahbudin H, eds. Acute myocardial infarction. 2nd ed. NewYork: Chapman & Hall, 1996.

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David, McCall, ed. Acute myocardial infarction. New York: Churchill Livingstone, 1991.

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J, Gersh Bernard, and Rahimtoola Shahbudin H, eds. Acute myocardial infarction. New York: Elsevier, 1991.

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Blocker, William P. Rehabilitation after myocardial infarction. Basle: CIBA-Geigy, 1986.

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E, Bush David, United States. Agency for Healthcare Research and Quality., and Johns Hopkins University. Evidence-based Practice Center., eds. Post-myocardial infarction depression. Rockville, MD: Agency for Healthcare Research and Quality, 2005.

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NHS Centre for Reviews & Dissemination., ed. Aspirin and myocardial infarction. York: NHS Centre for Reviews and Dissemination, University of York, 1995.

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E, Manson JoAnn, ed. Prevention of myocardial infarction. New York: Oxford University Press, 1996.

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F, Oliver M., Vedin Anders, and Wilhelmsson Claes, eds. Myocardial infarction in women. Edinburgh: Churchill Livingstone, 1986.

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Minatoguchi, Shinya. Cardioprotection Against Acute Myocardial Infarction. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-15-0167-8.

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Williams, John. Marker proteins in Myocardial Infarction. [s.l: The Author], 1990.

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Book chapters on the topic "Myocardial infarction"

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Becker, Christoph R. "Myocardial Infarction." In Integrated Cardiothoracic Imaging with MDCT, 251–56. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-72387-5_17.

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Selvester, Ronald H., David G. Strauss, and Galen S. Wagner. "Myocardial Infarction." In Electrocardiology, 169–264. London: Springer London, 2011. http://dx.doi.org/10.1007/978-0-85729-874-4_4.

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Seaver, Robert L. "Myocardial Infarction." In When Doctors Get Sick, 29–38. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4899-2001-0_4.

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Roth, Elliot J. "Myocardial Infarction." In Encyclopedia of Clinical Neuropsychology, 2316–17. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_2192.

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Saclarides, Theodore J. "Myocardial Infarction." In Common Surgical Diseases, 103–6. New York, NY: Springer New York, 1998. http://dx.doi.org/10.1007/978-1-4757-2945-0_24.

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Liu, Peijun, Yining Wang, and Zheng-yu Jin. "Myocardial Infarction." In Cardiac CT, 9–14. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5305-9_2.

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Roth, Elliot J. "Myocardial Infarction." In Encyclopedia of Clinical Neuropsychology, 1–2. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-56782-2_2192-2.

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Ko, Hanjo. "Myocardial Infarction." In Anesthesiology, 13–18. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-50141-3_2.

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Blake, Thomas M. "Myocardial Infarction." In The Practice of Electrocardiography, 173–85. Totowa, NJ: Humana Press, 1994. http://dx.doi.org/10.1007/978-1-4612-0291-2_11.

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Miura, Tetsuji, Derek M. Yellon, and James M. Downey. "Myocardial Infarction." In Physiology and Pathophysiology of the Heart, 955–74. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0873-7_47.

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Conference papers on the topic "Myocardial infarction"

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Mehri, Sounira, Wided Khamlaoui, and Mohamed Hammami. "Acute myocardial infarction." In the Fourth International Conference. New York, New York, USA: ACM Press, 2018. http://dx.doi.org/10.1145/3234698.3234741.

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Discher, Dennis, and Adam Engler. "Mesenchymal Stem Cell Injection After Myocardial Infarction Improves Myocardial Compliance." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176754.

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Cellular therapy for myocardial injury has improved ventricular function in both animal and clinical studies, though the mechanism of benefit is unclear. This study was undertaken to examine the effects of cellular injection after infarction on myocardial elasticity. Coronary artery ligation of Lewis rats was followed by direct injection of human mesenchymal stem cells (MSC) into the acutely ischemic myocardium. Two weeks post-infarct, myocardial elasticity was mapped by atomic force microscopy. MSC-injected hearts near the infarct region were two-fold stiffer than myocardium from non-infarcted animals but softer than myocardium from vehicle-treated infarcted animals. After eight weeks, the following variables were evaluated: MSC engraftment and left ventricular geometry by histologic methods; cardiac function with a pressure-volume conductance catheter; myocardial fibrosis by Masson trichrome staining; vascularity by immunohistochemistry; and apoptosis by TUNEL assay. The human cells engrafted and expressed a cardiomyocyte protein but stopped short of full differentiation and did not stimulate significant angiogenesis. MSC-injected hearts showed significantly less fibrosis than controls, as well as less left ventricular dilation, reduced apoptosis, increased myocardial thickness, and preservation of systolic and diastolic cardiac function. In summary, MSC injection after myocardial infarction did not regenerate contracting cardiomyocytes but reduced the stiffness of the subsequent scar and attenuated post-infarction remodeling, preserving some cardiac function. Improving scarred heart muscle compliance could be a functional benefit of cellular cardiomyoplasty.
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Maneska, Marijana, and Vladimir Ristovski. "Not a myocardial infarction." In RAD Conference. RAD Centre, 2023. http://dx.doi.org/10.21175/rad.abstr.book.2023.24.1.

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Sills, T. H., and S. Heptinstall. "BLOOD TAURINE AFTER MYOCARDIAL INFARCTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643021.

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Taurine, an amino acid that is present in high concentrations in the heart, is released from the heart after myocardial damage. There is evidence that the concentration of taurine in whole blood is raised after myocardial infarction (MI), and it has been suggested that blood taurine may be a measure of the degree of infarction. We have obtained serial measurements of blood taurine in patients admitted to a coronary care unit and have compared the results with those obtained for two cardiac enzymes (AST and HBD) and other blood parameters.The patients were divided into two groups: those for whom there was a peak of AST activity (> 40 i.u./l) (Group 1, n = 24) and those for whom AST and HBD was not raised (Group 2, n = 15). For Group 1 patients, mean results were obtained for each of the parameters for the day on which AST peaked (designated Day 0) and for preceeding and subsequent days. For Group 2 a single mean was obtained. Results marked * in the table differ significantly (p < 0.05 or lower) from those for Group 2:It can be seen that blood taurine was significantly raised after MI and followed a pattern similar to the neutrophil count. Furthermore, several positive correlations (r = 0.63-0.79) were obtained between taurine and neutrophil count in both groups, but not between taurine and AST or HBD.In another investigation we measured the amounts of taurine in neutrophils, platelets and plasma from patients with MI (n = 5) and controls (n = 9). We found no differences in the amounts present per neutrophil, per platelet or per ml of plasma.Our data suggest that the increased level of taurine in blood after MI merely reflects the increased number of neutrophils present in blood following the event.
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Mehri, Sounira, and Mohamed Hammami. "Clinical and biochemical factors associated with acute myocardial infarction: Risk factors for acute myocardial infarction." In 2017 International Conference on Engineering & MIS (ICEMIS). IEEE, 2017. http://dx.doi.org/10.1109/icemis.2017.8273109.

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Zhang, Pei, Tieluo Li, Katrina Williams, Shuyin Li, Xufeng Wei, Hosung Son, Pablo Sanchez, Bartley P. Griffith, and Zhongjun J. Wu. "Analysis of Infarct Size on Myocardial Infarction Remodeling." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53117.

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In the United States, over one million patients sustain left ventricular (LV) injury after myocardial infarction (MI). LV remodeling is an adaptive process of hypertrophy that includes infarct expansion, reduced contractility and LV dilation. Progressive enlargement of non-ischemic, hypocontractile myocardium in the adjacent zone (AZ) following the transmural MI has been identified clinically, which contributes to the development post-MI cardiomyopathy in patients. Till now, how the early regional biomechanical and cellular changes, particularly in the AZ, relate to LV remodeling process remains incompletely understood. This study aims to investigate the temporal and/or spatial variations of strain/stress and myocyte size in an ovine model with various MI sizes.
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Zhang, Song, John A. Crow, Robert C. Cooper, Ronald M. McLaughlin, Shane Burgess, Ali Borazjani, and Jun Liao. "Detection of Myocardial Fiber Disruption in Artificial Lesions With 3D DT-MRI Tract Models." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193121.

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In the United States, it is estimated that in 2008 approximately 1.2 million people will suffer a new or recurrent myocardial infarction. In 2005, the latest full year for which statistics are available, 16 million Americans (7.3% of the population) had some form of coronary heart disease. Loss of myocardium as a result of myocardial infarction increases wall stress locally and globally and triggers adaptive responses at the molecular, cellular, and tissue levels. These adaptive responses can lead to left ventricular dilation and congestive heart failure. Accurate non-invasive evaluation of myocardial structural degeneration (damage) and left ventricular remodeling following an infarct would have both prognostic and therapeutic value clinically.
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Villemant, D., P. Barriot, and P. Bodenan. "THROMBOLYSIS AND ACUTE MYOCARDIAL INFARCTION (AMI)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642981.

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AMI is a major cause of morbidity and mortality in modern society Conventional treatment has no benefic effect on the size of infarct, alteration of left ventricular (LV) function and mortality. Intravenous (IV) thrombolysis reduces in hospital mortality by 23 % if infused within 3 hours of ischemia, 47 % if within 1 hour. It reduces the size of infarct by 51 % if reperfusion occurs within 1 hour of ischemia, 31 % if between 1 and 2 hours and 13 % if between 2 and 4 hours. The preservation of LV function is of 28 to 42%. These benefic effects, thanks to IV thrombolysis, can be obtained only if reperfusion occurs within 3 or 4 hours of ischemia. Unfortunately, a french prospective study “ENIM 84” estimates that the mean delay between onset of chest pain and arrival at hospital is 10,3 hours.Goals of the study were to show that “at home” thrombolysis: 1) is a feasible and a safe technique, 2) is responsible of a significant saving of time, 3) preserves LV function according to the precocity of treatment.Two groups of patients (pts) are compared : group A : 62 pts had “at home” thrombolysis by a trained medical staff aboard a mobile emergency care unit. Group B : 53 pts had thrombolysis at arrival at CCU. Protocol is simular in both groups : An IV infusion of 1 5 M iu of streptokinase over 45 to 60 min after an IV bolus of 100 mg Hydrocortisone. Criteriae and contra-indications are those usually used for thrombolysis. Radionuclide angiography was performed 4 days and 1 month after AMI to evaluate global and regional ejection fraction (EF). Only 1 hemorrhagic complication (a mild melaena) and 2 reversible ventricular fibrillations were reported. Reperfusion arrythmias were frequent (55 %) but do not need treatment. The number of candidates for thrombolysis is then increased. The saving of time is 73 min. Difference between the 4 days and 1 month EF is not significant in pts with conventional treatment or if reperfusion occurs after 4 hours of ischemia 48 ± 11 % vs 51 ± 13 %.But it is significant if before 4 hours 49 ± 11 % vs 56 ± 12 % and highly significant if before 2 hours 48 ± 12 % vs 59 ± 10 %.
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Zhong, Jianing. "Acute Myocardial Infarction and Related Drugs." In The International Conference on Biomedical Engineering and Bioinformatics. SCITEPRESS - Science and Technology Publications, 2022. http://dx.doi.org/10.5220/0011238600003443.

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Tsgoev, Ch A. "REACTION-DIFFUSION MODEL OF MYOCARDIAL INFARCTION." In OpenBio-2023. ИПЦ НГУ, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-35.

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A series of numerical studies of the necrotic cell death process and inflammatory response in ischemic myocardial infarction has been performed using a minimal mathematical model of aseptic inflammation dynamics. The main attention is focused on the analysis of regularities of spatial and temporal development of the process. Evaluations of the efficacy of a number of hypothetical therapeutic strategies have been performed. The modeling results are in agreement with experimental data.
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Reports on the topic "Myocardial infarction"

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Li, Xiao, Fayang Ling, Wenchuan Qi, Sanmei Xu, Bingzun Yin, Zihan Yin, Qianhua Zheng, Xiang Li, and Fanrong Liang. Preclinical Evidence of Acupuncture on infarction size of Myocardial ischemia: A Systematic Review and Meta-Analysis of Animal Studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0044.

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Review question / Objective: Whether acupuncture is effective for infarction size on myocardial ischemia rat models. Condition being studied: Myocardial ischemia is a typical pathological condition of coronary heart disease (CHD), which has been a global issue with high incidence and mortality. Myocardial infarction caused by myocardial ischemia leads to cardiac dysfunction, and the size of myocardial infarction also determines the recovery and prognosis of cardiac function. Acupuncture, a long history of traditional Chinese medicine, is widely used to treat symptoms like thoracalgia and palpitation. Many researches based on rat experiments have shown that acupuncture affects infarction size, cardiac function, myocardial enzyme or arrhythmias severity on myocardial ischemia models; nevertheless, few literatures have systematically reviewed these studies, assessing the risk of bias, quality of evidence, validity of results, and summarizing potential mechanisms. A systematic review of animal studies can benefit future experimental designs, promote the conduct and report of basic researches and provide some guidance to translate the achievements of basic researches to clinical application in acupuncture for myocardial ischemia. Therefore, we will conduct this systematic review and meta analysis to evaluate effects of acupuncture on infarction size on myocardial ischemia rat models.
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Dejong, Marla J., Kyungeh An, Candace C. Cherrington, and Debra K. Moser. Predictors of Symptom Appraisal for Patients with Acute Myocardial Infarction. Fort Belvoir, VA: Defense Technical Information Center, November 2004. http://dx.doi.org/10.21236/ada427523.

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Crowley, James P., C. R. Valeri, and Joseph Chazan. Myocardial Infarction and Transfusion Requirements in Transfusion Dependent Anemic Patients. Fort Belvoir, VA: Defense Technical Information Center, May 1990. http://dx.doi.org/10.21236/ada360239.

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Naydenov, Stefan, Nikolay Runev, Emil Manov, Nadya Naydenova, Mikhail Matveev, and Plamen Krastev. Diagnostic Potential of Signal-Averaged Orthogonal Electrocardiography in Acute Myocardial Infarction. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, February 2021. http://dx.doi.org/10.7546/crabs.2021.02.16.

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Liu, Sihan, Shuo Han, Yingzi Lin, and Yingzhe Jin. The obesity paradox in patients with ST-segment elevation myocardial infarction. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2021. http://dx.doi.org/10.37766/inplasy2021.6.0015.

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Zhang, John Q. Post-Myocardial Infarction and Exercise Training on Myosin Heavy Chain and Cardiac Function. Science Repository, April 2019. http://dx.doi.org/10.31487/j.jicoa.2019.01.08.

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Yin, Ruoyun, Fan Zhang, Zhaoya Fan, Lei Tang, and Yuan Yang. Association between Abacavir Use With Myocardial Infarction: A systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2020. http://dx.doi.org/10.37766/inplasy2020.10.0054.

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De Jong, Marla J. A Cross-Sectional Examination of Changes in Anxiety Early After Acute Myocardial Infarction. Fort Belvoir, VA: Defense Technical Information Center, August 2003. http://dx.doi.org/10.21236/ada416443.

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Ratib, Karim, and Jim Nolan. ST-segment Elevation Myocardial Infarction Intervention in a Patient with Variant Radial Artery Anatomy. Radcliffe Cardiology, June 2017. http://dx.doi.org/10.15420/rc.2017.m007.

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De Jong, Marla J., Kyungeh An, Sharon McKinley, Bonnie J. Garvin, and Lynne A. Hall. Using a 0-10 Scale for Assessment of Anxiety in Patients with Acute Myocardial Infarction. Fort Belvoir, VA: Defense Technical Information Center, January 2003. http://dx.doi.org/10.21236/ada424770.

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