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Journal articles on the topic 'Myocardial infarction'

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

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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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2

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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3

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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5

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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6

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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7

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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8

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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9

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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10

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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11

I, Morild. "Unrecognized myocardial infarction in the elderly." Journal of Forensic Science and Research 1, no. 1 (2017): 077–86. http://dx.doi.org/10.29328/journal.jfsr.1001009.

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12

Jin, Jiyang, Min Chen, Yongjun Li, YaLing Wang, Shijun Zhang, Zhen Wang, Lin Wang, and Shenghong Ju. "Detecting Acute Myocardial Infarction by Diffusion-Weighted versus T2-Weighted Imaging and Myocardial Necrosis Markers." Texas Heart Institute Journal 43, no. 5 (October 1, 2016): 383–91. http://dx.doi.org/10.14503/thij-15-5462.

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We used a porcine model of acute myocardial infarction to study the signal evolution of ischemic myocardium on diffusion-weighted magnetic resonance images (DWI). Eight Chinese miniature pigs underwent percutaneous left anterior descending or left circumflex coronary artery occlusion for 90 minutes followed by reperfusion, which induced acute myocardial infarction. We used DWI preprocedurally and hourly for 4 hours postprocedurally. We acquired turbo inversion recovery magnitude T2-weighted images (TIRM T2WI) and late gadolinium enhancement images from the DWI slices. We measured the serum myocardial necrosis markers myoglobin, creatine kinase-MB isoenzyme, and cardiac troponin I at the same time points as the magnetic resonance scanning. We used histochemical staining to confirm injury. All images were analyzed qualitatively. Contrast-to-noise ratio (the contrast between infarcted and healthy myocardium) and relative signal index were used in quantitative image analysis. We found that DWI identified myocardial signal abnormity early (&lt;4 hr) after acute myocardial infarction and identified the infarct-related high signal more often than did TIRM T2WI: 7 of 8 pigs (87.5%) versus 3 of 8 (37.5%) (P=0.046). Quantitative image analysis yielded a significant difference in contrast-to-noise ratio and relative signal index between infarcted and normal myocardium on DWI. However, within 4 hours after infarction, the serologic myocardial injury markers were not significantly positive. We conclude that DWI can be used to detect myocardial signal abnormalities early after acute myocardial infarction—identifying the infarction earlier than TIRM T2WI and widely used clinical serologic biomarkers.
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13

Huda, MN, MZ Sayeed, MK Rahman, MMR Khan, and ARMS Ekram. "Right Ventricular Myocardial Infarction : Presentation and Acute Outcomes." TAJ: Journal of Teachers Association 25 (November 28, 2018): 42–46. http://dx.doi.org/10.3329/taj.v25i0.37557.

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Right Ventricular Infarction (RVI) complicating inferior wall myocardial infarction (MI) is common and associated with significant morbidity and mortality. We try to systematically assess the incidence, clinical presentation and in hospital outcomes of right ventricular myocardial infarction in a tertiary-care set up. This study was a descriptive, cross sectional observational series of consecutive patients with RVMI. All patients with acute inferior myocardial infarction (n=100) were enlisted. RVMI was diagnosed by ≥1mm ST elevation in lead V4R in right sided electrocardiogram. RVI occurred in 31% (n=31) of patients of acute inferior infarctions. Patients with isolated inferior myocardial infarction served as controls (n=69). Echocardiography was performed within 24 hours of admission. From both groups, 51% were qualified for thrombolysis. The incidence of hypotension (96.7%), cardiogenic shock (64.5%), bradycardia and heart block were much higher in RVI than in inferior myocardial infarction. Clinically manifest RV dysfunction (raised jugular venous pulse, hypotension and tricuspid regurgitation) and right ventricular dilatation detected by echocardiography was seen in a variable number of patients. In hospital mortality rate was significantly higher (n=13, 41.9%) in right ventricular infarction group than in inferior myocardial infarction group (n=2, 2.9%)TAJ 2012; 25: 42-46
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14

Libova, L., P. Minarik, A. Solgajova, T. Sollar, D. Zrubcova, J. Turzakova, and G. Vorosova. "Gender, Age, previous Myocardial Infarction, and Personality as Predictors of Anxiety in Patients after Myocardial Infarction." Clinical Social Work and Health Intervention 12, no. 3 (September 30, 2021): 97–103. http://dx.doi.org/10.22359/cswhi_12_3_17.

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Objectives: The first research objective was to study the prevalence of anxiety in patients after myocardial infarction; next objective was to investigate demographic and personality predictors of anxiety. Methods: 100 hospitalized patients after myocardial infarction were studied. The Mini IPIP tool was used for the evaluation of personality characteristics and HADS-A scale was used for the evaluation of anxiety. Multiple regression was used as an analytical framework. Results: The prevalence of significant anxiety among patients after myocardial infarction was high, almost one half of patients reported abnormal anxiety symptoms. Female gender, higher age, higher neuroticism and lower conscientiousness explain 66% of the variability of anxiety. Personality traits of extraversion, openness, agreeableness and previous myocardial infarctions do not show as significant predictors. Conclusion: The prevalence of anxiety in the group of patients after myocardial infarction is high. Knowing predictors of anxiety is important for better provision of care.
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15

KANMATSUSE, Katsuo, Ken NAGAO, and Nagao KAJIWARA. "Myocardial Infarction." Japanese Journal of Thrombosis and Hemostasis 1, no. 1 (1990): 25–29. http://dx.doi.org/10.2491/jjsth.1.25.

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16

Van Dijk, Maico, Jolanda Schuur, Jan Van Ree, and Eric Van Wijlick. "Myocardial Infarction." European Journal of General Practice 3, no. 4 (January 1997): 138–42. http://dx.doi.org/10.3109/13814789709160349.

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17

Smith, Edward A. "Myocardial infarction." Postgraduate Medicine 102, no. 5 (November 1997): 77–78. http://dx.doi.org/10.3810/pgm.1997.11.352.

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18

Rafflenbeul, W., and F. Ebner. "Myocardial Infarction." Drugs 42, Supplement 2 (1991): 38–42. http://dx.doi.org/10.2165/00003495-199100422-00007.

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19

Ahmed, Saeed, Hina Zubair, Khawaja Abdul Hamid, Faisal Bashir, and Muhammed Shahbaz Bakth Kayani. "MYOCARDIAL INFARCTION;." Professional Medical Journal 24, no. 03 (March 7, 2017): 392–97. http://dx.doi.org/10.29309/tpmj/2017.24.03.1555.

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Coronary artery disease is one of the major cause of mortality in the modernworld and will become the leading cause of death by 2020, percutaneous coronary interventionhas proven to be most efficient in STEMI to decrease the mortality. Objectives: This studywas designed to determine the procedural success of Primary PCI in patients with Acute STsegment elevation Myocardial infarction. Study Design: It was an observational study. Placeand Duration: Cardiology unit of P.I.M.S, Islamabad, conducted from 2nd November 2011 to2nd May 2012. Patients and Methods: This study included 43 patients with Acute STEMI. Allof them had primary PCI. The main outcome variable was frequency of procedural successdescribed as TIMI flow II or III, which was described as frequency distribution table. Results:Procedural success was achieved among all (100%) patients. Conclusions: The proceduralsuccess of primary PCI is high (almost successful in every case) and should be offered to thepatients with Acute STEMI whenever the facility is available.
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ALI, LIAQAT, ABDUL REHMAN ABID, JAHANGIR AHMED, Nusrat Niaz, Tahira Abdul Rehman, and Muhammad Azhar. "MYOCARDIAL INFARCTION." Professional Medical Journal 18, no. 03 (September 10, 2011): 418–25. http://dx.doi.org/10.29309/tpmj/2011.18.03.2359.

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Objective: To determine clinical predictors of in-hospital complications in patients presenting with acute ST elevation myocardial infarction. Design: Descriptive Study. Period: from October 2010 to January 2011. Setting: Faisalabad Institute of Cardiology, Faisalabad.. Materials and methods: A total 342 patients with AMI were recruited in this study. All patients presenting with acute ST elevation myocardial infarction and fulfilling inclusion and exclusion criteria were included in the study. A full history was taken, particularly age, sex, occupation, address, history of smoking, diabetes mellitus, hypertension, ischemic heart disease and family history of ischemic heart disease. Primary end point was death while secondary end point were patients who had mechanical, ischemic or electrical complications or all of them. Results: Mean age of the study population was 56.3±12.7 years. There were 255(74.6%) males and 87(25.4%) females. There were 103(30.1%) diabetics, 137(40.1%) hypertensive and 174(50.9%) smokers. Family history of IHD was present in 34(9.9%). Obesity was observed in 60(17.5%). Dyslipidemia was observed in 45(13.2%). Majority of patients 123(36%) presented between 4-8 hours after the onset of symptoms. Only 72(21.1%) patients presented to the hospital within 4 hours of onset of symptoms. Overall 194(56.7%) patients had anterior wall myocardial infarction followed by Inferior wall myocardial infarction 84(24.6%) patients. Streptokinase therapy for thrombolysis was given to 236(69%) patients. Overall in-hospital mortality was 28(8.2%). Most frequent in-hospital complication was cardiogenic shock occurring in 38(11.1%) followed by Ischemic complications (Post MI angina and Re-MI) 37(10.8%), heart failure in 37(10.8%) and 1st and 2nd degree AV blocks in 36(10.5%) patients. In-hospital mortality was most significantly associated with site of MI i.e. anterior wall myocardial infarction (X2=28.88, p=0.0001) followed by patients not receiving Streptokinase therapy (X2=18, p=0.001), Age (X2=10.13, p=0.006). Site of MI had the highest Contingency Coefficient value of 0.279 followed by Streptokinase therapy 0.195 and age 0.170. Conclusions: Cardiogenic shock was the most frequent complication. Major predictors of in-hospital mortality were anterior wall myocardial infarction, patients not receiving streptokinase therapy and old age.
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KHAN BABAR, HAROON AZIZ, ZAHID RAFIQUE BUTT, and JAMIL AHMAD. "MYOCARDIAL INFARCTION." Professional Medical Journal 19, no. 04 (August 7, 2012): 442–45. http://dx.doi.org/10.29309/tpmj/2012.19.04.2248.

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Objective: To assess the frequency of hyperhomocysteinemia in patients of first attack of ST-segment elevated myocardialinfarction under age of 40 years. Design: Cross sectional study. Period: December 2009 to June 2010. Setting: Ch. Pervaiz Elahi Institute ofCardiology, Multan. Material and methods: A total of 65 patients of acute myocardial infarction were included in the study on the basis of chestpain, ECG changes and increased cardiac enzyme. Results: A total of 65 patients fulfilled the inclusion criteria were included the study. Meanage was 35.68 years. Out of the 65 patients, 87.7% were male and 12.3% were female, 41.5% patients has increased homocysteine level while68.5% had normal homocysteine level. Conclusions: Plasma Hcy is an important risk factor for the development of the acute myocardialinfarction.
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AHMAD, SHIEKH NADEEM, SYED SAUD HASAN, and MUHAMMAD YOUSUF SALAT. "MYOCARDIAL INFARCTION." Professional Medical Journal 18, no. 04 (December 10, 2011): 671–77. http://dx.doi.org/10.29309/tpmj/2011.18.04.2667.

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Thrombolytic therapy for Acute Myocardial Infarction has been one of the most potent treatment ever developed for condition that kill more patients worldwide than any other. Objective: To evaluate the benefit and efficacy or observational studies of streptokinase therapy on ST-segment elevation resolution in different types of myocardial infarction that focus especially on the younger age group less than forty years. Study design: To observe the streptokinase therapy, in ST-segment elevation resolution, in age less than 40 years and in different types of myocardial infarction. Place & duration of study: The study was conducted at national institute of cardiovascular diseases (NICVD) of Pakistan, Karachi. Subject and Methods: All patients fulfilling the inclusion criteria for thrombolytic therapy were included. Baseline ECG recorded before streptokinase infusion and repeated at completion of infusion i.e. 90 minutes, day 1 and day 2. Results: Streptokinase therapy on blood pressure, CKMB, and ST-segment resolution at 90 minutes, day 1, and Day2 in less than 40-year of age patient. The mean systolic blood pressure was 124+ 3.32 and 112+3.00 pre and post SK therapy reflecting a percentage decrease of 6.67 and highly significant (P<0.001). The Diastolic blood pressure was decrease to 6.25% with a mean value of 76.80+ 2.70 and 72+1.91 before and after the Streptokinase therapy’s, segment resolution at 90 minutes was decreased to 52.01 percent from the baseline and continued to decrease at Day-1 and Day-2 with a percentage reduction of 70.65 and 83.69 % respectively. The P values were highly significant (P<0.001). Conclusions: Thrombolysis improves survival when given within 12 hours of the onset of symptoms. The magnitude of benefit is greatest when reperfusion is established early. Age itself should not be considered a contraindication for fibronolysis
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Anjum, Muhammad, Muhammad Ammar Rashid, Aamir Hussain, and Sadia Imam. "MYOCARDIAL INFARCTION;." Professional Medical Journal 24, no. 09 (September 8, 2017): 1280–85. http://dx.doi.org/10.29309/tpmj/2017.24.09.814.

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Objectives: To determine the frequency of new onset heart failure after acutemyocardial infarction and factors contributing it. Methods: A total of 228 patients were studiedfor occurrence of new onset clinical heart failure within24 hours after admission with anacute Myocardial Infarction. Clinical parameters were used to diagnose heart failure. Variousrisk factors were analyzed which contributed to occurrence of heart failure after MI. Patientsundergoing primary angioplasty were not included into this study as medical thrombolysis wasthe most common mode of therapy (in >90% of patients). Results: Among the 228 patientsstudied 77.2 %( 176) were males and 22.8 %(52) were females. Mean age of the populationwas 56.3(±12.1) years. Women were relatively older on presentation as compared to men(mean age 58.9±10.9yr vs 55.5±12.3yr). Similarly mean age for NSTEMI was higher ascompared to STEMI (58.59±11.1 vs 54.2±12.6yr.). A total of36.8 %( 84) patients exhibitedclinical signs of heart failure within24 hours of their admission. These patients tend to be olderthan patients without HF (mean age 60±11years vs 54±12 years). Females after MI showed agreater frequency for going into HF as compared to males (42.3% vs 35.2% respectively). Nowregarding the association of HF with various factors it was seen that, having a previous historyof MI was found to be the strongest factor associated with occurrence of HF, with HF beingnearly three times more common in these patients (i.e. 73% vs 26.1%, p value < 0.05). Thecurrent type of MI on presentation also showed a direct relationship with HF, being highest inpatients with NSTEMI (i.e. up to 50 %) followed by AWMI (35.5%) and lowest in inferior wall MI (pvalue < 0.05). Diabetes, hypertension and smoking also showed a higher but statistically nonsignificantrelationship with HF development (41.2% vs 34.3%, 41% vs 32.2% and 44% vs 32%respectively p value > 0.05). The blood pressure on presentation however was significantlyassociated with HF in these patients. Patients having high BP (> 140/80) on presentationdepicted an overall higher incidence of HF as compared to patients having BP equal to or lessthan 140/80 (45.2% vs 31.3% p value < 0.05). Conclusion: Heart failure is a fairly commonentity after acute MI, being the commonest in patients suffering an NSTEMI. Previous history ofan MI showed to be the strongest coexisting factor associated with HF.
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24

Kuhn, MM. "Myocardial infarction." Critical Care Nurse 11, no. 1 (January 1, 1991): 14–19. http://dx.doi.org/10.4037/ccn1991.11.1.14.

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25

&NA;. "Myocardial Infarction." AJN, American Journal of Nursing 85, no. 1 (January 1985): 108–13. http://dx.doi.org/10.1097/00000446-198501000-00042.

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26

Hennekens, Charles H. "Myocardial infarction." Current Opinion in Cardiology 4, no. 4 (August 1989): 535–39. http://dx.doi.org/10.1097/00001573-198908000-00014.

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27

Dinerman, Jay, Larry Lopez, and Jawahar Mehta. "Myocardial infarction." Current Opinion in Cardiology 4, no. 4 (August 1989): 540–46. http://dx.doi.org/10.1097/00001573-198908000-00015.

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28

Kukin, Marrick, and Milton Packer. "Myocardial infarction." Current Opinion in Cardiology 4, no. 4 (August 1989): 547–50. http://dx.doi.org/10.1097/00001573-198908000-00016.

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29

Goldich, Guy. "Myocardial infarction." Nursing 35, no. 9 (September 2005): 32CC1–32CC6. http://dx.doi.org/10.1097/00152193-200509000-00021.

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30

KIMATA, SHIN'ICHI. "Myocardial infarction." Rinsho yakuri/Japanese Journal of Clinical Pharmacology and Therapeutics 25, no. 1 (1994): 335–37. http://dx.doi.org/10.3999/jscpt.25.335.

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31

Davies, M. K. "Myocardial infarction." Heart 87, no. 4 (April 1, 2002): 315. http://dx.doi.org/10.1136/heart.87.4.315.

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32

Evanoski, Carol Ann M. "Myocardial Infarction." Critical Care Nursing Clinics of North America 9, no. 4 (December 1997): 489–96. http://dx.doi.org/10.1016/s0899-5885(18)30242-9.

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33

Gwilt, D. J. "MYOCARDIAL INFARCTION." Lancet 341, no. 8843 (February 1993): 469–70. http://dx.doi.org/10.1016/0140-6736(93)90214-2.

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34

Espiner, Eric. "MYOCARDIAL INFARCTION." Lancet 341, no. 8851 (April 1993): 995–96. http://dx.doi.org/10.1016/0140-6736(93)91078-z.

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35

Lumsden, Karen. "Myocardial infarction." Emergency Nurse 19, no. 4 (July 5, 2011): 11. http://dx.doi.org/10.7748/en.19.4.11.s10.

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36

Meyer, Judy, and Medfilms Inc. "Myocardial Infarction." American Journal of Nursing 85, no. 1 (January 1985): 108. http://dx.doi.org/10.2307/3463697.

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37

Ryan, M. F. "Myocardial infarction." BMJ 296, no. 6637 (June 11, 1988): 1669. http://dx.doi.org/10.1136/bmj.296.6637.1669-d.

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38

BECKER, D., M. BIRGER, E. SAMUEL, and S. FLORU. "Myocardial Infarction." Journal of Nervous and Mental Disease 176, no. 6 (June 1988): 377–78. http://dx.doi.org/10.1097/00005053-198806000-00010.

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39

JOSE, JOSMY. "MYOCARDIAL INFARCTION." Nursing Journal of India LXXXXIII, no. 02 (2002): 29–30. http://dx.doi.org/10.48029/nji.2002.lxxxxiii201.

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40

Sulo, Gerhard, Jannicke Igland, Stein Emil Vollset, Marta Ebbing, Grace M. Egeland, Inger Ariansen, and Grethe S. Tell. "Trends in incident acute myocardial infarction in Norway: An updated analysis to 2014 using national data from the CVDNOR project." European Journal of Preventive Cardiology 25, no. 10 (May 29, 2018): 1031–39. http://dx.doi.org/10.1177/2047487318780033.

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Background We updated the information on trends of incident acute myocardial infarction in Norway, focusing on whether the observed trends during 2001–2009 continued throughout 2014. Methods All incident (first) acute myocardial infarctions in Norwegian residents age 25 years and older were identified in the Cardiovascular Disease in Norway 1994–2014 project. We analysed overall and age group-specific (25–64 years, 65–84 years and 85 + years) trends by gender using Poisson regression analyses and report the average annual changes in rates with their 95% confidence intervals. Results During 2001–2014, 221,684 incident acute myocardial infarctions (59.4% men) were identified. Hospitalised cases accounted for 79.9% of all incident acute myocardial infarctions. Overall, incident acute myocardial infarction rates declined on average 2.6% per year (incidence rate ratio 0.974, 95% confidence interval 0.972–0.977) in men and 2.8% per year (incidence rate ratio 0.972, 95% confidence interval 0.971–0.974) in women, contributed by declining rates of hospitalisations (1.8% and 1.9% per year in men and women, respectively) and deaths (6.0% and 5.8% per year in men and women, respectively). Declining rates were observed in all three age groups. The overall acute myocardial infarction incidence rates continued to decline from 2009 onwards, with a steeper decline compared to 2001–2009. During 2009–2014, gender-adjusted acute myocardial infarction incidence among adults age 25–44 years declined 5.3% per year, contributed mostly by declines in hospitalisation rates (5.1% per year). Conclusion Acute myocardial infarction incidence rates continued to decline after 2009 in Norway in both men and women. The decline started to involve individuals aged 25–44 years, marking a turning point in the previously reported stagnation of rates during 2001–2009.
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V.N., Priyanka, Anil Kumar V.R., and Nagamalesh U.M. "Acute Myocardial Infarction Presenting with Atypical Symptoms." Indian Journal of Emergency Medicine 4, no. 3 (2018): 161–64. http://dx.doi.org/10.21088/ijem.2395.311x.4318.8.

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42

Connors, KF, and GA Lamas. "Postmyocardial infarction patients: experience from the SAVE trial." American Journal of Critical Care 4, no. 1 (January 1, 1995): 23–28. http://dx.doi.org/10.4037/ajcc1995.4.1.23.

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Improving patient survival is the ultimate goal after acute myocardial infarction. Although thrombolytics, aspirin, and beta-blockers have greatly decreased mortality, structural changes such as ventricular dilatation evolving within the myocardium during and after acute myocardial infarction indicate a poor prognosis. The Survival and Ventricular Enlargement trial demonstrated that when administered 3 to 16 days after acute myocardial infarction in selected patients, captopril, the angiotensin-converting enzyme inhibitor, reduces ventricular dilatation, prevents the development of congestive heart failure, and reduces morbidity and mortality. This paper reviews results of that trial and presents guidelines for effective captopril dosage after acute myocardial infarction.
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43

Doggen, Carine J. M., Frits R. Rosendaal, and Joost C. M. Meijers. "Levels of intrinsic coagulation factors and the risk of myocardial infarction among men: opposite and synergistic effects of factors XI and XII." Blood 108, no. 13 (December 15, 2006): 4045–51. http://dx.doi.org/10.1182/blood-2005-12-023697.

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Abstract The role of the intrinsic coagulation system on the risk of myocardial infarction is unclear. In the Study of Myocardial Infarctions Leiden (SMILE) that included 560 men younger than age 70 with a first myocardial infarction and 646 control subjects, we investigated the risk of myocardial infarction for levels of factor XI (factor XIc) and factor XII (factor XIIc). Furthermore, the risks for factor VIII activity (factor VIIIc) and factor IX activity (factor IXc) were assessed. Factor XIc was 113.0% in patients compared with 109.8% in control subjects (difference, 3.2%; 95% CI, 1.1%-5.4%). The risk of myocardial infarction adjusted for age for men in the highest quintile compared with those in the lowest quintile was 1.8-fold increased (ORadj, 1.8; 95% CI, 1.2-2.7). In contrast, factor XIIc among patients with myocardial infarction was lower than in control subjects, respectively, 93.0% and 98.6% (difference, 5.6%; 95% CI, 3.3%-7.9%). The odds ratio of myocardial infarction for men in the highest quintile versus those in the lowest quintile was 0.4 (ORadj, 0.4; 95% CI, 0.2-0.5). The highest risk was found among men with both high factor XIc and low factor XIIc (analyses in tertiles: ORadj, 6.4; 95% CI, 2.2-18.0). Factor VIIIc increased the risk of myocardial infarction although not dose dependently. Factor IXc increased the risk; odds ratio of myocardial infarction for men in the highest quintile versus those in the lowest quintile was 3.2 (ORadj, 3.2; 95% CI, 2.0-5.1). Thus, factors XIc and XIIc have opposite and synergistic effects on the risk of myocardial infarction in men; factor VIIIc and factor IXc increase the risk.
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44

Dzhyhaliuk, O. V., D. A. Lysenko, D. G. Smolko, I. M. Kyrychenko, and S. V. Prokopenko. "Morphological changes in the conditions of adrenaline myocardial dystrophy against the background of the introduction of the compound PC-66 and amiodarone to rats." Reports of Morphology 26, no. 1 (May 22, 2020): 48–53. http://dx.doi.org/10.31393/morphology-journal-2020-26(1)-07.

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Adrenaline damage to the myocardium is an important element in the pathogenesis of myocardial infarction in humans. Despite the use of modern methods of treatment of myocardial infarction, the issue of cardioprotection of reperfusion myocardial damage remains open. Promising in this direction is the use of quinazolone derivatives, which have already shown cardioprotective properties in other models of myocardial infarction. The aim of the study was to establish morphological changes in the conditions of adrenaline myocardiodystrophy (AMD) against the background of the introduction of the compound PC-66 and amiodarone in rats. The study was performed on 100 nonlinear rats of both sexes weighing 165-220 g, divided into four groups of 25 animals each: 1 – intact rats; 2 – rats with a model of adrenaline myocardial infarction without treatment (control); 3 – rats with AMD treated with amiodarone (10 mg/kg, intraperitoneally); 4 – rats with AMD treated with compound PC-66 (10 mg/kg, intraperitoneally). It was found that control rats under conditions of cardiotoxic dose of adrenaline in the left ventricular myocardium for up to 8 days of the experiment does not fully restore the myocardial structure, dystrophic and necrobiotic changes were found in both cardiomyocytes and walls of vessels of a blood microcirculatory channel of a myocardium. Course intraperitoneal administration to rats of the compound PC-66 in the conditions of adrenaline myocardial infarction as well as amiodarone, contributes to the attenuation of signs of dystrophic and destructive processes. The degree of protective effect on the myocardium under conditions of cardiotoxic dose of adrenaline compound PC-66 was not lower to the reference drug – amiodarone. Thus, it is morphologically confirmed that in adrenaline myocardial infarction the compound PC-66, similar to the action of amiodarone, has a cardioprotective effect.
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45

Huda, Nazmul, Zahidus Sayeed, ARMS Ekram, MMR Khan, and MK Rahman. "Right Ventricular Myocardial Infarction as an Independent Predictor of Prognosis in Acute Inferior Myocardial Infarction." TAJ: Journal of Teachers Association 26 (November 28, 2018): 8–13. http://dx.doi.org/10.3329/taj.v26i0.37578.

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Background: Acute inferior myocardial Infarction frequently involves the right ventricle and associated with significant morbidity and mortality. We hypothesized that right ventricular involvement may affect the prognosis of patients with inferior myocardial infarctions.Methodology: In 100 consecutive patients admitted to the hospital with acute inferior myocardial infarction, we assessed the incidence and prognostic factors for in-hospital outcome. RVMI (Right ventricular myocardial infarction) was diagnosed by ≥1mm ST elevation in lead V4R in right sided electrocardiogram.Result: RVMI was found in 31(31%) of patients of acute inferior myocardial infarctions. Major complications as hypotension and cardiogenic shock occurred in 96.7% and 64.5% patients respectively and in-hospital mortality was 41.9%. Whereas major complications as hypotension and cardiogenic shock occurred in 10.1% and 2.8% patients respectively and in hospital mortality was 2.8% of patients without right ventricular infarction among the inferior myocardial infarction. Multiple logistic regression analysis showed right ventricular infarction to be independent of and superior to all other clinical variables available on admission for the prediction of in hospital mortality (relative risk 88.37 percent, 95% confidence interval 7.33 to 1064.80; p=0.000) and major complications as hypotension (relative risk 394.22, 95% confidence interval 32.04 to 4849.07; p=0.000) and cardiogenic shock (relative risk 272.36, 95% confidence interval, 16.38 to 4526.35; p=0.000).Conclusion: RVMI commonly occurs in inferior myocardial infarction. It is a strong and independent predictor of major complications and in-hospital mortality. Early detection and appropriate monitoring can reduce its high mortality rate.TAJ 2013; 26: 8-13
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46

Chen, Chih-Hung, Shu-Yuan Hsu, Chien-Chih Chiu, and Steve Leu. "MicroRNA-21 Mediates the Protective Effect of Cardiomyocyte-Derived Conditioned Medium on Ameliorating Myocardial Infarction in Rats." Cells 8, no. 8 (August 19, 2019): 935. http://dx.doi.org/10.3390/cells8080935.

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Conditioned medium derived from ischemic myocardium improves rodent cardiac function after myocardial infarction. Exosomal miRNA-mediated intercellular communication is considered to mediate the protective effect of conditioned medium against ischemic injury. Oxygen–glucose-deprivation (OGD)-treated cardiac cells and a rat model with acute myocardial infarction (AMI) were applied. The expression profiles of myocardial-disease-associated miRNAs in cardiomyocytes, cardiac fibroblasts, ventricular myocardium, and conditioned medium derived from cardiomyocytes under ischemic stresses were analyzed. Primary cultured cell model and a rat model with myocardial infarction were applied to examine the role of miRNA in regulating cardiomyocyte apoptosis, fibroblast activation, immune cell infiltration, and myocardial infarction. Results showed that expression levels of miR-21 in cardiomyocytes, cardiac fibroblasts, and conditioned medium (CM) derived from cardiomyocytes were up-regulated with OGD treatment. With the depletion of miR-21, the protective effect of CM on cardiomyocytes against oxidative stress, enhanced fibroblast activation, and promotion of angiogenesis in endothelial cells were reduced. Administration of CM reduced the infarcted size and immune cell infiltration in myocardium of rats with AMI, while depletion of miR-21 reduced the effect of CM. In conclusion, miR-21 plays a role in intercellular communication among ischemic cardiac cells. The expression of miR-21 is important for the protective effect of conditioned medium against myocardial infarction.
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Michaud, Katarzyna, Cristina Basso, Giulia d’Amati, Carla Giordano, Ivana Kholová, Stephen D. Preston, Stefania Rizzo, et al. "Diagnosis of myocardial infarction at autopsy: AECVP reappraisal in the light of the current clinical classification." Virchows Archiv 476, no. 2 (September 14, 2019): 179–94. http://dx.doi.org/10.1007/s00428-019-02662-1.

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Abstract Ischemic heart disease is one of the leading causes of morbidity and death worldwide. Consequently, myocardial infarctions are often encountered in clinical and forensic autopsies, and diagnosis can be challenging, especially in the absence of an acute coronary occlusion. Precise histopathological identification and timing of myocardial infarction in humans often remains uncertain while it can be of crucial importance, especially in a forensic setting when third person involvement or medical responsibilities are in question. A proper post-mortem diagnosis requires not only up-to-date knowledge of the ischemic coronary and myocardial pathology, but also a correct interpretation of such findings in relation to the clinical scenario of the deceased. For these reasons, it is important for pathologists to be familiar with the different clinically defined types of myocardial infarction and to discriminate myocardial infarction from other forms of myocardial injury. This article reviews present knowledge and post-mortem diagnostic methods, including post-mortem imaging, to reveal the different types of myocardial injury and the clinical-pathological correlations with currently defined types of myocardial infarction.
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48

Kovalchuk, E. Yu, and A. V. Rysev. "POST-INFARCTION CARDIAC RUPTURE." HERALD of North-Western State Medical University named after I.I. Mechnikov 7, no. 3 (September 15, 2015): 97–101. http://dx.doi.org/10.17816/mechnikov20157397-101.

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The field of post-infarction myocardial ruptures is still a nearly blind spot of cardiology; there are many facts about it which are ambiguous and simply too vague. For example, the dispersion in frequency rate is quite self-explanatory: from 0 to 30 or even 35 per cent. A number of clinical studies concerning the 30 days mortality due to acute myocardial infarctions just ignores myocardial ruptures as being the cause of death. This probably comes from a certain confusion as the post-infarction myocardial ruptures and the cardiogenic shock have almost similar manifestations. However pathologists participating in those not so numerous clinical studies concerning the 30 days mortality due to acute MIs presume that the real frequency rate of myocardial ruptures is much higher and stands at 20 to 36 per cent among all cases.
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V. P. Novoselov, S. V. Savchenko, N. G. Oshchepkova, and R. V. Skrebov. "Morphological diagnostics of myocardial infarction." Bukovinian Medical Herald 17, no. 3 (67) p.1 (August 2, 2013): 111–13. http://dx.doi.org/10.24061/2413-0737.xvii.3.67.2013.154.

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The data of an expert assessment of changes of the coronary arteries of the heart, the myocardium are presented in the paper both at the macroscopic and at microscopic level with the use of modern methods of diagnostics in case of myocardial infarction.
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50

Raziyeva, Kamila, Aiganym Smagulova, Yevgeniy Kim, Saltanat Smagul, Ayan Nurkesh, and Arman Saparov. "Preconditioned and Genetically Modified Stem Cells for Myocardial Infarction Treatment." International Journal of Molecular Sciences 21, no. 19 (October 2, 2020): 7301. http://dx.doi.org/10.3390/ijms21197301.

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Ischemic heart disease and myocardial infarction remain leading causes of mortality worldwide. Existing myocardial infarction treatments are incapable of fully repairing and regenerating the infarcted myocardium. Stem cell transplantation therapy has demonstrated promising results in improving heart function following myocardial infarction. However, poor cell survival and low engraftment at the harsh and hostile environment at the site of infarction limit the regeneration potential of stem cells. Preconditioning with various physical and chemical factors, as well as genetic modification and cellular reprogramming, are strategies that could potentially optimize stem cell transplantation therapy for clinical application. In this review, we discuss the most up-to-date findings related to utilizing preconditioned stem cells for myocardial infarction treatment, focusing mainly on preconditioning with hypoxia, growth factors, drugs, and biological agents. Furthermore, genetic manipulations on stem cells, such as the overexpression of specific proteins, regulation of microRNAs, and cellular reprogramming to improve their efficiency in myocardial infarction treatment, are discussed as well.
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