Relevant bibliographies by topics / Atrial fibrillation; myocardial infarction

Academic literature on the topic 'Atrial fibrillation; myocardial infarction'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Atrial fibrillation; myocardial infarction"

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Vermond, Rob A., Isabelle C. Van Gelder, Harry J. Crijns, and Michiel Rienstra. "Does Myocardial Infarction Beget Atrial Fibrillation and Atrial Fibrillation Beget Myocardial Infarction?" Circulation 131, no. 21 (May 26, 2015): 1824–26. http://dx.doi.org/10.1161/circulationaha.115.016595.

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Bhattarai, Radha, and Sergey Anatolevich Sayganov. "Atrial Fibrillation in Acute Myocardial Infarction." Nepalese Heart Journal 12, no. 1 (March 24, 2015): 15–20. http://dx.doi.org/10.3126/njh.v12i1.12327.

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Background and Aim: New-onset atrial fibrillationfrequently complicates acute myocardial infarction.The incidence ranges from 6 - 21% “1”.We aim todetermine the incidence of atrial fibrillation in thesetting of acute myocardial infarction.Methods: This was a single center prospective study,conducted in the coronary care unit of Saint-PetersburgPokrovskaya city hospital, Russia, during the period,June 2013 to June 2014. Sixty consecutive patientsof acute myocardial infarction with atrial fibrillationwere included in this study. Onset, duration, and modeof termination of atrial fibrillation, clinical factorsassociated with its presentation and its relation withpatient outcome were evaluated.Results: Among the 60 patients 33 (55%) had inferiorwall myocardial infarction and 27 (45%) patientshad anterior wall myocardial infarction. In patientswith inferior wall myocardial infarction the onsetof atrial fibrillation occurred within 24 hours in 30(91%) patients, after 24 hour in 3 (9%) patients. Theepisode lasted for less than 24 hours in 12 (36%), andmore than 24 hours in 21 (64%) patients. In anteriorwall myocardial infarction atrial fibrillation occurredwithin 24 hours in 2 (7%) patients, on the second dayin 25 (93%). The episode lasted less than 24 hoursin 3 (11%), 48 hours in (85%), 72 hours in 1 (4%)patients. There was a significant difference in theonset and duration of atrial fibrillation in relation tothe location of infarction (P < 0.0001). Anterior wallmyocardial infarction was associated with late onsetof atrial fibrillation, increased frequency of heartfailure and higher CCU mortality.Conclusion: The onset of atrial fibrillation in anteriorwall myocardial infarction occurred later and lastedlonger in comparison to inferior wall myocardialinfarction. Increased incidence of heart failure andhigher CCU mortality was associated with anteriorwall myocardial infarction.DOI: http://dx.doi.org/10.3126/njh.v12i1.12327 Nepalese Heart Journal Vol.12(1) 2015: 15-20
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Nambiar, Dr Supriya D. "Cardiac and Extra Cardiac Predictors and Complications of Acute Atrial Fibrillation Complicating ST Elevation Myocardial Infarction (STEMI) ST Elevation myocardial infarction Acute Atrial Fibrillation (STAAF) Study." Journal of Medical Science And clinical Research 05, no. 05 (May 23, 2017): 22124–34. http://dx.doi.org/10.18535/jmscr/v5i5.139.

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Jortveit, Jarle, Are H. Pripp, Jørund Langørgen, and Sigrun Halvorsen. "Poor adherence to guideline recommendations among patients with atrial fibrillation and acute myocardial infarction." European Journal of Preventive Cardiology 26, no. 13 (April 9, 2019): 1373–82. http://dx.doi.org/10.1177/2047487319841940.

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Background The prevalence of atrial fibrillation in patients with acute myocardial infarction is largely unknown. The aims of the present study were to assess the prevalence of atrial fibrillation in a nationwide cohort of patients with acute myocardial infarction, to assess the prescription of anticoagulation therapy, and to study the long-term outcomes. Design A nationwide registry-based cohort study. Methods All patients registered in the Norwegian Myocardial Infarction Registry between 2013 and 2016 were included and followed up through 2017. Stroke rates during follow-up were obtained through linkage with the Norwegian Patient Registry. Results In total, 47,204 patients were registered in the Norwegian Myocardial Infarction Registry. Atrial fibrillation on admission was recorded in 5393 (11%) patients, and 2190 (5%) additional patients developed atrial fibrillation during their hospital stay. Only 45% of patients with atrial fibrillation on admission and CHA2DS2-VASc score ≥ 2 were treated with anticoagulation therapy prior to myocardial infarction, and 56% of patients with atrial fibrillation and CHA2DS2-VASc score ≥ 2 were prescribed anticoagulation therapy at discharge. Patients with myocardial infarction and atrial fibrillation had an increased risk of stroke or death during 822 (426, 1278) days of follow-up compared with patients without atrial fibrillation (multivariate adjusted hazard ratio 1.4, 95% confidence interval 1.3–1.4). Conclusions Almost half of patients with atrial fibrillation and myocardial infarction were not prescribed the guideline recommended treatment with anticoagulation therapy at discharge, and their long-term risk of stroke and death was increased compared with patients without atrial fibrillation. Increased efforts to improve the treatment of patients with myocardial infarction and atrial fibrillation are needed.
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Alasady, Muayad, Nicholas J. Shipp, Anthony G. Brooks, Han S. Lim, Dennis H. Lau, David Barlow, Pawel Kuklik, et al. "Myocardial Infarction and Atrial Fibrillation." Circulation: Arrhythmia and Electrophysiology 6, no. 4 (August 2013): 738–45. http://dx.doi.org/10.1161/circep.113.000163.

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Dukes, Jonathan W., and Gregory M. Marcus. "Atrial Fibrillation Begets Myocardial Infarction." JAMA Internal Medicine 174, no. 1 (January 1, 2014): 5. http://dx.doi.org/10.1001/jamainternmed.2013.11392.

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Neobutov, Nikolai, and Sergey Kolbasnikov. "The state of the myocardium, the vascular wall and the severity of anxiety-depressive disorders in patients with myocardial infarction and atrial fibrillation." Archiv Euromedica 9, no. 1 (April 30, 2019): 109–12. http://dx.doi.org/10.35630/2199-885x/2019/9/1/109.

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In patients with myocardial infarction with atrial fibrillation, the relationship between vascular wall parameters, structural and functional changes in the myocardium, and the severity of emotional disorders were clarified. 138 inpatients of the cardiology department were closely monitored. It turned out that patients with myocardial infarction and a constant form of atrial fibrillation, unlike patients with paroxysmal form, show significant structural changes in the myocardium, endothelial dysfunction with a reduction in wall elasticity, which must be considered during therapeutic and preventive, rehabilitation measure
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Tomcsányi, János, Katalin Takó, and Balázs Sármán. "Recidív akut myocardialis infarctus pitvarfibrilláció miatt." Orvosi Hetilap 157, no. 5 (January 2016): 191–93. http://dx.doi.org/10.1556/650.2016.30349.

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Coronary thromboembolism with subsequent myocardial infarction is a rare complication of atrial fibrillation. The authors present the history of a 55-year-old male with a history of acute myocardial infarction caused by thromboembolism in the distal part of left anterior descending coronary artery and paroxysmal atrial fibrillation, who presented one year later with new chest pain, ST-segment elevation and atrial fibrillation. Coronarography confirmed the presence of thrombus in the circumflex coronary artery. Transesophageal echocardiogram showed left atrial appendage thrombus. To the knowledge of the authors this is the first report of recurrent myocardial infarction caused by atrial fibrillation. Orv. Hetil., 2016, 157(5), 191–193.
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Cheng, Liting, and Yongquan Wu. "Mesenteric Ischemia and Myocardial Infarction Associated with Atrial Fibrillation." Case Reports in Cardiology 2018 (2018): 1–3. http://dx.doi.org/10.1155/2018/7860397.

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Atrial fibrillation is a common disease correlated with embolism incidents. However, there is lack of report on atrial fibrillation causing myocardial infarction and mesenteric ischemia at the same time. Our patient is a 69-year-old woman who had undergone thoracic surgery a month before presented to our hospital with newly discovered atrial fibrillation, abdominal pain, and ST-elevated myocardial infarction. This is a rare case that atrial fibrillation took place one month after surgery and caused embolism incidents in both coronary artery and mesenteric artery.
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Radha, B., S. A. Sayganov, and T. Y. Gromiko. "ATRIAL FIBRILLATION IN PATIENTS WITH INFERIOR MYOCARDIAL INFARCTION." HERALD of North-Western State Medical University named after I.I. Mechnikov 7, no. 1 (March 15, 2015): 46–52. http://dx.doi.org/10.17816/mechnikov20157146-52.

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Objective: To elucidate the mechanism of atrial fibrillation and evaluate left atrium function after restoration of sinus rhythm in patients with acute posterior wall myocardial infarction ( MI). Materials and Methods: The study included 53 patients with posterior wall MI.All patients were divided into 2 groups. The first group consisted of 33 a people with paroxysms of atrial fibrillation (AF), and the second included 20 control subjects without arrhythmia. All percutaneous intervention was performed within the first 24 hours. Patients were evaluated for time and duration of paroxysms, the size of the heart chambers and the recovery time of the left atrium (LA)function. Results: Patients with posterior wall myocardial infarction developed AF in the early stages of the disease (in 91% on the first day), with short duration of paroxysms, stopped spontaneously and often within 1 hour (in 11 people). There were no significant differences in the size of the heart chambers, left ventricular contractility and hemodynamic disturbances in patients of both groups. AF in most cases developed in patients without left ventricular failure (in 27 people; 82%). Wherein the proximal right coronary artery occlusion was observed more frequently in patients with atrial fibrillation, than in the control group (17 vs 2; p <0,001). Approximately half patients(16 ) with AF before the appearance of atrial fibrillation bradysystolya of atria (less than 50 in 1 min) was recorded, due to acute sinus node dysfunction. After the reversion of sinus rhythm mechanical function of the LA was absent in only 4 people with left ventricular failure. Effective systole of LA was restored only 7 days after reversion to sinus rhythm. The rare occurrence of mechanical dysfunction after discontinuation of arrhythmia indicates a low probability of thrombosis and embolism in the systemic circulation. Conclusion: In cases of patients with posterior wall localization of MI main causes of AF include acute ischemia of atria due to occlusion of the right coronary artery above the branches supplying atrium. Atrial bradysystolya due to acute sinus node dysfunction often contributes to the development of AF as a substitute atrial rate (acute syndrome of tachy-bradycardia). In case of patients with posterior wall MI AF episodes were rarely accompanied by hemodynamic disturbances and the risk of systemic thromboembolism after reversion to sinus rhythm was low.
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Dissertations / Theses on the topic "Atrial fibrillation; myocardial infarction"

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Hedberg, P. (Pirjo). "Advances in routine measurement of cardiac damage and cardiovascular risk markers." Doctoral thesis, University of Oulu, 2005. http://urn.fi/urn:isbn:9514276388.

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Abstract The development of commercially available assays from the measurement of enzyme activity to mass concentrations of proteins, especially the assays of cardiac troponin I and T, has been the most important innovation in the field of cardiovascular laboratory diagnostics over the decade. The availability of a simple, rapid test using whole blood to facilitate processing and to reduce the turnaround time could improve the management of patients presenting with chest pain. The aim of this study was to evaluate the analytical and clinical performance of a new time-resolved fluorometry-based immunology technology using the cardiac marker and high-sensitivity C-reactive protein assays. In addition, the use of high-sensitivity C-reactive protein assay for the investigation of patients with acute atrial fibrillation and the influence of heparin for cardiac marker assays were studied. The levels of precision attained with pooled serum and plasma samples and control materials were acceptable. The assays were found to be linear within the ranges tested. The correlation coefficient between the Innotrac Aio! 1st generation cTnI and Abbott AxSYM cTnI assays was 0.960, and the slope was 0.07. The correlations between the 2nd generation Innotrac Aio!, Access AccuTnI and Abbott AxSYM assays were good, but there were biases between the methods. The correlation coefficients between the Innotrac Aio! and Abbott AxSYM CK-MB and myoglobin assays were 0.995 and 0.971, respectively, but the Innotrac Aio! CK-MB assay yielded about 9% higher values than the Abbott assay. The correlations between Innotrac Aio! usCRP and Cobas Integra CRP latex and between Innotrac Aio! usCRP and Hitachi CRP (Latex ) HS were good. Furthermore, the sample material correlation studies showed no significant differences when the Innotrac Aio! System was used. However, the mean Abbott AxSYM CK-MB values and the cTnI values for heparin plasma samples were 17% higher and about 15% lower than for serum samples, respectively. In the investigation of CRP levels in patients with acute atrial fibrillation CRP tended to be higher in the patients with acute FA, and there was a positive correlation between the concentrations of CRP and IL-6. The results demonstrate the excellent analytical performance of the Innotrac Aio! 2nd generation cTnI, myoglobin, CK-MB and usCRP assays, and all the matrices, including serum, plasma and whole blood, are suitable sample matrices to be used with these methods without further standardization.
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Batra, Gorav. "Atrial Fibrillation in the setting of Coronary Artery Disease : Risks and outcomes with different treatment options." Doctoral thesis, Uppsala universitet, Kardiologi, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-320541.

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Coronary artery disease (CAD) is the leading cause of mortality worldwide and atrial fibrillation (AF) is a prevalent arrhythmia associated with increased risk of mortality and morbidity. Despite improved outcome in both diseases, there is a need to further describe the prevalence, outcome and management of CAD in patients with concomitant AF. AF was a common finding among patients with MI, with 16% having new-onset, paroxysmal or chronic AF. Patients post-MI with concomitant AF, regardless of subtype, were at increased risk of composite cardiovascular outcome of mortality, MI or ischemic stroke, including mortality and ischemic stroke alone. No major difference in outcome was observed between AF subtypes. At discharge, an oral anticoagulant was prescribed to 27% of the patients with MI and AF undergoing percutaneous coronary intervention (PCI). Aspirin or clopidogrel plus warfarin versus dual antiplatelet therapy with aspirin plus clopidogrel were associated with similar 0-90-day and lower 91-365-day risk of cardiovascular outcome, without increased risk of major bleeding events. Triple therapy with aspirin, clopidogrel plus warfarin versus dual antiplatelet therapy was associated with non-significant lower risk of cardiovascular outcome, but with increased risk of bleeding events. Treatment with renin-angiotensin system (RAS) inhibitors post-MI was associated with lower risk of all-cause and cardiovascular mortality in patients with and without congestive heart failure and/or AF. However, RAS inhibition in patients without AF was not associated with lower risk of new-onset AF. Approximately 1 in 3 patients undergoing isolated coronary artery bypass grafting (CABG) had pre- or postoperative AF. Patients with AF, regardless of subtype, were at higher risk of all-cause mortality, cardiovascular mortality and congestive heart failure. Furthermore, postoperative AF was associated with higher risk of recurrent AF. In conclusion, AF was a common finding in the setting of MI and CABG. AF, irrespectively if in the setting of MI or CABG was associated with higher risk of ischemic events and mortality. Also, postoperative AF was associated with recurrent AF. Oral anticoagulants post-MI and PCI in patients with AF was underutilized, however, optimal antithrombotic therapy is still unknown. RAS inhibition post-MI seems beneficial, however, it was not associated with lower incidence of new-onset AF.
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Gibbons, David D. "Stabilization of the Cardiac Nervous System During Cardiac Stress Induces Cardioprotection." Digital Commons @ East Tennessee State University, 2012. https://dc.etsu.edu/etd/1219.

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The cardiac nervous system consists of nested reflex feedback loops that interact to regulate regional heart function. Cardiac disease affects multiple components of the cardiac nervous system and the myocytes themselves. This study aims to determine: 1) how select components of the cardiac nervous system respond to acute cardiac stress, including myocardial ischemia (MI) and induced neural imbalance leading to cardiac electrical instability, and 2) how neuromodulation can affect neural-myocyte interactions to induce cardioprotection. Thoracic spinal cord stimulation (SCS) is recognized for its anti-anginal effects and ability to reduce apoptosis in response to acute MI, primarily via modulation of adrenergic efferent systems. The data presented here suggest that cervical SCS exerts similar cardioprotective effects in response to MI, but in contradistinction to thoracic SCS, uses both adrenergic and cholinergic efferent mechanisms to stabilize cardiomyocytes and the arrhythmogenic potential. SCS potentially can use efferent and/or anti-dromically activated cardiac afferents to mediate its cardioprotection. Thoracic SCS mitigates the MI-induced activation of both nodose and dorsal root ganglia cardiac-related afferents, doing so without antidromic activation of the primary cardiac afferents. Instead, thoracic SCS acts through altering the cardiac milieu thereby secondarily affecting the primary afferent sensory transduction. In response to cardiac stressors, reflex activation of efferent activity modifies mechanical and electrical functions of the heart. Excessive activation of neuronal input to the cardiac nervous system can induce arrhythmias. Stimulation of intrathoracic mediastinal nerves directly activates subpopulations of intrinsic cardiac neurons, thereby inducing atrial arrhythmias. Neuromodulation, either thoracic SCS or hexamethonium, suppressed mediastinal nerve stimulation (MSNS)-induced activation of intrinsic cardiac neurons and correspondingly reduced the arrhythmogenic potential. SCS exerted its stabilizing effects on neural processing and subsequent effects on atrial electrical function by selectively targeting local circuit neurons within the intrinsic cardiac nervous system. Together these data indicate that neuromodulation therapy, using SCS, can mitigate the imbalances in cardiac reflex control arising from acute cardiac stress and thereby has the potential to slow the progression of chronic heart disease.
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Leal, João Carlos Ferreira. "Troponina I cardiaca como marcador de risco para fibrilação atrial no pos-operatorio imediato de pacientes submetidos a revascularização miocardica." [s.n.], 2008. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308835.

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Orientador: Domingo Marcolino Braile
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
Made available in DSpace on 2018-08-11T14:35:59Z (GMT). No. of bitstreams: 1 Leal_JoaoCarlosFerreira_D.pdf: 5038174 bytes, checksum: ad94b28be3168b7ddcb5c89801eef75f (MD5) Previous issue date: 2008
Resumo: Objetivo: avaliar se há ou não associação na ocorrência de fibrilação atrial (FA) e os níveis séricos de troponina I cardíaca no pós-operatório imediato da revascularização do miocárdio (RM). Casuística e Método: estudo retrospectivo incluindo 95 pacientes submetidos à revascularização cirúrgica do miocárdio, entre dezembro de 1996 a março de 1998. Os pacientes foram divididos em 2 grupos: Grupo I constituído de 25 pacientes (26,31%) com fibrilação atrial (FA); Grupo II constituído de 70 pacientes (73,69%) sem FA. As variáveis avaliadas foram: tempos de circulação extracorpórea (CEC), pinçamento aórtico e isquemia, fração de ejeção e o diâmetro do átrio esquerdo. O ritmo cardíaco foi avaliado por monitorização contínua por exames eletrocardiográficos durante o período de internação. Todos os pacientes foram submetidos à dosagens dos níveis séricos de troponina-I cardíaca no pré e pós-operatório imediato da RM pelo método de quimioluminiscência, admitindo-se como normais valores abaixo de 0,1 ng/ml. Resultados: Os grupos I e II não apresentaram diferenças significantes quanto à fração de ejeção, diâmetro do átrio esquerdo, tempos de pinçamento da aorta e de isquemia. O tempo de CEC mostrou diferença significante entre os grupos. A análise pareada dos valores séricos da troponina I cardíaca dos pacientes dos grupos I e II no pré-operatório não mostrou diferença significante, com valor de P=0,9689. No pós-operatório, houve diferença significante entre os grupos, sendo que o grupo I mostrou maior aumento em relação ao II com P=0,0018. O valor de corte de troponina I cardíaca que melhor se associou com ocorrência de FA foi = 0,936 µg/ L. Conclusão: A ocorrência da FA está associada com os níveis séricos de troponina I cardíaca no pós-operatório imediato da RM quando considerado o valor de corte = 0,936 µg/L, sugerindo que a troponina I cardíaca é um marcador para FA e alertando para a necessidade de medidas diagnósticas ou terapêuticas preventivas
Abstract: Objective: To evaluate if there is any association among atrial fibrillation (AF) events and serum cardiac Troponin I levels in the immediate postoperative period of myocardium revascularization (MR). Patients and method: A retrospective study was made of 95 patients who underwent myocardial revascularization surgery between December 1996 and March 1998. The patients were divided into 2 groups: Group I comprised 25 patients (26.31%) who presented with atrial fibrillation (AF) and Group II 70 patients (73.69%) without AF. The variables evaluated were: time of extracorporeal circulation (ECC), aortic clamping and ischemia, ejection fraction and the diameter of the left atrium. The heart rhythm was evaluated by continuous monitoring by electrocardiography during hospitalization. The serum cardiac Troponin I levels were measured for all patients in the pre- and immediate postoperative periods of MR by chemoluminescence; normal values were consider to be below 0.1 ng/mL. Results: There were no significant differences between groups in respect to the ejection fraction, diameter of the left atrium and duration of aortic clamping and ischemia. The ECC time gave a significant difference between the groups. A comparison of the serum cardiac Troponin I levels of the patients in both groups in the preoperative period did not prove to be statistically significant (P-value = 0.9689). In the postoperative period however, there was a significant difference; Group I presented with a greater increase when compared to Group II (P-value = 0.0018). Levels of cardiac Troponin I =0.936 µg/L were associated with a risk of AF. Conclusion: AF events are associated with serum cardiac Troponin I levels =0.936 µg/L in the immediate postoperative period of MR. This suggests that cardiac Troponin I is a marker for AF, highlighting the necessity of diagnostic investigations and preventive therapeutic procedures
Doutorado
Cirurgia
Doutor em Cirurgia
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Stamboul, Karim. "La fibrillation atriale, silencieuse ou symptomatique, compliquant un infarctus du myocarde : déterminants, impact pronostique et rôle des dérivés méthylés de la L-arginine et du stress oxydatif." Thesis, Dijon, 2015. http://www.theses.fr/2015DIJOMU01/document.

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La fibrillation atriale (FA) est une complication fréquente de la phase aiguë de l’infarctus (IDM) avec un moins bon pronostic des patients. Sa forme silencieuse pourrait être fréquente après un IDM. Cependant, toutes les études ayant porté sur la FA se sont focalisées sur les formes symptomatique, paroxystique ou persistante. De plus, la réduction de la biodisponibilité du •NO et la dysfonction endothéliale peuvent altérer le pronostic des patients en FA. Or, l’asymétrique diméthylarginine (ADMA) en inhibant de façon endogène l’action des NO synthases peut conduire à une dysfonction endothéliale, une inflammation ou encore à un stress oxydatif, qui sont impliqués dans de nombreuses pathologies cardiovasculaires. Cependant, au-cune étude n’a évalué la relation potentielle entre le taux plasmatique d’ADMA et la survenue d’une FA après un IDM.Notre objectif a été d’évaluer dans le cadre d’une étude prospective le pronos-tic hospitalier et à un an des patients présentant de la FA silencieuse en phase ai-guë d’IDM, et évaluer le lien potentiel entre les dimethylarginines et l’apparition d’une FA. Notre première étude prospective montre pour la première fois que la FA si-lencieuse est plus fréquente que la FA symptomatique et est associée à un moins bon pronostic après un IDM.Notre second travail, démontre que l’impact négatif de la FA silencieuse sur le pronostic des patients se maintient à un an après l’IDM.Notre troisième travail montre également, que l’ADMA est associée de ma-nière indépendante à la survenue d’une FA symptomatique après un IDM. Ces données suggèrent qu’un dépistage et qu’une prise en charge spécifiques de la FA après un IDM pourraient améliorer le pronostic des patients. L’ADMA pourrait ainsi être utilisée comme un marqueur de risque de passage en FA après un IDM
Atrial fibrillation (AF) is a frequent complication of acute myocardial infarction (AMI) with a poorer prognosis. Silent atrial fibrillation has been suggested to be frequent after AMI. However, most part of the studies has targeted only paroxysmal or persistent AF. Thus, Reduced Nitric Oxide availability and endothelial dysfunction has been recently recognized as a possible contributor to altered prognosis in AF. Asymmetric dimethylarginine (ADMA) can inhibit nitric oxide synthase and leads to endothelial dysfunction, inflammation and oxidative stress in multiple cardiovascular diseases. However, any study has addressed the relationship between ADMA levels and the occurrence of AF in AMI.We aimed to assess in-hospital and 1-year prognosis in patients experiencing silent AF in AMI and evaluate the potential relationship between dimethylarginines plasma levels and the occurrence AF after acute myocardial infarction.Our first prospective study shows for the first time that silent AF is more frequent than symptomatic AF after AMI and is associated with a worse prognosis.Our second work confirms the impact of silent AF on prognosis, with a prognosis that remains worse one year after the acute phase of MI. Our third work proved that ADMA is independently associated with symptomatic AF after AMI and strengthen the capacity to estimate symptomatic AF occurrence. In conclusion our studies highlight that AF is not a negligible event after AMI, in particular silent AF. That suggests that systematic screening and specific management should be investigated in order to improve outcomes of patients. ADMA appears to be a potential predictor of AF after AMI, because of its significant association
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Hållmarker, Ulf. "Epidemiological Studies on Long Distance Cross-Country Skiers : Participants in the Vasaloppet 1955-2010." Doctoral thesis, Uppsala universitet, Uppsala kliniska forskningscentrum (UCR), 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-260994.

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The overall aim of this thesis was to study the influence of physical activity on health. Risks and benefits of physical activity is of particular interest since there is a global trend of less physical activity among youths and adults. In order to investigate this aim we used a database from a large cross country ski race, Vasaloppet, with participants with a wide age range, and with both elite athletes and ordinary people who exercise and promote their health. The most serious risk of strenuous exercise is sudden death and it is challenging to identify preventive effects of major endemic diseases. Using epidemiological methodology we studied 200 000 Vasaloppet skiers and compared them with the general population. Based on personal identification numbers we added data from Swedish national personal and health registers, clinical registers as the cancer register, Swedeheart, or Swedish stroke register, and socioeconomic information from Statistics Sweden. In the Vasaloppet database we collected data on age, gender, finish time and number of races during the period 1989 to 2010. We evaluated risk of death during the race in two papers (I,II). During 90 years of annual races, cardiac arrest occurred in 20 skiers, of which five survived. The death rate is in average two per 100 000 skiers. We also studied the association with cancer incidence (paper III). The overall reduction of cancer was modest among skiers compared with the general population, but for cancers related to lifestyle the risks were markedly lower. We investigated the risk for recurrent myocardial infarction and found a 30% reduction among skiers (paper IV). In paper V we showed that skiers with a first stroke have a lower incidence of all-cause death. The skiers had a higher frequency of atrial fibrillation but had less severe stroke and no increased risk of recurrent stroke. Thus our data suggest that a lifestyle with a high level of physical activity may work as a protection after a cardiovascular event. Summary: The short excess mortality in endurance physical activity is by far outweighed by the long term protective effect of exercise in cardiovascular diseases and cancer.
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Conic, Rosalynn Ruzica Zoran. "USING PSORIASIS AS A MODEL TO IDENTIFY UNIQUE BIOMARKERS." Case Western Reserve University School of Graduate Studies / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=case1554485554569272.

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Le, Quang Khai. "Troubles du rythme cardiaque dans les modèles murins transgéniques." Thèse, Nantes, 2010. http://hdl.handle.net/1866/4903.

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Les maladies cardio-vasculaires sont la première cause de mortalité dans le monde. L’hypertrophie cardiaque est un processus de remodelage provoqué par une surcharge de travail du muscle cardiaque afin de mieux répondre à la demande de l’organisme. Bien que bénéfique à court terme, une hypertrophie trop accentuée conduira à long terme, à une insuffisance cardiaque. L’hypertrophie est associée à un remodelage électrique qui conduit généralement à un allongement du potentiel d’action, une des causes des arythmies ventriculaires et de la mort subite. Généralement, le mécanisme causal est la fibrillation ventriculaire, un trouble du rythme irréversible dont les mécanismes sont complexes et méconnus. Si les conséquences fonctionnelles in vitro des mutations génétiques ou du remodelage ionique sont relativement simples à étudier ou à prévoir, leur rôle dans les mécanismes des troubles du rythme in vivo sont plus difficiles à appréhender. Parmi les nombreux modèles animaux développés pour la recherche sur les troubles du rythme, la souris est de plus en plus utilisée en raison de notre capacité à muter, invalider ou sur-exprimer les gènes d'intérêt chez ces animaux. L'objectif de mon travail de thèse était de mieux comprendre le rôle des canaux ioniques en physiopathologie cardiaque, en particulier dans la survenue des troubles du rythme in vivo. Ces travaux ont permis d'améliorer notre connaissance du rôle des anomalies génétiques impliquant des canaux ioniques et du remodelage ionique dans la physiopathologie des troubles du rythme et pourrait ainsi ouvrir de nouvelles perspectives thérapeutiques dans le traitement anti-remodelage cardiaque et la prévention de la mort subite.
Cardiovascular disease is the leading cause of death in the world each year. If no action is taken to improve cardiovascular health and current trends continue, WHO estimates that 25% more healthy life years will be lost to cardiovascular disease globally by 2020. Cardiac hypertrophy is the consequence of an excessive workload of the heart muscle leading to cardiac remodeling process. As the workload increases, the ventricular walls grow thicker, lose elasticity and eventually may fail to pump with as much force as a healthy heart. Furthermore, hypertrophied myocardium is not physiologically normal and may confer a predisposition to potentially fatal arrhythmias. Generally, the causal mechanism is ventricular fibrillation, a cardiac rhythm disorder which is irreversible but the pathophysiological mechanisms are complex and poorly understood. The functional consequences of mutations or ionic remodeling are relatively simple to study in vitro, but their role in the pathophysiology of arrhythmias in vivo is more difficult to grasp. Among the different animal models developed in cardiac arrhythmias research, the mouse is increasingly used because of our ability to mutate, knock-out or over-express genes of interest. The objective of my thesis was to study the role of ion channels in physiology as well as cardiac pathophysiology, particularly in the involvement of the occurrence of cardiac arrhythmias in vivo. This thesis will improve our understanding of the role of genetic abnormalities involving ionic remodeling in the pathogenesis of the heart and may also open new therapeutic perspectives in the treatment of cardiac remodeling as well as sudden cardiac death.
Thèse en cotutelle avec Université de Nantes - Pays de La Loire - France (2005-2010)
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9

Legallois, Damien. "Paramètres biologiques et échocardiographiques et remodelage ventriculaire gauche après syndrome coronarien aigu avec sus-décalage du segment ST Definition of left ventricular remodelling following ST-elevation myocardial infarction: a systematic review of cardiac magnetic resonance studies in the past decade Left atrial strain quantified after myocardial infarction is associated with ventricular remodeling The relationship between circulating biomarkers and left ventricular remodeling after myocardial infarction: an updated review Serum neprilysin levels are associated with myocardial stunning after ST-elevation myocardial infarction Is plasma level of Coenzyme Q10 a predictive marker for left ventricular remodeling after revascularization for ST-segment elevation myocardial infarction ?" Thesis, Normandie, 2020. http://www.theses.fr/2020NORMC429.

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Le remodelage ventriculaire gauche est une complication fréquente des patients ayantprésenté un syndrome coronarien aigu, pouvant conduire à terme à une situation d’insuffisancecardiaque. Il est donc important de connaître les facteurs associés à la survenue d’un remodelageventriculaire afin de dépister plus précocement les patients à plus haut risque d’insuffisance cardiaqueet ainsi optimiser leur prise en charge. Ce travail comprend deux axes. Le premier porte sur larecherche de nouveaux paramètres d’imagerie associés à la survenue du remodelage. Nous avonsdans un premier temps réalisé une revue de la littérature concernant la définition du remodelageventriculaire gauche en imagerie par résonance magnétique. Puis, nous avons conduit deux étudesayant pour but de rechercher une association entre (i) le strain atrial gauche et, (ii) le gradient depression intraventriculaire gauche diastolique, évalués en échocardiographie 24-48 heures après lesyndrome coronarien aigu et le remodelage ventriculaire gauche au cours du suivi. Le second axe portesur les biomarqueurs associés au remodelage ventriculaire post-infarctus. Nous avons réalisé une revuede la littérature au sujet des biomarqueurs qui, dosés lors de l’hospitalisation initiale, sont associés àl’existence d’un remodelage lors du suivi. Nous avons ensuite étudié la valeur prédictrice de deuxbiomarqueurs (la néprilysine et le coenzyme Q10) pour la survenue d’un remodelage ventriculairegauche
Left ventricular remodeling is a common complication in patients following acutemyocardial infarction and may lead to heart failure. Some baseline parameters are associated withremodeling at follow-up, allowing to better discriminate patients with an increased risk of heart failureto optimize therapeutics. This work has two axes, focused on imaging and biological parametersassociated with left ventricular remodeling, respectively. First, we reviewed past studies that definedremodeling using cardiac magnetic resonance imaging. Then, we studied the association betweensome echocardiographic parameters (left atrial strain and diastolic intraventricular pressure gradient)and left ventricular remodeling after ST-elevation myocardial infarction. In the other axis, wereviewed biomarkers that have been associated with left ventricular remodeling in prior studies. Then,we investigated the association between neprilysin and coenzyme Q10 levels and left ventricularremodeling in STEMI patients
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Sambola, Antonia, Pau Rello, Toni Soriano, Deepak L. Bhatt, Vinay Pasupuleti, Christopher P. Cannon, C. Michael Gibson, et al. "Safety and efficacy of drug eluting stents vs bare metal stents in patients with atrial fibrillation: A systematic review and meta-analysis." Elsevier Ltd, 2020. http://hdl.handle.net/10757/655507.

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Objective: A systematic review and meta-analysis was performed to evaluate the safety and efficacy of drug-eluting stents (DES) vs bare-metal stents (BMS) in atrial fibrillation (AF) patients. Methods: We systematically searched 5 engines until May 2019 for cohort studies and randomized controlled trials (RCTs). Primary outcomes were major bleeding and major adverse cardiac events (MACE) including cardiac death, myocardial infarction, target vessel revascularization (TVR) or stent thrombosis. Effects of inverse variance random meta-analyses were described with relative risks (RR) and their 95% confidence intervals (CI). We also stratified analyses by type (triple [TAT] vs dual [DAT]) and duration (short-vs long-term) of antithrombotic therapy. Results: Ten studies (3 RCTs; 7 cohorts) including 10,353 patients (DES: 59.6%) were identified. DES did not show higher risk of major bleeding than BMS (5.6% vs 6.9%, RR 1.07; 95%CI, 0.89–1.28, p = 0.47; I2 = 0%) or MACE (12% vs 13.6%; RR 0.96; 95%CI 0.81–1.13, p = 0.60; I2 = 44%). Although, DES almost decreased TVR risk (6.4% vs 8.4%, RR 0.78; 95%CI, 0.61–1.01, p = 0.06; I2 = 15%). Stratified analyses by type and duration of antithrombotic therapy showed no differences in major bleeding or MACE between both types of stents. In DES, long-term TAT showed higher major bleeding risk than long-term DAT (7.7% vs 4.7%, RR 1.48, 95%CI 1.08–2.03, p = 0.01; I2 = 12%). For both types of stents, MACE risk was similar between TAT and DAT. Conclusions: In patients with AF undergoing PCI, DES had similar rate of major bleeding and MACE than BMS. DAT seems to be a safer antithrombotic therapy compared with TAT.
Janssen Pharmaceuticals
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Books on the topic "Atrial fibrillation; myocardial infarction"

1

Meyer, Mark Louis. Silent cerebral infarction in patients with nonrheumatic atrial fibrillation. [New Haven, Conn: s.n.], 1994.

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Johannes, Janse Michiel, ed. The ventricular arrhythmias of ischemia and infarction: Electrophysiological mechanisms. Mount Kisco, NY: Futura Pub. Co., 1993.

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Braidwood Commission on Conducted Energy Weapon Use (B.C.). Restoring public confidence: Restricting the use of conducted energy weapons. Victoria, B.C: Braidwood Commission on Conducted Energy Weapon Use, 2009.

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Bowker, Lesley K., James D. Price, Ku Shah, and Sarah C. Smith. Cardiovascular. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198738381.003.0010.

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This chapter provides information on the ageing cardiovascular system, chest pain, stable angina, acute coronary syndromes, myocardial infarction, hypertension, treatment of hypertension, presentation of arrhythmias, management of arrhythmias, atrial fibrillation, rate/rhythm control in atrial fibrillation, stroke prevention in atrial fibrillation, bradycardia and conduction disorders, common arrhythmias and conduction abnormalities, heart failure assessment, acute heart failure, chronic heart failure, dilemmas in heart failure, heart failure with preserved left ventricular function, valvular heart disease, peripheral oedema, preventing venous thromboembolism in an older person, peripheral vascular disease, gangrene in peripheral vascular disease, and vascular secondary prevention.
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Brady, Peter A. Specific Arrhythmias and Syncope. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0044.

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Bradycardia is defined as a heart rate less than 60 beats per minute at rest or a decreased heart rate response to exercise. Causes of bradycardia include high vagal tone (most cases occur in asymptomatic and often fit and healthy persons), sinus node dysfunction, drug therapy, heart block, and myocardial infarction. A conduction system disorder is present when there is a delay in impulses from the sinus node reaching the ventricles or when some impulses do not reach the ventricles because of block within the AV node or distal conduction system (His-Purkinje system). Conduction system disorders can be divided into first-degree, second-degree, and third-degree (complete) heart block. The tachycardias (atrial fibrillation and atrial flutter) and syncope (as a transient loss of consciousness with spontaneous recovery) are also reviewed.
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Turc, Guillaume, David Calvet, and Jean-Louis Mas. Cardiac aetiology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198722366.003.0005.

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Cardiac aetiology accounts for approximately 20% of strokes in young adults. Although atrial fibrillation is a leading cause of stroke in the general population, it is uncommon in young adults. In such patients, more diverse causes of ischaemic stroke are observed, including valvular heart diseases, infective endocarditis, Libman–Sacks endocarditis, dilated cardiomyopathies, congenital heart diseases, myocardial infarction, and intracardiac tumours. Patent foramen ovale is commonly observed in young adults with ischaemic stroke, but this association may be incidental in a sizeable proportion of patients. Young adults who are the most likely to have a stroke-related patent foramen ovale are also those with the lowest recurrence risk.
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Banerjee, Ashis, and Clara Oliver. Cardiac emergencies. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198786870.003.0009.

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Chest pain is a common presenting complaint for patients in the emergency department. This chapter focuses on the management and recent changes to non-ST-segment elevation myocardial infarction (NSTEMI) and STEMI pathways, in keeping with national guidance. Arrhythmia management including atrial fibrillation as well as the use of scoring systems as the CHADVASC score also commonly appears in the short-answer question (SAQ) paper, which is covered in this chapter in line with current NICE guidance. In addition, there is also a section on the diagnosis and differentiation on managing a patient with a transient loss of consciousness and the associated risk factors of sudden cardiac death. This chapter also includes sections on hypertensive emergencies and the management of heart failure.
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Kelley, Roger E. Cardiac Disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0188.

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Heart disease is a major contributor to stroke and other neurologic disorders in adults. Cardioembolic stroke accounts for roughly 15% of all stroke, and the most common mechanism is cardiac arrhythmia, with atrial fibrillation the leading contributor. Anticoagulation such as using aspirin or warfarin is chosen based on the presence of associated risk factors including congestive heart failure, hypertension, age, and diabetes mellitus. Heart failure ranks second in the incidence of stroke from cardioembolism, with other risk factors being endocarditis, severe cardiomyopathy, acute myocardial infarction, and patent foramen ovale. Recent clinical trials indicate that induction of total body hyopthermia after cardiac arrest to a target temperature of 32°C to 34°C, for 24 hours, had a more favorable neurological outcome compared with a normothermia group.
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Sinnaeve, Peter, and Frans Van de Werf. Fibrinolytic, antithrombotic, and antiplatelet drugs in acute coronary syndromes. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0044.

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Antithrombotic therapy is a major cornerstone in the treatment for acute coronary syndromes, as thrombus formation upon a plaque rupture or an erosion plays a pivotal role in non-ST-segment elevation as well as ST-segment elevation acute coronary syndromes. Both acute and long-term oral antiplatelet therapies, targeting specific platelet activation pathways, have demonstrated significant short- and long-term benefits. The use of anticoagulants is currently largely confined to the acute setting, except in patients with a clear indication for long-term treatment, including atrial fibrillation or the presence of intraventricular thrombi. Despite the benefit of primary percutaneous coronary intervention in ST-segment elevation myocardial infarction, fibrinolysis continues to play an important role throughout the world as well. In this chapter, the fibrinolytic, antiplatelet, and anticoagulant agents used in the management of acute coronary syndrome patients are discussed.
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Sinnaeve, Peter, and Frans Van de Werf. Fibrinolytic, antithrombotic, and antiplatelet drugs in acute coronary syndromes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0044_update_001.

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Antithrombotic therapy is a major cornerstone in the treatment for acute coronary syndromes, as thrombus formation upon a plaque rupture or an erosion plays a pivotal role in non-ST-segment elevation as well as ST-segment elevation acute coronary syndromes. Both acute and long-term oral antiplatelet therapies, targeting specific platelet activation pathways, have demonstrated significant short- and long-term benefits. The use of anticoagulants is currently largely confined to the acute setting, except in patients with a clear indication for long-term treatment, including atrial fibrillation or the presence of intraventricular thrombi. Despite the benefit of primary percutaneous coronary intervention in ST-segment elevation myocardial infarction, fibrinolysis continues to play an important role throughout the world as well. In this chapter, the fibrinolytic, antiplatelet, and anticoagulant agents used in the management of acute coronary syndrome patients are discussed.
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Book chapters on the topic "Atrial fibrillation; myocardial infarction"

1

Musat, Dan L., Jonathan S. Steinberg, Delia Cotiga, and Eyal Herzog. "Arrhythmias Complicating Acute Myocardial Infarction: Atrial Tachyarrhythmias Including Atrial Fibrillation and Atrial Flutter." In Acute Coronary Syndrome, 175–89. London: Springer London, 2008. http://dx.doi.org/10.1007/978-1-84628-869-2_17.

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Gargiulo, Giuseppe, and Davide Capodanno. "Atrial Fibrillation on Vitamin K Antagonist Undergoing Primary Percutaneous Coronary Intervention for Acute ST-Elevation Myocardial Infarction." In Atrial Fibrillation and Percutaneous Coronary Intervention, 79–94. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-42400-2_5.

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Kiviniemi, Tuomas O., and K. E. Juhani Airaksinen. "Atrial Fibrillation on Vitamin K Antagonist Oral Anticoagulant Undergoing Primary Percutaneous Coronary Intervention for ST-Elevation Acute Myocardial Infarction." In Atrial Fibrillation and Percutaneous Coronary Intervention, 95–120. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-42400-2_6.

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Zuin, G., M. Celestre, and F. Di Pede. "Prognosis and Management of Atrial Fibrillation in Different Clinical Settings: Acute Myocardial Infarction." In Cardiac Arrhythmias 2005, 127–30. Milano: Springer Milan, 2006. http://dx.doi.org/10.1007/88-470-0371-7_17.

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De Ferrari, Gaetano M., Valentina De Regibus, Vincenzo Gionti, Daniela Civardi, Roberto Insolia, Matteo Pedrazzini, Davide Gentilini, Annamaria Di Blasio, Lia Crotti, and Peter J. Schwartz. "PREDESTINATION: PRimary vEntricular fibrillation and suDden dEath during a firST myocardIal iNfArcTION: Genetic Basis." In Contributions to Statistics, 85–96. Milano: Springer Milan, 2013. http://dx.doi.org/10.1007/978-88-470-5379-3_6.

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Marciniak, Maciej, Hermenegild Arevalo, Jacob Tfelt-Hansen, Kiril A. Ahtarovski, Thomas Jespersen, Reza Jabbari, Charlotte Glinge, et al. "A Multiple Kernel Learning Framework to Investigate the Relationship Between Ventricular Fibrillation and First Myocardial Infarction." In Functional Imaging and Modelling of the Heart, 161–71. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-59448-4_16.

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MacMahon, Stephen, and Salim Yusuf. "Effects of Lidocaine on Ventricular Fibrillation, Asystole, and Early Death in Patients with Suspected Acute Myocardial Infarction." In Acute Coronary Care 1987, 51–60. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2337-2_4.

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Hiremath, Jagdish, and Kaushik Sheth. "Atrial Fibrillation Complicating Acute Myocardial Infarction." In Atrial Fibrillation Update: A Textbook of Cardiology, 407. Jaypee Brothers Medical Publishers (P) Ltd., 2017. http://dx.doi.org/10.5005/jp/books/13034_66.

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Kumar, Sunil, and Manish Ruhela. "Takotsubo Mimicking Acute Myocardial Infarction and Atrial Fibrillation." In Atrial Fibrillation Update: A Textbook of Cardiology, 219. Jaypee Brothers Medical Publishers (P) Ltd., 2017. http://dx.doi.org/10.5005/jp/books/13034_41.

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Prescott, Eva. "Sex and gender differences overview." In ESC CardioMed, edited by Noel Bairey Merz, 2827–30. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0675.

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There are well-described differences between men and women in epidemiology, pathophysiology, presentation, and outcome of heart disease. Although risk factors responsible for cardiovascular disease are similar in men and women their relative importance differs. Puzzlingly, women have more angina yet less obstructive coronary artery disease. Also, when they suffer myocardial infarction, women more often present with myocardial infarction with non-obstructed coronary arteries (MINOCA) and takotsubo cardiomyopathy. Women have less systolic heart failure than men but more heart failure with preserved ejection fraction, a condition yet to find evidence-based treatment. Atrial fibrillation is also less common in women than men of similar age, but women with atrial fibrillation have higher risk of stroke than their male counterparts.
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Conference papers on the topic "Atrial fibrillation; myocardial infarction"

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Ali, M., A. Ibrahim, P. Kyaw, A. Kulkarni, and M. Siddique. "Right Atrial Thrombus Associated with Concurrent Myocardial Infarction and Pulmonary Embolism." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a3467.

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Funamoto, Kenichi, Ryo Koizumi, Toshiyuki Hayase, Muneichi Shibata, and Tomoyuki Yambe. "Hemodynamic Changes in the Left Atrium due to Atrial Fibrillation." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53817.

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The left atrium (LA), which connects four pulmonary veins (PVs) to the left ventricle (LV), has a characteristic shape called the left atrial appendage (LAA) under the left PV. Atrial fibrillation (AF) is a heart disease, by which irregular electrical signals with high-frequency contraction (> 400 bpm) occur in the LA. Although AF itself is not fatal, it may cause thrombus formation, resulting to cerebral infarction. In this study, hemodynamics in the LA with/without AF was investigated by means of fluid-structure interaction simulation.
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HONJO, HARUO. "ELECTROPHYSIOLOGY OF PULMONARY VEIN MYOCARDIAL SLEEVES AND THEIR ROLE IN ATRIAL FIBRILLATION." In Proceedings of the 31st International Congress on Electrocardiology. WORLD SCIENTIFIC, 2005. http://dx.doi.org/10.1142/9789812702234_0004.

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Ogawa, Emiyu, Arisa Ito, and Tsunenori Arai. "Fundamental study on photodynamic therapy for atrial fibrillation: effect of photosensitization reaction parameters on myocardial necrosis in vitro." In SPIE BiOS, edited by E. Duco Jansen and Robert J. Thomas. SPIE, 2012. http://dx.doi.org/10.1117/12.907176.

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Wong, Jonathan, Serdar Göktepe, and Ellen Kuhl. "Computational Simulation of Traveling Arrhythmic Waves in Myocardial Tissue." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206552.

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Cardiac arrhythmias are common cardiac disorders characterized by irregular electrical activity of the heart. Each year in the United States alone, about half a million deaths and 835,000 hospital discharges result from arrhythmias. In fact, atrial fibrillation is responsible for 15–20% of all ischemic strokes [1]. Due to the complexity of the electrical conduction pathways in myocardium, computational models are useful platforms for gaining insight into the origin of arrhythmias, as well as the development of corrective options. For these purposes, a quantitative finite element model based on the phenomenological Aliev and Panfilov model [2] was implemented to characterize the electrical behavior of cardiac tissue. Several examples of simulated re-entrant spiral waves demonstrate that our implementation can indeed capture the electrical aspects of cardiac tissue.
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6

Julian, D. G., L. S. Borthwick, D. Reid, K. P. Jennings, R. J. Wainwright, J. C. Rodger, D. Wood, J. S. Flax, and W. S. Phillips. "APSAC versus placebo: A Multicenter Study of Safty and Early Morality in Acute Myocardial Infarction." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643619.

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A prelimiry study was carried out of obtain data on mortality,benefit and the safety of anisoylated plasminogen streptokinase activator complec (APSAC).90 patients from 7 centers,with symptons of acute myocardial infarction of not more than 4 hours duration,were randomised to receiveeithere 30U of APSAC as an intravenous injection over 4 to 5 minutes or placebo given by the same route.45 patients recevied APSAC and placedo,mean time to treatment was 3 hours 20 minutes and 3 hours, respectively.Mortality at 30 days was 7 deaths in theplacebo group and 1 death in the APSAC group (p=0.058),these were all related either directly or indirectly to the infarct:cardiogenic shock (2),ventricular asystole(2) further acute myocardial infraction(2),ventricular fibrillation (1) and pulmonry embolism (1).The patient who died after APSAC therany had presented with an anterior infraction; 5 patients who died inthe placebo group presented with anterior infarcts and 2 with inferior infarcts. Most daeths occured in the group randomised 2 hours 30 minutes to 4 hours post-infarcation.Both systolic and diastolic blood pressure were generally similar in each groupfrom 1 hour to 1 month after treatment. 35 percent of petients in the placebo group experienced cardiovasular events (2 of whom died from cardiogenic shock) compared with 20 percent of APSAC of treated patients (1 of whom died from pulmonary embolism).Minor haematuria was apparent in a grater number of patients in the APSAC group after 12 hours, but there was no differnce between groups after 1 or 2 weeks.The result of this study ,although encouraging,should be interpreted with caution,mainly due to the small numbers of patients enrolled.There was however a trend towards incresed survival in the APSAC treated group (97.8 per cent) compared with84.4 cent survival in the placenbo groupat 30 days post-infarction.
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Mattison, Lars M., Chloe Johnson, and Paul A. Iaizzo. "Biomechanical Responses of Swine Esophagus Tissue to Irreversible Electroporation." In 2018 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/dmd2018-6963.

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Atrial Fibrillation (AF) is a common disease that may occur in the heart, especially as we age. AF is due to non-normal myocardial ectopic foci that then causes an uncoordinated atrium contraction. This effectively reduces the atrial kick to the ventricles, which can account for up to 20% of ventricular filling. While not an immediately fatal disease, it can cause reduced quality of life for patients and also puts them at increased risk for stroke. AF as a disease, is expected to affect over 50 million people in the United States alone by 2050 [1].
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Shenoi, Mithun M., Xiaoqing Zhang, Ramji T. Venkatasubramanian, Erin D. Grassl, Lenny George, Stephen Schmechel, James E. Coad, and John C. Bischof. "CT Visualization and Histopathological Assessment of Cryoablation in Pulmonary Veins." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206640.

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Over 2 million adults in the United States are affected by atrial fibrillation (AF), a common cardiac arrhythmia that is associated with decreased survival, increased cardiovascular morbidities, and a decrease in quality of life. Atrial fibrillation can be initiated by ectopic beats originating in the myocardial sleeves surrounding the pulmonary veins [1]. Pulmonary vein (PV) isolation via radiofrequency ablation is the current gold standard for treating patients with drug-refractory AF [2]. However, cryoablation is emerging as a new minimally-invasive technique to achieve PV isolation. Cryoablation is fast gaining acceptance due to its minimal tissue disruption, decreased thrombogenicity, and reduced complications (RF can lead to low rate of pulmonary vein stenosis) [2]. One important question in regard to this technology is whether the PV lesion is transmural and circumferential and to what extent adjacent tissues are involved in the freezing process. As ice formation lends itself to image contrast in the body, we hypothesized that intraprocedural CT visualization of the iceball formation would allow us to predict the extent of the cryolesion and/or provide us with a measure of the adjacent tissue damage.
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9

Teixeira, Davi Vargas Freitas, Arthur da Veiga Kalil Coelho, Camila Alves Pereira, Luciana Zelante Ambiel Magalhães, Marcele Schettini, and Sônia Maria Cesar de Azevedo Silva. "Bilateral anterior cerebral infarction associated with anatomical variation in a patient with COVID-19: a case report." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.338.

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Context: Cardiovascular diseases are the main cause of death in Brazil. Amongst them, cerebrovascular disease is the second greater cause of death and the first in disability. Despite its overall high incidence, initial presentation with bilateral anterior circulation involvement is rare. The association between COVID-19 and stroke is still unclear, nethertheless, a prothrombotic state has been consistently described. Case report: A 80-years-old male, with past medical history of atrial fibrillation in regular use of apixaban, treated for severe COVID-19 Pneumonia for 13 days of hospitalization, was admitted seven days after discharge, presenting loss of consciousness followed by a not witnessed fall. At first evaluation the patient was somnolent, eye opening to tactile stimulation, motor aphasia, right central facial palsy and crural predominant double hemiparesis. Tomography study revealed bilateral hypoattenuation at superior frontal and cingulate girus. Angiotomography identified a hipoplasic A1 segment of anterior cerebral artery. Addtional findings included segmental pulmonary embolism and aorta intraluminal thrombus. The patient evolved to mutism and worsening level of consciousness, followed by death after several clinical complications. Conclusions: Anatomical variants of anterior circulatian are common although tipically assintomatic. When related to cerebrovascular disease, cardioembolic event is frequently accountable. This case exhibits an unusual stroke presentation during COVID-19 convalescence period among other thrombotic events despite anticoagulant therapy. Therefore, reinforces literature findings that SARS- CoV-2 infection and stroke simultaneously increase mortality and highlights that more physiolopathology knowlegde regarding this association is required, as well as efficiency trials of oral anticoagulants in these scenarios.
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10

Mant, M. J., P. V. Greenwood, C. T. Kappagoda, and B. C. Hamacher. "TRANSCORONARY PLATELET ACTIVATION AND CONSUMPTION IN CORONARY ARTERY DISEASE (CAD): STUDIES DURING PACING TACHYCARDIA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643025.

Full text
Abstract:
Plasma platelet factor 4 (PF4), beta-thromboglobulin (BTG) and platelet counts (PC) were measured in blood from the aortic root (Ao) and the coronary sinus (CS) in 13 subjects with CAD immediately after atrial pacing to a heart rate of 130/min, to ischemic ECG changes or to angina. The same studies were performed on peripheral vein (PV) blood before and after pacing. Blood was collected before heparinisation. Blood from the Ao and CS was collected through catheters containing an anti-coagulant/antiplatelet solution. This technique has been shown to cause minimal or no platelet activation. Of the 13 subjects, 9 underwent investigation for exertional angina, 3 for myocardial infarction (MI) within 6 months, and 1 subject for both reasons. At coronary angiography after our studies, 9 subjects had hemodynamically significant 2 or 3 vessel CAD with at least 1 vessel of a dominant system and 4 had a lesser degree of CAD. Mean values in blood from the PV before pacing, and from the Ao, CS and PV after pacing were respectively: PF4 (ng/ml) -3.7, 8.8, 10.5, 9.6; BTG (ng/ ml) -17.2, 25.9, 28.7, 25.1; and PC (x109/1) - 213, 206, 200, 209. There was no significant difference (analysis of variance) between means in blood obtained from the Ao, CS and PV after pacing. For PF4 and BTG each of these 3 values was significantly higher than the PV values before pacing. Of the 13 subjects, 5 had angina during pacing. Mean results in these 5 subjects from the Ao and CS were not significantly different and were respectively: PF4 - 9.6 and 12.9-, BTG - 27.9 and 34.0, and PC - 204 and 197. Results in the 8 subjects who did not have angina during pacing were similar, as were results in the 4 subjects who had sustained a recent MI and in the 9 subjects who had not. These results indicate that the presence of the catheters and/or the pacing procedure causes slight platelet activation. However, they provide no support for the hypothesis that transcoronary platelet activation occurs during tachycardia and thus could contribute to angina. They also provide no support for the hypothesis that transcoronary platelet activation occurs during angina in patients with stable CAD, whether as a cause of it or a result.
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