Browsing by Subject "Myocardial infarction"

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  • Mattila, Tiina; Vasankari, Tuula; Rissanen, Harri; Knekt, Paul; Puukka, Pauli; Heliövaara, Markku (2018)
    Chronic obstructive pulmonary disease (COPD) has been associated with coronary mortality. Yet, data about the association between COPD and acute myocardial infarction (MI) remain scarce. We aimed to study airway obstruction as a predictor of MI and coronary mortality among 5576 Finnish adults who participated in a national health examination survey between 1978 and 1980. Subjects underwent spirometry, had all necessary data, showed no indications of cardiovascular disease at baseline, and were followed up through record linkage with national registers through 2011. The primary outcome consisted of a major coronary event-that is, hospitalization for MI or coronary death, whichever occurred first. We specified obstruction using the lower limit of normal categorization. Through multivariate analysis adjusted for potential confounding factors for coronary heart disease, hazard ratios (HRs) (with the 95% confidence intervals in parentheses) of a major coronary event, MI, and coronary death reached 1.06 (0.79-1.42), 0.84 (0.54-1.31), and 1.40 (1.04-1.88), respectively, in those with obstruction compared to others. However, in women aged 30-49 obstruction appeared to predict a major coronary event, where the adjusted HR reached 4.21 (1.73-10.28). In conclusion, obstruction appears to predict a major coronary event in younger women only, whereas obstruction closely associates with the risk of coronary death independent of sex and age.
  • Tuomikoski, Pauliina; Salomaa, Veikko; Havulinna, Aki; Airaksinen, Juhani; Ketonen, Matti; Koukkunen, Heli; Ukkola, Olavi; Kesaniemi, Y. Antero; Lyytinen, Heli; Ylikorkala, Olavi; Mikkola, Tomi S. (2016)
    Objectives: The role of postmenopausal hormone therapy (HT) in the incidence of acute coronary syndrome (ACS) has been studied extensively, but less is known of the impact of HT on the mortality risk due to an ACS. Study design and main outcome measures: We extracted from a population-based ACS register, FINAMI, 7258 postmenopausal women with the first ACS. These data were combined with HT use data from the National Drug Reimbursement Register; 625 patients (9%) had used various HT regimens. The death risks due to ACS before admission to hospital, 2-28, or 29-365 days after the incident ACS were compared between HT users and non-users with logistic regression analyses. Results: In all follow-up time points, the ACS death risks in HT ever-users were smaller compared to non-users. Of women with FIT ever use, 42% died within one year as compared with 52% of non-users (OR 0.62, p <0.001). Most deaths (84%) occurred within 28 days after the ACS, and in this group 36% of women with ever use of FIT (OR 0.73, p = 0.002) and 30% of women with >= 5 year FIT use (OR 0.54, p <0.001) died as compared to 43% of the non-users. Age 60 years at the HT initiation was accompanied with similar reductions in ACS mortality risk. Conclusions: Postmenopausal HT use is accompanied with reduced mortality risk after primary ACS. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
  • Abraham, Gad; Havulinna, Aki S.; Bhalala, Oneil G.; Byars, Sean G.; De Livera, Alysha M.; Yetukuri, Laxman; Tikkanen, Emmi; Perola, Markus; Schunkert, Heribert; Sijbrands, Eric J.; Palotie, Aarno; Samani, Nilesh J.; Salomaa, Veikko; Ripatti, Samuli; Inouye, Michael (2016)
    Aims Genetics plays an important role in coronary heart disease (CHD) but the clinical utility of genomic risk scores (GRSs) relative to clinical risk scores, such as the Framingham Risk Score (FRS), is unclear. Our aim was to construct and externally validate a CHD GRS, in terms of lifetime CHD risk and relative to traditional clinical risk scores. Methods and results We generated a GRS of 49 310 SNPs based on a CARDIoGRAMplusC4D Consortium meta-analysis of CHD, then independently tested it using five prospective population cohorts (three FINRISK cohorts, combined n = 12 676, 757 incident CHD events; two Framingham Heart Study cohorts (FHS), combined n = 3406, 587 incident CHD events). The GRS was associated with incident CHD (FINRISK HR = 1.74, 95% confidence interval (CI) 1.61-1.86 per S.D. of GRS; Framingham HR = 1.28, 95% CI 1.18-1.38), and was largely unchanged by adjustment for known risk factors, including family history. Integration of the GRS with the FRS or ACC/AHA13 scores improved the 10 years risk prediction (meta-analysis C-index: +1.5-1.6%, P <0.001), particularly for individuals >= 60 years old (meta-analysis C-index: +4.6-5.1%, P <0.001). Importantly, the GRS captured substantially different trajectories of absolute risk, with men in the top 20% of attaining 10% cumulative CHD risk 12-18 y earlier than those in the bottom 20%. High genomic risk was partially compensated for by low systolic blood pressure, low cholesterol level, and non-smoking. Conclusions A GRS based on a large number of SNPs improves CHD risk prediction and encodes different trajectories of lifetime risk not captured by traditional clinical risk scores.
  • Wlodarczak, Adrian; Inigo Garcia, Luis Antonio; Karjalainen, Pasi P.; Komocsi, Andras; Pisano, Francesco; Richter, Stephan; Lanocha, Magdalena; Ramon Rumoroso, Jose; Leung, Kwok Fai (2019)
    Background The Magmaris bioresorbable magnesium scaffold was successfully tested in in-vitro and in clinical premarket studies. Subsequently the Magmaris postmarket program aimed to review intraprocedural data of at least 2000 patients to assess user preferences, guideline adherence and intraprocedural performance in clinical routine. Methods This international multicentre survey encompasses data from 356 hospitals across 45 countries. As part of the certification for Magmaris implantation, each hospital had to complete consecutive post-market evaluation forms of their first 10 commercial Magmaris patients. Results From June 2016 to May 2018, data on 2018 implantations were collected. Main reasons for selecting Magmaris was patients' life expectancy (67%, n = 1359) and low or not calcified lesions, (67%, n = 1357). Magmaris was successfully deployed in 99% of cases (n = 1995), predilatation was performed in 95% (n = 1922) and post-dilatation in 87% (n = 1756). Physicians rated the overall performance and the pushability as good or very good in 96% of cases (n = 1799). Guide wire friction, trackability, and conformability were rated as good or very good in 94% of cases, and crossability in 93%. The majority of patients were scheduled to receive dual antiplatelet therapy for up to 12 months. Conclusion Generally, implantation guidelines were adhered to and theoretical advantages of the metal scaffold observed in in-vitro tests have translated into practice with good intraprocedural performance outcomes, confirming the controlled roll-out of this novel technology into clinical practice. (C) 2019 The Authors. Published by Elsevier Inc.
  • Stassen, Willem; Wallis, Lee; Lambert, Craig; Castren, Maaret; Kurland, Lisa (2017)
    Introduction: The incidence of myocardial infarction is rising in Sub-Saharan Africa. In order to reduce mortality, timely reperfusion by percutaneous coronary intervention (PCI) or thrombolysis followed by PCI is required. South Africa has historically been characterised by inequities in healthcare access based on geographic and socioeconomic status. We aimed to determine the coverage of PCI-facilities in South Africa and relate this to access based on population and socio-economic status. Methods: This cross-sectional study obtained data from literature, directories, organisational databases and correspondence with Departments of Health and hospital groups. Data was analysed descriptively while Spearman's Rho sought correlations between PCI-facility resources, population, poverty and medical insurance status. Results: South Africa has 62 PCI-facilities. Gauteng has the most PCI-facilities (n = 28) while the Northern Cape has none. Most PCI-facilities (n = 48; 77%) are owned by the private sector. A disparity exists between the number of private and state-owned PCI-facilities when compared to the poverty (r = 0.01; p = 0.17) and insurance status of individuals (r = -0.4; p = 0.27). Conclusion: For many South Africans, access to PCI-facilities and primary PCI is still impossible given their socio-economic status or geographical locale. Research is needed to determine the specific PCI-facility needs based on geographic and epidemiological aspects, and to develop a contextualised solution for South Africans suffering a myocardial infarction. (C) 2017 African Federation for Emergency Medicine. Publishing services provided by Elsevier B.V.
  • Smidtslund, Patrik (Helsingin yliopisto, 2021)
    Personer med typ 1-diabetes har en ökad risk att insjukna i en akut hjärtinfarkt. Studiens mål är att undersöka prognosen efter första hjärtinfarkten vid typ 1-diabetes samt att utreda hur olika diabetesrelaterade och hjärtinfarktrelaterade faktorer påverkar prognosen. Studien består av 132 personer som deltog i nationella FinnDiane-studien mellan åren 1995– 2011 och insjuknade i sin första hjärtinfarkt under uppföljningstiden. Information om hjärtinfarkten och diabetesrelaterade faktorer samlades från sjukjournaler. För bedömning av prognosen erhölls information om tidpunkt för eventuell död från Statistikcentralen. Under medianuppföljningstiden om 2,5 (0,0–7,2) år efter hjärtinfarkten dog 91 (68,9 %) av personerna i studien. I studien hade personer med kronisk njursjukdom den sämsta överlevnadsprognosen efter hjärtinfarkten och ju sämre njurfunktionen var, desto sämre blev prognosen. Personer med diabetesnefropati hade också en klart sämre prognos, speciellt om de var i dialysvård. De personer till vilka subakuta revaskularisering gjordes hade en betydligt bättre prognos medan akuta vården inte påverkade prognosen. I vår studie påverkade inte ålder, kön, durationen av diabetes, tidigare medicinering, lipidprofilen eller blodsockerbalansen prognosen. Resultaten i vår studie tyder på att för att förhindra hög mortalitet bland de personer som insjuknar i hjärtinfarkt måste vi förebygga utvecklingen av kronisk njursjukdom vid typ 1- diabetes. (197 ord)
  • Yliheljo, Emil (Helsingin yliopisto, 2017)
    Denna studie är en del av ett större projekt där man strävar efter att utveckla nya mikroRNA- riktade terapier för hjärtats regeneration. Studien utreder ifall man kan se en ökning i proliferationen av kardiomyocyter efter en induce- rad hjärtinfarkt. Den centrala frågeställningen är ifall neonatalmöss med inducerad hjärtinfarkt under dag 1 uppvisar bättre regenerationsförmåga av hjärtvävnaden än neonatalmöss med indu- cerad infarkt under dag 7. Infarkterna inducerades kirurgiskt genom att ligera LAD-kranskärlet med ett stygn. Till studien användes också referensgrupper med möss utan infarkt, som vid 1 eller 7 dagars ålder genomgått en kirurgisk öppning och slutning av bröstkorgen. Hjärtana avlägsnades 21 dagar efter ingreppen och frystes ner i tissue-TEK gel med hjälp av isopentan, varefter de snittades och markerades med antikroppar mot troponin I och mot Ki-67, ett protein som förekommer i prolifererande celler. Sedan användes fluorecerande sekundäranti- kroppar och färgen DAPI för att markera proverna immunohistokemsikt. Studiens andra mål var att få markeringen att fungera, en förutsättning för att kunna räkna andelen prolifererande kar- diomyocytkärnor. I beräkningen av kardiomyocytkärnor användes ett Matlab-baserat program, Nuquantus. Där- med utreder studien även möjligheterna för automatiserad beräkning av cellkärnor. Programmet lyckades räkna mängden kardiomyocytkärnor men de prolifererande kardiomyocytkärnorna var man tvungen att räkna skiljt för hand. Andelen prolifererande kardiomyocytkärnor jämfördes till slut mellan mössen med infarkter och deras referensgrupper. I studien upptäcktes en signifikant skillnad i den naturliga regenerationsförmågan hos mössen med infarkt under dag 1 och deras referensgrupp. Ingen signifikant skillnad kunde konstateras mellan mössen med infarkt under dag 7 och den andra referensgruppen. Detta indikerar att det neonatala mushjärtat innehar potential för vidare regenerativ forskning, även för det större pro- jektet och stöder tanken att hjärtats naturliga regenerationsförmåga avtar fort efter födseln. (275 ord)
  • Heliste, Juho; Jokilammi, Anne; Paatero, Ilkka; Chakroborty, Deepankar; Stark, Christoffer; Savunen, Timo; Laaksonen, Maria; Elenius, Klaus (BioMed Central, 2018)
    Abstract Background Receptor tyrosine kinases (RTK) are potential targets for the treatment of ischemic heart disease. The human RTK family consists of 55 members, most of which have not yet been characterized for expression or activity in the ischemic heart. Methods RTK gene expression was analyzed from human heart samples representing healthy tissue, acute myocardial infarction or ischemic cardiomyopathy. As an experimental model, pig heart with ischemia-reperfusion injury, caused by cardiopulmonary bypass, was used, from which phosphorylation status of RTKs was assessed with a phospho-RTK array. Expression and function of one RTK, ROR1, was further validated in pig tissue samples, and in HL-1 cardiomyocytes and H9c2 cardiomyoblasts, exposed to hypoxia and reoxygenation. ROR1 protein level was analyzed by Western blotting. Cell viability after ROR1 siRNA knockdown or activation with Wnt-5a ligand was assessed by MTT assays. Results In addition to previously characterized RTKs, a group of novel active and regulated RTKs was detected in the ischemic heart. ROR1 was the most significantly upregulated RTK in human ischemic cardiomyopathy. However, ROR1 phosphorylation was suppressed in the pig model of ischemia-reperfusion and ROR1 phosphorylation and expression were down-regulated in HL-1 cardiomyocytes subjected to short-term hypoxia in vitro. ROR1 expression in the pig heart was confirmed on protein and mRNA level. Functionally, ROR1 activity was associated with reduced viability of HL-1 cardiomyocytes in both normoxia and during hypoxia-reoxygenation. Conclusions Several novel RTKs were found to be regulated in expression or activity in ischemic heart. ROR1 was one of the most significantly regulated RTKs. The in vitro findings suggest a role for ROR1 as a potential target for the treatment of ischemic heart injury.
  • Heliste, Juho; Jokilammi, Anne; Paatero, Ilkka; Chakroborty, Deepankar; Stark, Christoffer; Savunen, Timo; Laaksonen, Maria; Elenius, Klaus (2018)
    BackgroundReceptor tyrosine kinases (RTK) are potential targets for the treatment of ischemic heart disease. The human RTK family consists of 55 members, most of which have not yet been characterized for expression or activity in the ischemic heart.MethodsRTK gene expression was analyzed from human heart samples representing healthy tissue, acute myocardial infarction or ischemic cardiomyopathy. As an experimental model, pig heart with ischemia-reperfusion injury, caused by cardiopulmonary bypass,was used, from which phosphorylation status of RTKs was assessed with a phospho-RTK array. Expression and function of one RTK, ROR1, was further validated in pig tissue samples, and in HL-1 cardiomyocytes and H9c2 cardiomyoblasts, exposed to hypoxia and reoxygenation. ROR1 protein level was analyzed by Western blotting. Cell viability after ROR1 siRNA knockdown or activation with Wnt-5a ligand was assessed by MTT assays.ResultsIn addition to previously characterized RTKs, a group of novel active and regulated RTKs was detected in the ischemic heart. ROR1 was the most significantly upregulated RTK in human ischemic cardiomyopathy. However, ROR1 phosphorylation was suppressed in the pig model of ischemia-reperfusion and ROR1 phosphorylation and expression were down-regulated in HL-1 cardiomyocytes subjected to short-term hypoxia in vitro. ROR1 expression in the pig heart was confirmed on protein and mRNA level. Functionally, ROR1 activity was associated with reduced viability of HL-1 cardiomyocytes in both normoxia and during hypoxia-reoxygenation.ConclusionsSeveral novel RTKs were found to be regulated in expression or activity in ischemic heart. ROR1 was one of the most significantly regulated RTKs. The in vitro findings suggest a role for ROR1 as a potential target for the treatment of ischemic heart injury.
  • Raatikainen, M. J. Pekka; Penttilä, Tero; Korhonen, Pasi; Mehtälä, Juha; Lassila, Riitta; Lehto, Mika (2018)
    Aims The impact of the quality of warfarin therapy on cardiovascular outcomes excluding stroke is largely unknown. The aims of this study were to evaluate the association between the warfarin control and the incidence and outcome of myocardial infarction (MI) and to validate the predictive value of the CHA2DS2-VASc score for MI in atrial fibrillation (AF) patients taking warfarin. Methods and results The nationwide FinWAF Registry consists of 54 568 AF patients (mean age 73.31 +/- 10.7 years, 52% men) taking warfarin. The quality of warfarin therapy was assessed continuously by calculating the time in therapeutic range within a 60-day window using the Rosendaal method (TTR60). Adjusted Cox proportional hazards models were prepared for the incidence of MI and cardiovascular mortality in six different TTR60 categories. During the 3.2 +/- 1.6 years of follow-up, the annual incidence of MI (95% confidence interval) was 3.3% (3.0-3.5%), 2.9% (2.6-3.3%), 2.4% (2.1-2.7%), 1.9% (1.7-2.2%), 1.7% (1.5-2.0%), and 1.2% (1.1-1.3%) among patients with TTR60 80%, respectively. Well-managed warfarin therapy (TTR60 >80%) was associated also with a lower cardiovascular mortality, whereas a high CHA(2)DS(2)-VASc score correlated with poor outcome. Conclusion Cardiovascular outcome was superior among AF patients with good warfarin control and in those with a low CHA(2)DS(2)-VASc score. The inverse association between the TTR60 and incidence of MI and cardiovascular mortality indicate that in AF patients the quality of warfarin therapy is critical not only for prevention of stroke but also with regard to cardiovascular outcome.
  • Kelloniemi, Annina; Aro, Jani; Näpänkangas, Juha; Koivisto, Elina; Mustonen, Erja; Ruskoaho, Heikki; Rysä, Jaana (2015)
    Background: The transforming growth factor (TGF)-beta is one of the key mediators in cardiac remodelling occurring after myocardial infarction (MI) and in hypertensive heart disease. The TGF-beta-stimulated clone 22 (TSC-22) is a leucine zipper protein expressed in many tissues and possessing various transcription-modulating activities. However, its function in the heart remains unknown. Methods: The aim of the present study was to characterize cardiac TSC-22 expression in vivo in cardiac remodelling and in myocytes in vitro. In addition, we used TSC-22 gene transfer in order to examine the effects of TSC-22 on cardiac gene expression and function. Results: We found that TSC-22 is rapidly up-regulated by multiple hypertrophic stimuli, and in post-MI remodelling both TSC-22 mRNA and protein levels were up-regulated (4.1-fold, P <0.001 and 3.0-fold, P <0.05, respectively) already on day 1. We observed that both losartan and metoprolol treatments reduced left ventricular TSC-22 gene expression. Finally, TSC-22 overexpression by local intramyocardial adenovirus-mediated gene delivery showed that TSC-22 appears to have a role in regulating collagen type III alpha 1 gene expression in the heart. Conclusions: These results demonstrate that TSC-22 expression is induced in response to cardiac overload. Moreover, our data suggests that, by regulating collagen expression in the heart in vivo, TSC-22 could be a potential target for fibrosis-preventing therapies.
  • Vihonen, Hanna; Tierala, Ilkka; Kuisma, Markku; Puolakka, Jyrki; Westerbacka, Jukka; Nurmi, Jouni (2014)