Universal definition of myocardial infarction: Kristian Thygesen, Joseph S. Alpert and Harvey D. White on behalf of the Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction

Thygesen, Kristian; Alpert, Joseph S.; White, Harvey D.; Jaffe, Allan S.; Apple, Fred S.; Galvani, Marcello; Katus, Hugo A.; Newby, L. Kristin; Ravkilde, Jan; Chaitman, Bernard R.; Clemmensen, Peter; Dellborg, Mikael; Hod, Hanoch; Porela, Pekka; Underwood, Richard; Bax, Jeroen J.; Beller, George A.; Bonow, Robert O.; Wall, Ernst E. van der; Bassand, Jean‐Pierre; Wijns, William; Ferguson, T. Bruce; Steg, Philippe Gabríel; Uretsky, Barry F.; Williams, David O.; Armstrong, Paul W.; Antman, Elliott M.; Fox, Keith A; Hamm, Christian W.; Ohman, E. Magnus; Simoons, Maarten L.; Poole‐Wilson, Philip A.; Gurfinkel, Enrique P.; López‐Sendón, José‐Luis; Пайс, Прем; Mendis, Shanti; Zhu, Jun-Ren; Wallentin, Lars; Fernández‐Avilés, Francisco; Fox, Kim; Parkhomenko, Alexander; Priori, Silvia G.; Tendera, Michał; Voipio‐Pulkki, Liisa‐Maria; Vahanian, Alec; Camm, A. John; Caterina, Raffaele De; Dean, Veronica; Dickstein, Kenneth; Filippatos, Gerasimos; Funck‐Brentano, Christian; Hellemans, Irene; Kristensen, Steen Dalby; McGregor, Keith; Sechtem, Udo; Silber, Sigmund; Widimský, Petr; Zamorano, José Luís; Morais, João; Brener, Sorin J.; Harrington, Robert A.; Morrow, David A.; Lim, Michael; Martínez-Ríos, Marco Antonio; Steinhubl, Steve; Levine, Glen N.; Gibler, W. Brian; Goff, David; Tubaro, Marco; Dudek, D; Al‐Attar, Nawwar

doi:10.1093/eurheartj/ehm355

Cited by 1,693 publications

(322 citation statements)

References 89 publications

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“…Necrosis of the cells in the ischemic zone completes 2-4 hours after the onset of decreased perfusion. The individual sensitivity of myocytes to ischemia or any preconditioning effect in the past can influence the extension and the rate of cell death (49). In the acute phase of MI, and especially in reperfusion, polymorphonuclear leukocytes migrate to the infarcted area, and they aggravate tissue damage by producing reactive oxygen species (ROS).…”

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confidence: 99%

The cardioprotective potential of hydrogen sulfide in myocardial ischemia/reperfusion injury (Review)

Dongó

Hornyák

Benkö

et al. 2011

Acta Physiologica Hungarica

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Myocardial infarction is responsible for the majority of cardiovascular mortality and the pathogenesis of myocardial damage during and after the infarction involves reactive oxygen species. Serious efforts are under way to modulate the developing ischemia/reperfusion injury and recently the use of hydrogen sulfide (H 2 S) emerged as a new possibility. H 2 S has been best known for decades as a pungent toxic gas in contaminated environmental atmosphere, but it has now been recognized as a novel gasotransmitter in the central nervous and cardiovascular systems, similarly to nitric oxide (NO) and carbon monoxide (CO). This finding prompted the investigation of the potential of H 2 S as a cardioprotective agent and various in vitro and in vivo results demonstrate that H 2 S may be of value in cytoprotection during the evolution of myocardial infarction. Although several questions remain to be elucidated about the properties of this new gasotransmitter, increased H 2 S levels may have therapeutic potential in clinical settings in which ischemia/reperfusion injury is encountered. This review article overviews the current understanding of the effects of this exciting molecule in the setting of myocardial ischemia/reperfusion.

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confidence: 99%

The cardioprotective potential of hydrogen sulfide in myocardial ischemia/reperfusion injury (Review)

Dongó

Hornyák

Benkö

et al. 2011

Acta Physiologica Hungarica

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“…Using a retrospective cohort design, we identified all the admissions for AMI (Non-ST segment elevation AMI -NSTEMI, and ST segment elevation AMI -STEMI) 13 within the four facilities of MHS from October 2011 to September 2014. We used the Crimson Database (performance improvement software) to identify the cases, and then performed a manual review of the electronic medical records.…”

Section: Methodology Study Designmentioning

confidence: 99%

Risk Factors for 30-Day Readmissions after Acute Myocardial Infarction

Rodríguez

Acharya

Olson

et al. 2015

ICFJ

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BackgroundThe hospital readmission rate has been thought to reflect the quality of patient care. Understanding the risk factors for these can guide strategies to reduce them.MethodsRetrospective cohort design that included all the admissions for AMI from October 2011 to September 2014. Primary outcome was 30-day readmission rate. Secondary outcomes were 7-day readmission rate, reasons for readmission and cardiac-related readmission rate. Univariate and multivariate logistic regression were conducted with Hosmer-Lemeshow goodness-of-fit statistics for model calibration and ROC curve for model discrimination.ResultsWe identified 2958 cases of AMI and 334 readmissions (11.3%). The final sample for analysis included 310 readmitted and 652 non-readmitted patients. The principal causes of readmission were cardiac related (42%), followed by respiratory (15%) and gastrointestinal (11%). Separate analysis for the early readmissions showed the same pattern. 42% of the readmissions happened during the first week and 68% in the first 2 weeks after discharge. Median time for readmission was 10 days. Older age, days from admission to catheterization, complete medical therapy at discharge, diabetes, hypertension, stroke, major psychiatric disorders, insurance status, chronic kidney disease and congestive heart failure were independently associated with 30-day readmission. The final multivariate model discriminated well with a ROC of 0.753 (95% CI 0.72-0.79).ConclusionReasons for readmission found in our study were consistent with previous studies. Absolute readmission rates reported in this study were lower than in some prior publications. We present novel and addressable patient risk factors derived from the index admission that can be used to predict readmission.

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“…Klasifikacija IM-a s obzirom na patofiziološke, kliničke i prognostičke čimbenike razlikuje pet tipova infarkta. 12 Infarkt miokarda s urednim koronarnim arterijama (MINCA) pripada u tip 1 (neaterosklerotski uzroci) (tablica 1). Ne postoji jedinstveno objašnjenje nastanka AIM-a s normalnim koronarnim arterijama, ali predloženo je nekoliko mogućih mehanizama: latentna ateroskleroza, vazospazam, tromboza in situ i hiperkoagulabilno stanje, embolizacija i upala.…”

Section: Cardiologia Croaticaunclassified

“…MI classification recognizes five types of infarction depending on pathophysiological, clinical, and prognostic factors. 12 Myocardial infarction with angiographically normal coronary arteries (MINCA) falls under type 1 (nonatherosclerotic causes) ( Table 1). There is no definite explanation of the causes of MINCA, but several mechanisms have been suggested: latent atherosclerosis, vasospasms, thrombosis in situ and a hypercoagulable state, embolization, and inflammation.…”

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Thrombophilia and Other Conditions Associated with Acute Forms of Cardiovascular Disease.

Cmrečnjak¹,

Kursar²

2015

Cardiol Croat.

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SaŽeTaK: Svjedoci smo sve češćih slučajeva akutnih koronarnih sindroma u mlađih bolesnika, odnosno u bolesnika u kojih ne nalazimo prisutne tipične preinačive ili nepreinačive čimbenike rizika. Veći-na studija defi nira mlađe pacijente kao osobe dobi do 45 godina. U takvih se bolesnika obično dijagnosticira akutni infarkt miokarda (AIM) s normalnim koronarnim arterijama, odnosno koronarne arterije ne pokazuju intraluminalne nepravilnosti (stroga defi nicija) ili arterije s manjim stupnjem stenoze, ali hemodinamski bez značenja (u većini slučajeva < 30% stenoza). Nedavno objavljena studija (APPROACH) utvrdila je učestalost akutnog infarkta miokarda s normalnim koronarnim arterijama u iznosu od 2,8% u bolesnika podvrgnutih koronarnoj angiografi ji kod AIM-a. Diferencijalna dijagnoza takvih akutnih koronarnih zbivanja uključuje miokarditis, stres miokardiopatije i sindrom baloniranja vrška lijeve klijetke. Ne postoji jedinstveno objašnjenje nastanka AIM-a s normalnim koronarnim arterijama, ali predloženo je nekoliko mogućih mehanizama: latentna ateroskleroza, vazospazam, tromboza i hiperkoagulabilno stanje, embolizacija i upala. Postoje stečeni i nasljedni sindrom trombofi lije.U ovom ćemo prikazu opisati povezanost između nasljednih oblika trombofl ije u koje ubrajamo mutaciju faktora V Leiden, mutacija gena za protrombin, manjak proteina C i proteina S, manjak antitrombina i mutacija gena za glikoprotein inhibitor plazminogen aktivatora-1 s akutnim oblicima srčanožilnih bolesti. SUMMaRY:We are witnessing increasingly frequent cases of acute coronary syndrome in younger patients, or in patients who did not present the typical risk factors. Most studies defi ne younger patients as persons under 45 years of age. Such patients are typically diagnosed with acute myocardial infarction (AMI) with normal coronary arteries, i.e. the coronary artery does not show intraluminal anomalies (strict defi nition) or with a smaller artery stenosis but hemodynamically insignifi cant (in most cases <30% stenosis). A recently published study (APPROACH) determined the prevalence of AMI with normal coronary arteries was 2.8% in patients who underwent coronary angiography for AMI. Differential diagnosis of such acute coronary events includes myocarditis, stress cardiomyopathy, and Takotsubo syndrome. There is no single explanation for the origin of AMI with normal coronary arteries, but a few possible mechanisms have been suggested: latent atherosclerosis, vasospasm, thrombosis and hypercoagulability, embolization, and infl ammation. We differentiate between acquired and inherited thrombophilia syndrome.In this report, we will describe a link between hereditary forms of trombophilia (a mutation of factor V Leiden, prothrombin gene mutation, defi ciency of protein C and protein S, antithrombin defi ciency, and mutations in the gene for glycoprotein plasminogen activator inhibitor-1) and acute forms of cardiovascular disease.KlJUČNe RIJeČI: trombofi lija, akutni koronarni sindrom, infarkt miokarda s urednim koronarnim arterijama.KeYWORDS:...

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Universal definition of myocardial infarction: Kristian Thygesen, Joseph S. Alpert and Harvey D. White on behalf of the Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction

Cited by 1,693 publications

References 89 publications

The cardioprotective potential of hydrogen sulfide in myocardial ischemia/reperfusion injury (Review)

The cardioprotective potential of hydrogen sulfide in myocardial ischemia/reperfusion injury (Review)

Risk Factors for 30-Day Readmissions after Acute Myocardial Infarction

Thrombophilia and Other Conditions Associated with Acute Forms of Cardiovascular Disease.

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