Pre-Infarction Angina and Outcomes in Non-ST-Segment Elevation Myocardial Infarction: Data from the RICO Survey

Lorgis, Luc; Gudjoncik, Aurélie; Richard, Carole; Mock, Laurent; Buffet, Philippe; Brunel, Philippe; Janin-Manificat, Luc; Beer, Jean‐Claude; Brunet, Damien; Touzery, Claude; Rochette, Luc; Cottin, Yves; Zeller, Marianne

doi:10.1371/journal.pone.0048513

Cited by 25 publications

(26 citation statements)

References 47 publications

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“…Data has shown a decrease in severity of stroke or myocardial infarction when preceded by transient ischemic attack or angina. This was supported with measurement and analysis of creatine kinase, infarct size on imaging, development of malignant arrhythmia, mortality and neurologic disability (Abete et al, 1997; Castillo et al, 2003; Lorgis et al, 2012; Moncayo et al, 2000; Wegener et al, 2004). Also, patients with peripheral vascular disease (PVD) and sleep apnea (through repetitive hypoxic crises) may have experienced naturally occurring ischemic preconditioning (Connolly et al, 2013; Koch et al, 2007).…”

Section: Clinical Considerationsmentioning

confidence: 84%

Ischemic conditioning-induced endogenous brain protection: Applications pre-, per- or post-stroke

Wang

Reis

Applegate

et al. 2015

Experimental Neurology

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In the area of brain injury and neurodegenerative diseases, a plethora of experimental and clinical evidence strongly indicates the promise of therapeutically exploiting the endogenous adaptive system at various levels like triggers, mediators and the end-effectors to stimulate and mobilize intrinsic protective capacities against brain injuries. It is believed that ischemic pre- or post-conditioning are actually the strongest known interventions to stimulate the innate neuroprotective mechanism to prevent or reverse neurodegenerative diseases including stoke and traumatic brain injury. Recently, studies showed the effectiveness of ischemic per-conditioning in some organs. Therefore the term ischemic conditioning, including all interventions applied pre-, per- and post- ischemia, which spans therapeutic windows in 3 time periods, has recently been broadly accepted by scientific communities. In addition, it is extensively acknowledged that ischemia-mediated protection not only affects the neurons but also all the components of the neurovascular network (consisting of neurons, glial cells, vascular endothelial cells, pericytes, smooth muscle cells, and venule/veins). The concept of cerebroprotection has been widely used in place of neuroprotection. Intensive studies on the cellular signaling pathways involved in ischemic conditioning have improved the mechanistic understanding of tolerance to cerebral ischemia. This has added impetus to exploration for potential pharmacologic mimetics, which could possibly induce and maximize inherent protective capacities. However, most of these studies were performed in rodents, and the efficacy of these mimetics remains to be evaluated in human patients. Several classical signaling pathways involving apoptosis, inflammation, or oxidation have been elaborated in the past decades. Newly characterized mechanisms are emerging with the advances in biotechnology and conceptual renewal. In this review we are going to focus on those recently reported methodological and mechanistic discoveries in the realm of ischemic conditioning. Due to the varied time differences of ischemic conditioning in different animal models and clinical trials, it is important to define optimal timing to achieve the best conditioning induced neuroprotection. This brings not only an opportunity in treatment of stroke, but challenges as well, as data is just becoming available and the procedures are not yet optimized. The purpose of this review is to shed light on exploiting these ischemic conditioning modalities to protect the cerebrovascular system against diverse injuries and neurodegenerative disorders.

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Section: Clinical Considerationsmentioning

confidence: 84%

Ischemic conditioning-induced endogenous brain protection: Applications pre-, per- or post-stroke

Wang

Reis

Applegate

et al. 2015

Experimental Neurology

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“…Similarly, some medications induce cardioprotection, such as nitroglycerin taken to relieve angina 52–54 . And angina itself may be protective if it precedes coronary thrombosis by a short time interval 55 . Or if coronary thrombosis occurs gradually rather than abruptly as in the experimental studies, there could be some activation of cardioprotective signaling during the transient moderate-flow state.…”

Section: Introductionmentioning

confidence: 99%

Cardioprotection and Myocardial Reperfusion

Heide

Steenbergen

2013

Circulation Research

102

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With the advent of thrombolytic therapy and angioplasty, it has become possible to reduce myocardial infarct size through early reperfusion. Enormous effort has been expended to find therapies that can further reduce infarct size after early intervention. Animal studies have identified many cardioprotective pathways that have the potential to reduce infarct size if activated before the onset of ischemia. More recently interventions effective at the onset of reperfusion have been described. Although basic research has identified many targets, most has been conducted in rodent models which may not be directly applicable to human disease and even promising agents have been disappointing in large scale clinical trials. There are many potential explanations for this failure which is the subject of this review. Potential factors include (1) the variability inherent in the patient population whereas animal studies usually use single gender homogeneous groups maintained on standard diets in carefully controlled environments; (2) the duration of ischemia is generally shorter in animal studies, resulting in potentially more salvageable myocardium than is often the case in patients; (3) that the animals are usually young without co-morbidities whereas the patient population is generally older and has significant co-morbidities; (4) animals are not treated with medications a priori whereas the patient population is often taking medications that may affect ischemic injury; and (5) animal studies may not involve thorough assessment of effects on organs other than the heart whereas patients can experience adverse effects of treatment in other organs that can preclude clinical use.

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“…Recently Lorgis et al suggested a beneficial effect of pre-infarction angina on short-term outcomes, especially ventricular arrhythmias and infarct size in NSTEMI pa- 38 . This beneficial effect is less apparent in patients with CV risk factors (hypertension, obesity), or under chronic use of CV drugs such as aspirin or nitrates.…”

Section: Discussionmentioning

confidence: 99%

Unstable angina pectoris prior to ST elevation myocardial infarction in patients treated with primary percutaneous coronary intervention has no influence on prognosis

Kluz¹,

Pařenica²,

Kubková³

et al. 2015

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Background. Pre-infarction unstable angina pectoris (UAP) can be considered ischemic preconditioning. The aim of this study was to compare short and long term outcomes in patients with or without pre-infarction UAP and ST elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PCI). Methods. 593 patients with STEMI (388 without and 205 with UAP) were evaluated. Levels of biomarkers (troponin I, BNP, NT-ProBNP, neopterin, endoglin and pentraxin-3) at hospital admission and 24 h after STEMI onset were assessed. Echocardiography was undertaken on the fourth day after MI and after 12 months. The median follow-up was 37 months. Results. We found no significant differences in sex, age or risk factors for atherosclerosis between the UAP and non-UAP group. As the median time from the onset of chest pain to admission was significantly longer in the UAP group (228 min vs 258 min; P=0.009), we used a propensity score to obtain comparable matched groups for use in further analyses. The levels of NT-proBNP were significantly higher on admission and after 24 hours in the UAP group. Left ventricular functions according to invasive and echocardiographic parameters were entirely comparable at hospitalization and after 12 months. No differences were found in severity index of acute heart failure during hospitalization. The incidence of major acute coronary events during follow-up was comparable for the groups. Conclusions. In patients with STEMI treated with primary PCI, pre-infarction UAP has no beneficial clinical effect during hospitalization or during long-term follow-up.

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Pre-Infarction Angina and Outcomes in Non-ST-Segment Elevation Myocardial Infarction: Data from the RICO Survey

Cited by 25 publications

References 47 publications

Ischemic conditioning-induced endogenous brain protection: Applications pre-, per- or post-stroke

Ischemic conditioning-induced endogenous brain protection: Applications pre-, per- or post-stroke

Cardioprotection and Myocardial Reperfusion

Unstable angina pectoris prior to ST elevation myocardial infarction in patients treated with primary percutaneous coronary intervention has no influence on prognosis

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