Myocardial infarction (MI) type 2 (T2MI) has been a focus of attention since it was first described in 2007. T2MI is due to a critical imbalance between myocardial oxygen supply and demand resulting from various pathological mechanisms other than an acute atherosclerotic plaque disruption in the coronary arteries. Patients may or may not have atherosclerotic coronary artery disease. Often, myocardial oxygen supply/demand imbalance is related to tachycardia, hypotension/ shock, coronary artery spasm, myocardial microvascular dysfunction, coronary embolism, coronary artery dissection, or other conditions reducing coronary artery flow, but also altered myocardial oxygen carrying capacity secondary to anaemia or hypoxaemia associated with severe respiratory failure. Distinguishing patients with T2MI from those with type 1 MI (T1MI) is often straightforward but challenging at other times. Patients with T1MI usually present with spontaneous symptoms and signs suggesting acute myocardial ischaemia, with a rise and/or fall of cardiac troponin (cTn) values being diagnostic of acute MI that is considered to be related to an atherosclerotic plaque disruption. Patients with T2MI may also have symptoms and findings signalling acute myocardial ischaemia, which is considered to be the result of an important myocardial oxygen supply/demand imbalance, and which is accompanied by a rise and/or fall of cardiac troponin (cTn) values indicating acute MI. However, it appears from an all-comers’ study that cTn levels in T2MI patients tend to be lower compared to individuals with T1MI. This pattern is reflected in the present high sensitivity (hs)-cTnI study, to which patients with ST elevations MI (STEMI) were excluded, where the hs-cTnI values were lower at 0, 1, and 3 h after admission in T2MI patients, although a differentiation between T1MI and T2MI could not be done from a single elevated hs-cTnI value. In fact, this finding is unsurprising considering the varied cTn kinetics in non-STEMI (NSTEMI) patients. On the other hand, in an attempt to distinguish T2MI from T1MI patients utilizing hs-cTnI, the authors developed a logistic regression model that identified optimal hs-cTnI concentrations that were very strong predictors for T2MI at baseline and after 1 or 3 h. Furthermore, when inserting these predictors in addition to clinical parameters into a multivariable model, they developed a binary score showing that female sex, lack of typical chest pain, and a low baseline hs-cTnI <_40.8 ng/L were important forecasters for differentiation between T1MI and T2MI. However, it is important to emphasize that these calculations were made on an NSTEMI cohort rather than on an all-comers’ population. However, the issue of which population to include in a given study is important. Studies have shown variable frequencies of T2MI ranging from 2 30% of the total numbers of MIs. The present reported incidence of 34.5% of all MIs may not only reflect the exclusion of STEMI patients but also the inclusion of patients with pulmonary embolism (PE) or Takotsubo syndrome (TS) in the T2MI category. The Universal Definition of MI Task Force did not intend that conditions with non-ischaemic myocardial injury in the setting of PE or TS be designated as T2MI in the absence of clear evidence of acute myocardial ischaemia. Nevertheless, Neumann et al. have argued that these patients have had high cTnI dynamics together with symptoms and angiographic findings compatible with concomitant T2MI. As such, the inclusion of such patients may inadvertently increase the frequency of T2MI patients. Perhaps because of the manner in which the cohort of Neumann et al. was selected, the frequency of coronary artery disease (CAD) was lower in T2MI patients, who more often consisted of women, were older, did not present with typical radiating chest pain and were more likely to have atrial fibrillation, heart failure, hypertension, and worse renal function when compared to T1MI patients. Moreover, the high 1 year mortality rate of T2MI patients equals that of T1MI patients, in contrast to many other studies that have shown a poorer outcome for T2MI patients when compared to T1MI patients.

中文翻译：

---

检测 2 型心肌梗死：针对正确的患者

自 2007 年首次描述心肌梗塞 (MI) 2 型 (T2MI) 以来，它一直是关注的焦点。T2MI 是由于各种病理机制导致的心肌氧供需之间的严重失衡，而不是急性动脉粥样硬化斑块破坏。冠状动脉。患者可能有也可能没有动脉粥样硬化性冠状动脉疾病。通常，心肌氧供/需失衡与心动过速、低血压/休克、冠状动脉痉挛、心肌微血管功能障碍、冠状动脉栓塞、冠状动脉夹层或其他减少冠状动脉流量的情况有关，但也与贫血继发的心肌携氧能力改变有关或与严重呼吸衰竭相关的低氧血症。将 T2MI 患者与 1 型 MI (T1MI) 患者区分开来通常很简单，但在其他时候却具有挑战性。T1MI 患者通常会出现提示急性心肌缺血的自发症状和体征，心肌肌钙蛋白 (cTn) 值的上升和/或下降可诊断为急性 MI，这被认为与动脉粥样硬化斑块破坏有关。T2MI 患者也可能有提示急性心肌缺血的症状和表现，这被认为是重要的心肌氧供/需失衡的结果，并伴有心肌肌钙蛋白 (cTn) 值的上升和/或下降，表明急性心肌梗死。然而，一项全民研究表明，与 T1MI 患者相比，T2MI 患者的 cTn 水平往往较低。这种模式反映在目前的高敏感性 (hs)-cTnI 研究中，该研究排除了 ST 段抬高 MI (STEMI) 患者，其中 T2MI 患者入院后 0、1 和 3 小时 hs-cTnI 值较低，虽然 T1MI 和 T2MI 之间的区别不能通过单一升高的 hs-cTnI 值来完成。事实上，考虑到非 STEMI (NSTEMI) 患者中不同的 cTn 动力学，这一发现并不令人惊讶。另一方面，为了尝试使用 hs-cTnI 区分 T2MI 和 T1MI 患者，作者开发了一个逻辑回归模型，该模型确定了最佳的 hs-cTnI 浓度，这些浓度是 T2MI 在基线和 1 或 3 小时后的强预测因子。此外，当将这些预测变量和临床参数插入多变量模型时，他们开发了一个二元评分，显示女性、没有典型的胸痛和基线 hs-cTnI <_40.8 ng/L 是区分 T1MI 和 T2MI 的重要预测因素。然而，重要的是要强调这些计算是在 NSTEMI 队列而不是所有来者的人群中进行的。然而，在给定研究中包括哪些人群的问题很重要。研究表明，T2MI 的可变频率范围为 MI 总数的 2 30%。目前报告的所有 MI 的发病率为 34.5%，这不仅反映了 STEMI 患者的排除，而且还反映了肺栓塞 (PE) 或 Takotsubo 综合征 (TS) 患者被纳入 T2MI 类别。MI 工作组的通用定义并不打算在没有明确的急性心肌缺血证据的情况下将 PE 或 TS 的非缺血性心肌损伤情况指定为 T2MI。尽管如此，Neumann 等人。有人认为这些患者具有高 cTnI 动态以及与伴随的 T2MI 相符的症状和血管造影结果。因此，纳入此类患者可能会无意中增加 T2MI 患者的频率。也许是因为 Neumann 等人的队列的方式。经选择，T2MI 患者的冠状动脉疾病 (CAD) 频率较低，这些患者通常由女性组成，年龄较大，没有典型的放射性胸痛，并且更容易出现心房颤动、心力衰竭、高血压、与 T1MI 患者相比，肾功能更差。此外，T2MI 患者的 1 年高死亡率与 T1MI 患者相同，而许多其他研究表明，与 T1MI 患者相比，T2MI 患者的预后较差。