急診擁塞-過去.現況

2025-02-24 16:10 急診擁塞是很難解決的問題. 需要成本(錢). 偏偏各國都付不出成本(不想或無力)

2015年. 醫改會舉英國為例. 英國實施急診四小時清空(出院或住院). 但上有政策下有對策. 醫院遇到這個規定怎麼應對. 既然入急診需四小時完成清空. 那就不要讓救護車進急診唄..... 

結果當時的英國. 救護車乾脆被擋在急診之外不讓病患進去. 這樣就可以達成四小時清空急診的政策. 最後倒楣的還是生病的人. 

急診擁塞不是一紙公文就能解決的問題. 

2015年醫改季刊





2025年英國急診

而跟進四小時清空急診的澳洲呢? 澳洲急診四小時清空政策 也沒有解決問題

2024 AHA Scientific Statement on Management of Elevated Blood Pressure

2025-02-16 12:23中午

2024年美國心臟學會將 hypertensive urgency 及 hypertensive crisis 刪除. 急性高血壓的治療不依照高血壓數值分類. 應依照病患的風險等級給予相應的處置. 目的是要避免發生併發症 
(下面這段是張志華主任臉書的文字) 

New AHA 2024 guidelines have omitted these terms: hypertensive urgency and hypertensive crisis. These terms created ambiguity and inconsistent treatment. The new approach prioritizes risk stratification over solely focusing on blood pressure numbers. Effective management of elevated blood pressure remains the goal to prevent complications.

 
2024 AHA Scientific Statement on Management of Elevated Blood Pressure

AHA全文

Abstract
Over the past 3 decades, a substantial body of high-quality evidence has guided the diagnosis and management of elevated blood pressure (BP) in the outpatient setting. In contrast, there is a lack of comparable evidence for guiding the management of elevated BP in the acute care setting, resulting in significant practice variation. Throughout this scientific statement, we use the terms acute care and inpatient to refer to care received in the emergency department and after admission to the hospital. Elevated inpatient BP is common and can manifest either as asymptomatic or with signs of new or worsening target-organ damage, a condition referred to as hypertensive emergency. Hypertensive emergency involves acute target-organ damage and should be treated swiftly, usually with intravenous antihypertensive medications, in a closely monitored setting. However, the risk-benefit ratio of initiating or intensifying antihypertensive medications for asymptomatic elevated inpatient BP is less clear. Despite this ambiguity, clinicians prescribe oral or intravenous antihypertensive medications in approximately one-third of cases of asymptomatic elevated inpatient BP. Recent observational studies have suggested potential harms associated with treating asymptomatic elevated inpatient BP, which brings current practice into question. Despite the ubiquity of elevated inpatient BPs, few position papers, guidelines, or consensus statements have focused on improving BP management in the acute care setting. Therefore, this scientific statement aims to synthesize the available evidence, provide suggestions for best practice based on the available evidence, identify evidence-based gaps in managing elevated inpatient BP (asymptomatic and hypertensive emergency), and highlight areas requiring further research.

High blood pressure (BP) remains the leading modifiable risk factor for cardiovascular disease (CVD) in the United States, and a large body of high-quality evidence guides the diagnosis and management of elevated BP in the outpatient setting. However, fewer data are available for the management of elevated BP in the acute care setting. Throughout this scientific statement, we use the terms acute care and inpatient to refer to care received in the emergency department (ED) and after admission to the hospital. The presence of elevated BP in the acute care setting in the United States is exceptionally common. One study found that elevated inpatient BP, with or without evidence of new or worsening target-organ damage, was present in up to 72% of hospital admissions.1
Elevated inpatient BP can be broadly categorized into 2 groups: asymptomatic elevated BP and elevated BP with signs of new or worsening target-organ damage, also known as hypertensive emergency. Although the recommendation to treat hypertensive emergency in a timely manner is well accepted, there is less clarity about the risks and benefits of treating asymptomatic elevated inpatient BP with antihypertensive medication. Despite its ubiquity, there are no randomized trials on the risks and benefits of treating asymptomatic elevated inpatient BP with antihypertensive medication, and recent observational studies suggest potential harms.
This scientific statement synthesizes the available evidence for treatment of elevated inpatient BP (asymptomatic and hypertensive emergency), outlines the evidence gaps for management of elevated inpatient BP, and sets forth potential hypotheses to be tested in future high-quality studies.


DEFINITIONS
Figure 1 presents the terminology used to define elevated inpatient BP (≥130 mm Hg systolic BP [SBP] or ≥80 mm Hg diastolic BP [DBP]) to be consistent with the 2017 Hypertension Clinical Practice Guidelines definition of hypertension.2 Historical terms such as hypertensive crisis (markedly elevated BP, eg, SBP/DBP >180/110–120 mm Hg, with or without new or worsening target-organ damage) and hypertensive urgency (markedly elevated BP without evidence of new or worsening target-organ damage) fail to acknowledge the nuances of treatment decisions and, through the use of subjective emotive language such as crisis and urgency, may encourage unnecessary antihypertensive treatment. Therefore, we propose the following objective terminology: hypertensive emergency (SBP/DBP >180/110–120 mm Hg with evidence of new or worsening target-organ damage), asymptomatic markedly elevated inpatient BP (SBP/DBP >180/110–120 mm Hg without evidence of new or worsening target-organ damage), and asymptomatic elevated inpatient BP (SBP/DBP ≥130/80 mm Hg without evidence of new or worsening target-organ damage). It is imperative to underscore that BP-related target-organ damage might manifest even when BP is below the 180/110 to 120 mm Hg threshold in particular contexts, indicating that this benchmark should not be perceived as an unequivocal aspect of the definition criteria. BP-related target-organ damage refers to the acute harmful effects of elevated BP on vital organs. Specifically, it is defined by any symptom, sign, or diagnostic finding indicative of acute damage, including but not limited to injuries to the brain (eg, hypertensive encephalopathy, intracranial hemorrhage, and acute ischemic stroke), heart (eg, acute myocardial infarction, unstable angina, acute left ventricular failure with pulmonary edema), large vessels (dissecting aortic aneurysm), kidneys, and the microvasculature. Microvasculature manifestations may include conditions such as high-grade retinopathy, acute kidney injury, or microangiopathic hemolytic anemia and thrombocytopenia.


Figure 1. Terminology of elevated inpatient BP in the acute care setting. The blood pressure (BP) classifications depicted in this figure are based on established thresholds from recent hypertension guidelines, including the 2017 Hypertension Clinical Practice Guidelines, the 2018 European Society of Cardiology/European Society of Hypertension (ESH) clinical practice guidelines for the management of arterial hypertension, and the 2023 ESH guidelines on arterial hypertension management. Markedly elevated BP is defined by the 2017 Hypertension Clinical Practice Guidelines as systolic BP (SBP) >180 mm Hg or diastolic BP (DBP) >120 mm Hg in scenarios without new or worsening target-organ damage. The 2023 ESH guidelines categorize hypertensive emergency or urgency as grade 3 hypertension (SBP ≥180 mm Hg or DBP ≥110 mm Hg) without differentiating severity based solely on BP values among those showing no signs of target-organ damage progression. The depicted ranges for inpatient elevated BP align with recommendations for outpatient high BP management as the definition of stage I hypertension. Readers are encouraged to consult individual guidelines for detailed definitions and clinical context.

EPIDEMIOLOGY

In 2012, hypertension was the primary diagnosis for 1 040 000 ED visits, with ≈23% resulting in hospitalization.3 Data from the Nationwide Emergency Department Sample for 2006 to 2013 indicate that hypertensive emergencies occurred in ≈2 in 1000 adult ED visits overall and 6 in 1000 for individuals with a previous diagnosis of hypertension.4 Rates of hypertensive emergencies have increased over the past 20 years; however, mortality rates have decreased and range from 0.2% to 11%.4,5

Asymptomatic elevated inpatient BP is more common than hypertensive emergency, although the prevalence varies. In a systematic review involving 9 studies, asymptomatic elevated inpatient BP was present in 50% to 72% of hospitalizations.1 A multihospital study of 224 265 adults admitted for reasons other than hypertension found that 10% had asymptomatic markedly elevated inpatient BP.6 In another study, the presence of at least 1 elevated BP, defined as SBP >140 mm Hg, was seen in 78% of 22 834 adults admitted to a medicine service for noncardiac diagnoses.7 Certain patient populations appear to be more prone to hypertensive emergencies or asymptomatic elevated inpatient BP. These include older individuals, Black adults, and those with comorbidities such as diabetes, chronic kidney disease, and CVD.4,6,8 In addition, socioeconomically disadvantaged individuals who are underinsured or who live in low-income areas and individuals who are nonadherent to antihypertensive medication also face an increased risk for being hospitalized for hypertension.9–11 The prevalence of elevated inpatient BP likely varies by region as a result of challenges such as shortages of health care professionals in rural areas and other resource availability unique to specific geographies. Furthermore, sex and gender may also play a role. The prevalence of outpatient hypertension is lower in women until about the fifth decade of life and is higher later in life compared with men. However, there is no evidence suggesting that the threshold for initiating antihypertensive medication or indicating the type or combinations of antihypertensive medications to use should differ according to sex or gender. The management of hypertension in pregnancy in the inpatient setting has special requirements, and we refer the readers to recent guidelines and scientific statements on the management of hypertension in pregnancy.12,13

BP MEASUREMENT IN THE ACUTE CARE SETTING

The 2019 American Heart Association (AHA) scientific statement on BP measurement described best practices for outpatient BP measurement in and out of the office setting.14 However, BP measurement in the acute care setting was not addressed in that statement, largely because of the limited data on this topic. Although the contexts are different, the general principles of proper BP measurement technique apply as outlined in the AHA scientific statement on measuring BP.14 Most studies examining elevated inpatient BPs have relied on BP measurements taken during routine care and recorded in the electronic health record. However, BP recordings in the electronic health record typically omit critical contextual factors contributing to variability and inaccuracy (Figure 2). These factors may include the device type, validation and calibration status of the device, BP cuff placement, cuff size, patient position (eg, supine, seated), and situational factors (eg, anxiety, pain, patient woken up for BP measurement). The available data suggest significant variation in current BP measurement practices in the acute care setting, including discrepancies in patient position, arm support, relative position to the heart, leg crossing, and incorrect cuff sizing.14 For instance, 1 report found that 36 of 100 inpatient BP measurements in a UK hospital were performed with an inappropriately sized cuff.15 In addition, the technique and variability of inpatient BP measurements may differ depending on the hospital unit where the BP is measured. In the intensive care unit, BP is often measured with an arterial line; however, erroneous readings can occur because of movement artifacts or calibration errors.16 This variation in measurement practices can contribute to inaccurate BP readings and subsequent unnecessary treatment. However, arterial lines are preferred for hypertensive emergencies and for intravenous antihypertensives. Studies have found that when BPs are >180/100 mm Hg in critical care or surgical inpatient populations, oscillometric devices may underestimate BP by as much as 50/30 mm Hg compared with BP from an arterial line.17,18 Even research-quality manual auscultatory methods with aneroid or mercury devices exhibit notable discrepancies compared with arterial line readings.19,20 Thus, arterial lines are preferred for monitoring the rate of BP decline and the use of intravenous antihypertensive medications for hypertensive emergency. In asymptomatic elevated BP, when feasible, using standardized BP measurements in the acute care setting before making BP management decisions is reasonable and may help minimize variability and ensure appropriate treatment. Special populations, including pregnant individuals, older individuals, or patients with obesity, pseudohypertension, arrhythmias, pulseless syndromes, and left ventricular assist devices, require particular attention when BP is measured. For these special populations, we direct readers to the 2019 AHA scientific statement on the measurement of BP in humans.14 Another special population for BP management in the inpatient setting is patients in the perioperative period. BP management in this setting is influenced by many factors such as pain, anxiety, anesthesia, and procedural variables. Although this topic is beyond the scope of our current statement, it merits attention and a dedicated review because of its distinct clinical challenges. Furthermore, the timing of BP measurements, relative to the time of day and proximity to stressors such as blood draws and diagnostic tests, along with geographic practices and staffing considerations, can influence BP measurement quality in the acute care setting.

Hypertensive Emergency

Distinguishing hypertensive emergencies from asymptomatic elevated inpatient BP is the critical first step in management. After an accurate BP measurement is performed with the appropriate technique, the next step is to assess the severity of the reading and assess for evidence of new or worsening target-organ damage, the hallmark of hypertensive emergency. The BARKH acronym (brain, arteries, retina, kidney, heart) assists in quickly identifying potential target organs at risk (Table 1).21 A comprehensive evaluation of markedly elevated BP includes a thorough history and physical examination. A comprehensive history includes information on chronic hypertension, the patient’s current antihypertensive medications and adherence to the regimen, and ascertainment of any available outpatient BP readings. The physical examination includes a focus on comparing bilateral pulses, auscultating the heart and lungs, and performing a fundoscopic examination. Further diagnostic investigations include a basic metabolic panel, a complete blood count, a chest radiograph, a 12-lead ECG including heart rate, and an assessment of volume status and risk of orthostasis. If the BP reading is confirmed and evidence of new or worsening target-organ damage is present, then the treatment pathway for hypertensive emergency as outlined in the 2017 Hypertension Clinical Practice Guidelines should be promptly initiated.2

hypertensive emergency from 2024 ESC guidelines

2025-02-16 10:33AM

2024 ESC Guidelines for the management of elevated blood pressure and hypertension: Developed by the task force on the management of elevated blood pressure and hypertension of the European Society of Cardiology (ESC) and endorsed by the European Society of Endocrinology (ESE) and the European Stroke Organisation (ESO) 

10. Acute and short-term lowering of blood pressure
10.1. Acute blood pressure management in hypertensive emergencies
10.1.1. Definition and characteristics of hypertensive emergencies

Hypertensive emergency is defined as BP of ≥180/110 mmHg (see Figure 10) associated with acute HMOD, often in the presence of symptoms. Hypertensive emergencies are potentially life-threatening and require immediate and careful intervention to reduce BP, often with i.v. therapy.

Symptoms of hypertensive emergency depend on the organs affected but may include headache, visual disturbances, chest pain, shortness of breath, dizziness, and other neurological deficits. In patients with hypertensive encephalopathy, somnolence, lethargy, tonic–clonic seizures, and cortical blindness may precede a loss of consciousness; however, focal neurological lesions are rare and should raise the suspicion of stroke.

As outlined in Section 7, we define HMOD among patients with chronically elevated BP or hypertension as the presence of specific cardiac, vascular, and renal alterations.31,159 However, in the setting of hypertensive emergency, more acute manifestations of organ damage are relevant for management.

Acute manifestations of organ damage include:

Patients with severe acute hypertension associated with other clinical conditions likely to require urgent reduction in BP, e.g. acute onset of aortic dissection, myocardial ischaemia, eclampsia, or heart failure.

Malignant hypertension, defined as extreme BP elevations and acute microvascular damage (microangiopathy) affecting various organs.947 The hallmark of this condition is small-artery fibrinoid necrosis in the kidneys, retina, and brain. The acute microangiopathy is typically characterized clinically by retinopathy (flame haemorrhages, cotton wool spots, and/or papilloedema). Other manifestations of microangiopathy include disseminated intravascular coagulation, encephalopathy (in about 15% of cases), acute heart failure, and acute deterioration in renal function.


Patients with sudden severe hypertension due to phaeochromocytoma, which can result in severe acute organ damage.

The term ‘hypertension urgency’ describes severe hypertension in patients without clinical evidence of acute organ damage. While these patients require BP reduction, they do not usually require admission to hospital, and BP reduction is best achieved with oral medication according to the drug treatment algorithm presented in Section 8. However, these patients may require more urgent outpatient review to ensure that their BP is controlled.

Acute and severe increases in BP can sometimes be precipitated by sympathomimetics such as methamphetamine or cocaine, when caution around beta-blocker use is also needed. Many patients in an emergency department with acute pain or distress may have acutely elevated BP that will normalize when the pain and distress are relieved, rather than requiring any specific intervention to lower BP.

A diagnostic work-up is necessary for patients with a suspected hypertensive emergency (see Supplementary data online, Table S12).
10.1.2. Acute management of hypertensive emergencies

Key considerations in defining treatment are:

Establishing the affected target organ(s) and whether they require any specific interventions other than BP lowering.


Determining whether there is a precipitating cause for the acute rise in BP and/or another concomitant health condition present that might affect the treatment plan (e.g. pregnancy).


The recommended timing and magnitude of BP lowering required for safe BP reduction.

These considerations will inform the type of BP-lowering treatment required. Regarding BP-lowering drugs, i.v. treatment using a short half-life drug is typically ideal to allow careful titration of the BP response to treatment. This requires a higher dependency clinical area with facilities for continuous or near-continuous haemodynamic monitoring. Recommended drug treatments for specific hypertensive emergencies are provided in the Supplementary data online, Table S13.

Rapid and uncontrolled or excessive BP lowering is not recommended in hypertensive emergency as this can lead to further complications. Although i.v. drug administration is recommended for most hypertensive emergencies, oral therapy with ACE inhibitors, ARBs, or beta-blockers (shorter-acting formulations like captopril or metoprolol) can also be effective. However, low initial doses should be used because these patients can be very sensitive to these agents, and treatment should take place in hospital. Further comprehensive details on the clinical management of hypertensive emergencies are available elsewhere.242
10.1.3. Prognosis and follow-up

The survival of patients with hypertensive emergencies has improved over the past few decades, but these patients remain at high risk and should be screened for secondary hypertension.
10.2. Acute blood pressure management in acute intracerebral haemorrhage

In acute intracerebral haemorrhage, an increased BP is common and is associated with a greater risk of haematoma expansion and death, and a worse prognosis for neurological recovery. In trials testing immediate BP lowering (within <6 h) to a systolic target of <140 mmHg, the achieved systolic BP in the intervention group was typically 140–160 mmHg and was reported to reduce the risk of haematoma expansion.948,949 Excessive acute drops in systolic BP (>70 mmHg) may be associated with acute renal injury and early neurological deterioration and should be avoided.950,951
10.3. Acute blood pressure management in acute ischaemic stroke

The beneficial effects of BP reduction in acute ischaemic stroke remain unclear. In patients not receiving i.v. thrombolysis or mechanical thrombectomy, there is no evidence for actively lowering BP unless it is extremely high (e.g. >220/120 mmHg). If BP is extremely high, an initial moderate relative reduction of 10%–15% over a period of hours may be considered.952 The reason for a more conservative approach to acute BP management is that cerebral autoregulation may be impaired in acute stroke, and maintaining cerebral perfusion relies on systemic BP.

In contrast, patients who are treated with i.v. thrombolysis or mechanical thrombectomy (or both) should have more proactive management of severe hypertension, because they have an increased risk of reperfusion injury and intracranial haemorrhage. In patients undergoing treatment with i.v. thrombolysis, BP should be lowered to <185/110 mmHg prior to thrombolysis and then maintained at <180/105 mmHg over the following 24 h.953 In patients undergoing treatment with mechanical thrombectomy (with or without i.v. thrombolysis) there is limited evidence from clinical trials, but BP should also be lowered to <180/105 mmHg prior to thrombectomy and maintained over the next 24 h.953,954 Therefore, patients with acute ischaemic stroke and a BP of <180/105 mmHg in the first 72 h after stroke do not seem to benefit from the introduction or reintroduction of BP-lowering medication.955 For stable patients who remain hypertensive (≥140/90 mmHg) ≥3 days after an acute ischaemic stroke, initiation or reintroduction of BP-lowering medication is recommended.



Recommendation Table 32



Recommendations for acutely managing blood pressure in patients with intracerebral haemorrhage or acute ischaemic stroke

10.4. Acute blood pressure management in pre-eclampsia and severe hypertension in pregnancy

10.4.1. Pre-eclampsia

Pre-eclampsia is discussed in Section 9. Here we focus on its management in the acute setting. Pre-eclampsia is cured by delivery. Most international societies, including the ESC, recommend an intensive approach to BP lowering in pre-eclampsia.89,964,965 In women with pre-eclampsia and severe hypertension, immediately reducing systolic BP to <160 mmHg and diastolic BP to <105 mmHg using i.v. labetalol or nicardipine (with administration of magnesium sulfate if appropriate and consideration of delivery if appropriate) was recommended in the 2018 ESC/ESH Guidelines on the management of arterial hypertension and the 2022 ESC Guidelines for management of cardiovascular disease in pregnancy.1,89 The objective of treatment is to lower BP within 150–180 min.

Magnesium sulfate [4 g i.v. over 5 min, then 1 g/h i.v.; or 5 g intramuscularly (i.m.) into each buttock, then 5 g i.m. every 4 h] is recommended for eclampsia treatment but also for women with pre-eclampsia who have severe hypertension and proteinuria or hypertension and neurological symptoms or signs.966 There is a risk of hypotension when magnesium is given concomitantly with nifedipine.967 If BP control is not achieved by 360 min despite two medications, consulting critical care is recommended for intensive care unit admission, stabilization, and delivery (if appropriate).966 Since plasma volume is reduced in pre-eclampsia, diuretic therapy should be avoided.

10.4.2. Severe acute hypertension in pregnancy

Severe hypertension in pregnancy (without pre-eclampsia) may necessitate acute BP-lowering therapies. Severe hypertension in pregnancy is defined in general as systolic BP of >160 mmHg and diastolic BP of >110 mmHg and is associated with adverse maternal and peri-natal outcomes independent of pre-eclampsia and potentially of the same magnitude as eclampsia itself.89,968

There are differences in rate of BP control between i.v. labetalol and i.v. hydralazine in severe hypertension in pregnancy.969 While evidence is conflicting,667,668 hydralazine may be associated with more peri-natal adverse events than other drugs.970 Nifedipine seems to provide lower BP with lower rates of neonatal complications than labetalol.971

Recommendation Table 33

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Recommendations for acutely managing blood pressure in patients with severe hypertension in pregnancy and pre-eclampsia (see Evidence Table 46)

10.5. Peri-operative acute management of elevated blood pressure

Details are provided in the ESC Guidelines on cardiovascular assessment and management of patients undergoing non-cardiac surgery.972 Peri-operative hypertension, hypotension, and BP variability are associated with haemodynamic instability and poor clinical outcomes for patients undergoing surgery.973 Pre-operative risk assessment for BP management, therefore, should involve assessing for underlying end-organ damage and comorbidities.974 Postponing necessary non-cardiac surgery is not usually warranted for patients with minor or moderate elevations in BP, as they are not at higher CVD risk.130,975

Avoiding large fluctuations in BP in the peri-operative course is important, and planning a strategy for a patient should account for the baseline office BP.974–977

There is insufficient evidence for reduced or increased peri-operative BP targets compared to usual care BP targets to lower peri-operative events.978 No specific measure of BP appears better than any other for predicting risk of peri-operative events.975

10.5.1. Blood pressure-lowering drugs in the peri-operative phase

Routine initiation of a beta-blocker peri-operatively is not necessary.979

Pre-operative initiation of beta-blockers in advance of high-risk, non-cardiac surgery may be considered in patients who have known coronary artery disease or myocardial ischaemia980 or two or more significantly elevated clinical risk factors in order to reduce the incidence of peri-operative myocardial infarction.979 Peri-operative continuation of beta-blockers is recommended for patients currently taking beta-blockers.981

Some studies suggest that continued use of ACE inhibitors is associated with a higher risk of peri-operative hypotension and subsequent end-organ damage including kidney injury, myocardial infarction, and stroke.982 In the Prospective Randomized Evaluation of Preoperative Angiotensin-Converting Enzyme Inhibition (PREOP-ACEI) trial, transient pre-operative interruption of ACE inhibitor therapy was associated with a decreased risk of intra-operative hypotension.983 A subsequent systematic review also showed a decreased risk of intra-operative hypotension with withholding ACE inhibitors/ARBs before surgery, but no association with decreased mortality or CVD outcomes.984 On the other hand, vigilance is needed because withholding ACE inhibitors has also been shown to increase post-operative hypertension.985 In patients with heart failure, loop diuretics can be continued in patients prone to volume overload.986 CCBs are generally considered safe pre-operatively.

EKG 新知 OMI 心肌梗塞

2025-02-06 分享自張志華醫師臉書

很重要的心電圖新知：什麼是OMI?

OMI ECG Patterns-Youtube

Occlusion Myocardial Infarction (OMI) refers to an acute coronary occlusion or near occlusion with insufficient collateral circulation, leading to myocardial infarction. Unlike STEMI, OMI is not solely defined by ECG patterns but involves clinical assessment, biomarkers, and angiography.

The OMI paradigm is preferred over STEMI for several reasons:

• Improved Diagnosis: OMI can identify occlusions even without typical STEMI ECG changes, reducing missed diagnoses and delays in treatment.

• Clinical Relevance: OMI focuses on the pathophysiological substrate (coronary occlusion) rather than just ECG signs, allowing for more accurate and timely interventions.

• Outcomes: Patients with STEMI(-) OMI have similar adverse outcomes to STEMI(+) OMI but experience delays in catheterization, highlighting the need for a more inclusive approach.