How is myocardial infarction diagnosed?

Myocardial infarction is not just the "classic" sudden chest pain. In women, the elderly, and patients with comorbidities, it often presents with shortness of breath, nausea, weakness, back pain, or jaw pain. Therefore, diagnosis today relies not on a single symptom but on a combination of data: clinical symptoms, an electrocardiogram, high-sensitivity troponin, and cardiac imaging. The physician's task is to quickly differentiate an infarction, which requires immediate reperfusion, from conditions that mimic it but are treated differently.

The modern approach begins at the emergency department entrance: an ECG within the first 10 minutes of any patient with suspected acute coronary syndrome, followed by a blood draw for high-sensitivity troponin. If the ECG shows ST-segment elevation or its equivalent, it's a "clear" scenario—urgent reperfusion is required. If there is no elevation, serial troponin measurement algorithms (e.g., 0/1-hour) are used, allowing for the safe exclusion of a significant proportion of patients without infarction and the timely recognition of those requiring invasive therapy.

A key concept is to distinguish between "myocardial injury" and "myocardial infarction." Injury is defined as an elevated troponin; infarction is injury plus evidence of ischemia (symptoms, ischemic ECG changes, recent regional contractility disturbances, or coronary artery occlusion). It is also important to distinguish type 1 infarction (thrombus/plaque rupture) from type 2 infarction (oxygen supply/demand imbalance without acute thrombosis): this determines the treatment plan—from emergency PCI to correction of anemia, hypoxia, or tachyarrhythmia.

Finally, "gray areas" require careful attention. In patients with chronic kidney disease, the elderly, and cancer patients, troponin is often elevated at baseline. Here, dynamics and context determine the outcome, and echocardiography, CT coronary angiography, and cardiac MRI can help. Standardized workflows (triage, temporary ECG and troponin targets, rule-out criteria, and indications for coronary angiography) minimize errors and expedite correct decisions—this is what saves the myocardium and lives today.

What is considered a heart attack today: basic definitions

In clinical practice, we distinguish between myocardial injury and myocardial infarction. Injury is defined as any increase in high-sensitivity troponin (hs-cTn) above the 99th percentile of the reference population, with acute injury requiring a dynamic (rise/fall). Infarction is defined as acute injury plus evidence of ischemia (symptoms, ischemic changes on ECG, presence of thrombus/occlusion on angiography, new regional contractility abnormalities or necrosis on imaging). This logic is enshrined in the Universal Definition of MI and underlies modern protocols. [1]

The classification by type is also clinically important: type 1 (coronary thrombus/plaque rupture), type 2 (oxygen supply-demand mismatch without acute thrombus), type 3 (sudden cardiac death), types 4-5 (associated with coronary interventions/surgeries). In reality, it is the distinction between type 1 and type 2 that determines the tactics: the former is more often indicated for an early invasive strategy, the latter - correction of the cause (hypoxia, tachyarrhythmia, anemia, etc.) during anatomical assessment of the coronary [2]

In 2023-2025, there will be active discussion about whether age/gender thresholds for hs-cTn are needed and how best to differentiate injury from MI in complex populations. European and American documents agree on one thing: a diagnosis of MI cannot be simply "stuck" to any elevated troponin – it must be interpreted contextually, taking into account the clinical presentation, ECG, and marker dynamics. [3]

Finally, the organizational standard: work must be carried out with highly sensitive troponin tests (hs-cTnI/hs-cTnT) and validated rapid serial measurement algorithms. Algorithms for "older" (less sensitive) tests are not applicable to these protocols. [4]

Table 1. "Damage" vs. "Infarction" (short cheat sheet)

What do we see?	Diagnostic thought
hs-cTn >99th percentile, there is dynamics	Acute myocardial injury
Plus ≥1 sign of ischemia (symptoms/ECG/angio/echo/MRI)	Myocardial infarction
No signs of ischemia (sepsis, pulmonary embolism, chronic kidney disease, myocarditis, etc.)	Non-ischemic myocardial injury
hs-cTn is consistently elevated, no dynamics	Chronic damage (common in CKD)

According to the Universal Definition of MI and ESC/ACC guidelines. [5]

When to suspect MI and what to do in the first minutes

The first filter is the clinical context: chest pain/discomfort, shortness of breath, nausea, cold sweat, irradiation; in the elderly and women, "atypical" complaints (shortness of breath, weakness, back/jaw pain) are common. Any patient with suspected acute coronary syndrome (ACS) should have an ECG within 10 minutes of contact with the medical system and a blood sample for hs-cTn. [6]

An ECG is the immediate deciding factor in cases of ST segment elevation and STEMI equivalents (e.g., new left bundle branch block + ischemic criteria, posterior infarction with ST depression V1-V3). This is an indication for immediate reperfusion (primary PCI or thrombolysis if PCI is not available in a timely manner) – this can be done concurrently, but there is no need to wait for troponin. In cases of unstable hemodynamics or threatening arrhythmias, ECG decisions are primary. [7]

If there is no ST elevation, the rapid troponin algorithm (below) comes into play. It is important to remember that in some patients, the early ECG may be nonspecific; repeat the recording if pain worsens, use right/posterior leads if the right ventricle/posterior wall is suspected. Any "doubtful" case with a high pre-test probability is best considered an MI until proven otherwise. [8]

Triage follows multidisciplinary pathways from recommendations: rapid risk stratification, early contact with the catheterization laboratory for STEMI, and standardized protocols for serial hs-cTn in suspected NSTE-ACS. This reduces errors and accelerates key decisions. [9]

Electrocardiogram: What constitutes evidence of ischemia?

Classic STEMI criteria include ST elevation above gender/lead-specific thresholds with clinical features suggesting acute coronary syndrome. STEMI equivalents include new or presumably new left bundle branch block with a high probability of MI (using the modified Sgarbossa/Smith criteria), and posterior MI (horizontal/downsloping ST depression in V1-V3 + high R wave). These situations require reperfusion, even if troponin has not yet risen. [10]

In the presence of NST changes, new or dynamic ST depressions/T-wave inversions, especially in several adjacent leads, are diagnostically valuable. However, an isolated ECG rarely provides a definitive answer—it becomes part of a mosaic along with symptoms and troponin. Repeat ECGs are critical if pain persists. [11]

When the ECG is non-diagnostic (pre-existing changes, pacemaker, hypertrophy), bedside echocardiography (looking for new regional wall motion abnormalities) and, if stable, CT coronary angiography to exclude obstructive lesions (in low/intermediate probability patients) are useful.[12]

A separate section is the differentiation of "double mimics": pericarditis (diffuse ST elevation with PR elevation), early repolarization, hyperkalemia, and pulmonary embolism. Mistakes here are costly, so suspicion of "pure" pericarditis or PE in the presence of typical pain and risk factors should be strongly substantiated. [13]

Table 2. ECG clues for and against coronary ischemia

Painting	More like IM	Most likely not IM
ST elevation	Territorial, with mirror depression	Diffuse elevation + PR elevation (pericarditis)
ST depression V1-V3	Posterior MI (STEMI equivalent)	Blockades/hypertrophy without dynamics
Left bundle branch block	New + IM clinic (Sgarbossa/Smith criteria)	Old, without dynamics and symptoms
Negative T	New, dynamic, multiple	Chronic, isolated

Integrate ECG into clinical and biomarker context. [14]

Biomarkers: How to Use High-Sensitivity Troponin Correctly

Hs-cTn is the main laboratory test. It is sensitive in the early hours of infarction, and its dynamics (Δ-change) helps differentiate acute from chronic infarction. All algorithms are based on the 99th percentile threshold of a specific test and serial measurements. Clinicians also consider pre-test probability and time since symptom onset. [15]

In Europe, the ESC 0/1 hour model (sometimes 0/2 hours or 0/3 hours) has become the baseline, while in the US, several validated pathways from the ACC Expert Consensus have been used (including "single" hs-cTn strategies in low-risk patients with pain >3 hours). Important: protocols are applicable only to hs-cTn assays and should use cutoff values and deltas validated for a specific reagent kit. [16]

The safety of rapid protocols is the subject of active research. For example, reports indicate that the "pure" 0/1 h ESC regimen may perform less well in patients with known coronary artery disease (lower NPV at 30 days), requiring a more conservative approach (additional serial measurements, clinical imaging, ECG, and imaging). This does not negate the use of algorithms, but requires sound clinical judgment. [17]

Certain groups (the elderly, CKD patients, and cancer patients) often have elevated hs-cTn levels at baseline. The key here is the dynamics and clinical relevance; even potential age thresholds are being discussed in future revisions of the Universal Definition of Myocardial Infarction. In doubtful situations, echocardiography, CT coronary angiography, or cardiac MRI (see below) can be helpful. [18]

Table 3. Serial hs-cTn: typical pathways

Approach	Where it is applied	The essence
ESC 0/1 h (or 0/2-0/3 h)	Ed/cardio reception, Europe	Collection upon admission and after 1 hour; “rule-out/observe/rule-in” algorithm
ACC Pathways (incl. single-draw at low risk)	ED, USA	For low risk and symptoms >3 h, a “single-dose” strategy is acceptable when hs-cTn is below the validated threshold.
Delta Approach	Everywhere	What matters is the dynamics (abs./rel. growth), and not just the fact of exceeding the 99th percentile

Imaging and Invasive Evaluation: Who, When, and Why

Bedside echocardiography is useful from the first minutes: it identifies new regional wall motion abnormalities (indirect confirmation of ischemia/necrosis), complications (mitral regurgitation, septal defect, tamponade), and helps with hemodynamic instability. Echo is especially valuable when the ECG is uninformative. [19]

In stable patients, CT coronary angiography (CTA) rapidly excludes obstructive coronary artery disease in the low/intermediate probability group, reducing hospitalizations and invasive procedures. If CTA shows no significant stenoses, the likelihood of ongoing type 1 MI is extremely low, and alternatives (myocarditis, Takotsubo, PE) should be sought. [20]

Invasive coronary angiography remains the gold standard for STEMI and high-risk NSTE-ACS. It not only confirms the diagnosis but also allows for immediate treatment (PCI). In the absence of obstruction and the continued suspicion of an ischemic mechanism, OCT/IVUS tools and vasospastic testing are used, especially with MINOCA. [21]

Cardiac MRI with late contrast is indispensable when it is necessary to differentiate MI from myocarditis/Takotsubo and to determine the duration and extent of necrosis. In MINOCA, MRI changes the clinical decision in a significant proportion of patients, directing them to the correct etiology. [22]

Table 4. Quick selection of visualization

Clinical situation	What to choose first
STEMI / instability	Invasive coronary angiography (reperfusion)
NSTE-ACS, moderate/high risk	Invasive assessment within risk timeframes
Low/intermediate probability, inconclusive ECG/troponin	CT coronary angiography
MINOCA, controversial etiology	Cardiac MRI; OCT/IVUS if necessary

According to ESC 2023 and multisociety recommendations 2021. [23]

Diagnostic algorithms in the emergency department: decision "flows"

The main goal of ED algorithms is to quickly differentiate: (1) overt STEMI → immediate reperfusion; (2) NSTE-ACS “rule-in” based on hs-cTn/ECG dynamics → early invasive strategy; (3) safe “rule-out” → discharge/outpatient reassessment; (4) “observation zone”. For this purpose, ESC 0/1 h and ACC pathways are used in combination with clinical assessment and risk scales. [24]

In the US, multisociety guidelines recommend a strategy of a single hs-cTn below the validated threshold with a clear ECG for low-risk patients with pain duration >3 hours, followed by a safe "rule-out." For higher-risk patients or early symptoms, serial testing is necessary. [25]

It's important to remember the limitations: in patients with known coronary artery disease and in certain comorbid groups, the NPV of rapid algorithms may decrease. In such cases, the series of measurements is expanded, imaging (CTAC/Echo) is added, and discharge is delayed. Safety is more important than speed. [26]

After the initial decision, a plan is developed: who needs an invasive assessment in the next few hours/day, who needs functional/anatomical tests on an outpatient basis, and who needs observation. Standardized protocols reduce variability and legal risks. [27]

Table 5. Rule-out/observe/rule-in logic (generalized)

Branch	What is usually required
Rule-out	Normal ECG + hs-cTn low/no change via validated pathway → discharge/outpatient evaluation
Observe	Borderline values/microdynamics → repeat hs-cTn, ECG, possibly CTCAG/Echo
Rule-in	Significant excess of the 99th percentile + dynamics and/or ischemic ECG changes → early invasive strategy

Specific thresholds depend on the test used and the local protocol. [28]

Special groups and "gray zones"

Women, the elderly, and CKD. These patients are more likely to have "atypical" symptoms and chronically elevated hs-cTn. Focus on dynamics and imaging; avoid a "diagnosis throne" based on a single number. Age/gender thresholds are being discussed and validated, but this is still an area of active research. [29]

Cancer patients and those receiving chemotherapy often have subacute myocardial injury with elevated hs-cTn levels without type 1 MI. Cardiac MRI and well-designed cardio-oncological routing are particularly important here. New studies even suggest tailored thresholds/deltas for this population. [30]

MINOCA (MI in non-occlusive coronary arteries) requires an exclusion algorithm: coronary spasm, dissection, thrombosis with lysis, myocarditis, and Takotsubo. MRI and invasive intravascular imaging radically improve diagnostic accuracy and change treatment. [31]

Competitors of MI include myocarditis, pulmonary embolism, aortic dissection, and severe pericarditis. If there is a discrepancy between troponin, ECG, and clinical findings and the "wrong" pain, it is better to expand the diagnostic search than to "drag on" MI. [32]

Table 6. Common causes of elevated hs-cTn "not in type 1 MI"

Category	Examples
Type 2 MI (imbalance)	Tachy/bradyarrhythmia, hypoxia, severe hypotension, anemia
Non-ischemic injury	Myocarditis, heart failure, renal failure, sepsis
Other acute conditions	PE, stroke/SAH, pericarditis/myopericarditis
Procedural/toxic	Cardioversion/ablation, cardiotoxic therapy

What decides next is context, dynamics and visualization. [33]