TIMI Risk Score for STEMI
Bedside estimation of 30-day all-cause mortality in patients presenting with ST-elevation myocardial infarction. Derived from the InTIME II trial (n = 14,114) and externally validated in TIMI 9.
Calculate TIMI Risk Score — STEMI
Select all criteria that apply to your patient at presentation. This score is intended for patients with confirmed STEMI (ST elevation on ECG or new LBBB with clinical context consistent with acute MI). It was originally derived in fibrinolytic-eligible patients but has been applied across reperfusion strategies.
The TIMI risk score for STEMI was derived and validated in fibrinolytic-eligible patients. It excluded patients with cardiogenic shock, SBP > 180 mmHg, DBP > 110 mmHg, prior cerebrovascular disease, or high bleeding risk. Apply with caution in these excluded populations. The score estimates population-level risk and does not replace individualised clinical assessment.
Understanding the TIMI Risk Score for STEMI
The TIMI Risk Score for STEMI was developed by Morrow et al. in 2000 using data from the InTIME II trial, which enrolled 14,114 patients with STEMI receiving fibrinolytic therapy across more than 800 hospitals worldwide. The score was designed to provide a simple, bedside-applicable tool for predicting 30-day all-cause mortality — an outcome that occurred in 6.7% of the study population.
From an initial multivariate logistic regression model containing all significant baseline predictors, 10 variables were selected that captured 97% of the model’s predictive capacity. These were then assigned integer weights based on their adjusted odds ratios, creating a score that can be summed on a pocket card or at the bedside without a calculator. The resulting score ranges from 0 to 14 and demonstrates a greater than 40-fold graded increase in 30-day mortality from the lowest to highest scores.
Scoring Formula
TIMI Score = sum of all applicable criteria
Age 65–74 → +2
Age ≥ 75 → +3
DM / HTN / Angina → +1
SBP < 100 → +3
HR > 100 → +2
Killip II–IV → +2
Weight < 67 kg → +1
Anterior STE or LBBB → +1
Time to Rx > 4 h → +1
Range: 0–14 points
Worked Example
A 70-year-old man with hypertension presents with an anterior STEMI. SBP 105 mmHg, HR 92 bpm, Killip class I, weight 80 kg. Time to thrombolysis: 3 hours.
Age 65–74 = 2
HTN = 1
SBP ≥ 100 = 0, HR ≤ 100 = 0
Killip I = 0, Weight ≥ 67 = 0
Anterior STE = 1
Time ≤ 4 h = 0
TIMI Score = 4 → 30-day mortality ≈ 7.3%
Key distinction: Unlike the TIMI Risk Score for UA/NSTEMI (a 7-point binary scale), the TIMI Score for STEMI is a weighted scoring system with a maximum of 14 points. The two scores use entirely different criteria and should never be interchanged. The STEMI version focuses on haemodynamic and demographic predictors of mortality, not on ischaemic recurrence.
Interpretation — 30-Day Mortality by Score
The table below shows the estimated 30-day all-cause mortality for each TIMI score value, as reported in the original InTIME II derivation cohort. The score demonstrates a continuous graded relationship with mortality — there are no formal “cutoffs,” but clinical practice generally groups patients into risk strata for decision-making.
| TIMI Score | 30-Day Mortality | Risk Stratum |
|---|---|---|
| 0 | 0.8% | Low risk |
| 1 | 1.6% | Low risk |
| 2 | 2.2% | Low risk |
| 3 | 4.4% | Low–moderate risk |
| 4 | 7.3% | Moderate risk |
| 5 | 12.4% | Moderate–high risk |
| 6 | 16.1% | High risk |
| 7 | 23.4% | High risk |
| 8 | 26.8% | Very high risk |
| > 8 | 35.9% | Very high risk |
Nearly two-thirds of patients in the derivation cohort had scores of 0–3, with a 5.3-fold gradient in mortality over this range alone. The score’s c-statistic of 0.779 is comparable to the full multivariate model (0.784), demonstrating that the simplified bedside score retains nearly all prognostic power. The score was also stable across time points from 1 day to 365 days.
Scoring Criteria in Detail
The eight scoring criteria (with age counted as one variable with three levels) capture the key haemodynamic, demographic, and clinical predictors of early mortality in STEMI. Each variable’s point weighting reflects its adjusted odds ratio for 30-day death.
Age carries the highest point weight in the score (up to 3 points for ≥ 75 years), reflecting the strong independent association between advancing age and mortality following STEMI. Elderly patients have higher rates of mechanical complications, heart failure, and cardiogenic shock. They are also more likely to present late with atypical symptoms, reducing the window for effective reperfusion.
- < 65 years: 0 points. Lower baseline mortality risk, though complications can still occur, particularly with large anterior MIs or delayed presentation.
- 65–74 years: 2 points. A transitional group where comorbidity burden increases and cardiac reserve diminishes.
- ≥ 75 years: 3 points. The highest weighting. These patients have the highest mortality and complication rates, and decisions regarding invasive strategies must balance benefit against bleeding and procedural risk.
Hypotension at presentation carries the joint-highest weighting (3 points, equal to age ≥ 75), reflecting its strong association with cardiogenic shock, large infarct size, and haemodynamic compromise. A systolic BP below 100 mmHg may indicate extensive myocardial damage with reduced cardiac output, right ventricular infarction (especially in inferior STEMI), or mechanical complications such as acute mitral regurgitation or ventricular septal defect.
Hypotension should prompt immediate evaluation for these causes. Volume status assessment, echocardiography, and consideration of inotropic or mechanical circulatory support may be needed alongside reperfusion therapy.
Tachycardia at presentation is an independent predictor of mortality, reflecting sympathetic activation in response to pain, anxiety, reduced cardiac output, or incipient heart failure. In the context of STEMI, a heart rate exceeding 100 bpm may suggest a large area of myocardium at risk, evolving heart failure, or hypovolaemia.
It is important to distinguish sinus tachycardia (a compensatory response) from pathological arrhythmias such as atrial fibrillation with rapid ventricular response, which carry additional prognostic significance. Beta-blockade to control heart rate may be appropriate if there is no contraindication (hypotension, acute heart failure, bradycardia risk).
The Killip classification is a bedside assessment of heart failure severity in the setting of acute MI. It has been one of the most consistent predictors of mortality across multiple ACS scoring systems. In the TIMI STEMI score, any Killip class above I scores 2 points.
- Class I: No clinical signs of heart failure. No rales, no S3, no JVD. (0 points)
- Class II: Mild-to-moderate heart failure. Rales in the lower half of the lung fields, elevated JVP, or S3 gallop. (2 points)
- Class III: Acute pulmonary oedema. Rales extending above the lower half of the lung fields. (2 points)
- Class IV: Cardiogenic shock. Hypotension (SBP < 90 mmHg), signs of end-organ hypoperfusion (oliguria, altered mental status, cool extremities). (2 points)
Note that the original TIMI STEMI study excluded patients presenting with cardiogenic shock, so the score’s predictive accuracy in Killip class IV patients may be limited. However, the inclusion of Killip class II–III substantially improves discrimination across the population.
Low body weight has been consistently associated with increased mortality following STEMI, an observation reproduced across multiple ACS registries. The mechanism is multifactorial: lower body weight may reflect frailty, sarcopenia, or chronic illness burden. Additionally, low-weight patients may be at higher risk of bleeding complications from anticoagulant and antiplatelet therapy, and from catheterisation procedures.
This variable serves as a proxy for overall constitutional vulnerability. It is worth noting that women are more frequently below this threshold than men, which may partially explain sex-based differences in STEMI outcomes.
Anterior STEMI (ST elevation in leads V1–V4, with or without extension to V5–V6, I, and aVL) typically results from occlusion of the left anterior descending artery and involves the largest territory of myocardium at risk. Compared to inferior or lateral STEMI, anterior infarctions carry higher rates of heart failure, cardiogenic shock, ventricular arrhythmias, and death.
New LBBB in the setting of chest pain was historically treated as a STEMI equivalent, prompting emergent reperfusion. Current guidelines have evolved — new LBBB alone is no longer considered sufficient for emergent catheterisation lab activation unless other clinical features strongly suggest acute ischaemia. The modified Sgarbossa criteria can help identify acute MI in the setting of LBBB.
Delay from symptom onset to reperfusion therapy is a well-established determinant of infarct size and mortality. The adage “time is muscle” reflects the progressive, time-dependent loss of viable myocardium during coronary occlusion. The greatest absolute benefit from reperfusion is achieved in the first 2–3 hours, with a steep decline in benefit thereafter.
A treatment delay exceeding 4 hours reflects either late presentation by the patient, system-level delays in diagnosis and transfer, or both. In the era of primary PCI, this variable should be interpreted as symptom-onset to balloon time exceeding 4 hours, or symptom-onset to fibrinolytic administration exceeding 4 hours if a pharmacological strategy is used.
This composite variable captures the presence of any one of three major cardiovascular comorbidities: diabetes mellitus, hypertension, or prior angina pectoris. Each of these conditions independently increases the risk of adverse outcomes after STEMI through different but overlapping mechanisms.
- Diabetes mellitus is associated with diffuse coronary disease, impaired collateral circulation, autonomic neuropathy (which may mask ischaemic symptoms), and worse outcomes across all ACS presentations.
- Hypertension contributes to left ventricular hypertrophy, diastolic dysfunction, and increased myocardial oxygen demand, all of which impair recovery from acute infarction.
- Prior angina indicates pre-existing obstructive coronary disease, though paradoxically, some studies suggest that prior angina may confer a degree of ischaemic preconditioning that partially offsets its risk contribution.
Only 1 point is awarded regardless of how many of these conditions are present, reflecting their relatively modest independent contribution to 30-day mortality compared to haemodynamic variables.
Special Populations & Considerations
The TIMI STEMI risk score was derived in a specific trial population. Understanding its applicability — and limitations — in different clinical contexts is essential for appropriate use.
Important limitation: The original derivation cohort excluded patients with prior cerebrovascular disease, SBP > 180 mmHg, DBP > 110 mmHg, and those at high risk of severe bleeding. The score has not been formally validated in these populations and may not accurately predict outcomes in these excluded subgroups.
Comparison with Other STEMI Risk Scores
Several risk stratification tools exist for STEMI patients. Understanding their differences helps clinicians select the most appropriate score for their clinical scenario and the data available.
The Global Registry of Acute Coronary Events (GRACE) score is a more complex model that predicts in-hospital and 6-month mortality across the full ACS spectrum (STEMI, NSTEMI, and unstable angina). It uses 8 variables including heart rate, systolic BP, creatinine, Killip class, cardiac arrest at admission, ST-segment deviation, elevated cardiac markers, and age. The GRACE score requires a computer or dedicated calculator for its nomogram-based computation, making it less practical at the bedside than the TIMI score.
The GRACE score generally provides superior discrimination for in-hospital mortality (c-statistic ≈ 0.83) compared to the TIMI STEMI score (0.78), but at the cost of greater complexity. The TIMI score’s advantage lies in its simplicity and ease of use at the point of care.
The Zwolle score was specifically developed for STEMI patients treated with primary PCI — unlike the TIMI score, which was derived in a fibrinolytic population. It includes 6 variables: Killip class, TIMI flow post-PCI, age, 3-vessel disease, anterior MI, and ischaemia time. The inclusion of angiographic data (TIMI flow, multi-vessel disease) means it can only be calculated after catheterisation, limiting its use for initial triage at presentation.
The Zwolle score is particularly useful for identifying very low-risk patients suitable for early discharge after primary PCI (within 48–72 hours).
The Dynamic TIMI Risk Score extends the original baseline score by incorporating in-hospital events — recurrent MI, arrhythmia, major bleed, stroke, heart failure, recurrent ischaemia, and renal failure — to provide an updated 1-year mortality estimate at discharge. The combined score ranges from 0 to 29 points. This allows reclassification of patients whose risk profile changed during hospitalisation, improving accuracy for post-discharge planning.
In the ExTRACT-TIMI 25 validation, 25.2% of patients were reclassified between risk categories when in-hospital events were added to the baseline score, with a net reclassification improvement of 33%.
Common Pitfalls & Limitations
The TIMI Study Group developed two entirely different risk scores: one for STEMI (this calculator, 0–14 points, weighted criteria, predicting 30-day mortality) and one for UA/NSTEMI (0–7 points, binary criteria, predicting 14-day ischaemic events). These scores use completely different variables, have different ranges, and answer different clinical questions. They are not interchangeable.
How to avoid: Always confirm which TIMI score you are using. The STEMI score requires confirmed ST elevation or LBBB and focuses on mortality prediction. The UA/NSTEMI score is for undifferentiated non-ST-elevation ACS and predicts composite ischaemic endpoints.
The derivation cohort excluded patients with cardiogenic shock (SBP < 90 with signs of hypoperfusion), severe uncontrolled hypertension (SBP > 180 or DBP > 110), prior cerebrovascular disease, and high bleeding risk. These exclusions mean the score has not been validated in these groups, and its predictions may be unreliable. Patients with cardiogenic shock, in particular, have substantially higher mortality than the score would suggest.
How to avoid: Recognise the score’s derivation boundaries. For patients with cardiogenic shock, use specialised tools (e.g., IABP-SHOCK II risk score) and prioritise immediate haemodynamic assessment over risk score calculation.
The InTIME II trial was conducted in the late 1990s, when fibrinolysis was the primary reperfusion strategy. In the current era of primary PCI, dual antiplatelet therapy, high-potency statins, and modern cardiac care, absolute mortality rates at each score level are likely lower than the 2000 derivation data. The relative risk stratification (i.e., higher scores still mean higher risk) remains valid, but the specific mortality percentages should be interpreted as approximate upper bounds.
How to avoid: Use the score for relative risk stratification and clinical decision-making rather than quoting exact mortality percentages to patients. Consider institutional and regional outcome data for absolute risk estimation.
Risk score calculation should never delay reperfusion therapy. In STEMI, “time is muscle” — every minute of coronary occlusion results in progressive myocardial necrosis. The TIMI score is designed to be calculated alongside (not instead of) the initiation of reperfusion protocols. All eight variables are available within minutes of presentation from basic demographics, vitals, and ECG.
How to avoid: Calculate the score in parallel with standard STEMI protocols. The score informs prognosis and may guide post-reperfusion care intensity, but it should not influence the decision to pursue reperfusion — all STEMI patients meeting criteria should receive timely reperfusion regardless of their score.
The time-to-treatment criterion (symptom onset to reperfusion > 4 hours) only contributes 1 point, which may suggest it is clinically less important than other variables. However, this variable was included because it adds independent prognostic information beyond the haemodynamic markers. Furthermore, time to treatment is the only modifiable variable in the score — all other criteria are fixed at presentation.
How to avoid: While the score appropriately weights time to treatment as a predictor (1 point based on odds ratio), do not interpret this low weighting as suggesting that treatment delays are clinically unimportant. Minimising time to reperfusion remains the single most impactful intervention in STEMI management.
Quick Reference Summary
| Criterion | Points | Weight Rationale |
|---|---|---|
| Age ≥ 75 years | 3 | Strongest demographic predictor |
| Age 65–74 years | 2 | Intermediate age risk |
| SBP < 100 mmHg | 3 | Haemodynamic compromise |
| HR > 100 bpm | 2 | Sympathetic / decompensation marker |
| Killip class II–IV | 2 | Clinical heart failure |
| DM, HTN, or angina | 1 | Comorbidity burden |
| Weight < 67 kg | 1 | Constitutional vulnerability |
| Anterior STE or LBBB | 1 | Large territory at risk |
| Time to Rx > 4 h | 1 | Delayed reperfusion (only modifiable variable) |
The Golden Rule: The TIMI STEMI score is for rapid bedside prognostication — it informs the intensity of post-reperfusion care and helps identify patients at highest risk of complications. It should never delay reperfusion, and it should never be confused with the TIMI UA/NSTEMI score (a completely different tool).
Disclaimer & References
For Educational Purposes Only. This calculator and the accompanying clinical information are intended as educational tools for healthcare professionals. They do not replace clinical judgement. Results should be interpreted in the full clinical context. Lab reference ranges vary by institution — verify with your own laboratory. Drug dosages should be confirmed against current prescribing information.
References
- Morrow DA, Antman EM, Charlesworth A, et al. TIMI risk score for ST-elevation myocardial infarction: A convenient, bedside, clinical score for risk assessment at presentation: An InTIME II substudy. Circulation. 2000;102(17):2031-2037. DOI: 10.1161/01.CIR.102.17.2031
- Morrow DA, Antman EM, Giugliano RP, et al. A simple risk index for rapid initial triage of patients with ST-elevation myocardial infarction: an InTIME II substudy. Lancet. 2001;358(9293):1571-1575. DOI: 10.1016/S0140-6736(01)06649-1
- Amin ST, Morrow DA, Braunwald E, et al. Dynamic TIMI risk score for STEMI. J Am Heart Assoc. 2013;2(1):e003269. DOI: 10.1161/JAHA.112.003269
- InTIME-II Investigators. Intravenous NPA for the treatment of infarcting myocardium early; InTIME-II, a double-blind comparison of single-bolus lanoteplase vs accelerated alteplase for the treatment of patients with acute myocardial infarction. Eur Heart J. 2000;21(24):2005-2013. DOI: 10.1053/euhj.2000.2371
- Killip T, Kimball JT. Treatment of myocardial infarction in a coronary care unit: A two year experience with 250 patients. Am J Cardiol. 1967;20(4):457-464. DOI: 10.1016/0002-9149(67)90023-9
- Ibanez B, James S, Agewall S, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J. 2018;39(2):119-177. DOI: 10.1093/eurheartj/ehx393
- O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction. J Am Coll Cardiol. 2013;61(4):e78-e140. DOI: 10.1016/j.jacc.2012.11.019
- Gallindo de Mello BH, Oliveira GBF, et al. Validation of the Killip-Kimball classification and late mortality after acute myocardial infarction. Arq Bras Cardiol. 2014;103(2):107-117. DOI: 10.5935/abc.20140091
- Claeys MJ, Vandersmissen L, Sinnaeve PR, et al. Gender, TIMI risk score and in-hospital mortality in STEMI patients undergoing primary PCI: results from the Belgian STEMI registry. EuroIntervention. 2020;16(5):e381-e387. DOI: 10.4244/EIJ-D-18-01137
- Antman EM, Cohen M, Bernink PJLM, et al. The TIMI risk score for unstable angina/non-ST elevation MI: A method for prognostication and therapeutic decision making. JAMA. 2000;284(7):835-842. DOI: 10.1001/jama.284.7.835