Myocardial Infarction Management for Septic Patients in the ICU: A Multidisciplinary Approach

Dr. Kamal Sharma
Critical Care, Heart Health, ICU Management

25

Aug 25

Sepsis

Sepsis is a life-threatening medical emergency resulting from the body’s overwhelming response to an infection.1 If not treated immediately, it can lead to tissue damage, organ failure, and death. Worldwide, sepsis accounts for 11 million deaths annually, representing 20% of all global deaths.

The Sepsis-3 definition (2016) defines sepsis as organ dysfunction combined with a dysregulated host response. Organ dysfunction indicative of sepsis is defined as an increase of 2 or more points in the SOFA (Sequential Organ Failure Assessment) score. The SOFA score evaluates the function of six organ systems on a scale of 0 to 4. Septic shock, a subtype of sepsis, is characterized by the need for vasopressors to maintain a mean arterial pressure of  ≥65 mmHg and a serum lactate level >2 mmol/L (>18 mg/dL) without hypovolemia.2

Sepsis can be caused by any type of infection, including bacterial, viral, or fungal. Common sites and types of infections that can lead to sepsis include:

  • Respiratory system: Lung infections such as pneumonia.
  • Urinary tract system: Especially catheter-related infections.
  • Gastrointestinal system: Appendicitis, bowel problems, peritonitis, and gallbladder or liver infections.
  • Bloodstream: Bacteremia.
  • Central nervous system: Infections of the brain or spinal cord.
  • Skin infections: Wounds, inflammation, openings from catheters and IVs, and cellulitis.

Symptoms of sepsis in adults include:

  • Feeling very unwell, extreme pain, or “the worst ever”
  • Fast breathing
  • Skin rash or clammy, sweaty skin
  • Feeling very hot or cold, chills or shivering
  • Fast heart beat
  • Feeling confused, disoriented, or slurring speech
  • Not passing much (or any) urine
  • Weakness or aching muscles

Symptoms of sepsis in children include:

  • Fit or convulsion
  • Fast breathing or long pauses in breathing
  • Very blotchy, blue or pale skin
  • Floppy
  • Feels abnormally cold to touch
  • Drowsy, difficult to wake up or confused
  • Rash that doesn’t fade when pressed (glass test).3

‘STEMI’

A clinical syndrome defined by characteristic symptoms of myocardial ischemia in association with persistent ST- elevation and subsequent release of biomarkers of myocardial necrosis.1

STEMI Complicating Septic Shock and Mortality

Patients with sepsis often show positive troponin levels, indicating myocardial damage. Sepsis-induced myocardial dysfunction affects 25% to 50% of adult septic shock patients.

The presence of ST-elevation myocardial infarction (STEMI) significantly worsens mortality in septic shock patients. Mortality rates are 23.5% without STEMI but rise to 52.3% with STEMI.4

STEMI is a clinical syndrome characterized by symptoms of myocardial ischemia, persistent ST-elevation on an ECG, and subsequent release of biomarkers of myocardial necrosis. Diagnosis of STEMI involves ST-segment elevation on ECG, and new pathological Q-waves indicate heart muscle necrosis. Elevated cardiac troponin (cTn) is diagnostic for acute MI when accompanied by evidence of myocardial ischemia (clinical symptoms, ECG abnormalities, or imaging evidence).5

Reperfusion Strategies in STEMI

Early reperfusion is critical in STEMI to limit myocardial damage and improve outcomes, emphasizing the concept of “Time = Muscle”. Delayed reperfusion negatively impacts patient outcomes. Treating patients within the first hour of symptom onset can save 65 lives for every 1000 treated.6

Reperfusion strategies for STEMI include:

  • Invasive primary PCI (Percutaneous Coronary Intervention): Recommended over fibrinolysis and within ≤12 hours of symptom onset in the absence of contraindications. It is indicated for all patients with ischemic symptoms for ≤12 hours and persistent ST elevation.
  • Pharmacological induction of thrombolysis: If timely PCI is not possible, fibrinolytic therapy is recommended, ideally within ≤10 minutes of STEMI diagnosis, even in the pre-hospital setting.
  • Pharmaco-invasive: A combination of both approaches.

The choice of reperfusion strategy depends on the expected delay to PCI from STEMI diagnosis. For delays between 3 and 12 hours, primary PCI should be given more consideration over fibrinolytic therapy.

Fibrinolysis: Agents and Safety Concerns

Fibrin-specific fibrinolytic agents (e.g., alteplase, reteplase, tenecteplase) are preferred due to their lower risk of bleeding compared to non-fibrin-specific agents like streptokinase. Fibrin-specific agents activate the conversion of fibrin-bound plasminogen to plasmin, leading to clot dissolution. Non-fibrin-specific agents act on both free and fibrin-bound plasminogen.7

A comparison of fibrinolytic agents shows:

  • Alteplase (rt-PA): Fibrin specificity ++, plasma half-life 4-6 min, dose 15 mg bolus plus 90 min infusion up to 85 mg.
  • Reteplase (rPA): Fibrin specificity +, plasma half-life 18 min, dose 10+10MU double bolus 30 min apart.
  • Tenecteplase (TNK-tPA): Fibrin specificity +++, plasma half-life 20 min, dose ±0.5 mg/kg single bolus over approximately 10 seconds.

Contraindications to fibrinolysis include:

  • Absolute contraindications: Prior intracranial hemorrhage or stroke of unknown origin, ischemic stroke within the previous 6 months, CNS damage or neoplasms or arteriovenous malformation, GI bleeding within the past month, known bleeding disorder, aortic dissection, and non-compressible punctures in the past 24 hours.
  • Relative contraindications: TIA in previous 6 months, oral anticoagulant therapy, pregnancy or 1 week postpartum, refractory hypertension (SBP >180 mmHg and/or DBP >110 mmHg), advanced liver disease, infective endocarditis, active peptic ulcer, and prolonged or traumatic resuscitation.

In sepsis, coagulopathy and systemic inflammation increase bleeding risks. Thrombolytics carry a 1.8% stroke risk and 5% transfusion-requiring bleeding in AMI patients. Fibrin-specific agents may reduce bleeding compared to non-specific agents like streptokinase, which has been linked to higher hemorrhage rates. Adjunctive anticoagulants like enoxaparin reduce reinfarction risk but require cautious dosing in sepsis due to potential renal impairment and thrombocytopenia.8

Importance of a Pharmaco-Invasive Strategy

The Strategic Reperfusion Early After Myocardial Infarction (STREAM) study assessed the impact of increasing time delay on outcomes in patients randomized to a pharmaco-invasive strategy or primary PCI. The study found that as PCI-related delay increased, outcomes with a pharmaco-invasive strategy became superior to primary PCI. This suggests that in circumstances where timely PCI is not possible, a pharmaco-invasive strategy may offer an effective alternative reperfusion option.9

For older, early-presenting STEMI patients, a pharmaco-invasive approach is an effective reperfusion strategy. Novel thrombolytics like tenecteplase (TNK-tPA) and reteplase (rPA) are fibrin-specific and administered as a single bolus, achieving comparable angiographic patency rates to accelerated infusion alteplase (tPA). These agents simplify administration, which is crucial in time-sensitive acute myocardial infarction (AMI) management. However, lanoteplase (nPA) showed higher rates of intracranial hemorrhage compared to tPA, limiting its clinical use.

Clinical Recommendations and Gaps in Evidence

Clinical recommendations include prioritizing fibrin-specific agents (TNK-tPA, rPA) over streptokinase or urokinase to minimize systemic bleeding. Administration should be within 12 hours of symptom onset, balancing sepsis-related hemodynamic instability. Close monitoring of coagulation parameters (INR, platelets) and signs of hemorrhage is essential, especially with concurrent anticoagulants.10

Despite the advantages of novel thrombolytics in AMI, there are gaps in evidence. There are no direct trials addressing thrombolysis specifically in AMI patients with sepsis, and current data are extrapolated from general AMI populations, highlighting the need for sepsis-specific studies. If sepsis-related hypotension or organ failure prevents thrombolytic safety, alternative reperfusion strategies like PCI may be preferable. Therefore, in cases of AMI complicated by sepsis, individualized risk-benefit assessment is necessary, favoring fibrin-specific agents with vigilant monitoring.

Authors of this article

Dr. Kamal Sharma, MD, DM (Cardiology), DNB (Cardiology), DNB (Medicine), MNAMS, FACC, FSCAI, FESC, B J Medical College, Ahmedabad.

Reference

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8.         Ren C, Li Y xuan, Xia D meng, et al. Sepsis-Associated Coagulopathy Predicts Hospital Mortality in Critically Ill Patients With Postoperative Sepsis. Front Med. 2022;9. doi:10.3389/fmed.2022.783234

9.         ST–Segment-Elevation Myocardial Infarction Patients Randomized to a Pharmaco-Invasive Strategy or Primary Percutaneous Coronary Intervention | Circulation. Accessed July 13, 2025. https://www.ahajournals.org/doi/10.1161/circulationaha.114.009570

10.       Czempik PF, Wiórek A. Management Strategies in Septic Coagulopathy: A Review of the Current Literature. Healthcare. 2023;11(2):227. doi:10.3390/healthcare11020227