Acute myocardial infarction with cardiogenic shock

Risk stratification and role of mechanical circulatory support devices

Cardiogenic shock (CS) is a primary cardiac disorder that result in clinical and biochemical evidence of tissue hypoperfusion due to extensive damage of myocardium due to acute myocardial infarction (AMI). It is characterised clinically by a systolic blood pressure less than or equal to 90mmHg for greater than or equal to 30 minutes and urine output less than or equal to 30mlo / hr or cool extramitres and hemodynamically by depressed cardiac index (less than or equal to 2.2L/min/M2 body surface area and an elevated pulmonary capillary wedge pressure greater than 15mmHg.

Approximately 5-8% of ST elevation myocardial infarction (STEMI) and 2-3% of non ST elevation myocardial infarction (NSTEMI) cases can result in cardiogenic shock. CS associated with AMI (AMI – CS) can lead to a mortality rate of nearby 40% at 30 days and 50% at 1 year1.

Inspite of widely available cardiology specific intensive care units, marked improvement in percutanous and surgical revascularization and increased availability of mechanical circulatory support, the mortality rate for CS has not shown significant decline2,3.

Risk stratification in AMI – CS

Many classification systems have been developed for risk-stratification of CS.

  1. Killip and Kimbel: In 1957 Killip and Kimbel put forward a classification based on the severity of heart failure in AMI. It consists of 4 classes.

Class I – No evidence of heart failure.

Class II – Presence of mild to moderate heart failure characterised by rates (crepitations) in lungs, so gallop and jugular venous congestion

Class II – Overt pulmonary edema

Class IV – Cardiogenic shock (with low blood pressure, cold clamy skin and reduced urine output.

  1. Forrester classification: In 1976 Forrestor etal developed a classification system for AMI based on their hemodynamic profile, specifically cardiac index (CI) and pulmonary artery wedge pressure (PAWP) into 4 profiles.

Profile I  (Warm and dry) Normal cardiac index (CI >2.2L/min/M2) and normal PAWP (<18mmHg) indicates adequate perfusion and no congestion

Profile II (Warm and wet) – Normal CI and elevated PAWP (>18mmHg). This indicates adequate perfusion, but with signs of congestion

Profile III (Cold and dry) – Low CI (2.2L/min/M2) and normal PAWP. Indicates impaired perfusion but no congestion.

Profile IV (Cold and wet) – Low CI and elevated PAWP indicates both impared perfusion and congestion.

This classification was used for guiding treatement (use of inotropic agents, vaso pressors and address volume status)

Eventhough it effectively categorizes patients based on perfusion and congestion, its ability to accurately predict cardio renal events or other specific complcations in advanced stages is not clear. Further more it relies on invasive hemodynamic measurement, which are not always readily available

Later, 2 risk scores (IABP – Shock II and card – shock) were developed to evaluate short term mortality, but did not became popular

  1. Card-Shock Score: It utilizes seven variables assessed at admission to categorize patients in to low (0-3 points) Intermediate (4-5 points) or high risk (6-9 points) groups5.

The variables were age, eGFR, blood lactate level, confusion on admission, left ventricular ejection fraction, previous myocardial infarction or coronary artery bypass grafting and etiology of cardiogenic shock (ACS vs non ACS). The score has demonstrated good predictive performance in assessing in hospital mortality in patients with shock.

  1. The IABP – SHOCK II Score: It is based on six variables. Age (greater than 73 years), prior stroke, admission glucose (greater than 191mg/dL) S. Creatinine (>1.5mg/dl) Lactate (>5mm/L) Post – PCI TIMI flow grade (less than 3). Categorized in to 3. Low risk (0-2 points) Intermediate risk (3-4 points) and high risk (5-9 points)6.
  2. TIMI risk score for ST elevation AMI: This is a tool developed to assess the risk of mortality and other adverse events (heart failure, cardiogenic shock) in patients with STEMI. It is based on eight clinical indicators assessed at the time of presentation the score helps to categorise patients into risk levels (low, medium or high)
  3. Sequential Organ Failure Assessment Score (SOFA#SCORE): The SOFA SCORE was developed in 1994 to assess the extent of organdysfunction / failure in the patient population as quantitatively and objectively as possible. It evaluates six organ systems, each receiving a score from normal to 4 (most abnormal). Respiratory, cardiac vascular, hepatic, coagulation, renal and neurological. A higher SOFA SCORE indicates more severe organ dysfunction. The score provides an objective measures of the progression of multi organ failure in the context of AMI – CS guiding clinical decision. The score in re-calculated every 24hrs in the ICU to track a patient’s condition and predict outcome7.
  4. The SCAI-SHOCK stage classificaiton: In 2019 the society for cardiac vascular intervention released a classification system for evaluating severity of CS (Later in 2022 an update of this system also was released). This system consists of 5 stages.

Stage A (No shock) At risk, patient has a cardiac condition with risk for CS. But not symptomatic.

Stage B (Pre shock): Clinical evidence of hemodynamic instability, but no hypo perfusion.

Stage C (Established shock): Clinical evidence of hypo perfusion requiring intervention

Stage D (Worsening shock): Worsening hemodynamics and lactate. Failed initial intervention

Stage E (Refractory shock): Actual or impending circulatory collapse.

This classification system help to assess the severity of CS, guide treatment decisions and predict patient outcomes. The classification has been validated in multiple studies, demonstrating its effectiveness in risk stratification for patients with CS. Higher SCAI stages are consistantly associated with increased – in hospital and post discharge mortality.

Role of mechanical supportive devices in the management of AMI-CS.

The use of vasoactive drugs (inotropes) is the first line of treatment in almost all patients with CS. These agents increase myocardial contractility by which increase cardiac output and blood pressure (BP), thereby maintain end organ perfusion.

  1. Vasopressors: Are agents with vasoconstrictive effects that increase BP (eg Vasopressor and Phenylephrine)
  2. Inopressors: These drugs have dual actions – vasopressor and inotropic effects (eg Epinephrine, norepinephrine and Dopamine).
  3. Inodilators are group vasoactive agents which have inotropic and vasodilatory properties. (Eg. Dobutamine, Milrinone and levosimendan)

Data on comparative efficacy of different inotropic agents in CS is limited. No single agent has proves clear superiority. They are used singly or in different combinations as per situation demands.

Vaso active inotropic score (VIS): It is a numerical score used to quantify the degree of hemodynamic support provided to a patient with CS, following AMI-CS. Higher VIS values reflect greater dependence on vasoactive drugs, having a more challenging hospital course with increased in – hospital and followup mortality9.

Early revascularization by means of coronary angioplasty or CABG is byfar the most effective treatment strategy for early and long term survival for patients with AMI-CS. This has became evident by the shock trial. In this trial patients with AMI-CS was randomly asigned to emergency revascularization (PTCA / CABG) or initial medical stabilization. Although overall mortality at 30 days did not differ in both groups (46.7% Vs 56%; P=0.11), the 6 months mortality was lower in the early revascularization group than medical therapy group (50.3% Vs 63.1%; P=0.027)10. Moosvi AR etal reported that revascularization (PTCA / CABG) is associated with improved survival in AMI-CS compared with medical stabilization this improvement in survival is most evidence of revascularization is performed early (within 24hrs of onset of CS)11.

Mechanical support devices for CS include Intra Arotic Balloon Pumps (IABP), Extra Corporeal Membrane Oxygenation (ECMO) and percutanous ventricular assist devices (PVAD) like the impella. These devices improve blood flow, support organ perfusion and reduced the hearts work load, acting as a bridge to heart recovery11.

IABP

In 1968 Dr. Adrian Kantro Witz and collegues reported the first successful use of IABP, in the treatment of CS. Since then it has been widely used in cath labs for managing percutaneous coronary interventions in AMI with CS.

This device work by inflating a long balloon in the descending aorta (introduced through femoral artery) during diastole and deflating during systole, timed by a machine that monitors ECG. When the balloon is inflated, it helps to increase blood pressure in aorta and help coronary perfusion. There can be an augmentation of cardiac output by approximately 0.5-1.0L/min when the balloon is deflated, it creates low pressure in aorta that reduces resistance and thereby after load and cardiac work strain.

IABP was also used for AMI with CS with mechanical complications like, acute mitral regurgitation and acute ventricular septal rupture. But its use is not recommended is patient with moderate to severe AR, Aortic dissection and aortic Aneurysm.

Initial studies between 1970 and 1990 reported that use of IABP is beneficial to provide hemodynamic support in the form of an increase in cardiac index, decrease in pulmonary capillary wedge pressure and decrease in multiorgan dysfunction. But subsequent trials have shown negative results. In the SHOCK II trial, patients with AMI.CS were randomised in IABP (n= 301) vs no IABP (n=299). All patient received early revascularization and best possible medical supportive therapy. At 30 days, all cause mortality had occurred in 39.7% of the IABP group Vs 41.3% of the non IABP group (P=0.69). More over IABP did not demonstrate any positive effects is time to achieve hemodynamic stability, length of intensive care unit stay, peripheral tissue / organ perfusion as measured by S.Lactic Acid levels and the dose of Catecholamine required to maintain adequate organ perfusion.

A followup study of the shock II trail (IABP- SHOCK II trial) found that there was no benefit in the primary end point of mortality at 30 days 3 and 12 months12. Based on the IABP shock II trial results routine use of IABP in AMI-CS has been down graded from class 2 (level of evidence A) in the 2013 STEMI guideline to class 3 in the 2025 ACC/ AHA / ACEP / NAEMSP / SCAI guidelines for managed of ACS. Routine IABP use in AMI-CS has been carried a class III recommentation in European guidelines since 2014.

ECMO

ECMO is a life support system used when a patient’s heart and lungs are unable to function adequately on their own. The Veno-Arterial (V-A) ECMO acts as a heart – lung bypass machine circulating blood outside the body adding oxygen, removing carbon dioxide and then returning the blood to the patient, thus allowing the patients heart and lungs to rest and potentially recover.

The usefulness of V-A ECMO in AMI-CS was studied in various trials13.

Studies showed that the benefit was better, when the ECMO was initiated early in the course of cardiogenic shock.

Micro Axial Flow Pumps

Impella is a catheter based micro axial flow pump. It is a short term device insereted in to the left ventricle (LV), actively pumping blood out of the heart in to the aorta. It unloads the LV decreasing LV filling pressures and increases cardiac output, improving hemodynamic stability in patients with AMI-CS. There are different types of impella which offers different levels of hemodynamic support. Impella 2.5 (2.5L/min) Impella CP (3.0-4.0L/min) Impella 5.0 (5.0 L/min) and impella 5.5 (>6.0 L/min).

Few small previous studies (Impella – STIC, IMPRESS in Severe shock, ISAR- shock (all IABP vs IMPELLA) etc did not show any mortality benefit of micro axial flow pumps in AMI-CS.

In a meta analysis of 5 randomised trails (Thiele etal, n=503) with 6 months mortality data compared early routine active mechanical supportive devices use vs control in patients with AMI-CS. No significant difference were observed for LV unloading devices Vs control, no mortality benefit (p=0.075). Major bleeding and vascular complications were more with the use of MCS14.

In the recent DanGer – shock trial, patients with AMI-CS were randomised in to (1) micro axial flow pumps group (n=179) and (2) to standard care group (n=176). Death from any cause occurred in 82/179 patients (45.8%) in the micro axial group and 103/176 (58%) in the standard case group (p=0.04). A composite safety end point (severe bleeding, limb ischemia, hemolysis, device failure or worsening aortic regurgitation) occurred in 43 patient (24.0%) in group I and 11 (6.2%) in group 2. So the conclusion of the study was that the routine use of a micro axial flow pump with standard care in patient with AMI-CS led to a lower risk of death from any cause at 180 days than standard care alone. There was a higher incidence of adverse events when the micro axial pump was used15.

Based on the DanGer – shock trial results the use of micro axial flow pumps in AMI-CS received an upgraded class II (level of evidence A) recommendation (use is reasonable) in the 2025 ACC / AHA / AECP / NAEMSP / SCAI guidelines for the management of ACS from class II (Level of evidence B) recommendation of 2013 guidelines. In conclusion, optimum use of vasoactive drugs and early revascularization remains the corner stone in the management of AMI-CS. Available data regarding the mortality benefit of various mechanical supportive devices are uncertian. A multi disciplinary approach, early initiation of mechanical supportive devices tailored to the severity of CS is important. Further research are vital to optimise device use and improve patient survival.

Reference

  1. Sansky MD, Morrow DA, Proudfoot AG et al – Cardiogenic shock after acute myocardial infarction – A review JAMA 2021, 326(18) 1840-1850.
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  9. Hu Y, Wang L, Yang F et al. Prognostic implications of vasoactive inotropic score is adult patients with cardiogenic shock on veno arterial extra corporeal membrane oxygenation. J. Thoracic DIS 2024. 16: (2) 1097-1107.
  10. Hochman JS, Sleeper LA et al. Early revascularization in acute myocardial infarction complicated by cardiogenic shock N Eugl J Med 1999; 341: 625-634.
  11. MOSVI AR, Khaja F et al. Early revascularization improves survival in cardiogenic shock complicating acute myocardial infarction JACC. 1992; 19: 907-914.
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  13. Ostradal P Rokyta R, Karosek J et al. Extra corporeal membrane oxygenation in the therpay of cardiogenic shock; results of the ECMO – CS randomised – clinical trial, circulation. 2022 – 147 (6) 327 – 333.
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  15. Moller JE, Engstram T, Jensen Lo et al. DanGer – Shock investigators. Micro axial flow pump or standard care in infarct related cardiogenic shock. N Engl J Med 2024 390:15: 1382 – 1393.
  16. Rao VS, O Donogue MC, Ruel et al. 2025 ACC / AHA / AECP / NAEMSP / SCAI guideline for the management of patients with acute coronary syndrome. A report of the American college of cardiology. American Heart association joint committee on cinical practice guidelines. Circulation 2025 – 151, 13: No 13.

Authored by:

Dr. Devarajan K. A.
MBBS, MD, DM
Consultant Cardiologist

Dr. KM Cherian Institute of Medical Sciences is a pioneer in delivering world-renowned treatment procedures at affordable costs. We continually upgrade the quality of the healthcare ecosystem and enable faster recovery for patients from all backgrounds.