Acute MI complicated by cardiogenic shock Mechanical complications of MI Mechanical circulatory support

1. Cardiogenic shock following
Acute MI
Dr. Lokesh Khandelwal
DM Cardiology
GB Pant Hospital, Delhi

2. Introduction
• Cardiogenic shock - leading cause of death from AMI.
• AMI with LV dysfunction- most frequent cause.
• A loss of >40% of functional myocardium is required to cause CS.
• Prevalence- 10% of all MI.*
*Kolte D, Trends in the incidence, management, and outcomes of cardiogenic shock complicating ST-elevation myocardial
infarction in the United States. J Am Heart Assoc 2014.
**Thiele H, Management of cardiogenic shock. Eur Heart J 2015;36:1223–30.
Mortality - 40% to 50%.**

3. Definition*
• Clinical criteria: SBP <90 mm Hg for ≥30 min OR Support to maintain SBP ≥90 mm Hg
• End-organ hypoperfusion: (urine output <30 mL/h or cool extremities)
• Hemodynamic criteria: CI of ≤2.2 L/min/m2 AND
PCWP ≥15 mm Hg
*Hochman JS, Sleeper LA, Webb JG et al. Early revascularization in acute myocardial infarction complicated by cardiogenic shock:
SHOCK Investigators: Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock. N Engl J Med.
1999;341:625–634.

4. Hemodynamic Presentations*
1. Cold and wet – Two thirds
2. Cold and dry – 28%
3. Warm and wet – SIRS features, lower SVR, and a higher risk of sepsis and mortality
4. Normotensive CS – 5.2%
5. RV CS – 5.3%
*Contemporary Management of Cardiogenic Shock- AHA Scientific Statement. Oct 2017

5. *Reynolds HR, Hochman JS. Cardiogenic shock: current concepts and improving outcomes. Circulation. 2008;117:686–697.
The CS Spiral

6. ECHO
• EF and severity of MR
• Pulmonary artery systolic pressure and PCWP, short mitral deceleration time
(<140 ms) is highly predictive of an increased PCWP of >20 mmHg in CS.*
• Volume status
• Exclude mechanical complications
• Help to guide medical and mechanical therapeutic decisions.
*Reynolds HR, Anand SK, Fox JM, Harkness S, Dzavik V, White HD, et al. Restrictive physiology in cardiogenic shock:
observations from echocardiography. Am Heart J. 2006

8. Critical Care Unit Monitoring

9. Medical therapy

11. A total of six studies
with 842 eligible
patients
Some evidence to avoid
dopamine due to
increased rates of
arrhythmias.
Some evidence, which
suggests to prefer
norepinephrine in
comparison to
epinephrine as
vasopressor.

12. In cardiogenic shock is to avoid bolus dosing in order to minimize the risk of
hypotension and to administer a 24-h infusion at a rate of 0.05–0.1
µg/kg/min.
Or infusion rate of 0.2 µg/kg/min for the first 60 min if a more rapid onset of
effect is required.
May in addition be beneficial in acutely decompensated HF, including ACS
and cardiogenic shock.

13. Shown to improve
hemodynamics
compared to other
inotropes
Should be used
when urinary output
is insufficient after
diuretics
Should be preferred
over adrenergic
inotropes in patients
with beta-blockers
Use in CS - Improvements
in cardiac fuction,
hemodyanamics and end-
organ function. Re-
hospitalization rates are
decreased
Requires continuous
monitoring due to
the risk of
hypotension

14. Fibrinolytic Therapy
• If early invasive approach cannot be completed in a timely fashion, fibrinolysis can
be considered in CS associated with STEMI with CS upto 12 hours.
• Effectiveness of thrombolytic therapies may be dependent on a higher systemic
perfusion pressure.*
*Prewitt RM et al. Effect of a mechanical vs a pharmacologic increase in aortic pressure on coronary blood flow and thrombolysis
induced by IV administration of a thrombolytic agent. Chest. 1997;111:449–453.

15. Fibrinolytic Therapy
*Fibrinolytic therapy in patients with ST-segment elevation myocardial infarction, J Cardiovasc Thorac Res. 2017; 9(4): 209–214

16. Alteplase, tenecteplase, and reteplase should be considered over
streptokinase.
The addition of glycoprotein IIb or IIIa inhibitors to fibrinolytic therapy should
be discouraged.

17. Invasive Strategy
• Invasive strategy is preferred in suspected ACS-associated CS, regardless of the time
delay from MI onset.*
*Contemporary Management of Cardiogenic Shock- AHA SCIENTIFIC STATEMENT. Oct 2017

18. SHOCK TRIAL

19. • Randomized 302 patients
• Invasive strategy (within 12 hours) or initial
medical stabilization.
• 30-day all-cause mortality – Primary end point
• Lower in the invasive arm (46.7% vs 56.0%;
P=0.11)
• Six-month mortality
• Lower in the invasive arm( 50.3 percent vs. 63.1
percent, P=0.027).
SHOCK TRIAL
N Engl J Med. 1999
Early revascularization should be strongly considered for patients with
acute myocardial infarction complicated by cardiogenic shock.

20. SHOCK-2 TRIAL

21. Randomized 600 patients with CS
complicating AMI to IABP or no IABP.
30 days mortality-
39.7% patients in the IABP group and 41.3%
patients in the control group (P = 0.69).
No significant differences in length of stay
in ICU,serum lactate levels, the dose and
duration of catecholamine therapy, and
renal function, major Bleeding
Use of IABP did not significantly reduce 30-day mortality in
patients with CS complicating AMI for whom an early
revascularization strategy was planned.

22. CULPRIT-SHOCK TRIAL

23. Randomly assigned 706 patients
with multivessel disease
At 30 days-
Death or renal-replacement
therapy-
45.9% in the culprit-lesion-only
PCI group and in 55.4% in the
multivessel PCI group ( P = 0.01).
In patients with AMI and CS culprit only PCI has lower rate
of 30 days mortality compared to multivessel PCI.

24. Mechanical circulatory
support (MCS)
Temporary MCS
IABP
Impella 2.5, CP,
and 5.0
TandemHeart
Investigational devices
iVAC 2L
HeartMate Percutaneous
Heart Pump
Durable MCS
HeartMate II
and 3
HeartWare
HVAD

25. MCS
Bridge to recovery
Bridge to transplantation
Bridge to a bridge
Destination therapy

26. Temporary MCS
• Patients with persistent CS, with or without end-organ hypoperfusion.
• Temporary MCS – Multiorgan system failure or relative C/I to durable MCS or heart
transplantation to allow clinical optimization before the consideration of a longer-
term device. (AHA recommendation (Class IIa, Level of Evidence C)

27. Yancy et al, jacc 2013 62 147-239. ACC-GUIDELINE-HF

28. IABP

29. IABP

30. IABP
• Role of IABP in AMI with CS and mechanical complications- well proven.
• Patients presenting in cardiogenic shock without mechanical complications – no role of IABP.
• Maximum advantage of IABP is when patient is not in frank CS.
• Increases diastolic blood pressure and reduces SBP.
• Minimal improvement in MAP, CI, serum lactate, and catecholamine requirements with
IABP.*
*Prondzinsky R et al. Hemodynamic effects of intra-aortic balloon counterpulsation
in patients with acute myocardial infarction complicated by cardiogenic shock: the prospective, randomized IABP shock trial. Shock.
2012;37:378–384.

31. IABP
• IABP-SHOCK II*, which enrolled patients with MI-associated CS, found no differences
in the primary end point of 30-day mortality, prespecified secondary end points, or
1-year outcomes between those with and those without IABP support.
*Thiele H et al; Intra-aortic balloon counterpulsation in acute myocardial infarction complicated by cardiogenic shock (IABP-SHOCK
II): final 12 month results of a randomised, open-label trial. Lancet. 2013;382:1638–1645

32. IABP
• Currently Class IIIA recommendation.*
• CS with acute MR or a VSD (Class IIA, LOE C).
*2014 ESC/EACTS guidelines on myocardial revascularization

33. Impella

34. Impella
• Mechanism - Unloading of LV into aorta so providing hemodynamic support –
increased MAP and increased CO (2.5 L/min with Impella 2.5 and 5 L/min with
Impella 5)
• Impella CP, which can be inserted percutaneously provides a CO of 4 L/min.

35. Impella
• USpella registry of patients with CS treated with Impella
devices before PCI, MCS placement resulted in improved
survival to hospital discharge.*
* O’Neill WW et al. The current use of Impella 2.5 in acute myocardial infarction complicated by
cardiogenic shock: results from the USpella Registry. J Interv Cardiol. 2014;27:1–11.

36. ISAR-SHOCK TRIAL JACC Vol. 52, No. 19, 2008

37. ECMO
Veno-venous
Isolated
respiratory failure
despite MV and no
significant cardiac
dysfunction.
Veno-arterial
Support both CVS
and respiratory
systems and is
used in CS.
Extracorporeal Membrane Oxygenation
It involves right atrial–aorta connection and leads to indirect LV unloading.

39. Extracorporeal Membrane Oxygenation
• Indications - poor oxygenation that is not expected to rapidly improve with an
alternative temporary MCS device or during CPR.
• Complications - distal limb ischemia, thromboembolism, stroke, bleeding, hemolysis,
infection, and aortic valve insufficiency.
• Increase LV afterload.

40. • Analyzed the use of ECMO or Impella (2.5, CP, or 5.0) for CS following AMI , from a cohort
of patients who underwent TCS within 72 hours after admission for emergency PCI from
January 2009 to April 2015.
• 42 had early TCS: 23 ECMO and 19 Impella.
• ECMO patients were sicker than Impella patients (higher blood lactate level at ICU
admission, higher vasoactive-inotroic and ENCOURAGE scores before TCS implantation, p ≤
0.02).
ECMO is the technique of choice in case of profound CS, whereas Impella
devices seem more appropriate for less severe hemodynamic compromise.

41. Tandem heart

42. Tandem heart
• Mechanism : Indirect LV unloading (connecting left atrium to common iliac artery) :
increased MBP and increased CO (4 L/min).
• Ischemic benefit : unloading LV (so reducing LVEDP).
• Limitations- risk of limb ischemia-highest among all and so is the bleeding risk and
requirement of transfusion.

45. Durable MCS
• Ventricular assist devices (VADs) - pump-flow devices that can temporarily or
permanently support a patient’s circulatory system, used in end-stage/failing heart.
• Divert blood away from the failing ventricle, give rest to the ventricle and maintain
adequate cardiac output

46. Durable MCS
Continuous-flow devices,
include an inflow cannula placed
directly into the LV cavity and an
outflow graft sutured into the
ascending aorta (hemodynamic
support -5 to 10 L/min).

47. Durable MCS
HeartMate II and 3
BTT and
destination
therapy
HeartWare HVAD
BTT device

48. HeartMate 3
The blood pump is positioned within the pericardial space, with its integral inflow conduit in the left
ventricle and outflow graft attached to the ascending aorta.

49. HeartMate 3
• HM3 uses a centrifugal flow pump that has a capacity to pump blood up
to 10 L/min.

50. HeartMate II
Continuous-flow rotary pump with axial design. Flow 3-8L/min.
The device is positioned outside the pericardial space in preperitoneal pump pocket.

51. HeartWare HVAD
Continuous-flow rotary pump with centrifugal design.
The pump is positioned within the pericardial space.

52. Heartmate 2 and HeartWare HVAD trials

53. HeartWare HVAD- ADVANCE TRIAL

54. Durable
MCS
Group 1 (BTT indication) –
Heart transplant candidates waiting for donor heart.
Significantly symptomatic (Stage D or NYHA Class IV),
low peak VO2 (<14 ml/kg/ min), are inotrope
dependent, may have starting end-organ damage due
to chronic low cardiac output.
Group 2 (DT indications) –
NOT SUITABLE for heart transplant due to above
cutoff age limit, diabetes, significant pulmonary
hypertension, established renal dysfunction or recent
malignancy.
Indian Heart Journal 70S (2018) S1–S72

55. INTERMACS
• An important milestone in the advance of MCS therapy has been the development
of the Interagency Registry for Mechanically Assisted Circulatory Support
(INTERMACS).
• Is the largest available data repository for the study of durable MCS outcomes.
• Began prospective patient enrollment and data collection in June 2006.
The Journal of Heart and Lung Transplantation, Vol 32, No 2, February 2013

56. INTERMACS Grading
• Sophisticated Grading used to assess prognosis and sickness level of patients with
advanced HF.
• This is also widely used to select patients who need Mechanical assist before Heart
Transplants or Implantable VAD’s.

57. Durable MCS
• INTERMACS grade ≤3, cardiogenic shock or advanced HF and may need MAS
(Temporary) or permanent LVAD as a BTT.
• INTERMACS grade >3 can be stabilized on Drugs before taking up for Heart
Transplantation.
**Contemporary Management of Cardiogenic Shock- AHA SCIENTIFIC STATEMENT. Oct 2017

58. Indian perspective
• Worldwide – more than 18000 VADs
• India – less than 100
• Heartmate II INR 40–60lakhs
• Heartware INR 60–80 lakhs
• Heartmate III INR 90–100 lakhs

59. SynCardia Total Artificial Heart–Temporary (TAH-t)

60. SynCardia Total Artificial Heart–Temporary (TAH-t)
• The TAH-t consists of a right and left prosthetic ventricle.
• Two atrial connectors on the cuffs, and two connectors on the end of the grafts are
sewn to the aorta and pulmonary artery.
• The prosthetic ventricles, made of biocompatible polyurethane, have a capacity of
70 mL.
• The ventricles are pneumatically driven.

61. SynCardia Total Artificial Heart–Temporary (TAH-t)
• When compressed air is forced into the air sacs simultaneously, compression is
effected onto the blood sac and ejection occurs in simulation of cardiac systole.
• As the air sac is deflated, the blood sac is filled passively from the atrial connection

62. Heart Transplantation
• Only hope for meaningful, long-term recovery in ESHF on OMT.
• Low number of available organs - unreliable primary therapy.
• 44% of MCS device implantations in INTERMACS profile 1 and 2 patients are
performed with a BTT strategy.*
*Kirklin JK et al. Second INTERMACS annual report: more than 1,000 primary left ventricular assist device implants. J Heart Lung
Transplant. 2010

63. Indications
• LVEF less than 30%, NYHA Class 3–4) after OMT therapy or CRT device
• Vo2 max <14 ml/kg/m2 or NT pro BNP more than 1000 units’ pg/ml
• Recurrent Heart failure episodes
• Intractable Ventricular arrhythmias
• Survival Chances less than 80% at one year
• Age less than 70 years

64. Absolute contraindications
• Age >75
• Biologically unfit or Frail
• Advanced malignancies
• HIV/AIDS
• Severe renal dysfunction
• Moderate Liver Cirrhosis

65. Heart Transplantation
• All patients being evaluated for MCS implantation should concurrently be assessed
for transplantation.
• Heart transplantation - MCS device implantation in suitable candidates in whom
heart function is not expected to recover.*
• Limitations- Low number of available organs, unpredictable donor availability, high
cost, limited expertise.
*Contemporary Management of Cardiogenic Shock- AHA SCIENTIFIC STATEMENT. Oct 2017

66. Surveillance
• Endomyocardial (EM) biopsies are routinely advocated every month in the first
year after heart Transplant
• Since Cost of EM biopsies is prohibitively high, it is prudent to limit the EM
Biopsies to two in the first Year – one at one month and another at one year
after Heart Transplant.*
*Indian Heart Journal 70S (2018) S1–S72

67. Survival
• Registry of the International Society of Heart and Lung Transplantation indicates a
current 1-year survival of 84.5% and a 5-year survival of 72.5%.*
*The registry of the International Society for Heart and Lung Transplantation: thirty-first official adult heart transplant report--2014
Indian perspective*
Started in 2008
50-100 transplants per year
*Indian Heart Journal 70S (2018) S1–S72

68. Mechanical causes leading to CS
• Ventricular septal rupture
• Papillary muscle rupture
• Free wall rupture

69. Ventricular septal rupture

70. Ventricular septal rupture
CHARACTERISTIC VENTRICULAR SEPTAL
RUPTURE
Incidence 1-3% without and 0.2-0.3%
with fibrinolytic therapy.
3.9% in patients with cardiogenic shock
Time course Bimodal peak; within 24 hr and 3-5 days;
range, 1-14 days
Clinical manifestations Chest pain, shortness of breath,
hypotension
Physical findings Harsh holosystolic murmur, thrill, S3,
accentuated S2, pulmonary edema, RV
and LV failure, cardiogenic shock
Echo findings VSR, left-to-right shunt, RV
overload
Right-heart catheterization Increase in oxygen saturation from the RA
to RV, large v waves

71. Ventricular septal rupture

72. Ventricular septal rupture
• Anterior infarction - apical septum perforation
• Inferior infarctions - basal septum perforation

73. Ventricular septal rupture
• Hemodynamic monitoring
• SBP ≥ 90mmHg - vasodilator therapy - nitroglycerin or nitroprusside
• Inotropes – SBP < 90mmHg
• IABP- If pharmacologic therapy fails to achieve hemodynamic stability, it should be
instituted rapidly. Acts as bridge to definitive repair.

74. • Surgical repair
• Transcatheter closure - inoperable and the anatomy is amenable to application of a
device.
Ventricular septal rupture complicating acute myocardial infarction: a contemporary review
Eur Heart J. 2014;35(31):2060-2068.

75. Percutaneous closure of an apical ventricular septal rupture

76. Major trials of percutaneous closure of ventricular septal rupture

77. Papillary muscle rupture
• IWMI - PM papillary muscle rupture, more
frequent, single blood supply
• ALMI – AL papillary muscle rupture

78. Papillary muscle rupture
CHARACTERISTIC PAPILLARY MUSCLE RUPTURE
Incidence Approximately 1%
Time course Bimodal peak; within 24 hr and 3-5 days;
range, 1-14 days
Clinical manifestations Abrupt onset of shortness of breath and
pulmonary edema; hypotension
Physical findings A soft murmur, no thrill, severe pulmonary
edema, cardiogenic shock
Echo findings Hypercontractile LV, torn papillary muscle or
chordae tendineae, flail leaflet, severe MR
Right-heart catheterization No increase in oxygen saturation from the RA to
RV, large v waves, very high PCWP

79. Papillary muscle rupture

81. Ventricular free wall rupture
• Early tear leading to tamponade and immediate
death
• Late tear- due to infarct expension -hypotension,
and pericardial discomfort

82. Ventricular free wall rupture
CHARACTERISTIC RUPTURE OF THE VENTRICULAR
FREE WALL
Incidence Approximately 1%
T ime course Bimodal peak; within 24 hr and 3-5 days; range,
1-14 days
Clinical manifestations Anginal, pleuritic, or pericardial chest pain;
syncope; hypotension; sudden death
Physical findings Jugular venous distention, pulsus
paradoxus, electromechanical dissociation,
cardiogenic shock
Echo findings >5 mm pericardial effusion, signs of
tamponade

83. Fibrinolysis and cardiac rupture
MICHAEL B . HONAN JACC Vol, 16, No . 2 August 1990:359-67

84. 1375 patients who received a fibrinolytic agent or underwent primary angioplasty; the incidence of rupture was
3.3 and 1.8 percent, respectively. Angioplasty was a significant independent protective factor (odds ratio 0.46)

85. Ventricular free wall rupture

86. Ventricular free wall rupture
• Large infarct and occurs near the junction of the infarct and normal muscle.
• More common in the anterior or lateral LV wall
• Aggressive medical management including fluid therapy, inotropes, MCS and
pericardiocentesis.
• Definitive treatment - prompt surgical closure

87. • Patients having AMI complicated with CS should undergo early invasive therapy
for revascularization targeting only culprit vessel and an optimal supportive
intensive care treatment.
• Patients in which timely PCI is not possible should be given fibrinolytic therapy.
• MCS should be instituted if CS is persistent despite supportive therapy.
CONCLUSIONS

88. THANK YOU