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Ventricular Septal Rupture with Cardiogenic
Shock follows by Infero-posterior Myocardial
Infarct
Dr Han Naung Tun MBBS, MD, FACTM
Heart and Vascular Centre , Yangon and Tuft University Medical Centre , Boston
National Representative Heart Failure Specialist of Tomorrow for Myanmar in HFA and Ambassador
of Echocardiography in EACVI, ESC
Council of Clinical Practice and Working Groups of European Society of Cardiology , France
@HanCardiomd
Disclosure
None to declare
Preamble
Main Topic: Acute Cardiac Care – Cardiogenic Shock with VSR
Patient presentation
58 year-old man with known history of Type II DM and hypertension with the
complaint of central chest pain for 2 days which is associated with dyspnoea, sweating
and nausea.
He had chest pain in cardiac origin, off and on for 2 days. typical chest pain and
worsening dyspnea (Killip 3)
Physical Examination : he was afebrile, blood pressure 130/70 mmHg, heart rate
161/min, oxygen saturation 80% on air, auscultation of heart revealed 1st and 2nd
heart sounds with no added sound and lungs had crepitation in both fields.
Investigation at the time of admission
WBC 19.72
Hb % 14.2
Plt 378
Trop-T 130
NT Pro BNP 3831
Arterial Lactate 4 mmol/l
Urea 4.2
Na+ 144.1
K+ 2.89
Cl- 104
HCO3- 16.5
Creatinine 114
eGFR 60.82
AST 104
ALT 85.5
ALPO4 139
T.Bilirubin 0.378
CRP 116.98
ESR 70
RBS 320 mg/dl
Cholesterol 220.2
Triglyceride 154.2
HDL 53.7
LDL 154.2
HbA1C 6.8
ECG at the time of admission
According to this ECG, what would you like to do first?
1. Immediate activation of Cath Lab to do Primary PCI
2. Emergency assessment of Echocardiography without delaying of Cath lab
activation while activating Cath Lab
3. Treat arrhythmia without delaying of Cath lab activation
4. All of above
Initial work up
He was also given IVI insulin for blood sugar controlled ,IVI Amiodarone loading
dose follow by maintenance dose for arrhythmia ,IV Frusemide for pulmonary
congestion .
Immediate bedside echo showed LVEF – 60% with RCA territory and posterior
wall hypokineisa without any structural lesion was noted.
CVP line and urinary catheter were inserted .
The patient was started on loading DAPT , atorvastatin 80 mg, and
Anticoagulation was achieved with intravenous heparin and also given empirical
Antibiotic Therapy.
SCAI stages A-B (pre-shock) are
associated with the lowest mortality
but a higher proportion of those who
experience a late deterioration is
going to die in hospital.
Therefore, it is crucial to recognise
patients in pre-shock (SCAI shock
stages A and B) and to monitor and
treat them rapidly and appropriately.
Non-invasive mechanical respiratory support (CPAP) was initiated b/c ABG
showed Type 1 respiratory failure with SPO2 – 80 % on high flow face mask
and fast breathing – RR- 30/min .
His haemodynamic parameters were suddenly compromised with BP -80/60
mmHg . IVI Noradrenaline was initiated and titrated with the response,
and Cath Lab was activated immediately.
The patient was immediately transferred to the cath-lab and CAG is
performed
We observed there was high LV-EDP .
Coronary Angiogram shows Distal RCA bifurcation
with ostial PDA branch stenosis assumed as culprit
lesion
In the Cath Lab
Which is the appropriate next step according to the current ESC
guidelines?
A. Systemic thrombolysis
B. PCI of all stenotic vessels
C. PCI of the infarct-related artery
Successful PCI of Distal RCA across ostial PDA
branch with good TIMI 3 flow result.
After 72 hrs of post PCI, his hemodynamic state was suddenly deteriorated
with BP- 70/40 mmHg, severe breathless in NYHA IV, Oxygen saturation was
80% under NIV .
Immediate bedside echo was checked again that showed LVEF -40 % , shunt
between LV and RV (assumed VSR after AMI) , dilated IVC were noted .
He was intensively treated with IVI inotropes and optimal medical treatment,
including mechanical respiratory support (under care of anaesteologist) and
circulatory support (IAPB).
Physical examination at the time of admission revealed a coarse, grade 4/6
holosystolic murmur, with a precordial thrill. Rales were heard over the lower
third of the bilateral lung fields
Bedside TTE showed the VSD in the mid-ventricular inferoseptum, with a left-to-right shunt
Transthoracic echocardiography showed LVEF -30 % the VSD in the mid-ventricular
inferoseptum, with a left-to-right shunt. (assumed VSR after AMI)
After Diagnosed of VSR due to acute MI , what would be your next management ?
A. Plan for surgical closure after consultation with cardiac surgery team
B. Immediate percutaneous device closure
C. Conservative medical therapy
Seemed to be improved haemodynamic parameter ; with BP- 90/60 mmHg
under inotropes and SPO2 with 92% by O2 5L/min , but Arterial lactate 2.3
mmol/L; on approipiate OMT .
We tried percutaneous closure of the VSD under transesophageal
echocardiographic (TEE) guidance
As the defect was extensive and larger for percutaneous closure, and the
procedure was failed and aborted.
We were planning with cardiac surgery team for VSR repair
In day 7 of ICCU Stay ,
Still in the Cardiac ICU
Chest X- Ray
Rechecked TTE
In the meantime we were consulting with cardiac surgery team for VSR repair, the patient was
expired with cardiogenic shock with severe acute pulmonary edema in 9th day of post PCI.
Mortality and Timing of Repair
Amit Goyal et al JACC, 2018
Brandon M. Jones et al , EHJ ,2014
Outcome and profile of ventricular septal
rupture with cardiogenic shock after
myocardial infarction: a report from the
SHOCK Trial Registry
Although patients with rupture had less severe coronary disease, their in-
hospital mortality was higher (87% vs. 61%, p < 0.001). Surgical repair was
performed in 31 patients with rupture (21 had concomitant bypass surgery); 6
(19%) survived. Of the 24 patients managed medically, only 1 survived
Venu Menon, FACC Shock Trial Registry, JACC 2000
A multidisciplinary approach for managing acute ventricular septal rupture.
Brandon M. Jones et al , EHJ , 2014
(α) If deemed suitable for percutaneous repair, transcatheter septal closure (TSC) may be used as primary repair, bridge to surgery,
in conjunction with surgery, or as salvage of residual defect following surgical repair. (β) Candidacy for total artificial heart and/or
cardiac transplantation should be considered for any unstable patient whether as an alternative to, in addition to, or following failure
of repair. (MCS = mechanical circulatory support; OHT = orthotopic heart transplant; TAH = total artificial heart.)
Amit Goyal et al JACC, 2018
VSR Management Algorithm
ACVC pMCS Postcard
ACVC pMCS Postcard
 It is Important to recognise patients in pre-shock (SCAI shock stages A and B)
 Ventricular septal rupture (VSR) remains a devastating complication following
acute myocardial infarction (MI).
 Once diagnosed, management includes any combination of aggressive medical
management, MCS, surgical repair, transcatheter closure, novel
surgical/percutaneous hybrid procedures, and palliative care.
 In hemodynamically stable patients with preserved end-organ function and
favourable anatomy, early corrective surgery should be considered
 A multidisciplinary heart team must collaborate at an experienced center to
devise a strategy that is tailored to each patient.
Learning Points
Acknowledgment
 Subspecialty communities - Association for Acute
CardioVascular Care Education
 Association for Acute CardioVascular Care
 European Society of Cardiology
Thank You

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Ventricular septal rupture with cardiogenic shock follows by Inferior AMI

  • 1. Ventricular Septal Rupture with Cardiogenic Shock follows by Infero-posterior Myocardial Infarct Dr Han Naung Tun MBBS, MD, FACTM Heart and Vascular Centre , Yangon and Tuft University Medical Centre , Boston National Representative Heart Failure Specialist of Tomorrow for Myanmar in HFA and Ambassador of Echocardiography in EACVI, ESC Council of Clinical Practice and Working Groups of European Society of Cardiology , France @HanCardiomd
  • 3. Preamble Main Topic: Acute Cardiac Care – Cardiogenic Shock with VSR
  • 4. Patient presentation 58 year-old man with known history of Type II DM and hypertension with the complaint of central chest pain for 2 days which is associated with dyspnoea, sweating and nausea. He had chest pain in cardiac origin, off and on for 2 days. typical chest pain and worsening dyspnea (Killip 3) Physical Examination : he was afebrile, blood pressure 130/70 mmHg, heart rate 161/min, oxygen saturation 80% on air, auscultation of heart revealed 1st and 2nd heart sounds with no added sound and lungs had crepitation in both fields.
  • 5. Investigation at the time of admission WBC 19.72 Hb % 14.2 Plt 378 Trop-T 130 NT Pro BNP 3831 Arterial Lactate 4 mmol/l Urea 4.2 Na+ 144.1 K+ 2.89 Cl- 104 HCO3- 16.5 Creatinine 114 eGFR 60.82 AST 104 ALT 85.5 ALPO4 139 T.Bilirubin 0.378 CRP 116.98 ESR 70 RBS 320 mg/dl Cholesterol 220.2 Triglyceride 154.2 HDL 53.7 LDL 154.2 HbA1C 6.8
  • 6. ECG at the time of admission
  • 7. According to this ECG, what would you like to do first? 1. Immediate activation of Cath Lab to do Primary PCI 2. Emergency assessment of Echocardiography without delaying of Cath lab activation while activating Cath Lab 3. Treat arrhythmia without delaying of Cath lab activation 4. All of above
  • 8. Initial work up He was also given IVI insulin for blood sugar controlled ,IVI Amiodarone loading dose follow by maintenance dose for arrhythmia ,IV Frusemide for pulmonary congestion . Immediate bedside echo showed LVEF – 60% with RCA territory and posterior wall hypokineisa without any structural lesion was noted. CVP line and urinary catheter were inserted . The patient was started on loading DAPT , atorvastatin 80 mg, and Anticoagulation was achieved with intravenous heparin and also given empirical Antibiotic Therapy.
  • 9. SCAI stages A-B (pre-shock) are associated with the lowest mortality but a higher proportion of those who experience a late deterioration is going to die in hospital. Therefore, it is crucial to recognise patients in pre-shock (SCAI shock stages A and B) and to monitor and treat them rapidly and appropriately.
  • 10. Non-invasive mechanical respiratory support (CPAP) was initiated b/c ABG showed Type 1 respiratory failure with SPO2 – 80 % on high flow face mask and fast breathing – RR- 30/min . His haemodynamic parameters were suddenly compromised with BP -80/60 mmHg . IVI Noradrenaline was initiated and titrated with the response, and Cath Lab was activated immediately. The patient was immediately transferred to the cath-lab and CAG is performed We observed there was high LV-EDP .
  • 11. Coronary Angiogram shows Distal RCA bifurcation with ostial PDA branch stenosis assumed as culprit lesion In the Cath Lab
  • 12. Which is the appropriate next step according to the current ESC guidelines? A. Systemic thrombolysis B. PCI of all stenotic vessels C. PCI of the infarct-related artery
  • 13. Successful PCI of Distal RCA across ostial PDA branch with good TIMI 3 flow result.
  • 14. After 72 hrs of post PCI, his hemodynamic state was suddenly deteriorated with BP- 70/40 mmHg, severe breathless in NYHA IV, Oxygen saturation was 80% under NIV . Immediate bedside echo was checked again that showed LVEF -40 % , shunt between LV and RV (assumed VSR after AMI) , dilated IVC were noted . He was intensively treated with IVI inotropes and optimal medical treatment, including mechanical respiratory support (under care of anaesteologist) and circulatory support (IAPB). Physical examination at the time of admission revealed a coarse, grade 4/6 holosystolic murmur, with a precordial thrill. Rales were heard over the lower third of the bilateral lung fields
  • 15. Bedside TTE showed the VSD in the mid-ventricular inferoseptum, with a left-to-right shunt
  • 16. Transthoracic echocardiography showed LVEF -30 % the VSD in the mid-ventricular inferoseptum, with a left-to-right shunt. (assumed VSR after AMI) After Diagnosed of VSR due to acute MI , what would be your next management ? A. Plan for surgical closure after consultation with cardiac surgery team B. Immediate percutaneous device closure C. Conservative medical therapy
  • 17. Seemed to be improved haemodynamic parameter ; with BP- 90/60 mmHg under inotropes and SPO2 with 92% by O2 5L/min , but Arterial lactate 2.3 mmol/L; on approipiate OMT . We tried percutaneous closure of the VSD under transesophageal echocardiographic (TEE) guidance As the defect was extensive and larger for percutaneous closure, and the procedure was failed and aborted. We were planning with cardiac surgery team for VSR repair In day 7 of ICCU Stay ,
  • 18. Still in the Cardiac ICU Chest X- Ray Rechecked TTE In the meantime we were consulting with cardiac surgery team for VSR repair, the patient was expired with cardiogenic shock with severe acute pulmonary edema in 9th day of post PCI.
  • 19. Mortality and Timing of Repair Amit Goyal et al JACC, 2018
  • 20. Brandon M. Jones et al , EHJ ,2014
  • 21. Outcome and profile of ventricular septal rupture with cardiogenic shock after myocardial infarction: a report from the SHOCK Trial Registry Although patients with rupture had less severe coronary disease, their in- hospital mortality was higher (87% vs. 61%, p < 0.001). Surgical repair was performed in 31 patients with rupture (21 had concomitant bypass surgery); 6 (19%) survived. Of the 24 patients managed medically, only 1 survived Venu Menon, FACC Shock Trial Registry, JACC 2000
  • 22. A multidisciplinary approach for managing acute ventricular septal rupture. Brandon M. Jones et al , EHJ , 2014
  • 23. (α) If deemed suitable for percutaneous repair, transcatheter septal closure (TSC) may be used as primary repair, bridge to surgery, in conjunction with surgery, or as salvage of residual defect following surgical repair. (β) Candidacy for total artificial heart and/or cardiac transplantation should be considered for any unstable patient whether as an alternative to, in addition to, or following failure of repair. (MCS = mechanical circulatory support; OHT = orthotopic heart transplant; TAH = total artificial heart.) Amit Goyal et al JACC, 2018 VSR Management Algorithm
  • 26.  It is Important to recognise patients in pre-shock (SCAI shock stages A and B)  Ventricular septal rupture (VSR) remains a devastating complication following acute myocardial infarction (MI).  Once diagnosed, management includes any combination of aggressive medical management, MCS, surgical repair, transcatheter closure, novel surgical/percutaneous hybrid procedures, and palliative care.  In hemodynamically stable patients with preserved end-organ function and favourable anatomy, early corrective surgery should be considered  A multidisciplinary heart team must collaborate at an experienced center to devise a strategy that is tailored to each patient. Learning Points
  • 27. Acknowledgment  Subspecialty communities - Association for Acute CardioVascular Care Education  Association for Acute CardioVascular Care  European Society of Cardiology