TREATMENT OF MECHANICAL COMPLICATIONS POST...

Καρδιαγγειακή Απεικόνιση 2016

TREATMENT OF MECHANICAL

COMPLICATIONS POST AMI

Ioannis Iakovou, MD, PhD

Onassis Cardiac Surgery Center

Athens, Greece


• Ventricular Septal Rupture

• Papillary Muscle Rupture

• Acute Mitral Regurgitation

• Free Wall Rupture

• Ventricular Aneurysm

• Left Ventricular Failure and Cardiogenic Shock

• Right Ventricular Failure

Mechanical Complications post ΑΜΙ


•Can occur with either anterior or

inferior MI

•May develop as early as 24 hrs; most

commonly seen 3 to 7 days after MI in

the prefibrinolytic era and 2 to 5 days

currently

•Causes an abrupt left-to-right “shunt”

Ventricular Septal Rupture

• loud systolic murmur and thrill medial to the apex along the left sternal border in

the 3rd or 4th intercostal space, accompanied by hypotension with or without signs

of LV failure

• The GUSTO-I trial has demonstrated an incidence of VSR of approximately 0.2%


Oxygen saturation “step-up”

IV C sat

7 0 %

SV C sat

6 5 %

RA sat

6 8 %

RV sat

8 8 %

PA sat

8 8 %


MI Case (ST)

72 y, female with anterior MI (late-12 hrs- presentation) hemodynamicaly unstable,

killip IIII, tachycardia

• 10 yrs ago anterior Mi

thromb,

• 13 mos ago PCI LAD

(DES),

• Dc Plavix 5 days ago


MI Case (ST)

Thromboaspiration and PPCI LAD (DES)

• Pt stabilized

hemodynamically

• ST resolution

• ½ hour later cardiac

arrest, AV dissociation

• Bedside echoIVS “shunt”


Independent Predictors of Ventricular Septal

Rupture Occurrence

• Older age

• Female gender

• Nonsmoker

• Anterior infarct

• Worse Killip class on admission

• Increasing heart rate on admission


• Rapid diagnosis

• Afterload reduction

• Inotropic support

• Intra-aortic balloon pump

• Surgical repair of ruptured septum

Ventricular Septal Rupture


Ventricular Septal Rupture -Treatment

• Μortality rate in patients with VSD treated medically is 24% at 72 hours and

75% at 3 weeks. patients should be considered for urgent surgical

repair, even if the patient's condition is stable.

• Aim Intensive medical management should be started to support the

patient before surgery. Unless there is significant aortic regurgitation, an

IABP should be inserted urgently as a bridge to a surgical procedure.


Mitral Regurgitation

• Papillary muscle rupture was reported to occur between days 2 and 7 in the

prefibrinolytic era,

• the SHOCK Trial Registry demonstrated a median time to papillary muscle rupture of 13

hours. Papillary muscle rupture is found in 7% of patients in cardiogenic shock and contributes to

5% of the mortality after acute MI.

• In some patients, permanent mitral regurgitation is caused by papillary muscle or

free wall scar.

• Frequent auscultation during the first few hours of infarction often reveals a

transient late apical systolic murmur thought to represent papillary muscle

ischemia with failure of complete coaptation of the mitral valve leaflets.


Development of giant “V waves”

P. A. pressure

V-wave

P.C. Wedge pressure


Acute Mitral Regurgitation:

Treatment Rapid diagnosis

Afterload reduction Nitroprusside (decreases SVR,

thereby reducing the regurgitant fraction and increasing

the forward stroke volume and cardiac output).

Inotropic support

IABP (decrease LV afterload, improve coronary

perfusion, and increase forward cardiac output. Patients

with hypotension may tolerate vasodilators after the

insertion of an IABP)

Surgical valve replacement


Free wall rupture

• Free wall rupture occurs in 3% of MI patients and accounts for

approximately 10% of mortality after MI (almost always fatal). The

timing of cardiac rupture is within 5 days in 50% of patients and

within 2 weeks of MI in 90% of patients.

• Free wall rupture occurs only among patients with transmural MI.

• Risk factors include advanced age, female gender, hypertension,

first MI, and poor coronary collateral vessels.


Cardiac Tamponade

Equalization of diastolic pressures

Hypotension

J.V.D.

Clear lung fields

Pulsus paradoxus

Pseudoaneurysm

Enlarged cardiac silhouette

Echocardiographic diagnosis

Free wall rupture


Rapid diagnosis

Pericardiocentesis The procedure may be dangerous

because of reopening of communication with the

pericardium as the intrapericardial pressure is relieved

Emergency open heart surgery to correct the rupture

Free wall rupture


Pseudoaneurysm

• may remain small or undergo progressive enlargement.

• The outer wall is formed by the pericardium and mural thrombus.

• Pseudoaneurysms may remain clinically silent and be discovered during routine investigations. However, some patients may have recurrent tachyarrhythmia, systemic embolization, and heart failure.

• Some patients may have systolic, diastolic, or to-and-fro murmurs related to the flow of blood across the narrow neck of the pseudoaneurysm during LV systole and diastole.


Left Ventricular Failure and

Cardiogenic shock

• The clinical definition of cardiogenic shock is decreased cardiac

output and evidence of tissue hypoxia in the presence of adequate

intravascular volume

• 5-10% of pts after a heart attack

• 60000-70000 pts in Europe/year

• In the past decade the mortality rate was reduced mainly by early

reopening of the infarct-related artery.

• Still extremely high, approx. 50% @ 30 days


Schematic drawings of current percutaneous mechanical

support devices for CS: (A) intra-aortic balloon pump; (B)

TandemHeartTM; (C) Impella®.

Thiele H et al. Eur Heart J 2010;31:1828-1835


Percutaneous Assist Devices -

Overview

Thiele et al, Eur Heart J 2007; 28:2057-2063

Tandem Heart™ Impella Recover®

LP 5.0

Impella Recover®

LP 2.5

Catheter size (French) - 9 9

Cannula size (French) 21 venous

12-19 arterial

21 12

Flow (l/min) Max. 4.0 Max. 5.0 Max. 2.5

Pump speed (rpm) Max. 7,500 Max. 33,000 Max. 33,000

Insertion/

Placement

Peripheral

(Femoral artery + LA)

Peripheral surgical

(Femoral artery)

Percutaneous

(Femoral artery)

Anticoagulation + + +

Recommended duration of

use

- 14 days 7 days 5 days

CE-Certification + + +

FDA PMN IDE Trial IDE Trial

Relative costs in

comparison to IABP

+++++ +++ +++


Antman et al. Circulation. 2004;110:82-292

O’Gara et al. Circulation. 2013;127:e362-e425

Van de Werf et al. Eur Heart J. 2008;29:2909-2945

Steg et al. Eur Heart J. 2012;33:2569-2619

Guidelines

IABP in STEMI complicated by cardiogenic shock


LVAD or IABP?

Bleeding

Invasiveness

+ -

Implantation procedure

LVAD

Hemodynamic support

Better LV-unloading

Costs


Recommendations on how to

approach shock

If a pt has a SBP of 75-80 mm Hg the aim is to increase BP over the

next couple of days while keeping them out of shock; use IABP

Do not use IABP in all high risk pts; but consider in the following

situations:

Severe HF

Bridge to surgery

Impeding CS

Mild CS


For more severe cases of CS (SBP approx 40,50,60, 70 mmHg) or pts

requiring high doses of inotropes or vasopressors we (may) have the

option of percutaneous LVAD (Tandemheart or Impella) which provide

superior hemodynamic support compared to IABP

Cardiac arrestECMO & bypass

Percutaneous LVAD did not reduce 30-day mortality

Percutaneous LVAD is associated with higher rate of bleeding, especially

the TandemHeart

Until now, we cannot recommend to replace IABP by percutaneous

LVAD as first-choice approach in the mechanical management of

cardiogenic shock

Recommendations on how to

approach shock (2)


Right Ventricular Failure-treatment

• Mild RV dysfunction is common (approximately 40%) after MI of the inferior

or inferoposterior wall; however, hemodynamically significant RV

impairment occurs in only 10% of patients with inferior or inferoposterior

wall MI

• Only proximal occlusions (proximal to the acute marginal branch) of the

RCA result in marked dysfunction



• volume loading to increase left ventricular preload and cardiac output is

key to the management of RV infarction.

• hemodynamic monitoring with a pulmonary artery catheter in these

patients, because overzealous fluid administration can further decrease LV

output. The target central venous pressure for fluid administration is

approximately 15 mm Hg.

• When volume loading is insufficient to improve cardiac output, inotropes

are indicated. Dobutamine (increases cardiac index, improves RV ejection

fraction)> than afterload reduction with nitroprusside.


• Patients may benefit from reperfusion therapy,

• because patients who undergo successful reperfusion of RV branches have

enhanced RV function and a lower 30-day mortality rate.

• Patients with RV infarction and bradyarrhythmias or loss of sinus rhythm

may have significant improvement with AV sequential pacing.

• IABP + dobutamine improve the cardiac index (CI).

• Pericardiectomy (reverses the septal impingement on left ventricular

filling) .

• An RV assist device is indicated for patients who remain in cardiogenic

shock in spite of these measures.



Ventricular Aneurysm

• Common, especially with a large transmural infarct (most commonly anterior) and good residual myocardium.

• Aneurysms may develop in a few days, weeks, or months. may be suspected when paradoxical precordial movements are seen or felt, accompanied by persistent elevation of ST segments on the ECG or a characteristic bulge of the cardiac shadow on x-ray.

• They do not rupture but may be associated with recurrent ventricular arrhythmias and low cardiac output.

• Administration of ACE inhibitors during acute MI modifies LV remodeling and may reduce the incidence of aneurysm


• Anticoagulation is indicated for patients with a mural thrombus. target

international normalized ratio (INR) of 2 to 3 for 3 to 6 months.

• Patients with LV aneurysms and a low global EF (less than 40%) have a

higher stroke rate and should take anticoagulants for at least 3 months

after the acute event.

• Refractory heart failure or refractory ventricular arrhythmias surgical

resection. Surgical resection may be followed by conventional closure or

newer techniques to maintain LV geometry. Revascularization is

beneficial for patients with a large amount of viable myocardium around

the aneurysm.

Ventricular Aneurysm- Treatment


• Rapid diagnosis

• Patient stabilization (afterload reduction, inotropic support)

• Intra-aortic balloon pump or LVADs

• Surgical repair

Conclusions

Treatment of mechanical complications of AMI is based on


Thank You!

Email: [email protected]

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