ARRHYTHMIAS in ACS PATIENTS

PRACTICAL ASPECTS

14 Feb 2562

Roj Rojjarekampai , MD

OUTLINES AF VAs

• Epidemiology and

consequences

• Management in acute

and long term phase

• - rate and rhythm

management

• - stroke prevention

• Epidemiology and

pathophysiology

• Acute Management in

Vas related ACS

• : Medications

• : Non-medications

STEMI with AF

INCIDENCE

AF & short-term Mortality in ACS

STEMI NSTEMI

HR = 1.65 HR = 2.30

AF & long-term Mortality in ACS

STEMI NSTEMI

HR=2.37 HR =1.67

Mortality in AF with MI

OR = 1.46 New AF ; OR =1.37

AF and ACS • AF occurred in ACS 10-20 %

[ more frequently in more

severe setting and advance

ages ]

• In pooled analysis of 120,566

pts of STEMI , NSTEMI show

in-hospital AF 8% and 6.4%

respectively

AF and ACS • Ass with increase of in-hospital

and long term mortality

• Both pre-existing and new onset

AF increase equivalent mortality rate in ACS patients

Management of AF complicating ACS

• Acute Phase

Management of AF complicating ACS

• Acute Phase

AF in ACS

Rate control

Amiodarone BB , Digitalis

DCCV

Amiodarone

Hemodynamic instability YES NO

Management of AF complicating ACS

• Long term phase : focus on stroke prevention

• Triple Therapy [ OAC +ASA+P2Y12inh] should be

considered in all ACS with AF whose CHA2DS2VASc ≥ 2

Triple Therapy

Triple Therapy vs DAT

Triple Therapy vs DAT

Trial design: Patients with an indication for oral anticoagulation (OAC) and undergoing DES PCI

were randomized to either 6 weeks or 6 months of triple therapy (aspirin + clopidogrel + OAC

initially, aspirin + OAC indefinitely). Patients were followed for 9 months.

9.8 8.8

0

10

20 Primary endpoint: Composite of death, MI, stent thrombosis, stroke, TIMI major bleeding at 9 months for 6 weeks vs. 6 months of triple therapy: 9.8% vs. 8.8%, HR 1.14, 95% CI 0.68-1.91, p = 0.63

Cardiac death, MI, stent thrombosis, ischemic stroke: 4.0% vs. 4.3%, p = 0.87; TIMI major bleeding: 5.3% vs. 4.0%, p = 0.44

Stent thrombosis: 0.7% vs. 0%

ISAR-TRIPLE trial

N.Sarafoff et al.TCT 2014

Primary endpoints at 9 months

Duration of triple therapy

PIONEER AF-PCI

ACS 50 % , high stroke risk90%

PIONEER AF-PCI:BLEEDING

PIONEER AF –PCI :MACE

ROW, rest of

world

RE-DUAL PCI: dual antithrombotic therapy with dabigatran after percutaneous coronary

intervention in patients with atrial fibrillation

Dabigatr

an 110

mg dual

therapy

(n=981)

Warfarin triple

therapy

(n=981)

Dabigatran 150

mg dual therapy

(n=763)

Corresponding

Warfarin triple

therapy (n=764)

Age, years, mean 71.5 71.7 68.6 68.8

≥80 (US, ROW), ≥70 (Japan),

%

22.9 22.9 1.0 1.0

Full analysis set presented. HRs and Wald CIs from Cox proportional-hazard model. For the dabigatran 110 mg vs warfarin comparison, the model is

stratified by age, non-elderly vs elderly

(

ACS c Stenting c AF (high stroke risk)

Strategies of antithrombotic therapy • : triple therapy [ OAC +ASA+P2Y12inh] [ Class I ] for

4-6 weeks [ class II b]then dual therapy [ P2Y12 inh

+ OAC ] until 1 year and OAC monotherapy lifelong

• : Dual therapy [ OAC + P2Y12 inh ] for 1 year [ II a ]

• - VKA + Clop [ or Tica ]

• - NOACS [ Riv 15 mg od or Dab 150 bid ] + Clop

VAs

VAs and ACS • In STEMI : incidence decrease

from 10 % in fibrinolytic era

[ GUSTO-1] to near 6 % in

primary PCI era [ APEX-AMI]

• 90% occurred in first 48 hrs

• Ass with increase mortality

Predictors for VAs

Should be considered at increased risk of

Ventricular Tachyarrhythmias

outcome

VT/VF in ischemia

1 2

3

Myocardial ischemia(1) • Net cellular K loss

• Net cellular Na gain

• Decrease intracellular ATP

content

• Increase intracellular proton

generation ( acidosis )

Mechanisms (2) 1)increase RMP [ -80 to -60 mv ]

2)Reduction in AP amplitude ,

velocity, duration

3)Early cellular uncoupling

Types of VAs • Acute : VT in ischemic zone [ re-entry]

• : PVC triggers

• : often irregular and degeneration to VF

• Reperfusion and subacute :recovering from brief

duration of ischemia

• : ↑ iCa lead to increase automatism & triggers activity [ DAD ]

• Chronic { > 1 MONTH } mostly from re-entry around scar tissue : stable anatomic circuit MMVT

Accerelated Idioventricular Rhythm

BENIGN

AIVR ; CAVEAT • AIVR is one of the reperfusion arrhythmias

• AIVR is not specific sign of successful reperfusion Rx

• Most AIVR does not need for specific Rx

• Clinical correlation of patients is essential

• Regular rhythm.

• Rate 50-110 bpm.

• Three or more ventricular complexes.

• QRS complexes >120ms.

• Fusion and capture beats.

https://lifeinthefastlane.com/ecg-library/basics/vt_vs_svt/

Treatment of VAs

in ACS

• prophylactic AADs not suitable

• optimal revascularization ,early Rx with BB

, balancing Elyte ,sedation, DCCV /

overdrive stimulation should be considered

first

• if AADs is needed ( recurrent VAs related-

ACS after failure available Rx) ,IV

Amiodarone and followed by IV Lidocaine

is reasonable

Management of VAs in STEMI

Amiodarone vs Lidocaine

Management of VAs in STEMI ( 2 )

Management of VAs in STEMI ( 3 )

Beta Blockers Which , How to start ?

Beta-Blocker Heart Attack Trial: impact of

propranolol therapy on ventricular

arrhythmias.

• Trial started in 1978 • Double blinded RCT compared propranolol

[ n=1,926]vs placebo [n=1,921]in pts of 5-21 days

after MI

• Propranolol started at 120 mg /day and titrated to

180-240 mg / day

• Average 25 months F/U

BHAT trial

BHAT : cause of death

IV BB • Limited availibilty of IV BB which recommended for

ACS patients [ IV Metoprolol , IV Propranolol ] in

Thailand

• Ultra-short acting BB ; Esmolol was shown as

effective treatment for refractory VF in OHCA, post

MI patients [ 500 ug/kg IV bolus then 50-100 ug/kg/min infusion IV ]

Esmolol in OHCA

Esmolol in MI • The first case is about a 47-year-old woman, who came to our attention for anterior myocardial

infarction (STEMI). A primary percutaneous coronary intervention on the left anterior descendant artery was performed in a single vassel disease. Circulation was supported by an intra-aortic balloon pump (IABP) and epinephrine infusion. The left ventricular function was depressed (LVEF 30% at echo). The patient was then stabilized; IABP was removed and epinephrine infusion was stopped. Eight days later, she suffered an episode of sustained monomorphic VT at 220/min perceived as simple palpitations; blood pressure was 73/49 mmHg (85/50 mmHg during sinus rhythm). Lidocaine 100 mg was administered unsuccessfully, so she was sedated and converted to sinus rhythm with 200J synchronized DC shock. From that moment on six other arrhythmic relapses occurred, for a total of seven DC shocks, despite the infusion of amiodaron (20 mcg/kg/min) and lidocaine (20 mcg/kg/min). After the last cardioversion an infusion of esmolol 50 mcg/kg/min was started and the patient stabilized, without any other relapse. There was no mechanical cause for the arrhythmia (Figure 1A) The second case is about a 71-year-old man with an idiopathic dilated cardiomyopathy (LVEF 28% at echo) and normal coronary arteries. He was admitted because of an appropriate ICD intervention. During the hospitalization he suffered another episode of VT refractory to antitachycardia pacing (ATP) and evolving into ventricular flutter treated with DC shock. In the following hours he had incessant episodes of haemodynamically well-tolerated VT, not responding to medical treatment with intravenous lidocaine (100 mg bolus and then infusion 20 mcg/kg/min), intravenous flecainide (1 mg/kg), amiodarone (150 mg plus 300 mg bolus), and several attempts of ATP. The patient was cardioverted eight times with external and internal DC shock. The arrhythmias stopped when esmolol therapy was instituted, with an initial bolus of 40 mg followed by an infusion of 50 mcg/kg/min for two hours. No relapse of ventricular arrhythmia was observed and in the following days (Figure 1B).

Emergency Care Journal 2016; volume 12:6097

REVASCULARIZATION

BB , SEDATION

RATE & RHYTHM CONTROL

Non – Medication Treatments

Overdrive Pacing

Cardiac sympathetic denervation

Bradyarrhythmias in MI • High grade AVB

• - in acute RCA occlusion : narrow complex ,

good prognosis

• - in acute LAD occlusion : wide complex [ CRBBB

with LAFB ], bad prognosis

• BBB had no longer associated with long term

mortality except in case with new LBBB within 60 minutes after admission

STEMI inf wall with CHB

STEMI ant wall with CHB

Rx of Bradyarrhythmias related ACS

CHB and STEMI

US database from 2003-2012 2,273,853 STEMI 2.2% CHB In hosp mortality 20.4 % vs 8.7% OR 2.47

In Hospital Moratlity rate In STEMI complicating CHB

Medications for AVB ass MI

Take Home Messages • 1) Both SVAs and VAs are not uncommon in ACS

patients despite aggressive revascularization

strategy widely used

• 2) DCCV not be delayed in case with arrhythmias

induced hemodynamic worsened

• 3) Beta Blockers must be prescribed in all patients

of ACS if no contraindication , esp in first 48

hours

• 4) Non Pharmacological treatments should be considered in patients who failed for medication