LVOT Obstruction: Patients at Risk

Edwin G. Avery, M.D.

Chief, Case Cardiac Anesthesia Group

Fall 2011 Cardiac Anesthesia TEE Conference

Disclosures

Covidien: funded research, consultant

Alere: funded research

The Medicines Company: funded research, speaker’s

bureau

Overview

Discuss the most common perioperative clinical

presentations of LVOT obstruction associated with

Hypertrophic Cardiomyopathy (HCM) and the

interventional options available to treat this

pathology

Present a clinical case of HCM with LVOT

obstruction as assessed with intraoperative TEE

HCM and LVOT Obstruction

HCM and LVOT Obstruction Hypertrophic cardiomyopathy (HCM) is a clinical syndrome

with multiple variants that all involve an increase in LV

myocardial mass

Estimated prevalence 0.2% (inherited and acquired)

The clinical symptoms vary but most commonly include:

dyspnea, angina and dizziness

Dizziness may present as lightheadedness, presyncope,

syncope and sudden death

HCM

Normal

HCM and LVOT Obstruction

HCM variants include:

Concentric LVH (RV may also be involved)

Asymmetric upper septal hypertrophy (ASH)

ASH with or without systolic anterior motion of the

anterior mitral leaflet (SAM)

SAM with or without mitral regurgitation (commonly a

posteriorly directed jet of variable severity)

Malposition of the anterior papillary muscle

Mid-cavitary hypertrophy (with or without a gradient)

Apical hypertrophy

LV free wall hypertrophy

HCM and LVOT Obstruction TEE presentation of HCM concentric LVH (PWT or SWT ≥ 11 mm)

HCM and LVOT Obstruction TEE presentation of HCM concentric LVH ± RVH

HCM and LVOT Obstruction TEE presentation of HCM concentric LVH (PWT or SWT ≥ 11 mm)

PWT = 21 mm

End diastole

HCM and LVOT Obstruction TEE presentation of ASH SWT:PWT ≥ 1.3

HCM and LVOT Obstruction TEE presentation of ASH SWT:PWT ≥ 1.3

SWT = 34 mm

SWT:PWT = 34 / 21 = 1.62

End Diastole

LV long axis

(SWT measured perpendicular

to LV long axis)

Distance to maximal septal

thickness from aortic annulus

HCM and LVOT Obstruction TEE presentation of HCM ASH with or without SAM

HCM and LVOT Obstruction TEE presentation of HCM ASH with or without SAM†

†Mild posteriorly directed MR

HCM and LVOT Obstruction TEE presentation of HCM HOCM: LVOT gradient (latent or provocative)†

†Latent ≥30 mmHg, Provocative ≥50 mmHg

HCM and LVOT Obstruction TEE presentation of HCM HOCM: LVOT gradient (latent or provocative)†

†Latent ≥30 mmHg, Provocative ≥50 mmHg

Peak 92 mmHg

Mean 53 mmHg Note sharper peak associated

with dynamic obstruction

HCM and LVOT Obstruction HOCM: LVOT gradient (dynamic obstruction)

Characteristic

“Spike and

Dome” A-line

tracing in

dynamic

obstruction

HCM-LVOT Obstruction:Treatment Medical therapy: β-blockers, verapmil, disopyramide

Permanent pacemaker (DDD) or ICD implantation

Ethanol injection for septal ablation (1st septal perforator

coronary artery)

Mitral valve replacement with low profile mechanical

prosthesis (e.g., St. Jude bileaflet tilting disc)

Surgical myectomy

HCM-LVOT Obstruction:Treatment TEE exam of patients undergoing septal myectomy should include

a complete multiplanar assessment of the aortic valve for evidence

of AI as the surgical approach to the septum may result in damage

to the valve

HCM-LVOT Obstruction:Treatment

Pre-Myectomy Post-Myectomy

Minor AV Injury

HCM-LVOT Obstruction Summary

In some cases, even aggressive septal myectomy may

not relieve the resting or provocative gradient (even

when combined with medical therapy).

In such cases the implantation of a low profile mitral

mechanical prosthesis can be helpful in relieving the

gradient.

There is no evidence that ANY therapy alters the

progressive course of this disease.

Edwin G. Avery, M.D.

Chief, Case Cardiac Anesthesia Group

University Hospitals Case Medical Center

You’re the Intraoperative Echocardiography Consultant

Preinduction Hemodynamics

Induction

Systemic BP: 75/37

Pulmonary BP: 82/44

Fentanyl + Versed + Cisatracurium

Diagnosis? Treatment?

Phenylephrine + Volume + Ventilation

Stable hemodynamics and ready for TEE

ME 4C View

ME 4C Color MV

ME Long Axis View

ME 4C View w/Color

TG Short Axis Mid-pap View

20 mm

TG Short axis mid-pap View

ME Long axis

SWT = 30 mm

End Diastole

LV long axis

(SWT measured perpendicular

to LV long axis)

Distance to maximal septal

thickness from aortic annulus

SWT:PWT = 30 / 20 = 1.5

TG LV Long axis

TG Modified LA View

TG Modified Long axis w/color

LVOT pre-CPB Gradient

Peak 92 mmHg

Mean 63 mmHg C.O. = 1.7 L/min

HCM patients may have low C.O. secondary to low stroke volumes as a result of

decreased LV chamber size and noncompliance/diastolic dysfunction

Deceleration time postCPB

135 msec (Restrictive < 150 msec)

8.6 cm/sec

TDI Lateral MV annulus

Vp post-CPB

Vp 39 cm/sec (Restrictive < 45 cm/sec)

IVRT 200 msec

(Restrictive < 60 msec; Delayed Relaxation > 100)

IVRT Post-CPB

TG SA RV

Membranous septum pre-CPB

ME AV SA w/color

On CPB – Septal Myectomy

ME 4C View post-CPB

ME 4 C view w/color

TG Modified Long axis post-CPB

TG Modified long axis w/color post-CPB

Peak 5 mmHg

Mean 2 mmHg

Post-CPB LVOT gradient

C.O. = 2.0 L/min

Improved a-line tracing

Pre-CPB Post-CPB

TG SA RV post-CPB

AV SA post-CPB w/ZOOM

AV LA Zoom post-CPB

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