ECG of the Week!!!

Dr. K. Manoj KumarProf. Dr.Gowrishankar Unit

A 55yr old Male, c/o shortness of breath – 7 days; chest pain – 6days

No h/o syncope ; no h/o oliguria; no h/o fatigue

Not a known Diabetic; known hypertensive for 5yrs

No h/o similar illness in the family

O/E Patient Conscious Mildly dyspneic,tachypneic Mild pallor – I0/PE0/L0/CL0

CVS S1 S2+ S4+; systolic murmur+ not radiating to carotid

RS NVBS heard P/A soft BP 130/80 mm hg PR 76/min

ON INVESTIGATION Blood Sugar, Urea Creatinine levels are

within normal limits CBC with normal limits Chest X-Ray

Mild cardiomegalyLung fields clear

ECG

ECG shows: Rate : 75/min Normal axis of 15 degree Normal ST segment PR interval normal normal sinus beat followed by atrial ectopic

Atrial bigeminal rhythm Tall R waves with deep symmetrical sharply

pointed inverted T waves in the mid precordial leads

The initial horizontality of ST Segment with well developed ST T angle – ST Segment shelf is seen

DIFFERENTIAL DIAGNOSIS OF THIS ECG Hypertrophic cardiomyopathy lV SYSTOLIC OVERLOAD like

hypertension Myocardial ischemia CVA with qrs st pattern Valvular aortic stenosis

HYPERTROPHIC CARDIOMYOPATHY Inheritable autosomal dominant disease

of heart muscle d/tmutation in beta mhc of chr14

characterized by thickened but non dilated left ventricle in the absence of another cardiac or systemic condition capable of producing magnitude of the hypertrophy evident

Small ventricular cavity and marked hypertrophy of myocardium with myofibril disarray w/wo dynamic outflow tract obstruction

Most common cause of sudden cardiac death in young people including trained athelets

WHO designated with HCM to describe this unique process of primary muscle hypertrophy

M mode echo define ASH

Myocardial disarray of muscle fibre result in WHORLING characteristic of HCM

3.1icknessPostwallth

knessSeptalThic

PATHOPHYSIOLOGY Diastolic dysfunction LV Out flow tract obstruction Mitral regurgitation due to elongated

mitral leaflets and chordae Intramyocardial ischaemia due to

partially obliterated intra mural coronary arteries

Arrythymias Autonomic dysfunction – systolic BP↓ on

exercise

EFFECT OF MANEUVER FOR HCM DIFFERENTIATION MANEUVER PHYSIOL EFFECT HCM AS

MR Valsalva vr,svr,co

squat&hand vr,svr,co Grip &phenyl

ephrine

Amylnitritevr, dec svr

Parameters associated with sudden deathsurvivor of cardiac arrestSustained VTFamily history of premature sudden deathMassive degree of ventricular hypertrophyHypotensive response to exerciseMyocardial bridgingSeptal thickness > 30mm Troponin t mutation

Courtesy Braunwald heart diseases & Harrison Medicine

ECHO FINDINGS LV hypertrophy with septum >1.3times

posterior LV wall thickness Ground glass appearance of septum Spade shaped LV Cavity small lv cavity SAM of mitral valve septal immobility premature closure of aortic valve resting gradient>30mm provocable gradient>50mm

ECHO CLASS OF LVH IN HOCM TYPE 1 ..ANT SEPTUM 10% TYPE 2…ANT AND POST SEPTUM 20% TYPE 3 ..ANT AND POST SEPTUM

INCLUDING LAT.FREE WALL 52% TYPE 4 ..REGION OTHER THAN SEPTUM

AND POST FREE WALL 18%

COMPLICATIONS Sudden death Infective endocarditis Systemic embolism Atrial fibrillation High incidence of SVT 46%, PVC 43%,

VT 26% AF 25-30%

TREATMENT Screening Echo for first degree relatives Avoid strenuous exercise IE prophylaxis Keep well hydrated Medical therapy like Beta blockers,

calcium channel blockers, diisopyramide Surgical options include septal

myectomy. Dual chamber pacing, septal ablation in patients not responding to surgery

AICD for prevention of sudden death

THANK U