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بسم الله الرحمن

الرحیم

Atrial and Ventricular Hypertrophy

ECG Features and Common Causes

ALI BARABADI

University of Guilan

Aims and Objectives.

Understand pathophysiology of types of hypertrophy.

Common patient presentation and symptoms.

ECG appearances associated with different types of hypertrophy.

CARDIAC HYPERTROPHY

CARDIAC HYPERTROPHY

Physiological hypertrophy

(Athlete’s Heart)

Physiological hypertrophy

(Athlete’s Heart)

Pathological hypertrophy (Cardiovascular disease)

Pathological hypertrophy (Cardiovascular disease)

Finding animal studyFinding animal study

Identified key signaling mechanisms Identified key signaling mechanisms

To diagnosis, New TherapeuticTo diagnosis, New Therapeutic

Increased heart mass Normal or Enhanced cardiac function Reversible

Increased heart mass Reduced cardiac function Irreversible Cell death and fibrosis Increased mortality

Pressure overload

Systolic wall stress

Mechanical transducers

Eccentric hypertrophy

Volume overload

Diastolic wall stress

Concentric hypertrophy

Responses to hemodynamic overload

hypertrophy

Extracellular and intracellular signals

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Signaling pathway in Signaling pathway in Physiological Cardiac Physiological Cardiac HypertrophyHypertrophy

PI3K PI3K (p110(p110αα))

PI3K PI3K (p110(p110αα))

Akt1Akt1Akt1Akt1Angiogenesis

Angiogenesis

Contractility

Contractility Heart

growthHeart

growth

Anti-apoptosis

Anti-apoptosis

Anti-fibrosisAnti-fibrosis

Pathological pathway

Pathological pathway

IGF-1IGF-1

IGF-1 IGF-1 ReceptorReceptor

Cell membrane Cell membrane

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Signaling pathway in Signaling pathway in Physiological Cardiac Physiological Cardiac HypertrophyHypertrophy

• mTOR dependent pathway

• mTOR independent pathway

» Regulation of protein synthesis and cell » Regulation of protein synthesis and cell sizesize

Akt1Akt1Akt1Akt1

mTORmTORmTORmTOR

Protein synthesisProtein synthesisProtein synthesisProtein synthesis Protein degradationProtein degradationProtein degradationProtein degradation

Cell sizeCell sizeCell sizeCell size

Distinct characteristics of physiological Distinct characteristics of physiological and pathological cardiac hypertrophyand pathological cardiac hypertrophy

PI3K PI3K (p110(p110αα))

PI3K PI3K (p110(p110αα))

Akt1Akt1Akt1Akt1

New therapeutic strategyactivate regulators of

PI3K (p110α) pathway,i.e. ‘PI3K–regulated microRNAs’

IGF-1IGF-1

IGF-1 IGF-1 ReceptorReceptor

Cell membrane

Lead Iextends from the right to the left arm

Lead IIextends from the right arm to the left foot

Lead IIIextends from the left arm to the left foot

Einthoven’s Triangle

+-

+

-

Normal Intervals

PR 0.20 sec (less than one large

box) QRS

0.08 – 0.10 sec (1-2 small boxes)

QT 450 ms in men, 460 ms in

women Based on sex / heart rate R-R interval with normal HR

Left Atrial Hypertrophy / Enlargement.

Thickening of wall. Dilatation of

chamber (enlargement).

Increased volume. Increased muscle

mass.

Some causes.

Mitral and / or aortic valve disease. Left ventricular systolic and diastolic

dysfunction. Cardiomyopathy - hypertrophic /

dilated. Atrial fibrillation. Left atrial mass. Hypertension.

Left Atrial Abnormality

II: wide P wave V1: negative P wave is “1 box wide, 1 box deep” wider; left atrial enlargement should prolong the P wave > 0.12 sec. V1 may show a bi-phasic P wave

Right Atrial Hypertrophy / Enlargement.

Some causes.

Tricuspid and / or pulmonary valve disease.

Lung disease. Congenital heart disease RV systolic and diastolic dysfunction. Mitral stenosis (pressure back-up).

Right Atrial Abnormality Criteria

Tall P waves in lead II Tall, peaked P wave (>2.5mm). Best seen lead II - often throughout ECG. Normal P wave is less than 2.5 mm tall and 0.12 seconds wide.With right atrial hypertrophy, P waves are typically taller than 2.5 mm but not wider than 0.12 sec.

Right Ventricular Hypertrophy.

Some causes of RVH.

Pulmonary hypertension Mitral stenosis. Pulmonary valve disease. Congenital heart disease RV systolic dysfunction

ECG Criteria for RVH.

Right axis deviation of +110 degrees or more. Dominant R wave in lead V1. R wave in lead V1 >7mm.

Other supporting criteria: ST segment depression T inversion V1 - V4. Deep S waves V5, V6, I and aVL.

Left Ventricular Hypertrophy.

Thickened walls. Dilated chamber. Increased muscle mass

or increased volume.

Some causes of LVH.

Aortic valve disease. Coarctation of the aorta. Cardiomyopathy - dilated,

hypertrophic. Hypertension. Heart Failure - systolic.

Commonly Used Criteria for LVH.

ECG Feature: Amplitude:

Largest R or S wave in limb leads >20mm.

S wave leads V1 and V2 >30mm.

R waves in leads V5 or V6 >30mm.

Left axis deviationQRS Duration of >0.09s.

• If S wave in V1 + R wave in V5 or V6 ≥ 35 mm (≥ 50 for under 35 yrs of age)

• R wave > 11 mm in aVL

R wave > 15 mm in lead I

LVH Types

Volume Over LoadPressure Over Load

LVH Types

Pressure Over load Like in hypertension, IHD) Ischemic heart

disease( LV strain pattern – ST depression with T ↓

in V5, V6, L1 and aVL leadsVolume Over load Like in Mitral or Aortic regurgitation Shows prominent positive T waves in V5, V6, L1 and aVL

Conclusion.

LAH – ECG appearance and common causes.

RAH – appearance and causes. LVH – appearance, certainty of

diagnosis, causes and pitfalls. RVH – appearance, causes and

pitfalls.

Web Site Instruction

Berne and Levy Physiology, 6th Edition Bruce M. Koeppen, Bruce A. Stanton R. Klablunde -Cardiovascular Physiology Concepts -Lippincott (2005) Leonard S. Lilly-Pathophysiology of Heart Disease_ A Collaborative Project of Medical Students a

nd Faculty , Fifth Edition-Lippincott Williams & Wilkins (2010) (Expert consult) Robert O Bonow_ Eugene Braunwald_ et al-Braunwald's heart disease _ a textboo

k of cardiovascular medicine-Elsevier Saunders (2012) http://www.madsci.com/manu/ekg_hypr.htm http://library.med.utah.edu/kw/ecg/ecg_outline/Lesson7/index.html http://library.med.utah.edu/kw/ecg/ecg_outline/Lesson8/index.html

Thank you

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