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The Heart -1Updated for Spring 2008

Dr. Amitabha Basu MD

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Topic

• Heart failure

• Ischemic heart disease

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Congestive heart failure

• Def: reduced cardiac output to meet the demand.

• In many pathologic states, the onset of heart failure is preceded by cardiac hypertrophy.

• Pathogenesis: flow chart next slide.

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Flow chat

Increased work load, MI, pressure/ volume overload

↓re-expression of embryonic/fetal type of protein

(β-myosin heavy chain)

+Reduced capillary density → reduced oxygen

supply ↓

Heart failure

These re-expression of embryonic/fetal type are associated with myocardial hypertrophy.

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Congestive heart failure

• So, it is long term process.

• Clinical: similar to RHF

• Often progress from the underling diseases like– Hypertension– Cor-pulmonale– Valvular disease– Multiple MI

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Morphology of congestive heart failure

Concentric hypertrophyPressure over load

Caused By: hypertensionNarrow chamber and thick wall

Eccentric hypertrophyVolume over load.Caused by valve regurgitations

Dilated chamber/thick wallEND

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Left Heart failure

• Left heart failure: etiology– Ischemic heart disease– Hypertension– Aortic / Mitral valve disease

• Presentation: acute onset of dyspnea, pulmonary edema, rales, S3 gallop.

• Complication: Cardiogenic shock

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Pulmonary congestion and edema. Intraalveolar pale pink, low protein, few lymphocytes

fluid: Transudate)

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Right heart failure

• Etiology:– Left heart failure and Cor-pulmonale

• Clinical: – jugular venous distension, hepatoslemegaly,

dependent edema, ascites, pleural effusion.

• Complication: – Chronic passive congestion of liver (nutmeg

liver)– Cardiac cirrhosis and centrilobular necrosis.

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A classic case of progression of heart failure

• Next slide

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LVF↓

Dyspnea ← Pul. Edema (T) + heart failure cells ← ↑Hydrostatic pr. ←PHT↓

reduced lung edema ← ↓ Flow of blood in the lung ←RHF↓

Increased (central) venous pressure ↓

↑ Hydrostatic pressure in peripheral blood vessels in the soft tissue = Pitting (dependent edema)

+Ascitis

+Develop Passive venous congestion of various organs

Liver: hepatomegaly (Nutmeg liver)/cardiac cirrhosisSpleen: congestive splenomegaly

Kidney : Hypoxia (Sec. hypertension)

PHT- pulmonary hypertension

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Ischemic Heart Disease (IHD)

Dr. Basu MD

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Do you know

• Propels over 6000 liters of blood through the body daily.

• Beats more than 40 million times a year.

• Yearly economic burden of ischemic heart disease is estimated to be in excess of $100 billion.

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Topic

• Definition

• Types of IHD

• Pathogenesis of Ischemic Heart Disease

• Myocardial infarction

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Ischemic Heart Disease

• There is an imbalance between the myocardial demand and the blood supply.

• Age: Male: middle age

– Female : post menopausal

• Epidemiology: leading cause of death for both males and females in the United States.

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Types of ischemic heart disease

1. Angina ( with > 75% narrowing) 1. Angina pectoris (classical, stable angina)

2. Prinzmetal variant

3. Unstable angina

2. Myocardial infarction (100% occlusion)

3. Sudden cardiac death

4. Chronic ischemic heart disease

Acute

Coronary

Syndrome

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Pathogenesis of IHD

1. Narrowing (stenosis) of coronary artery: • Mostly fixed arthrosclerosis.

2. Complete obstruction (occlusion) of the lumen of coronary artery:

1. Thrombus developed on an atheroma / embolism**.

1. 75% or more narrowing: Ischemic symptoms (angina).

2. Complete occlusion (100% ): Infarction

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Morphology- Angina

• Fixed Atherosclerotic narrowing of the coronary artery.

• This partial occlusion may produce angina.

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Coronary artery showing: >75% narrowing, which would be associated with angina.

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Nearly complete luminal occlusion. Following acute plaque change

This produce myocardial infarction

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Angina Pectoris• Angina pectoris is characterized by:

– Intermittent chest pain caused by transient, reversible myocardial ischemia.

• Type:1. Typical or stable angina pectoris.

• Fixed atherosclerotic narrowing (75% or greater).

2. Prinzmetal, or variant , angina.

3. Unstable angina pectoris (crescendo angina).• Preinfarction angina.

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Typical or stable angina pectoris

• Episodic chest pain associated with exertion or stress.

• Pathogenesis: Fixed coronary atherosclerotic narrowing without plaque change ( > 75% but not full)

• Pain is relived by rest or vasodilators (nitroglycerine) that reduce the venous return.

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Prinzmetal Angina

• Is a form of angina pectoris which

– occurs at rest and

– presumably stems from a coronary artery spasm with or without an obstructive lesion in the artery.

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Unstable Angina (crescendo angina)

• Pathogenesis: – acute plaques change but without 100%

occlusion.

• Clinical:– Increased frequency of anginal pain.– Pain precipitated by less exertion.– Pain is more intense and last longer.

• High risk for Myocardial infarction.

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Biochemical of angina

• C-reactive protein (CRP) may serve as a marker to predict the risk of MI in patients with angina.

• Also serve as a marker to predict the risk of new infarcts in patients who recover from infarcts.

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Myocardial Infarction

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Myocardial infarction

Sudden (> 30 min.) pain

May be in shock due acute LVF : Pulmonary edema.

Statistics:

In U.S. 1.5 million/yr. 25% die in acute phase within 1 hr.

At age 45 –55 : M:F::4:1

At age 80 equal incidence among sexes

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Pathogenesis of Myocardial Infarction –

100% Occlusive intracoronary thrombus By:-

1. Provoked by complications of Atheroma: E.g. : Rupture of plaque.

2. Coronary artery spasm: ? Smoking

3. Emboli (Source is the proximal part of same blood vessels).

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Types of Myocardial Infarction

• Subendocardial MI: – < 50% of the wall thickness

– Any MI typically begins in this area (most poorly perfused area of the myocardium).

• EKG: ST segment depression.

• Transmural MI:– Necrosis extend externally and involve entire

myocardium.– Most common type, take about 24 hrs to

develop.

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M.I: Sites of occlusion:infarction• LAD = Lt. Ant. Desc. A (40 –50%):-

– Lt.Ventricle : anterior and apical– Ant.2/3 of Inter Ventricular Septum (IVS)

• RCA= Rr. Coronary A (30 40%) – Lt.Ventricle : post. wall– I.V.S.post.1/3

• LCX= Lt. Circumflex A(15-20%):- – Lt.Ventricle -- lateral wall

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LAD occlusion Right Coronary occlusion

Left Circumflex occlusion

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Morphology

Time Gross Features

Light Microscope

Electron Microscope

0-½ hr

None None Relaxation of myofibrils; glycogen loss; mitochondrial swelling.

Reversible Injury

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Morphology of Myocardial Infarction

Time from Onset

Gross Morphologic Finding

18 - 24 Hours Pallor of myocardium

3 - 7 Days Hyperemic border with central yellowing

10 - 21 Days Maximally yellow and soft with vascular margins

7 weeks White fibrosis

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Acute myocardial infarct, predominantly of

the posterolateral left ventricle

SCAR

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Time from Onset Microscopic Finding

0-30 min. No change (E.M- Mitochondrial swelling)

Irreversible cell death

↓

1-3 hours Few wavy fibers at the margin of MI.

4-12 hours Loss of cross striations and edema.

12-24 hours Coagulative necrosis, Marginal contraction bands necrosis, ( and

PMNs infiltrate).

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Time from Onset Microscopic Finding

24 - 72 Hours Plenty of PMNs and coagulation necrosis

4-7 days Macrophage & mononuclear infiltration

10-21 Days prominent granulation tissue

7-8 Wk Fibrosis: Healing

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1 to 3 hourswavy fibers (elongated and narrow), compared with adjacent normal fibers (at right).

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12 -24 hrs. Contraction band necrosis : Note the many irregular darker pink wavy contraction bands extending across the fibers.

CONTRACTION BANDS

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Remote infarction ( left Trichrome stain: showing blue collagen).

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MECHANISM of reperfusion injury

• Generation of oxygen free radicals from infiltrating leukocytes

• And apoptosis.

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Effect of reperfusion injury

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Biochemistry of MIElevated by Peak Return to

normalMYOGLOBIN may rise immediately

CK- MB 4-8 hr 18-20hr 2-3 days

CK-MB Isoform 1 & 2 Normal ratio of 1 : 2 = 1.2

In MI the ratio of 1: 2 is >1.5

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Biochemistry of MIElevated

byPeak Return to

normal

Cardiac specific Troponin I and T

3-6 hr 16-20hr 7-10 days

LDH

( level depends on the amount of cell death)

24hr 3-6 days 8-14 days

In MI, LDH “Flip” occur.Normally LDH2 > LDH1, After MI : LDH1 > LDH2

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Enzymes

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Complications of MI

Arrhythmias with possible "sudden death”

(ventricular fibrillation)

Occur immediately

[ MOST COMMON cause of sudden death in MI]

Acute fibrinous pericarditis Typical onset: Second or third day

Late: Dressler syndrome

Rupture of the wall and tamponade or VSD

3-7 days after the MI

Papillary muscle rupture and mitral incompetence

3-7 days after the MI

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Cardiac tamponade

Occur due to hemopericardium.

↑ pericardial pressure = ↓ diastolic filling of the ventricles, and hence in stroke volume

Signs:

Sudden drop in systolic and well as diastolic blood pressure.

Distended jugular vein.Right ventricular and right atrial collapse.

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OTHERS complications

Mural thrombi and thrombo-embolism:

Infarct of Brain, kidney, Intestine

1wk or >

Carcinogenic shock (10% cases)

MI is the most common cause of Cardiogenic shock.

Multi-organ failure

Extension of infarct or repeat 2nd infarction- ? diagnosis

Any time and the most common cause of sudden death weeks after an MI

Ventricular aneurysms Late complication

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Myocardial rupture in an acute infarct in the

wall : ? consequence

Hemopericardium

Cardiac tamponade:-

Acute chest pain/ sudden drop of BP

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Rupture of the ventricular septum (L) and papillary muscle (R)

Left-to-right shunt and right heart failure.

Pan systolic murmur

Produce sudden mitral insufficiency.

Holosystolic murmur (laterally at the apex of the heart with the patient in the left lateral decubitus position) radiated to axilla .

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left ventricular aneurysm: does not contract , so the ejection fraction and

stroke volume of the heart are reduced- patient

feels week!.

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Clinical Features of Myocardial Infarction

• Severe, crushing substernal chest pain.

• Pain radiate to either:– Neck ,Epigastrium,Shoulder.– Or left arm.

• In up to 50% of cases, pain is preceded by episodes of angina pectoris.

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Diagnosis of Myocardial Infarction

– EKG – ST elevation changes, T wave inversion and Q wave- transmural infarct.

– Echo cardiogram– Myocardial enzyme markers

• Creatinine Kinase• Troponins• Lactate dehydrogenase, Myoglobin

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Sudden Cardiac Death (SCD)

Mechanism of SCD is most often a lethal arrhythmia .

Commonest cause = I.H.DOther causes:- 2. Aortic stenosis3. 2nd Myocardial infarct4. M.V. prolapse5. Cardiomyopathy6. Myocarditis

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Thank you