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The Heart -1
Updated 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 hypertrophy
Pressure over load
Caused By: hypertension
Narrow chamber and thick wall
END
Eccentric hypertrophy
Volume over load.
Caused by valve
regurgitations
Dilated chamber/thick
wall
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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 cirrhosis
Spleen: 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
Acute
Coronary
Syndrome
2. Myocardial infarction (100% occlusion)
3. Sudden cardiac death
4. Chronic ischemic heart disease
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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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Reversible Injury
Time Gross
Features
0-½
hr
None
Morphology
Light
Electron Microscope
Microsco
pe
None
Relaxation of
myofibrils; glycogen
loss; mitochondrial
swelling.
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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
Maximally yellow and soft with
vascular margins
White fibrosis
10 - 21 Days
7 weeks
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Acute myocardial infarct, predominantly of
the posterolateral left ventricle
SCAR
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Time from Onset
0-30 min.
Microscopic Finding
1-3 hours
No change (E.M- Mitochondrial
swelling)
Irreversible cell death
↓
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
10-21 Days
Plenty of PMNs and coagulation
necrosis
Macrophage & mononuclear
infiltration
prominent granulation tissue
7-8 Wk
Fibrosis: Healing
4-7 days
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1 to 3 hours
wavy 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 MI
Elevated by
Peak
MYOGLOBIN
may rise immediately
CK- MB
4-8 hr
18-20hr
Return to
normal
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 MI
Elevated
Peak
by
3-6 hr
16-20hr
Cardiac specific
Troponin I and T
LDH
24hr
( level depends
on the amount of
cell death)
3-6 days
Return to
normal
7-10 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)
Acute fibrinous pericarditis
Rupture of the wall and
tamponade or VSD
Papillary muscle rupture and
mitral incompetence
Occur immediately
[ MOST COMMON
cause of sudden death
in MI]
Typical onset: Second or
third day
Late: Dressler syndrome
3-7 days after the MI
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)
Multi-organ
failure
MI is the most common cause of
Cardiogenic shock.
Extension of infarct or repeat 2nd Any time and the most
infarction- ? diagnosis
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.
Produce sudden mitral
insufficiency.
Pan systolic murmur
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.D
Other causes:2. Aortic stenosis
3. 2nd Myocardial infarct
4. M.V. prolapse
5. Cardiomyopathy
6. Myocarditis
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Thank you
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