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ISCHEMIC HEART DISEASE

ATHEROSCLEROSIS
MAJOR RISK FACTORS OF ATHEROSCLEROSIS
Cigarette smoking
Hypertension (BP > 140/9o(mm/hg) or (on Antihypertensive medication)
Low HDL cholesterol
Diabetes mellitus
Family history of CHD
Age (Men > 45 years; Women > 55 years)
Life style risk factors
Obesity (BM1 > 30 kg/m)
Physical inactivity
Atherogenic diet

EMERGING RISK FACTORS.


Lipoprotein (a)
Homocystine
Prothrombotic factors (Fibrinogen)
Pro inflammatory factors( CRP)
Impaired fasting glucose
Subclinical atherogenesis
RISK FACTOR AND RELATIVE RISK OF FUTURE CARDIOVASCULAR ADVERSE EVENTS

Lipoprotein (a)
Homocystine
IL-6
Total Cholesterol
LDL-Cholesterol
sICAM-1
Serum amyloid-A
Apolipoprotein-B
TC:HDL ratio
hs-CRP
hs-CRP+TC:HDL

0.0

RELATIVE RISK OF FUTURE CARDIOVASCULAR ADVERSE EVENTS


hsCRP, high reactivity C-reactive protein;
siCAM-l, soluble intercellular adhesion molecule-1;
HDLC, high density lipoprotein cholesterol

LIPID FRACTIONS AND RELATIVE RISK OF FUTURE CARDIOVASCULAR ADVERSE EVENTS


RELATIVE RISK FOR FUTURE CARDIO
VASCULAR EVENTS

Decreasing Predictivity of Risk

LIPID FRACTION & LIPID RATIOS

TC:HDLC

Apo B100:HDLC

LDLC:HDLC

APO B100:APO A1

Non HDL cholesterol fraction

Apolipo-protein B1 fraction

HDL cholesterol fraction

Total cholesterol fraction

Apolipo-protein fraction

LDL cholesterol fraction

TYPE OF HVPERLIPIDEMIA AND RISK OF CORONARY ARTERY DISEASE


CONDITION

Type I (Familial Hyper Chylomicronemia)

RISK OF CORONARY ARTERY


DISEASE
Not increased

Type II A (Familial Hyper Cholesterolemia)


Type II B (Familial Combined Hyperlipidemia)

Accelerated
Accelerated

Type III (Familial Dysbetalipoprotenemia


Type IV (Familial Hyper Triglyceredemia)
Type V (Familial Mixed Hypertriglyceredemia)

Accelerated
Accelerated
Not increased

VARIOUS CHOLESTEROL VALUES


LDL CHOLESTEROL
<100 optimal
100-129 Above optimal
130-159 Boderline High
160-189 High
>190 Very high

TOTAL CHOLESTEROL
<200 Desirable
200-239 Boderline High
>200 High

HDL CHOLESTEROL
<40 Low
>60 High

DIETRY MANAGEMENT

BENEFICIAL CARDIOVASCULAR EFFECTS OF SELECTED DIETRY COMPONENTS


Omega 3 fatty acids
Triglycerides, Platelet Aggregation
High Fibre Diet
TC,
LDL cholesterol
Sterol esters
TC LDL cholesterol
Soya protein
Triglycerides LDL cholesterol
Vitamin E
LDL oxidative susceptibility
Vitamin C
Recycles Vitamin A
Folic acid/Vitamin B6
Homocystiene levels
Moderate alcohol consumption
HDL Cholesterol Blood Coagulation
OMEGA-3 FATTY ACIDS
OMEGA 3 PUFA
Marine Sources
Eicosapentaenoic acid(EPA)
Docosahexaenoic acid(DHA)

Protects From IHD/CAD


Reduction in Mortality From CAD/SCD

HYPOLIPIDEMIC EFFECT

ANTI-THROMBOTIC EFFECT

ANTI-ARRHYTHMOGENIC
EFFECT
Stabilisation of membrane
phospholipids

TC levels
LDL levels
HDL levels

THERAPEUTIC LIFE STYLE CHANGES


NCEP ATP-III (National Cholesterol Education Programme Adult Treatment Panel)
NUTRIENT
RECOMMENDED INTAKE
Saturated Fat
<7% of Total Calories(TC)
Polyunsaturated Fat
Upto 10% of TC
Carbohydrate
Upto 20% of TC
Fibre
20-30 gm/day
Proteins
Upto 15% of TC
Cholesterol
<200mg/day
Total calories
Balance Energy Intake & Expenditure
Salt
<6g/day

Anti-platelet
Anti-inflammatory effect

ANGINA

STABLE
Chest Pain or arm
discomfort on effort that
is:
Relieved in 10
min/rest/nitro-glycerine.
by exertion.
No in cardiac markers
ECG shows ST
depression.

TYPES
UNSTABLE
Angina pain when
It occurs at rest lasting
>10 min.
It is more severe, frequent
& prolonged.
No elevation in cardiac
markers
ECG shows ST
depression.

PRINZMETAL/VARIANT
Angina pain that occurs at
rest, not related to
exercise.
Occurs due to Vasospasm
ECG shows ST elevation.
No elevation in cardiac
markers

MYOCARDIAL INFARCTION
DEFINATION
MI RELATED TO ISCHEMIA DUE TO PRIMARY CORONARY EVENT
Detection of rise and/or fall of cardiac biomarkers (preferably troponin) with at least one value above
the 99th percentile of the upper reference limit (URL) together with evidence of myocardial ischemia
with at least one of the following:
Symptoms of ischemia.
ECG changes indicative of new ischemia (new ST-T changes or new left bundle branch block [LBBB])
Development of pathological Q waves in the ECG.
- Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality.
MI RELATED SUDDEN CARDIAC DEATH
Sudden, unexpected cardiac death, involving cardiac arrest, often with symptoms suggestive of
myocardial ischemia, and
accompanied by presumably new ST elevation, or new LBBB, and
evidence of fresh thrombus by coronary angiography and/or at autopsy, but death occurring before
blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the
Blood.
MI ASSOCIATED WITH PCI
By convention, increases of biomarkers greater than "3 x 99th percentile URL"
have been designated as defining "PCI-related myocardial infarction
MI ASSOCIATED WITH CABG
By convention, increases of biomarkers greater than "5x 99th percentile URL" +
new pathological Q waves or new LBBB, or angiographically documented new graft or
native coronary artery occlusion, or
imaging evidence of new loss of viable myocardium have been
Designated as defining CABG-related myocardial infarction.
CRITERIA FOR PRIOR MYOCARDIAL INFARCTION
Any one of the following criteria meets the diagnosis for prior myocardial infarction.
Development of new pathological Q waves with or without symptoms
Imaging evidence of a region of loss of viable myocardium that is thinned and fails to contract, in the
absence of a, non-ischemic cause.
Pathological findings of a healed or healing myocardial infarction.

ECG CHANGES

ECG

STABLE - ST
DEPRESSIO
N
UNSTABLE ST
DEPRESSIO
N
PRINZMETA
L - ST
ELEVATION
MI

STEMI - ST
ELEVATION
NSTEMI - ST
DEPRESSIO
N

ECG CHANGES OF MI IN ORDER

HYPER
ACUTE
'T'
WAVES
TERMINAL
QRS
CHANGES
ST
ELEVATION
T
WAVE
INVERSION
PATHOLOGI
CAL
Q
WAVE
THE SITE OF INVOLVEMENT OF ARTERIES AND THE CORRESPONDING SITES OF
MYOCARDIAL LESIONS
Left ant. Descending artery (40-50%)
Anterior wall of left ventricle near apex
Ant. portion of ventricular septum
Apex Circumferentially
RCA (30-40%)
Inf. post, wall of left ventricle
Post portion of ventricular septae
Inf. post, right ventricular free wall in some cases
Left circumflex (15-20%)
Lateral wall of left ventricle except at apex

COMMON

UNCOMMON

Left anterior descending


(LAD) artery (40-50%)
Right coronary artery (3040%)
Left circumflex coronary
artery (15-20%)

Left main coronary artery


Secondary branches e.g.,
Diagonal branches of
LAD artery
Marginal branches

RARE (NEVER
ENCOUNTERED)
Penetrating
intramyocardial branches
of coronary arteries

ANTERIORWALL MYOCARDIAL INFARCTION SUBDIVIDED INTO


TVPE OF M.I
LEADS INVOLVED
Extensive anterior wall M.I
Standard lead I
Lead AVL and
All precordial leads (V1-V6)
An anteroseptal wall M.I
Leads VI to V4
An anterolateral wall M.I.
Standard lead I, lead AVL and
Leads V4 to V6
Apical wall M.I.
V5-V6
Inferior wall M.I.

Standard leads II and III


Lead AVF
Standard lead II, III
Lead AVF
V1 V2
Standard lead II, III
Lead AVF
V5 V6

Inferoposterior wall M.I.

Inferolateral wall M.I.


DIAGNOSIS
CARDIAC MARKERS
ENZYME

SEEN AT

PEAKS AT

RETURNS TO
NORMAL

Creatinin phosphokinase

2-4 hrs

24 hrs

48-72 hrs.

Lactate dehydrogenase

24 hrs

4 - 5 days

After 10 days

Myoglobin
Troponin -I
Troponin - T

2-3 hrs within 4-8 hrs


within 4 - 8 hrs

48 hrs
48 hrs

7-12 hrs
7-10 days
7-10 days

THALLIUM SCANNING:
Thallium-201 is used is injected IV while pt. Is exercising on trade mill.
Interpretation:
Normal Myocardial Tissue:- hot spot.
Ischemic Myocardial Tissue:-hot spot during rest & cold on exertion.
Infracted Myocardial Tissue:-cold spot on both rest & exertion.
**NOTE** Thallium scan differentiate Normal, Ischemic & Infracted tissue.

HYBERNATION vs. STUNNED MYOCARDIUM


ACUTE CORONARY OCCLUSION
ISCHEMIC VENTRICULAR DYSFUNCTION

EARLY REPERFUSION
PERSISTENT VENTRICULAR DYSFUNCTION

CHRONIC SEVERE CORONARY STENOSIS


CHRONIC REDUCTION IN BLOOD FLOW &
ISCHEMIA
METABOLIC ADAPTATION
CHRONIC CONTRACTILE DYSFUNCTION
REVASCULARISATION

DELAYED SPONTANEOUS RECOVERY OF


VENTRICULAR FUNCTION

IMPROVED CONTRACTILE FUNCTION

STUNNED MYOCARDIUM

HYBERNATING MYOCARDIUM

TREATMENT OF MI & ANGINA


PRINZMETAL ANGINA
Sublingual Nitro-glycerine
Long Acting Nitrates
CCBs
-Blockers

Acute Episode
Prevent Recurrences
Prevention of Coronary Artery Spasm
Variable Response

MYOCARDIAL INFARCTION
ST-ELEVATION MI (STEMI)

Immediate Management With MONA


Morphine
Oxygen
Nitrates
Aspirin
Start Adjuvant Treatment
-blocker
Nitro-glycerine(IV)
Heparin(IV)

Reperfusion Therapy(<12hrs)
Thrombolysis (streptokinase)
Early Primary PCI
After 12hrs thrombolysis is of no use.

MANAGEMENT OF NSTEMI/ UNSTABLE ANGINA


Immediate treatment with MONA & Bed Rest
M- MORPHINE
O- OXYGEN
N- NITRATES
A- ASPIRIN
Antischemic Therapy: NITRATES, BLOCKER
Antithrombotic Threapy: ASPIRIN+CLOPIDOGREL
Anticoagulant Therapy: HEPARIN (UFH/LMWH)

Assess clinical risk


Low Risk

High Risk

Patient is Candidate for Early Conservative Treatment

Patient is Candidate for Early Invasive Treatment

CONSERVATIVE TREATMENT
Continue Antischemic Therapy
Continue Antithrombotic Threapy
Continue Anticoagulant Therapy
Watchful waiting
ECG & Cardiac markers monitoring

INVASIVE TREATMENT
Revascularisation with
PCI
CABG
THROMBOLYSIS CONTRAINDICATED

ST ELEVATED M.I.
Thrombolysis,
PCI,
Bypass Surgery

NON ST ELEVATED M.I.


PCI,
Bypass surgery
THROMBOLYSIS CONTRAINDICATED

THROMBOLYTICS
Drugs :
Streptokinase used mostly high benefit low risk (IC bleed)
rTPA
Alteplase
tenecteplase
reteplase
Indications:
Acute NSTEMI
Chest pain e new STEMI and LBBB
C/I:-

Prior I/C haemorrhage


Structural cerebral vascular lesion
Malignant I/C neoplasm
Ischemic Stroke within 3months
Suspected aortic dissection
Bleeding diathesis
Facial trauma
Timing:
Ideally e in 30 minutes 3 hours
But if delayed till 12 hour if PCI is not available
Can be till 24 hour only if PCI is not available
Complication of Streptokinase:
H Hypotension
I I/C haemorrhage
F Fever
I Anaphylaxis
Arrhythmias
**NOTE** MI with hypotension suggest carcinogenic shock and in these cases the reperfusion therapy is
Angioplasty / bypass not thrombolytics.
RV INFARCT TREATMENT
Best modality of t/t in inferior M.I.
Best modality of t/t in inferior M.I.
complicated by Right ventricular

Reperfusion therapy
Thrombolytic or
PCI
IV fluids

COMPLICATIONS OF MI
Arrhythmias VF(common cause of MI related deaths)
Interventricular septal rupture.
Free wall rupture-Haemopercardium
Papillary Muscle Rupture

CARDIOMYOPATHY
SYMPTOMATIC CARDIOMYOPATHY
DILATED
RESTRICTIVE
CARDIOMYOPATHY
CARDIOMYOPATHY
Systolic Dysfunction
Diastolic Dysfunction
EJECTION FRACTION<30%
EJECTION FRACTION>30%

HYPERTROPHIC
CARDIOMYOPATHY
Diastolic Dysfunction
EJECTION FRACTION>30%

HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY


PATHPHYSIOLOGY
Septal Hypertrophy
Asymmetrical septal hypertrophy.
Dynamic LV Outflow Obstruction
It is related to narrowing of the sub aortic area as a consequence of opposition of anterior mitral
valve leaflet against hypertrophied septum in mid systole (SYSTOLIC ANTERIOR MOTION
SAM)
CLINICAL SPECTRUM OF HOCM
ASYMPTOMATIC PATIENT
SUDDEN DEATH
First clinical manifestation of disease (commonly in young adults after sport)
SYMPTOMATIC
SYMPTOMS
SIGNS
Dyspnoea
Double or triple pericardial impulse
Angina
Brisk carotid upstroke
Fatigue
S4
syncope
Systolic murmur
Harsh, diamond shaped
Best heard at lower lt sterna border
as well as apex but no radiation to
neck
FACTORS AFFECTING INTENSITY OF MURMUR
CONDITION WHICH OBSTRUCTION &
CONDITION WHICH OBSTRUCTION &
INTENSITY OF MURMUR
INTENSITY OF MURMUR
FACTOR SING MYOCARDIAL
FACTOR THAT MYOCARDIAL
CONTRACTILITY
CONTRACTILITY
Exercise
-blockers
Sympathomimetic amines
CCBs
Digitalis
FACTOR WHICH VENTRICULAR
VOLUME
FACTOR WHICH SES VENTRICULAR
Passive leg raising
VOLUME
Valsalva manoeuvre
Expansion of blood volume
Sudden standing
Supine position
Nitroglycerine
AORTIC IMPEDENCE & AFTERLOAD
Amyl nitrate
Phnylephrine
Tachycardia
Hand grip
Squatting
AORTIC IMPEDENCE & AFTERLOAD
MANAGEMENT OF HOCM
Avoidance of strenuous physical activity
-blockers
HR
BP
Stiffness of LV
Fatal arrhythmias
CCBs (Verapamil Diltiazem)
Stiffness of LV

Elevated Diastolic Pressure


Amiadarone
Surgical Myomectomy

DRUGS C/I IN HOCM


DRUGS THAT SES MYOCARDIAL CONTRACTILITY
Sympathomimetic amines
Digitalis
-blockers
DRUGS THAT SES VENTRICULAR VOLUME
Nitrates
Diuretics
PERICARDIAL DISEASES
CARDIAC TAMPONADE
INTRODUCTION
It is a condition characterised by presence of fluid in pericardial space which leads to sed
intrapericardial pressure.
CAUSES:
Trauma
CLINICAL FEATURE:
SYMPTOMS:
Becks Triad.
JVP
Decreased BP
Muffled Heart Sounds
SIGNS:
JVP ses
Prominent X-decent.
Absent Y- wave.
Pulses Paradoxus
Kussumals sign-mostly absent but can also be present when pericardium starts organising.
INVESTIGATION:
ECG:- electrical Alternance.
2D echo: Shows pericardial effusion
RV size.
CONSTRICTIVE PERICARDITIS
INTRODUCTION:
It is a CHRONIC clinical condition characterized by organisation of pericardium leading to
pericardial space.
CAUSES:
Trauma
Cardiac operation
Mediastinal irradiation
Purulent infection
Neoplastic diseases
Rheumatoid arthritis (not acute rheumatic fever)


C/F:

O/E:

SLE
Fatigue
Hypotension
Reflex Tachycardia.
JVP-sed
Prominent X decent-absent
Prominent Y present.
Kussumals sign +ve
Pulses paradoxus ve
Tapping apex broad bent sign
square root sign
Equalisation of diastolic pressure

INVESTIGATION:
ECG:
Low voltage complexes
2D ECHO:
Thickened pericardium
Pericardial calcification
RV-size normal

CHARACTERISTIC

TAMPONADE

Clinical
Pulsus paradoxus
Common
jugular veins
Prominent y descent
Absent
Prominent x descent
Present
Kussmauls sign
Absent (Rare)
Third heart sound
Absent
Pericardial knock
Absent
Electrocardiogram
low ECG v o l t a g e
May be present May
Electrical alternans
be present
Echocardiography
Thickened pericardium
Absent
Pericardial calcification
Absent
Pericardial effusion
Present
RV size
Usually small
Myocardial thickness
Normal
Right atrial collapse and RVDC Present
Increased early filling,
Absent
mitral flow velocity
Exaggerated respiratory variation Present
in flow velocity
CT/MRI Thickened/calcific
Absent
pericardiumCardiac catheterization
Usually present
Equalization of diastolic
procedures
Cardiac biopsy helpful
No
Square Root Sign
+ve

CONSTRICTIVE RESTRICTIVE
PERICARDITIS CARDIOMYOPAT
HY

RVMI .

Usually absent

Rare

Rare

Usually present
Usually present
Present
Absent
Often present

Rare
Present
Present
Rare
Absent

Rare
Rare
Present
May be present
Absent

May be present
Absent

May be present
Absent

Absent
Absent

Present
Often present
Absent
Usually normal
Normal
Absent
Present

Absent
Absent
Absent
Usually normal
Usually increased
Absent
Present

Absent
Absent
Absent
Enlarged
Normal
Absent
May be present

Present

Absent

Absent

Present

Absent

Absent

Usually present

Usually absent

Absent or present

No
+++ve

Sometimes
+ve

No
-ve

**NOTE**
A Positive Kussumals Sign Is Rare In Cardiac Tamponade. Its Presence Suggests That An Organizing Process
& Epicedial Constriction Are Present In Addiction To Effusion.

CONGESTIVE HEART FAILURE


INTRODUCTION
It is characterized by of cardiac pump dysfunction leading to decrease in stroke volume, cardiac output,
blood pressure and perfusion.
PATHOPHYSIOLOGY:
Heart Failure

sed renal perfusion

Reduced Cardiac Output

Increased Renin

Sympathetic nervous activation

Increased Angiotensin

Increased peripheral resistance

Increased aldosterone

Vasoconstriction

hydrostatic pressure

Increased Sodium and


water retention
FEATURES OF LEFT HEART FAILURE & RIGHT HEART FAILURE
LEFT HEART FAILURE
Lt heart failure is defined as a clinical syndrome
where the dominant feature is fluid congestion in the
lungs (pulmonary) rather than in the systemic
circulation.
The pulmonary capillary wedge pressure is typically
elevated (PCWP)
Predominant symptoms are related to passive

RIGHT HEART FAILURE


Rt heart failure is defined as a clinical syndrome
where the dominant feature is fluid congestion in the
systemic circulation
The pulmonary capillary wedge pressure is normal
( normal PCWP) unless rt. Heart failure is caused
secondary to left sided heart failure (ed PCWP)
(PCWP is not elevated in isolated RHF)

congestion of lungs pulmonary edema


Dyspnoea
Orthopnea
PND
Cough with pink frothy sputum
Rales/Crackles

Peripheral edema
Ascites
Congestive hepatomegly
Congestive spleenomegaly
Wt. Gain
Nocturia
Raised JVP
Positive Hepatojugular Reflex.

THE FRAMINGHAM HEART STUDY CRITERIA


MAJOR CRITERIA
PND
Neck vein distension
Rales
Cardiomegaly
Acute pulmonary edema
S3 gallop
venous pressure ( >16 cm)
Circulation time>25s
Hepatojugualr reflex positive

MINOR CRITERIA
Ankle edema
Night cough
Hepatomrgaly
Pleural effusion
Vital capacity reduced by one third from predicted
Tachycardia (>120)

MAJOR OR MINOR CRITERIA


Weight loss of more than 4.5kg over 5 days in responce to treatment
DEFINITE TREATMENT
2 major criteria or one major & 2 minor criteria.
INVESTIGATIONS
SIGNS OF PULMONARY VENOUS HYPERTENSION
(In order of appearance with increasing pulmonary venous pressure)
Vascular Redistribution
Upper lobe venous distension
Interstitial edema
Kerley B lines
Perihilar haze
Bronchial cuffing
Alveolar edema
Airspace opacities
Perihilar bat wing distribution
Clears rapidly with diuretics
Pleural effusions
BRAIN NATRIURETIC PEPTIDE IN THE DIAGNOSIS OF HEART FAILURE
The natriuretic peptide system impacts salt and water handling and pressure regulation and ,may
influence myocardial structure and function.
Brain natriuretic peptide is a hormone that is released from myocardial cells in the atria and in some
cases the ventricles in response to volume expansion.
The release of both ANP and BNP is increased in heart failure as ventricular cells are recruited to
secrete both ANP and BNP in response to high ventricular filling pressures.
The plasma concentrations of both hormones are increased in patients with asymptomatic and
symptomatic left ventricular dysfunction, permitting their use in diagnosis.

HYPONATREMIA
Due to sed ADH
Due to sed ANP, BNP & CNP.
sed BNP, pro-BNP

MANAGEMENT OF HEART FAILURE

Once The Clinical Diagnosis Of Heart Failure Is Confirmed Assess For Fluid Retention. It Is Important
To Treat The Patients Fluid Retention Before Starting An ACE Inhibitor.
Beta Blockers Should Be Started Once The Fluid Retention Has Been Treated.
DRUGS USED:
AIM OF DRUG THERAPY IN CHF

Relief of congestive and low output symptoms and


restoration of cardiac performance

INOTROPIC DRUGS
Digoxin
Dobutamine
Dopamine
Amrinone
Milirinone

Arrest and reversal of disease progression


and prolongation of survival

ACE INHIBITORS
Captopril
Enalapril
Lisinopril
Ramipril
Trandolapril

DIURETICS
Furosemides
Thiazides
Bumetanide
Hydrochlorthiazide
Metolazone

AT-II ANTAGONISTS
Losartan
Candesartan
Irbesartan
Losartan

VASODILATOR
ACE inhibitor2
AT-1 antagonist
Hydralazine
Nitrate

BLOCKERS
Bisoprolol
Carvedilol
Metoprolol

BLOCKER
Metoprolol
Bisoprolol
Carvedilol
**NOTE**
ACEIs Reduces The Mortality By 20%