Ischemic Heart disease (IHD)

Or
Coronary artery disease(CAD)
 Introduction
Commonest cause of mortality and morbidity
Leading killer amongst CVD
Increasing incidence and prevalance every
year
Set of risk factors profile identified
Present day lifestyle predisposes for IHD
 Definition Of IHD
Condition causing hypoxia to the
myocardium due to inadequate perfusion
secondary to varied etiology
Atherosclerosis of epicardial arteries
commonest cause
 Types of IHD
Angina pectoris
Chronic stable angina
Unstable angina
Acute myocardial infarction
Sudden cardiac death (SCD)
 Epidemiology
Commonest cause of mortality /morbidity
Progress to UA NSTEMI STEMI
7 lakh hospital admissions in USA per year
 RISK FACTORS
MODIFIABLE NON MODIFIABLE
Cigarette Smoking
Obesity Genetic
Hypertension
Sex
Hyper-cholesterolemia
Diabetes mellitus Age
Personality A
Mental Stress & Physical
Inactivity
Increased lipoprotein A levels
>0.3 g/dl
Hyperhomocysteinemia
 Etiology of IHD /CAD
Atherosclerosis Embolism
Infective endocarditis
Arteritis
Left atrial /ventricular
SLE thrombus
PAN Left atrial/ventricular
RA tumour
Ankylosing Prosthetic valve
spondylitis thrombus
Takayasu disease Complication of cardiac
catheterization
 Etiology Continued
Coronary mural thickening
Amyloidosis
Radiation therapy
Hurlers syndrome
Pseudoxanthoma elasticum
Other causes of coronary luminal narrowing
Aortic dissection
Coronary spasm
Congenital coronary artery disease
Anomalous origin from pulmonary artery
Arteriovenous fistula
 Arteriosclerosis
(Thickening and hardening of arterial walls )
Atherosclerosis
Calcification (Monckebergs )
Congenital
Inflammatory
Granulomatous (Syphilitic aortitis )
Autoimmune
 Atherosclerosis
(patchy nodular type of arteriosclerosis )
Fatty streak Earliest lesion ,universal, by 10 years
of age , yellow /white patch in intima of aorta
Reversible
Fibrous plaque firm,elevated dome shaped
lesion , seen in aorta/coronaries/carotids
indicates advancing atherosclerosis
Complicated lesion calcified fibrous plaque
with necrosis ,thrombosis ,ulceration causes
obstruction to lumen/trigger plaque rupture
 Why and How of atherosclerosis
Exact etiology is not known
Complex interaction of genetic to environmental
factors
response to injury hypothesis considered
endothelial dysfunction basic problem
Endothelial injury by a variety of toxins tobacco,
oxidised LDL ,HTN ,viruses etc leading to
deposition of chronic inflammatory
cells,cholesterol and collagen
 Continued
Vascular smooth cells migrate from Tunica
media to tunica intima they hypertrophy
,proliferate to synthesise extracellular matrix
of connective tissue
Cholesterol accumulate in matrix covered by a
fibromuscular cap lined by smooth muscle
cells ,collagen and a layer of endothelial cells
 Pathology
Coronary atherosclerosis most common
pathology
atherosclerotic plaque final lesion and
hallmark of CAD
Directly /indirectly responsible for all CV
events
Proximal 6 cm of coronary arteries usually
involved
Distal vessels routinely spared
ANGINA PECTORIS
 Definition
discomfort felt in the chest or around chest
due to myocardial ischemia due to decreased
coronary blood flow or a mismatch between
myocardial O2 supply and demand
 Causes of angina
Reduced myocardial oxygen supply
Coronary artery disease
Severe anemia

Increased myocardial Oxygen demand

Left ventricular hypertrophy
Hypertension
Aortic stenosis
Aortic regurgitation
Hypertrophic cardiomyopathy
Rapid tachyarrhythmias
 Types of angina
Classic angina- Sudden ,sharp ,left sided chest
pain ,retrosternal ,varying intensity, radiation
to left arm ,jaw ,neck ,forearm ,any quality ,5-
10 min , on work and exercise , by rest \ SL
nitrates
Atypical angina- absence of one or more
criteria ( may not on work or by rest
 Types of angina
Angina equivalent Dyspnea as a sole
manifestation
Variant (prinzmetal angina ) Angina at rest
\periodic with ST segment elevation
Angina decubitus Angina in recumbent
position ( lying down )
Nocturnal angina angina at night ( like PND )
Angina inversus Pain increases at rest and
decreases on exercise
 Factors contributing to survival
Prognostic factors for the survival of angina
patients depends on
Extent \ severity of CAD
LV systolic function
Presence\severity of ischemia in exercise
 Angina at rest
(contributes to acute coronary syndrome )
Severe angina
Acute MI ( STEMI /NSTEMI )
Coronary spasm
 Symptoms
Typical /atypical chest pain
Chest discomfort
Breathlessness (angina equivalent )
Silent
CCF
Rarely as SCD (malignant VT )
 Conditions that provoke ischemia
Hyperthyroidism Renal disease
Hypertension Gross anemia
Hyperthermia AS/HOCM
Arrhythmias
Anxiety
Hypoxemia
AV fistulae
Polycythemia
 Clinical examination
Look for risk factors xanthelasma \xanthomas
Systemic disease DM /HTN /Thyroid
/anemia/
BP /Peripheral arteries /LVH /fundus /apex /
arterial bruits
Cardiac auscultation S3 /S4 /murmurs /clicks
 Investigations
ECG -12 lead ECG Doppler color flow
studies
CXR /fluoroscopy
Cardiac CT /MRI
TMT
Coronary
Radionuclide angiography
perfusion studies Blood chemistry
(thallium 201 ) Blood sugar ,lipid
2D Echo profile
 ECG in angina
Normal ECG does not rule out IHD
ST Segment depression ,t wave inversion are
usual features
ST elevation prinzmetal angina /early MI
Stress ECG ST depression > 1 mm for > 0.08
seconds is significant
 Management Non pharmacological
Patient education risk factors
Weight reduction
Smoking cessation
Moderation in alcohol intake
Avoid /decrease stress/anxiety
Regular exercise 30 minutes /day
Control comorbid conditions ( eg DM )
 Management pharmacological
Treat hyperlipidemia
Diet /exercise /drugs Statins
Goal TC <200 mg% ,LDL-C < 100 mg%
Treat hypertension Anti hypertensive drugs
Goal - < 140/90 mmHg
Cardioprotection Antiplatelet drugs
Aspirin 75-325 mg OD
Clopidogrel 75 mg od
 Antianginal drugs
Nitrates to relieve symptoms
Beta blockers to reduce ischemia
CCBs to decrease coronary spasm
ACEi for cardiac remodelling .Used in CAD
with LV dysfunction
 Nitrates in angina
Used in emergency /prophylaxis /maintenance
Cause systemic venodilatation and dilatation of
epicardial arteries decrease pre/post load of LV
and redistribute blood flow to ischemic
subendocardium
Nitrates decrease cardiac workload /o2 demand
Routes S/l ,oral ,transdermal patch ,spray
Anginal attack s/l (2-3 min) or spray and repeat
Side effects Headache ,dizziness ,flushing
,hypotension and tolerance
 Beta blockers in angina

Block beta 1 adrenoceptors in heart

Negative inotropic ,negative chronotropic
Decreases HR ,increases diastolic perfusion ,increases
LV perfusion and decreases Myocardial oxygen demand
Adverse effects Bradycardia ,Hypotension ,Impotence
,bronchospasm, dyslipidemia
Contraindications Heart blocks ,vasospastic angina
,severe bronchospasm ,Severe CCF
Used as antianginal /antiarrhythmic/anti HTN drugs
 CCBs in angina
Block calcium entry into vascular smooth cells
Resulting decrease contraction of muscle cells
Decrease coronary resistance ,increased coronary
blood flow (vasodilatation )
Acts through 4 channels L ,T (heart) ,N ,P (CNS)
Preffered in prinzmetal angina (diltiazem)
Side effects hypotension ,flushing
,headache,dizziness ,pedal edema
Preffered in beta blocker failure cases
 Other drugs in angina
ACEI indicated in CAD with DM /previous MI
/CCF : decrease preload
K channel activator Nicorandil increase
coronary blood flow by dilatation of coronary
arteries 5 mg tid
Ranolazine fatty acid oxidation inhibitor ,CHO
oxidation increases ,More oxygen efficient
Antioxidants Vitamin A ,C , E- role unclear
IV vascular endothelial growth factor (VEGF) and
basic fibroblast GF ( bFgF) proteins increases
coronary blood flow in animal models
 PTCA in angina
Angina with 2 or 3 vessel disease
Angina with proximal LAD blocks
Symptomatic angina with anatomy that is
suitable for catheter based therapy
PCI is no better than medical line of
treatment
 CABG in angina
Angina with 2 or 3 vessel disease
Angina with proximal LAD CAD
Refractory /highly symptomatic angina
Surgical techniques Internal mammary
artery grafts
CABG is better than PTCA and medical line of
treatment ( improve survival ,less recurrence )
 Complications of stable angina
Unstable angina
Acute MI
SCD
Cardiac arrhythmias
Sudden CCF
 Unstable angina (UA)
Other names

Intermediate coronary syndrome

Pre infarct Angina
Acute coronary syndrome /insufficiency
Status Angiosis
Crescendo Angina
Preocclusive /prethrombotic syndrome
Threatening MI
Accelerated Angina
 Symptom complex of UA
Severe frequent angina of new onset (> 3
attacks /day in last 3-6 months )
Crescendo angina -angina in frequency
/intensity /symptoms
Angina at rest
 Pathophysiology of UA
Plaque rupture
Thrombus formation
Vasospasm
Multiple lesions
Secondary causes - myocardial demand
(hyperthyroidism ,fever ,sepsis ,tachycardia
,gross anemia )
 Diagnosis of UA
Prolonged angina at rest
ECG ST and T ,transient ST elevation
Cardiac enzymes not elevated
Poor response to S/L nitroglycerine
 DD for unstable angina
Acute MI
Acute pulmonary embolism
Costochondritis
Pneumothorax
HTN emergency \urgency
Pericarditis
Severe systemic infection
 UA vs Acute Mi
Difficult to differentiate UA aand NSTEMI
Cardiac enzymes are markedly raised in
NSTEMI and normal in UA
20% NSTEMI have Normal ECG but have
cardiac enzymes
 Treatment of UA
Antiplatelet agents aspirin + clopidogrel
Antianginals Nitrates ,Beta blockers
Antithrombotics heparin /LMWH
Glycoprotein 2B /3A inhibitors in patients
undergoing early PCI
 Advantages of LMWH
Increased Bioavailability
Fixed dose regimen
More effective thrombin inhibition
chances of heparin induced
thrombocytopenia
cost
PTT levels do not have to be monitored
 Glycoprotein 2b/3a inhibitors
Platelet glycoprotein 2b/3a inhibitors inhibit
platelet aggregation and decrease thrombus
formation
Abciximab murine monoclonal antibodies
Eptifibatide peptide from snake venom
Trofiban ,lamifiban non peptide inhibitors
Used IV in patients undergoing PCI
Oral glycoprotein inhibitors not effective
 Imp points In UA
Mimic acute MI ( STEMI /NSTEMI )
Treat like MI ( ICCU care )
Cardiac enzymes normal
IV heparin /LMWH highly effective
Early PCI beneficial
 Flowchart for management of UA
Unstable angina

Hospitalisation
Medical line of treatment

Pain decreases Pain increases

Coronary angiography

Minimal /NCCP Left Main CA

1 VD 2 VD
3 VD
Medical CABG
/PTCA
 Variant ( prinzmetal angina )
Angina at rest
Not precipitated by stress
Associated with ST elevation
Maybe associated with AMI
Mechanism usually focal coronary artery
spasm
Hypercontractility of arterial wall in
atherosclerotic process present
 continued
Provocative test for diagnosis ergotamine
maleate test sensitive / specific test
Responds to nitrates S/l ,IV
Calcium blockers and alpha blockers effective
Beta blockers less useful
In severe cases -PTCA
 Syndrome -X
Typical exertional angina with angiographically
normal coronary arteries
Usually a presumptive diagnosis of exclusion
Female predominant (3 : 1) ,> post menopausal
group
Mechanism endothelial dysfunction
/microvascular ischemia / sympathetic tone /
pain perception /spasm
Lifestyle modification ,CCBs and nitrates
Prognosis same as general population
 Silent ischemia
Asymptomatic patients with documentary
evidence of ischemia in ECG ,Ambulatory ECG
,Nuclear scintigraphy and 2D echo
Exact mechanism unknown
Abnormality in perception of cardiac pain
,autonomic neuropathy etc
Nitrates+ CCBs + beta blockers (metoprolol )
tried
Prognosis same as symptomatic CAD