IHD By Dr G vamsi krishna SR dept.Of GM.

Ischemic heart disease

1. ISCHEMIC HEART DISEASE
DR. GADDE VAMSI KRISHNA
SENIOR RESIDENT
DEPARTMENT OF GENERAL MEDICINE
[email protected]

2. DEFINITION
•Ischemicheartdiseaseisagroupofheartdiseasesinwhichthereisan
imbalancebetweenmyocardialbloodsupplyanditsoxygendemand.
IHDistheleadingcauseofdeathinbothmalesandfemales.

3. RIGHT VENTRICLE vs LEFT VENTRICLE
WHICH IS MORE INVOLVED IN IHD?

4. CLINICO-PATHOLOGICAL SPECTRUM
•Ischemicheartdisease(IHD)formsaclinico-pathologicalspectrumof
diseasesandconsistsofstableanginaandacutecoronarysyndromes
(includesSTEMI,NSTEMIandunstableangina).

5. ETIOLOGY
•Coronaryarterialocclusionisthemaincauseofmyocardialischemia
mostlyduetocoronaryatherosclerosisanditscomplications.
Coronaryatherosclerosisnarrowsoneormoreoftheepicardial
coronaryarteries→decreasesthecoronarybloodflowinabout90%
ofcases.Hence,IHDisoftenknownascoronaryarterydisease(CAD)
orcoronaryheartdisease.
•Otherrarecauses:Emboli,vasculitis,coronaryvasospasm,
hematologicdisorderslikesicklecelldisease,diminishedavailability
ofbloodoroxygen(loweredsystemicbloodpressureasinshock).

6. ATHEROSCLEROSIS
Atherosclerosis is a progressive inflammatory disorder of the arteries characterized by
focal deposits of lipids in the intima.

7. SEQUENTIALCHANGES LEADING TO CAD

8. STABLE VS UNSTABLE PLAQUE

9. COMPLICATIONS OF ATHEROMATOUS PLAQUE
Rupture, ulceration, or erosion: Plaque protrudes into the lumen and can
disturb the blood flow → resulting in turbulent flow of blood → which can
damage the endothelium → cause rupture, ulceration or erosion of the
intimal surface of plaques.
Hemorrhage into a plaque: It may occur due to rupture of the fibrous cap
of the plaque or of the thin-walled vessels formed due to neovascularization.

10. COMPLICATIONS OF ATHEROMATOUS PLAQUE
Thrombosis and embolism: Ulceration/erosion/rupture of endothelial
surface → exposes the blood to highly thrombogenic subendothelial collagen
→ favors thrombus formation → can partially or completely occlude the
lumen (depending on the size of the lumen) → lead to ischemia. The
thrombus may become organized or fragment to form thromboemboli.
Atheroembolism: Plaque rupture → discharge atherosclerotic debris into the
bloodstream → results in atheroemboli.
Aneurysm formation: Atherosclerosis even though an intimal disease may
cause pressure or ischemic atrophy of the underlying media. It may also
damage the elastic tissue and cause weakening the wall → result in
aneurysmal dilation → which may rupture.
Calcification: It may occur in the central necrotic area of the plaque
(dystrophic calcification).

11. PATHOPHYSIOLOGY OF IHD

12. ANGINA PECTORIS
Angina pectoris is a clinical syndrome that presents as paroxysmal and
recurrent attacks of substernal or precordial chest discomfort due to
transient myocardial ischemia, which falls short of inducing necrosis of
myocardial cell.
Cause: Transient myocardial ischemia is due to:
(1) Obstruction of coronary flow by atherosclerosis,
(2) Coronary arterial spasm or
(3) Thrombosis of coronary artery.
(4) Others include embolus, coronary ostial stenosis, and coronary
arteritis (e.g. in SLE).

13. FACTORS PRECIPITATING ANGINA

14. STABLE ANGINA
•Coronary atherosclerosis reduces the lumen of the coronary arteries. It
cannot increases in perfusion when the demand for flow is increased
(e.g. during exertion or excitement). This leads to a situation where
when the demand for blood flow is increased (e.g. during exertion or
excitement), there cannot be a corresponding increase in perfusion due
to the atheroma.
•In stable angina is due to transient myocardial ischemia. Stable angina
shows a fixed reduction of at least 70% in the diameter of coronary
arteries which causes reduction in coronary blood flow. Inability to
increase oxygen extraction or reduced coronary blood flow, together
with increased myocardial demand, leads to angina.

15. STABLE ANGINA
Diagnosis of angina is mainly depends on the clinical history.
Classical or stable or exertional angina pectoris is characterized by:
•Chest pain: Constricting discomfort / squeezing / tightening /
heaviness / aching in the front of the chest. Pain may radiate to
left arm, neck (throat), jaw (chin) or less commonly to right arm,
back, and epigastrium. Typical chest pain lasting 2–5 minutes.
Levine’s sign (clenched fist held over the chest) may be positive.
•Brought on by physical exertion, such as after meals and in cold,
windy weather or by anger or excitement/emotion.
•Relieved (usually within minutes) with rest or sublingual glyceryl
trinitrate. Occasionally, it may disappear with continued exertion
(‘walking through the pain’). Pain seldom lasts > 20 minutes.

16. TYPICAL VS ATYPICAL CHEST PAIN

17. DIFFERENTIALS OF CHEST PAIN

18. TYPES OF ANGINA
•Stable angina
•Unstable angina
•Variant (Prinzmetal’s/vasospastic) angina
•Refractory angina: Patients with severe coronary disease in whom
revascularization is not possible and angina is not controlled by medical
therapy.
•Nocturnal angina: Unusual form of angina that develops in aortic
regurgitation especially syphilitic. It is characterized by paroxysmal,
nocturnal angina pains accompanied by nightmares, dyspnea, palpitations,
skin flushing, profuse sweating and wide pulse pressure. It does not relieved
by sublingual nitroglycerine.

19. TYPES OF ANGINA
•Angina decubitus: Pain develops while lying flat (raises end-diastolic left
ventricular volume, myocardial wall tension and hence oxygen demand).
•Cardiac syndrome X (microvascular angina): These patients have
angina-like pain, a positive exercise test and angiographically normal
coronary arteries. They form a heterogeneous group. It occurs in patients
with metabolic syndrome and is more common in women. This type has a
good prognosis. Response to nitrates is less reliable and they are difficult to
treat. The myocardium shows an abnormal metabolic response to stress,
indicating that the myocardial ischemia probably results from abnormal
dilator responses of the coronary microvasculature to stress. About 1% die
and 0.6% suffer a stroke within 1 year after their first hospital admission.

20. TYPES OF ANGINA
•Status anginosus: Frequent, recurrent, sustained angina refractory to usual
treatment.
•Walk-through angina: Angina with effort that disappears gradually during
activity that is sustained (although usually at reduced intensity) and after which
improved exercise tolerance results.
•Second-wind angina: A brief rest after an initial attack results in a markedly
improved threshold free from angina. A synonym is “warm-up” angina.
•Caudal angina: Angina symptoms occurring in the scalp or head via referred
pain.
•Silent angina: Objective manifestations of ischemia without symptoms.
•Angina equivalents: Symptoms other than pain or discomfort that are ischemic
related and serve as angina surrogates, e.g. dyspnea, diaphoresis, fatigue, or light-
headedness.

21. FUNCTIONAL CLASSIFICATION OF ANGINA

22. FUNCTIONAL CLASSIFICATION OF ANGINA

23. INVESTIGATIONS

24. INVESTIGATIONS

25. TREATMENT

26. TREATMENT

27. TREATMENT
It is conventional to start therapy with low-dose aspirin, a statin, sublingual GTN and a β-
blocker. If needed later add a calcium channel antagonist or a long-acting nitrate.

28. TREATMENT

29. VARIANT/PRINZMETAL ANGINA
•In 1959 Prinzmetal et al. described a syndrome of severe ischemic
pain that usually occurs at rest and is associated with transient ST-
segment elevation.
•Etiology: Focal spasm of an epicardial coronary artery is the cause of
Prinzmetal’s variant angina (PVA) and leads to severe transient
myocardial ischemia and occasionally infarction.
•The cause of the spasm is not well defined, but it may be related to
hypercontractility of vascular smooth muscle due to adrenergic
vasoconstrictors, leukotrienes, or serotonin.

30. Clinical Features:
•Pain occurs without exertion and usually at rest. It is more frequent in women.
•Associated with migraine, Raynaud’s phenomenon and aspirin-induced asthma.
Younger patients with history of cigarette smoking.
Investigation:
•Characteristically, it is associated with transient ST segment elevation on the ECG
during the pain.
•Coronary angiography is gold standard for diagnosis. Focal spasm commonly
accompanied by stenosis within 1 cm of spasm is the hallmark (most commonly in
right coronary artery).
•Provocation tests (e.g. hyperventilation, cold pressor testing or ergometrine or
intracoronary acetylcholine challenge) may be needed for demonstration of focal
spasm and establishing the diagnosis.
VARIANT/PRINZMETAL ANGINA

31. Management:
•Nitrates and calcium channel blockers are the main therapeutic agents.
•Aspirin may actually increase the severity of ischemic episodes,
possibly as a result of the sensitivity of coronary tone to modest
changes in the synthesis of prostacyclin.
•The response to β-blockers is variable but usually poor.
•Prazosin can be useful.
•Coronary revascularization may be helpful in patients with discrete,
flow-limiting, proximal fixed obstructive lesions.
Prognosis is usually better than those with fixed, significant obstructive
lesions.
VARIANT/PRINZMETAL ANGINA

32. ACUTE CORONARY SYNDROME
Acute coronary syndrome (ACS) is a term used for spectrum of clinical
presentations due to acute myocardial ischemia. It includes:
•ST elevation myocardial infarction (STEMI): Majority of STEMI has Q-
wave MI (QwMI).
•Non ST elevation myocardial infarction (NSTEMI): A small percentage of
STEMI and majority of NSTEMI have non- Q-wave MI (NQwMI,
previously known as subendocardial infarction). However, the terms Q-
wave or non Q-wave infarctions are not used at present.
•Unstable angina (UA): Includes patients with acute coronary syndrome but
with normal ECG, without elevation of cardiac injury markers and no ST
elevation in the ECG. Management of unstable angina and NSTEMI is
similar.

33. SPECTRUM OF ACS
•UNSTABLE ANGINA
•NSTEMI
•STEMI

34. NSTEMI
•Non-ST elevation MI (STEMI):
•It is usually shows ST depression and T inversion in the ECG along
with elevation in serum troponins or CKMB.
•Myocardial function (as shown by ejection fraction) in NSTEMI is
less deranged when compared to STEMI. However, in NSTEMI early
as well as late reinfarction rates are higher than in STEMI.

35. UNSTABLE ANGINA
Three principal presentations of unstable angina include:
•Rest angina: Angina occurring at rest and prolonged, usually >20 minutes.
•New-onset angina: New-onset angina of at least CCS Class III severity.
•Increasing angina: Previously diagnosed angina that has become distinctly
more frequent, longer in duration, or lower in threshold (i.e. increased by >1
CCS) class to at least CCS Class III severity.
Normal ECG (no ST elevation), without elevation of cardiac injury markers
(normal level of cardiac enzymes).
Patients with UA have a high risk of developing MI or sudden death when
compared to patients with stable angina. Thus, they need aggressive treatment
in the hospital.

36. RISK CATEGORIES AND MANAGEMENT IN NSTEMI/UA

37. STEMI
•Type 1: Spontaneous myocardial infarction with ischemia due to a primary
coronary event, e.g. plaque erosion/rupture, fissuring or dissection
•Type 2: Myocardial oxygen demand supply mismatch, i.e. secondary to ischemia
due to increased oxygen demand or decreased supply (e.g. coronary spasm,
coronary embolism, anemia, arrhythmias, hypertension, or hypotension).
•Type 3: Diagnosis of MI resulting in sudden cardiac death.
•Type 4: MI after percutaneous coronary intervention (PCI)—post PCI related.
•Type 5: MI after coronary artery bypass graft (CABG)—post CABG.
Transmural infarct is an infarct that involves the full thickness of myocardium.
Sub endocardial infarct is an infarct which involves subendocardial region.
However, these terms are no longer used. Silent infarct is infarct without symptoms
but with only ECG changes.

38. CLINICAL FEATURES OF ACS

39. COMPLICATIONS OF MI

40. INVESTIGATIONS

41. CORONARY ANATOMY & ECG LEADS

42. CARDIAC ENZYMES

43. MANAGEMENT

44. MANAGEMENT
Initial treatment:
•Admit in intensive coronary care unit, attach a cardiac monitor and secure an
intravenous line.
General treatment (‘M O N A C’):
•Morphine 2–4 mg q 5–10 minute to control chest pain.
•Oxygen 4 L/minute: Hypoxemia in uncomplicated MI is usually due to
ventilation-perfusion abnormalities and may be exacerbated by CHF. Therefore,
oxygen is given to patients suspected of having an acute coronary syndromes and
oxygen saturation <90%.
•NTG (nitroglycerine) sublingual or spray, followed by infusion for persistent chest
pain.
•Aspirin 160–325 mg chew and swallow or/and
•Clopidogrel 300 mg oral

45. Confirm diagnosis:
•By investigations namely: Electrocardiogram (ECG), 2D ECHO, Plasma
cardiac biomarkers: Troponin T or I and CK-MB.
Specific therapy:
•Thrombolysis or percutaneous coronary interventions.
•β-blockers unless contraindicated.
•Treat complications (arrhythmias, congestive failure and shock).
•Control of pain by analgesics
•Proper control of pain is necessary not only to relieve distress but also to
lower adrenergic drive which reduces vascular resistance, BP, infarct size
and susceptibility to ventricular arrhythmias.
MANAGEMENT

46. MANAGEMENT
•Intravenous opiates: Initially, morphine in the dose of 2–4 mg or
diamorphine 2.5–5 mg is administered along with antiemetics
(metoclopramide 10 mg) should be administered, and repeated until the
patient is comfortable. β-blockers, nitroglycerine and thrombolysis may also
help in reducing the pain.
•Anti-anginal therapy
•Anti-thrombotic therapy
•Anti-coagulant therapy
•Statins
•Thrombolysis or percutaneous coronary interventions.

47. MANAGEMENT

48. MANAGEMENT
Anticoagulants (antithrombin therapy):
Prophylactic anticoagulants are given to prevent deep vein thrombosis and
pulmonary embolism in patients who do not receive fibrinolytic agents. They
reduce the risk of thromboembolic complications, and prevent re-infarction in
the absence of reperfusion therapy or after successful thrombolysis.
•Unfractionated heparin
•Low molecular weight heparin
•Direct thrombin inhibitors
Antithrombin preparations should be continued for at least 48 hours and
preferably for 8 days or till discharge or coronary revascularization.

49. MANAGEMENT
Statins:
•High-dose statins are recommended in all patients during the first 24 hours of admission
for STEMI, irrespective of the patient’s cholesterol concentration, if there is no
contraindications (e.g. allergy, active liver disease). They are recommended during the
early phase of therapy up to at least four weeks. Patient on statin therapy presenting with
STEMI should continue statin.
Advantages:
•Lowers cholesterol, direct effects on endothelial function, oxidative stress, inflammation,
thrombosis as well as plaque stabilization. High dose atorvastatin (40-80 mg) or
rosuvastatin (20-40 mg) therapy before emergency percutaneous coronary intervention
has following advantages:
•Reduce periprocedural inflammatory response
•Reduce myocardial dysfunction
•Prevent contrast-induced nephropathy.

50. REPERFUSION THERAPY
Reperfusion options for STEMI
Fibrinolysis:
It is usually preferred in the following situations:
Early presentation (≤3 hours from symptom of onset) in patients where
primary PCI cannot done because of the following:
Catheterization laboratory occupied/unavailable
Vascular access difficulties
Lack of access to a skilled PCI laboratory– Delay to primary PCI
Door-to-balloon time minus door-to-needle time is >1 hour.
Door-to-balloon time is >90 minutes.

51. REPERFUSION THERAPY: THROMBOLYSIS
INDICATIONS:

52. REPERFUSION THERAPY: THROMBOLYTIC DRUGS

53. SIGNS OF REPERFUSION:
TIMI GRADING:
REPERFUSION THERAPY: THROMBOLYSIS

54. REPERFUSION THERAPY: THROMBOLYSIS
CONTRAINDICATIONS:

55. REPERFUSION THERAPY: PCI
Types of stents:
Two types namely (1) bare-metal stents and (2) drug-eluting stents. The drug eluting stents are coated
stents lined with substances (e.g. sirolimus and pacliltaxel) that prevent neo-intimal hyperplasia and
reduce the risk of coronary artery re-occlusion.

56. REPERFUSION THERAPY: PCI
Primary PCI:
In which PCI is used solely in acute MI.
It is indicated in cardiogenic shock, and in patients in whom thrombolytic therapy is
contraindicated.
It is generally preferred with following conditions:
Skilled PCI laboratory is available with good surgical backup.
Door-to-balloon time is ≤90 minutes.
Door-to-balloon time minus door-to-needle time is ≤1 hour.
High-risk STEMI
Cardiogenic shock: Killip class CHF ≥3
Contraindications to fibrinolysis including increased risk of bleeding and intracranial
hemorrhage.
Late presentation (>3 hours after symptom of onset).

57. REPERFUSION THERAPY: PCI
Rescue PCI:
•It is combination of PCI with thrombolytic therapy and PCI is performed within 12 after
failed thrombolysis/fibrinolysis for patients with continuing or recurrent myocardial
ischemia. Indications: STEMI in aged <75 years who received fibrinolytic therapy and
have cardiogenic shock, severe congestive heart failure (Killip class III) or
hemodynamically compromising ventricular arrhythmias. May be performed in patients
with symptoms of persistent ischemia.
Facilitated PCI:
•In this type PCI is done following initial pharmacological regimen aimed at improving
patency of coronary arteries before PCI. The pharmacological regimens include GB
IIB/IIIa inhibitors, full-dose or reduced-dose of fibrinolytic therapy, and combination of a
GP IIb/IIIa inhibitor and a reduced-dose fibrinolytic/thrombolytic agent. However, this
type of re-perfusion may be inferior to thrombolysis alone or primary PCI and is usually
not recommended in most patients with STEMI.

58. REPERFUSION THERAPY: CABG
Coronary artery bypass grafting:
•Recommended in failed PCI with persistent pain or hemodynamic instability in
patients with coronary anatomy suitable for surgery. Persistent or recurrent
ischemia refractory to medical therapy in patients who have coronary anatomy
suitable for surgery, and are not candidates for PCI or fibrinolytic therapy. Patients
with STEMI at the time of operative repair of mechanical defects.

59. REPERFUSION THERAPY: CABG
•In coronary artery bypass grafting, autologous veins (reversed
segments of the patient’s own saphenous vein) or arteries (internal
mammary artery/radial artery/gastroepiploic arteries) are anastomosed
to the ascending aorta at one end and to the native coronary arteries
distal to the area of occlusion/stenosis at the other end.
•Usually done under cardiopulmonary bypass but, in few cases, it can
be done in the beating heart (‘off-pump’ surgery). Aspirin (75–150 mg
daily) and clopidogrel (75 mg daily) both improve graft patency, and
one or other should be given indefinitely.

60. REPERFUSION THERAPY: CABG
Indications:
•Significant left main coronary disease.
•Triple vessel disease/two blood vessel disease with reduced left
ventricular function (left ventricular ejection fraction is <50%).
•Two vessel disease with significant proximal left anterior descending
artery disease and either LVEF <50% or demonstrable ischemic on
noninvasive testing.
•Failure of medical therapy and with acceptable risk for CABG.
•Prior CABG, PCI (percutaneous coronary interventions) with
recurrent restenosis

61. MANAGEMENT OF COMPLICATIONS
Ventricular dysfunction:
After STEMI ventricular remodeling occurs, ventricular dysfunction can be prevented by
ACE inhibitors and nitrates.
Killip classification of ventricular dysfunction. This classification has prognostic value with
highest mortality in class IV patients.
Cardiogenic shock:
This results when there is infarction of ≥40% of left ventricle. The patient has systolic BP
<90 mm Hg and pulmonary capillary wedge pressure >18 mm Hg.– Cardiogenic shock is
best managed by invasive means (Primary PCI). Use of intra-aortic balloon pump and IV
vasopressors may be beneficial.

62. MANAGEMENT OF COMPLICATIONS
Right ventricular infarction:
•Clinically significant right ventricular infarction is rare and occurs in patients with
inferior infarction.– ST elevation in V4R is common in first 24 hours.
•Signs of severe right ventricular failure: These include jugular vinous distension,
Kussmaul’s sign, hepatomegaly, with hypotension.
•Investigation: 2-D echocardiography is useful for diagnosis and assessment of
severity.
•Treatment: Volume expansion to maintain adequate right ventricular preload.
•Avoid use of diuretics, ACE inhibitors and nitrates. Inotropics and vasodilators
may be needed when a significant left ventricular dysfunction is also present.
Routinely considered for re-perfusion therapy (fibrinolysis or PCI).

63. MANAGEMENT OF COMPLICATIONS
Pericarditis:
•Common complication in first week of transmural myocardial infarct.
•Radiation of pain to trapezius muscle is helpful in distinguishing it from
ischemia.
•Pericardial rub may be present.
•Treatment: Aspirin 650 mg qid and withhold anticoagulants.
Management of other complications:
These include (1) thromboembolism, (2) left ventricular aneurysm, (3) sinus
bradycardia, (4) AV block, (5) ventricular tachycardia and fibrillation and
acute mitral regurgitation, VSR and tricuspid regurgitation.

64. AFTERCARE AND REHABILITATION
•Physical activities: To be restricted for 4–6 weeks because
replacement of infarct by fibrous tissue takes 4–6 weeks. Advised
gradual mobilization and return to work over 6 weeks. Exercise and
sexual activity within the limits.
•Patients who had complications, the regimen depends on the type of
complication.
•Lifestyle and risk factor modification: Control of risk factors such
as obesity by regular exercises, cessation of smoking, lifestyle
modifications and control of plasma lipids by diets and drugs.

65. THANK YOU
TO BE CONTINUED
LET’S DISCUSS HEART FAILURE IN NEXT CLASS