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ISCHEMIC HEART

DISEASE
Definition
• " Ischaemia " refers to an insufficient amount of blood. The
coronary arteries are the only source of blood for the heart muscle.
If this coronary arteries are blocked, the blood supply will reduce.
Physiology of coronary circulation
• Heart is supplied by two major coronary arteries,
originating from the aortic root

• Major branches of coronary arteries lie on the epicardial


surface of the heart so the direction of perfusion is from
epicardium to endocardium. Subendocardial layers of the
LV are most susceptible to ischemia

• Coronary ostia are being blocked while valve opens – no


coronary blood flow during systole

• During diastole blood is forced into coronary arteries.


Driving force of coronary perfusion is diastolic blood
pressure. Heart rate determines the duration of diastole:
the lower the HR the longer the duration of coronary
perfusion
Determinants of myocardial metabolic needs and
myocardial blood supply

Needs Supply
• Systolic BP • Diameter of coronary artery
• Heart rate • Blood O2 capacity – Hb
• Myocardial contractility and thickness concentration, oxygen concentration
• Myocardial wall stress
Main features of stable ischemic heart disease
DIAGNOSIS
Historical description of angina

This is a disorder of the breast, marked with strong and peculiar symptoms,
considerable for the kind of danger belonging to it . . . .The seat of it, and sense of
strangling and anxiety with which it is attended, may make it not improperly called
angina pectoris . . . .Those who are afflicted with it are seized . . . with a painful
and most disagreeable sensation in the breast, which seems as if it would take
their life away, if it were to increase or continue . . . . When a fit of this sort comes
on by walking, its duration is very short, as it goes off almost immediately upon
stopping. If it comes on in the night, it will last an hour or two.

William Heberden 1768


Angina Pectoris
• location – retrosternal with radiation to the neck,
shoulders, arms, jaw, epigastrium
• triggers – exercise, stress, cold, heavy meal,
smoking
• character
• vague discomfort, squeezing, burning, tight, choking,
heavy, cold sensation
• equivalents – dyspnea, fatigue, weakness,
lightheadedness, nausea, sweating, syncope
• duration
• tyoically 3-5 minutes
• > 20 minutes – myocardial infarction, noncardiac
• < 1 minute - noncardiac

11
Location and radiation of anginal pain
Chest pain (angina)
Clinical classification of chest pain
• Weak relationship between severity of pain and degree of oxygen supply-
there can be severe pain with minimal disruption of oxygen supply or no pain
in severe cases

• Four types:
 Stable angina
 Unstable angina
 Microvascular angina
 Prinzmetal’s angina
Stable angina

•Also called “Exercise angina”


•Discomfort is precipitated by activity
•Minimal or no symptoms at rest
•Symptoms disappear after rest/cessation of activity
• The pain and pattern of events is unchanged over a period of
time (months  years)
Classification and Severity of Angina
(Canadian Cardiovascular Society)
Unstable angina

• Acute coronary syndrome in which angina worsens


• May occur at rest
• Severe and of acute onset
• Crescendo pain - pain increases over time (duration, frequency), no
longer relieved by nitroglycerin
Microvascular angina

• Cause unknown
• Possible mechanisms
• endothelial dysfunction
• microvascular ischemia
• abnormal pain perception
• Angina, positive stress test, normal coronary arteries (at angiography)
• Good prognosis
Prinzmetal’s (variant) angina

• Prinzmetal’s angina is a variant form of angina with normal


coronary vessels or minimal atherosclerosis
• Usually occurs during the night (at same time)
• Longer duration, more difficult relieved ny nitroglycerin
• It is caused by spasm of coronary artery
• ECG – transient ST elevation
Differential diagnosis
Clinical examination
 Signs suggesting CAD (only present during chest pain)
S3 or S4 gallop, mitral regurgitation murmur, bibasilar rales,
high/low BP
 Signs of noncoronary atherosclerotic vascular disease
Carotid bruit, diminished / absent pedal pulses, abdominal
aneurysms
 Xanthelasma and xanthomas: hyperlipidemias
 Nicotin stain (tip of the fingers)
Investigations
 ECG
 may be normal in the absence of pain (50-60%)
 ST depression (downsloping, horizontal)
 T waves – negative, tall positive
 old myocardial infarction – Q wave
 Chest X-ray
 If no obvious noncardiac cause of chest pain

 Echocardiography
 Exclusion of alternative causes of angina
 Identification of regional wall motion abnormalities
 Measurement of LV ejection fraction
 Evaluation of diastolic function
Laboratory
• cardiac enzymes – troponin, CK-MB
• hemoglobin, hematocrit, WBC, platelets
• lipid profile – cholesterol, triglycerides, HDL-cholesterol, LDL-
cholesterol
• glycemia
• creatinine
Clinical pretest probability in patients with
chest pain
Stress testing
• Methods to induce ischemia
• exercise
• pharmacological – dobutamine, adenosine, dypiridamole

• Methods to assess ischemia


• ECG
• echocardiography
• radionuclide imaging (SPECT, PET)
Exercise ECG
• most commonly used noninvasive procedure for evaluationg inducible
ischemia
• may be combined with imaging (echo, nuclear)
• on treadmill or bicycle ergometer
• at least 85% of maximal heart rate (220 – age) to be conclusive
• positive if
• angina
• ST depression > 1 mm (downsloping or horizontal), 2 mm (upsloping)
• ST elevation > 1 mm
• BP decrease
• ventricular arrhythmias
• new LBBB
Other tests

 If exercise ECG can’t be interpreted / performed:


 If due to left bundle branch block: Pharmacologic stress test with imaging (radionuclide perfusion of
myocardium / ECHO)
 If due to other abnormalities: Exercise stress test with imaging (radionuclide perfusion of
myocardium / ECHO)
 If patient can’t exercise: Pharmacologic stress test with imaging (radionuclide perfusion of
myocardium / ECHO)

 Coronary artery calcium score (CT):


 Low coronary artery calcium score identifies people w/o CAD
 High score is less reliable in ruling in CAD
Coronary angiography
Gold standard for diagnosis and risk stratification in chronic IHD.
Indications for coronary angiography:
• Class III-IV angina (disabling angina), especially despite optimal
treatment
• Prior myocardial infarction
• Prior ventricular fibrillation/resuscitated sudden cardiac death
• Positive exercise testing compatible with high risk
• Recurrence of angina after revascularization
From the angiography standpoint coronary lesions can be classified into:

• Single-vessel disease
• Two-vessel disease
• Multi-vessel disease
• Left main disease
Stable angina management
General measures

• Smoking cessation
• Weight loss, diet and physical activity
• Control of blood pressure and diabetes
Pharmacological treatment of stable angina

Drugs for prognosis improvement (prevention of MI and death)

• Low-dose (75-100 mg) aspirin


• Clopidogrel 75 mg/day - if intolerant to aspirin
• Statins (simva, atorva, rosuva) – LDL cholesterol < 70 mg/dl or
decrease > 50% from baseline
• ACE inhibitors in patients with hypertension, diabetes mellitus
or heart failure – ARB in patients with intolerance (cough)
• Beta-blockers in patients with prior MI
Pharmacological treatment of stable angina

Drugs for symptom relief (antianginal drugs)

Short-acting nitroglycerine (NG) – sublingual tablets or spray


• Mode of action:
• donator of NO → mostly venodilatation → ↓ return of blood to the heart → reduced
preload and pressure in ventricles → reduced myocardial oxygen needs, enhanced
subendocardial perfusion.
• vasodilatation of subepicardial vessels
• Onset of action – up to 1 minute, duration of action – up to 5
minutes.
• Daily multiple doses are safe.
Long-acting nitrates
• Extended-release NG (Nitromint 2.6 mg) – 2x daily
• Isosorbide dinitrate (Isodinit 20 mg): 2 -3 x daily
• Isosorbide-5-mononitrate (Mononitron 60 mg, Olicard 40 mg): 1 x daily
• Nitroderm patch (5-10 mg) – every 24 h (12 h free interval)
• Low oral bioavailability due to first passage effect (high inactivation in liver) – better
with extended release formulations
• Limitations - development of tolerance. In order to prevent tolerance allow at least
12-14 hours nitrate-free interval per day. Usually first dose of long-acting nitrates is
given in the morning, second – at 4 -5 pm (if needed), then no nitrates (except
short-acting NG on demand)
• Side effects – headache, hypotension, flushing
• Contraindications – association with PDE 5 inhibitors (sildenafil - Viagra) – risk of
severe hypotension
Beta-blockers
• First-line antianginal therapy
• Mode of action:
• negative chronotropic effect → ↓HR → prolonged diastolic perfusion time
(increased supply)
• negative inotropic effect → ↓contractility → decreased myocardial
metabolic needs
• ↓ SBP → ↓afterload → decreased myocardial metabolic needs
• ↑ tone of intact coronary arteries → “reversed steal” phenomenon
(increased flow in affected artery)
• Coronary vasospasm is rare from the ß2-receptor blocking effect, but use of b-
blockers should be avoided among patients with known, active vasospasm.
• All beta-blockers are equally effective in preventing anginal episodes
Calcium channel blockers
• Verapamil & Diltiazem
• Negative chrono- and inotropic effects
• Vasodilatation
• Combination with beta-blockers prohibited! (risk of profound bradycardia
and complete heart block)

• Dihydropiridines (amlodipine, felodipine)


• Mostly vasodilatation, less negative inotropic effect
• Useful in vasospastic angina
• Can be combined with beta-blockers
Ivabradine

• Selective negative chronotropic effect on the sinus node – reduces heart


rate
• No effect on BP, LV contractility and conduction
• May be first-line antianginal if beta-blocker is contraindicated
• Can be combined with any other antianginal
• Indicated in sinus rhythm if heart rate > 70 b/min
Trimetazidine (Preductal MR)
• Oral 3-ketoacylthiolaze (3-KAT) inhibitor
• 3-KAT activity is responsible for fatty acid oxidation in muscles
• Inhibition of 3-KAT switches metabolism from aerobic fatty acid
oxidation to anaerobic glycolysis, thus favorably influencing myocardial
O2 demands and ATP balance in cell.
• No effect on BP, HR, contractility and conduction
• Well tolerated, few side effects
• Usually added to other antianginals as a second-line therapy
Revascularization in angina
UNSTABLE ANGINA/
NSTEMI
Pathophysiology
• Plaque rupture
• exposes thrombogenic components stimulating platelet deposition, activation, and
aggregation followed by activation of the coagulation cascade and thrombus formation
• Thrombus formation
• Exposure of circulating platelets to subendothelial contents results in platelet adhesion,
aggregation, and, ultimately, thrombus formation. With platelet activation, the
glycoprotein (GP) IIb/IIIa receptor on the platelet surface undergoes a conformational
change, facilitating further platelet activation and aggregation. This markedly increases
thrombin production, further expanding and stabilizing the thrombus.
• Vasospasm
• can be induced by the local production of vasoactive substances released from the
subendothelial matrix or propagating thrombus or it can occur as a primary
phenomenon. Severe localized spasm of a coronary artery segment (Prinzmetal’s angina)
may also result in UA. This vasospasm frequently occurs at sites of unstable plaque and is
thought to contribute to thrombus formation. Even angiographically normal coronary
arteries with underlying endothelial dysfunction may be subject to vasospasm.
Pathophysiology

• Secondary causes
• increased demand – tachycardia, severe hypertension, cocaine use, hyperthyroidism,
fever
• decreased supply – anemia, hypoxemia
Historical definition

. . . sudden onset of one or more anginal attacks a day from a previous


background of good health or . . . a dramatic change in the symptomatic
pattern of previously recognized coronary disease . . . . In patients with
unstable angina, the attacks, in addition to being more frequent, are also
often of longer duration and may occur at rest without an apparent
precipitating event . . . . The electrocardiogram shows no evidence of recent
infarction, and such serum enzymes as the glutamic oxaloacetic
transaminase or the creatine phosphokinase show no diagnostic alterations

Fowler 1971
Classification
Diagnosis
• Angina
• at rest/minimal exertion
• recent onset/increased severity
• more severe and protracted – requires several doses of NTG or prolonged rest
• ECG changes
• ST depression > 0.5 mm
• T wave inversion
• new BBB
• ST elevation in aVR – possible left main stenosis or multivessel disease
• Normal serial cardiac enzymes (troponin, CK-MB)
• NSTEMI – increased cardiac enzymes
• Coronary angiography – indicated in all patients
TREATMENT
Antiplatelets – mechanism of action
Antiplatelets
• Aspirin – 150-300 mg chewed, followed by 75 – 100 mg daily
+
• Clopidogrel – loading dose 300-600 mg, followed by 75 mg/day, or
• Ticagrelor – loading dose 180 mg, followed by 2x90 mg/day, or
• Prasugrel – loading dose 60 mg, followed by 10 mg/day

• Duration of dual antiplatelet therapy = 12 months, then only aspirin


• Side effects
• clopidogrel – bleeding
• ticagrelor – dyspnea, bleeding, bradycardia
• prasugrel - bleeding
Anticoagulants – mechanisms of action
Anticoagulants

• Heparin (unfractionated)
• iv bolus 4000 u, followed by infusion 1000 u/h or 4000 u iv every 4 h
• monitoring for dosage adjustment – aPTT
• side effects – bleeding, thrombocytopenia
• Low molecular weight heparins (LMWH)
• Enoxaparin 1 mg/kg sc every 12 h
• Fondaparinux 2,5 mg sc once daily
• no monitoring is necessary
• Duration of therapy = 5-7 days
Antiischemic, secondary prevention
• Nitrates
• Nitroglyerin –
• sublingual up to 3 consecutive tablets
• iv infusion 10 – 100 µg/min
• Betablockers
• Calcium channel blockers
• ACE inhibitors
• High dose statins
• Atorvastatin 80 mg, Rosuvastatin 40 mg
Revascularization
• PCI + stenting (drug eluting stents, bare metal stents)
• CABG

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