2. OUTLINE
• definition
• anatomy
• epidemiology
• Scope of CHD and definitions
• Pathophysiology of CHD
• Diagnosis of CHD(stable, Acute coronary syndrome)
• Differential diagnoses of acute chest pain
• Complications of acute coronary syndrome
• Drugs for CHD(list and rationale)
• Immediate management of acute coronary syndrome
3. DEFINITION
• Is a condition in which there is an
inadequate supply of blood and oxygen to
a portion of the myocardium.
• Occurs when there is an imbalance
between myocardial oxygen supply and
demand
4. Anatomy of coronary arteries
The right coronary artery
Right atrium
Right ventricle
Parts of the left atrium and left
ventricle and the atrioventricular
septum.
Left coronary artery divides into
1.An anterior interventricular branch
->> right and left ventricles and anterior
part of the ventricular septum
2.A circumflex branch.
A. Left marginal artery is a large branch
that supplies the left margin of the left
ventricle down to the apex.
B. Anterior and posterior ventricular
branches supply the left ventricle.
C. Atrial branches supply the left atrium.
5. EPIDEMIOLOGY
World wide: 17million died of CVD particularly CAD/year.
Africa: 10%30%
2001; 8th cause of death in africa, how ever above 60’s is number 1
leading cause of death in men and number two in women after stroke.
2005; 361,000 death in africa
2030; 2X increase fold.
Uganda: Very low CAD prevalence rates were reported from Kenya and
Uganda.
In Uganda, 449 out of the 15 176 admissions in a 1-year period had CVD
and, of these, only three were considered to be CAD
in Kampala, electrocardiographic evidence of possible CAD was found in
only one of 412 villagers over the age of 45 years.
However CAD is believed to be on rise due to lifestyle changes
Sex: mortality Male>female
6. RISK FACTORS
Non- modifiable
• Age >50 yrs
• Sex male>female
• Family Hx( x2 in 1st degree relatives)
• Ethnic background south
asians>caucasions>blacks
7. RISK FACTORS Cont…
Modifiable
• Smoking
• High amounts of LDLs and cholesterol and low HDL
• Physical inactivity and obesity
• diabetes
• Air pollution( particulate matter)
• High blood pressure
• Alcohol intake
• Hypertension
• Metabolic syndrome
• Atherogenic diet
• Dyslipidemias
10. Pathophysiology
– Arteriosclerosis – natural changes in the intima,
connective tissue, and diameter of artery
– Atherosclerosis – pathologic phenomenon occurring in
the coronary, carotid, iliac, and femoral arteries as
well as the aorta (coronary artery disease)
Coronary blood flow also can be limited by spasm,
arterial thrombi, and, rarely, coronary emboli as well
as by ostial narrowing due to aortitis
11. The atherosclerotic process
Response to Injury hypothesis
- inflammatory response resulting in proliferation of
tissue within the arterial wall which may result in
obstruction of blood flow
Causes:
-elevated levels of cholesterol and triglyceride in
the blood,
-high blood pressure – turbulent blood flow
-tobacco smoke
-glycosylated substances
12. Pathophysiology contd.
Response to Injury Hypothesis
1. Injury to endothelium causing to platelets adhere
to endothelium then release of growth factors
2. Monocytes attach to endothelium and penetrate
(also LDL receptor activation) – monocytes become
macrophages and take up LDL and SMC’s
3. Smooth muscle cell proliferation and migrate from
medial to intimal layer
4. Foam cells are formed - migration to the intima
smooth muscles with lipids form fatty streaks
5. Fibromuscular plaque – fibromuscular layer with
cholesterol core
13.
14.
15. ANGINA
Stable angina(Exertional); episodic clinical syndrome
due to transient myocardia ischemia lasts 2-5min,
aggravated by exertion or emotion and relieved by
nitroglycerin or rest. substernal discomfort (Levine's
sign).
Prinzmental angina; a form of angina pectoris xterised
by pain not ppted by cardiac work, is longer in
duration, more severe and has unusual ECG finding(ST-
segment elevation) (transmural ischemia) and responds
to nitroglycerin and calcium-channel blocker
(vasodilator)
16. ANGINA contd..
Unstable angina; angina pectoris or equivalent ischaemic
discomfort with at rest/minimal exertion of >10minutes
or severe and new onset or crescendo pattern
Decubitus angina is that occurring on lying down. It
usually occurs in association with impaired LVF, as a
result of severe coronary artery disease.
Nocturnal angina occurs at night and may wake the
patient from sleep. It can be provoked by vivid dreams.
occurs in patients with critical coronary artery disease
and may be the result of vasospasm.
17. TREATMENT FOR ANGINA
Nitrates
Glyceryl trinitrate( GTN)
Isosorbide trinitrate
May b used alone in stable angina
BBs
Atenolol
CCBs
Verapamil
Potassium channel activators
Nicorandin
Cause both arterial and venous dilation
18. RISK STRATIFICATION FOR
DEVELOPING MI
High Risk Low Risk
Clinical Post infarct angina
Recurrent pain at
rest
Heart failure
No history of MI
Rapid resolution of
symptoms
ECG Arrhythmia
ST depression
Transient ST
elevation
Persistent deep T-
wave inversion
Minor or no ECG
changes
Biochemistry Troponin T>0.1g/l Troponin T<0.1g/l
19. MYOCARDIAL INFARCTION
Due to formation of occlusive thrombus at the site of rupture
or erosion of an artheromatous plaque in a coronary artery.
The thrombus undergoes lysis over the course of the next
few days, by this time irreversible damage has occurred.
Sudden death from VF or asystole may occur immediately
and many deaths occur within the 1st hr , if the pt survives
the most critical stage the liability to dangerous arrythmias
remains but diminishes as each hr passes by. Those who
survive may die of cardiac failure. The process of infarction
takes around 8 hours and therefore most patient present
when it is still possible to save myocardium.
20. MYOCARDIAL INFRACTION
NSTEMI; angina pectoris or equivalent ischemic discomfort at rest/
minimal exertion> 10minutes or severe and new onset or crescendo
pattern + elevated cardiac biomarkers and ST segment depression/t
wave inversion
STEMI; Sudden onset of severe retrosternal pain
Lasts more than 30 to 45 minutes
Not relieved by nitroglycerin
Radiates down the left arm into the shoulders or into the jaw or
epigastrium
Associated with sweating (diaphoresis), anxiety, and hypotension
"Silent" acute MIs
May occur in the elderly and in individuals with diabetes mellitus
Due to high pain threshold or problems with nervous system
21. Clinical features of MI
Symptoms
severe chest pain lasts longer than that due to angina
breathlessness,
collapse or syncope,
nausea and vomiting
anxiety and fear of impending death.
22. CLINICAL FEATURES Cont…
Signs
Signs of sympathetic activation; pallor sweating,
tachycardia
Signs of vagal activation; vomiting, bradycardia
Signs of impaired myocardial function; hypotension,
oliguria, narrow pulse pressure, raised JVP, 3rd heart
sound, quiet 1st HS, diffuse apical impulse, lung
crepitations
Signs of tissue damage; fever
Signs of complications; MR, pericarditis
23. Diagnosis of CHD
Stable angina
history,
physical examination(abdominal aortic aneurysm, carotid
arterial bruits, and diminished arterial pulses in the
lower extremities, xanthelasmas and xanthomas, blood
pressure, fundi exam, signs of anemia, thyroid disease,
and nicotine stains on the fingertips from cigarette
smoking, Palpation may reveal cardiac enlargement and
abnormal contraction of the cardiac impulse,
Auscultation can uncover arterial bruits, a third and/or
fourth heart sound, or apical systolic murmur),
lab exam(urine, blood for lipid profile, glucose,
creatinine, hematocrit or Hb, TFTs, CXR, CRP),
ECG,
25. ECG changes in MI
Zone of Ischemia: T wave inversion
Zone of Injury: ST elevation
Inferior wall MI: leads I, II, AVF
Anterior wall MI; all chest leads
Zone of Necrosis: Abnormal Q wave
Remember
STEMI
NSTEMI
27. Myocardial Infarction WHO Diagnosis
- Typical history
- ECG finding
- Raised biochemical markers
ECG findings;
I. Hyper acute T waves- this is the earliest sign, changes are
only present for 5-30 mins.
II. ST segment elevation follows- within the 1st few hrs of
symptom onset.
III.Diminution of the R wave
IV.Pathological Q waves within 1-2hrs and these act as a
permanent marker of myocardial necrosis
V. Resolution of changes; ST segment elevation diminishes over a
period of weeks, T waves inversion may persists for many
28. MI WHO Diagnosis Cont…
Plasma biochemical markers
- Creatinine kinase (CK) or CK-MB that rises 4-6hrs then
peaks at 12hrs and falls to normal after within 48-72
hrs.
- Cardiac troponins T and I released within 4-6 hrs and
remain elevated for up to 2 weeks.
Leukocytosis
Raised ESR
Raised C reactive protein
CXR; pulmonary edema with pre existing myocardial
damage.
Echocardiography to assess left and right ventricular
function
29. Differential diagnoses of acute chest
pain
CHEST WALL PAIN
Musculoskeletal pain
Isolated musculoskeletal chest pain
syndromes
Rheumatic diseases
Nonrheumatic systemic diseases
Skin and sensory nerves
CARDIAC CAUSES OF CHEST PAIN
Coronary heart disease
Aortic dissection
Valvular heart disease
Pericarditis
Myocarditis
Stress-induced cardiomyopathy
Cardiac syndrome X
Pheochromocytoma
GASTROINTESTINAL CAUSES OF CHEST PAIN
Gastroesophageal reflux disease
Esophageal hyperalgesia
Abnormal motility patterns and achalasia
Esophageal rupture, mediastinitis, and
foreign bodies
Medication-induced esophagitis
Other gastrointestinal causes of chest pain
PULMONARY CAUSES OF CHEST PAIN
Pulmonary vasculature
Acute pulmonary thromboembolism
Pulmonary hypertension and cor
pulmonale
Lung parenchyma-
Pneumonia
Cancer
Sarcoidosis
Pleura and pleural space
30. MANAGEMENT
The goals are to:
Relieve symptoms
Resolve risk factors in a bid to slow, stop, or
reverse plaque buildup
Lower the risk of blood clot formation
Widen or bypass clogged arteries
Prevent complications of CHD
Entails
Lifestyle changes
Drugs
Invasive treatment
31. MANAGEMENT Cont…
Lifestyle Changes
Diet aimed at controlling HTN & lowering
cholesterol
low cholesterol & salt
fiber, fruits and vegetables
Increase physical activity-@least 30mins daily
Quit smoking
Reduce alcohol intake to about 2-4 units daily
Learn to cope with and reduce stress.
32. MANAGEMENT Cont…
DRUGS
Anti-platelets
aspirin 75mg o.d, clopidogrel 75mg o.d (in pts with S/E to ASA)
M.O.A- Inhibit platelet aggregation by selective blockade of platelet
cyclooxygenase
S/E- bleeding
Anti- anginal drugs
1. Nitrates
- Sublingual glyceryl trinitrate 400-500µg, isosobide
dinitrate10-20mg 8hrly
- MOA- act directly on vascular smooth muscle to produce
venous and arteriolar dilatation
- S/E-severe headaches
33. TREATMENT Cont…
2. Beta blockers
- Atenolol 50-100mg od, metoprolol 50-200mg od,
larsoprolol 5-10mg od
- MOA- lower myocardial O2 demand by reducing HR, BP
and myocardial contractility
- S/E- bronchospasms.
3. Calcium antagonists
- Nifedipine 5-20mg 8hourly, Amlodipine 2.5-10mg od,
Verapamil 40-80mg 8hourly
- MOA- inhibit the slow inward entry of extracellular
calcium through the cardiac cell membranes & lower
myocardial contractility.
35. TREATMENT Cont…
Early management of MI
Admit the patient
Defibrillation
bed rest
oral aspirin
high flow O2,
I.V analgesia with opiates
I.V antiemetic
Thrombolysis wth streptokinase
monitor ECG
Rx complications.
36. TREATMENT Cont…
Invasive treatment
- Percutaneous coronary intervention(PCI)
Performed by passing a fine guide wire a cross coronary
stenosis under radiological guidance a balloon is
inflated to dilate the stenosis. and CABG are used as
treatments.
- Coronary artery bypass graft (CABG)
Stenosed arteries are bypassed using sahenous vein grafts,
or by utilizing internal mammary artery.
38. PREVENTION
Recognize the symptoms
Reduce your risk factors:
Lose weight
Quit Smoking
Keep your cholesterol at a normal level.
Keep your blood pressure under control.
Use techniques to ease stress.
Control blood sugar level.
Eat Right
REGULER EXERCISE
39. COMPLICATIONS
ARRHYTHMIAS IN AMI
Ventricular fibrillation tachycardia
Atrial fibrillation and tachycardia
Heart block
ISCHAEMIA
ACUTE CIRCULATORY FAILURE
DRESSLER’S SYNDROME
Post MI syndrome characterized by pericarditis, pleurisy
and persistent fever.
MECHANICAL COMPLICATIONS
Pappilary muscle demage
Rupture of IV septa
Rupture of the ventrical
EMBOLISM
VENTRICULA ANEURSYM
40.
41. Ischemic Changes
T-waves, ST-segment, and Q-waves
1. T-waves
Hyperacute (tall and peaked)
Flattened
Inverted (symmetrical)
2. ST-segments
Elevated (Infarct)
Depressed (Ischemia or Infarct)
3. Q-Waves
Late change of Infarction
42. Ischemia – ST-Segment
ST-segment Elevation
A change of Infarction (concave down)
DDx: Prinzmetal angina, Aneurysm, LBBB,
Pericarditis, Hypothermia, Hyperkalemia,
Benign early repolarization
Benign Early Repolarization
(concave up)
Acute Infarction
(concave down)
44. Ischemia – Q-Waves
Q-waves
Indicates infarction
Occur several hours
to days after infarct
Persist lifelong
Pathological Q
Ensure there is no R
wave!
Should be > 0.04 s
(1 small block)
Should be > 25% of
the R wave
amplitude
Q waves
NOT Q waves (they are S waves)
45. Ischemic Changes
Remember the anatomical correlations
Especially important when diagnosing ischemia
or infarction
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Rhythm Strip (II)
46. Ischemia – Examples
Acute Anterior ST-elevation MI
ST-segment elevation
V1-V4
Reciprocal
ST-depression
II, III, aVF
Trends in coronary artery disease and associated risk factors in sub-Saharan Africans by
O Akinboboye1, O Idris2, O Akinboboye3 and O Akinkugbe4
Received 1 May 2002; Revised 1 October 2002; Accepted 17 October 2002.
Journal of Human Hypertension (2003) 17, 381–387. doi:10.1038/sj.jhh.1001562