Cardiology JC006: Chest Pain On Exertion: Ischaemic Heart Disease, Angina Pectoris Flashcards
Blood supply to the heart
- Left coronary artery
- LAD
- LCX - Right coronary artery
- Right marginal
- Posterior descending
***Pathophysiology of IHD
Myocardial ischaemia
1. **Critical coronary stenosis
2. Inflammation
3. Platelets + Coagulation
4. **Vasospasm
5. ***Microvascular dysfunction
6. Endothelial dysfunction
3 mechanisms leading to mismatch between demand vs supply (can co-exist!!!):
1. Epicardial coronary arteries
- ***Atherosclerotic disease
—> stable plaque / vulnerable plaque —>
—> reduction in CFR (coronary flow reserve)
—> Demand ischaemia +/- stable angina
or
—> plaque rupture leading to thrombosis
—> ACS or infarction
- ***Vasospastic disease —>
—> focal/transient vasospasm
—> Prinzmetal angina
or
—> persistent vasospasm
—> MI
- Coronary microcirculation dysfunction (despite patent lumen)
- ***Microvascular dysfunction
—> impair coronary physiology + myocardial blood flow
—> myocardial ischaemia in CAD and CMP + induce severe acute ischaemia “Takotsubo”
Mismatch between demand vs supply
Demand:
- HR
- Wall tension
- Contractility
- Heart hypertrophy
Supply:
- Spasm
- Diastolic time (depend on HR)
- AoP-LVEDP gradient (depend on Ao diastolic pressure + LVEDP)
- Local autoregulation
End result:
Ischaemia
—> **Lactic acidosis + **ST depression + **↓ Contractility + **Pain
Angina pectoris
Discomfort in chest / adjacent areas that occur predictably + reproducibly at a certain level of exertion + is relieved with rest / nitroglycerin
Mechanism of Ischaemia chest pain
Cardiac pain + neural pathways are poorly understood
Heart do not have its own direct nerve fibre
Angina pectoris:
- results from ischaemic episodes that excite chemosensitive + mechanosensitive receptors in the heart
—> stimulation of the receptors
—> release of **adenosine, **bradykinin, other substance that excite sensory ends of sympathetic + vagal afferent fibres
—> afferent fibres traverse nerves that connect to upper 5 thoracic **sympathetic ganglia + upper 5 distal **thoracic roots of spinal cord
—> within spinal cord, cardiac sympathetic afferent impulse may ***converge with impulses from somatic thoracic structures (i.e. same dermatome)
—> referred cardiac pain
(Silent ischaemia in diabetic patients: related to failed development of cardiac sensory system ∵ reduced nerve growth factor)
Epidemiology of IHD
- number 1 cause of death
- most common in middle aged, men
- 60-79 yo: 25% men, 16% women have CHD
- > 80: 37% men, 23% women
- presentation of women usually 10 years later than men (60 vs 50 yo)
- incidence of CHD / angina in post-menopausal women ~ men
- annual rate of MI in symptomatic angina: 3-3.5% per year
- within 12 months of initial diagnosis, 10-20% with stable angina progress to unstable angina / MI (if no treatment given)
Initial manifestation:
- Angina pectoris (50%)
- ACS (50%)
Etiologies of IHD
Primary cardiac cause
1. **Atherosclerosis (most common)
2. Coronary artery abnormality (spasm / arteritis / dissection / anomalies / radiation-induced)
3. Myocardial bridging
4. **Aortic stenosis (↑ demand)
5. **Hypertrophic cardiomyopathy (↑ demand)
6. **Dilated cardiomyopathy
7. ***Tachycardia (↑ demand)
Primary non-cardiac cause
1. **Anaemia
2. Sickle cell disease
3. **Hypoxaemia
4. CO poisoning
5. Hyperviscosity (e.g. Polycythaemia)
6. **Hyperthyroidism
7. **Phaeochromocytoma
Risk factors:
1. Smoking —> ↑ BP due to stimulation of chromaffin cells
2. Alcohol —> ↑ BP
3. **High cholesterol
4. **High BP
5. **Obesity
6. **Metabolic syndrome
7. ***Type 2 DM
8. Cocaine abuse —> ↑ Sympathetic stimulation —> Vasospasm + ↑ BP + Direct cardiotoxicity (suspect in young patients: acute MI, tachycardia, malignant HT)
Pathogenesis of Atherosclerosis
**Atherocyte phagocytise lipid (Fatty streak formation) + **Fibrocyte produce fibrous tissue (+ Ca deposition) + ***Inflammation of wall
—> Pathological intimal thickening with macrophages
—> Fat core (stable: with fibrous cap, unstable: ruptured)
—> Ruptured plaque
—> Platelet + Coagulation activation
—> ACS
2 Factors:
1. **Concentration of lipoprotein
2. **Susceptibility of arterial walls
***Diagnosis + Assessment of IHD
- History
- Clinical risk assessment
—> Demographics
—> Risk factors
—> Stability + Frequency of symptoms
—> Presence of HF
—> Prior MI
-
Chest pain symptoms: SOCRATES
—> Site: retrosternal / slightly to left, occasionally at extrathoracic site
—> Onset: gradual increase + fading away, usually 2-10 mins
—> Character: tightness, pressure, squeezing, heaviness, burning, aching, fullness, “heavy weight”, “band across chest”
—> Radiation: neck throat, lower jaw, **left shoulder / arm (ulnar distribution), occasionally to right arm, interscapular, epigastrium, back (never below abdomen)
—> Associations: SOB, dizziness, syncope
—> Time course: worsening, improving, fluctuating
—> Exacerbating / Relieving factors: **4Es: eating, exertion, emotion, environment vs ***rest, cessation of activity / stress, NTG
—> Severity: 0-10, may progress from asymptomatic —> pain on exertion —> pain at rest -
**Non-chest pain symptoms
—> Dyspnea
—> Non-chest locations of discomfort (exertional / at rest)
—> Mid-epigastric / Abdominal
—> Diaphoresis
—> Excessive fatigue + weakness
—> Dizziness + Syncope
- P/E (not much to see)
- Investigation
- **Resting ECG (look for previous MI, myocardial ischaemia)
- Fasting lipid profile + glucose
- **Echocardiogram (look at heart function)
- ***Exclude potential exacerbating factors e.g. anaemia, thyrotoxicosis - Assessment of myocardial ischaemia (Stress: Exercise to induce ischaemia)
- **Stress ECG
- Stress myocardial perfusion scintigraphy
- **Stress Echocardiogram
- Stress cardiac magnetic perfusion
Non-chest pain symptoms
- Dyspnea
- on exertion
- at rest
- PND
- temporal change of ↑ exertional dyspnea with ↓ effort tolerance - Non-chest locations of discomfort (exertional / at rest)
- neck / mandibular
- throat tightness
- shoulder discomfort
- upper arm / forearm discomfort (more often left side)
- interscapular / infrascapular - Mid-epigastric / Abdominal
- mid-epigastric burning, often postprandially
- sharp abdominal pain (atypical, more in women)
- RUQ pain (mimic gallbladder disease / pancreatitis)
- ***N+V (often associated with ↑ vagal tone secondary to inferior MI) - Diaphoresis
- Excessive fatigue + weakness
- discernible prodrome of ↑ fatigue with ↓ effort tolerance - Dizziness + Syncope
***P/E of Chest pain
- Majority of cases: ***Normal
-
**Risk factors for CAD
- BP
- Weight
- Lipid abnormalities
—> **corneal arcus
—> xanthomas
—> xanthelasma (xanthoma on eyelid)
- DM
—> retinal arteriolar changes
—> ***acanthosis nigricans
- Tobacco use / COPD
—> nail stain
—> prolonged expiration, wheezing, distant breath sounds
- Frank’s sign (ear lobe crease: potential marker for CAD) - ***Complications of IHD
- cardiomegaly
- heart failure
- MR (functional MR)
- arrhythmia
- peripheral arterial disease (PAD) - ***Implicating / contributing conditions for IHD
- thyrotoxicosis
- severe anaemia - Other causes of angina / dyspnea
- AS
- hypertrophic cardiomyopathy
- pulmonary HT
***Non-invasive investigations
- Lipid level
- ***LDL (very important modifiable risk factor by statin), HDL
- TG
- Lipoprotein(a) (lead to inflammation, oxidation of LDL-C) (genetic predisposition, cannot treat) - Metabolic evaluation
- FG
- **HbA1c
- Creatinine
- **Thyroxine - Markers of cardiac function, myocyte injury, ischaemia, haemodynamic stress
- High-sensitivity CRP (indicate higher risk of inflammation in coronary arteries)
- **Brain natriuretic peptide (indicate heart failure ∵ IHD)
- NT-proBNP
- **Troponin T / I (indicate heart injury)
—> prognostic implications as well - Exercise stress testing (**confirm diagnosis of IHD)
Indications of stress test: Dx of IHD **uncertain
—> if can exercise + ECG normal —> Treadmill exercise test
—> if can exercise + ECG abnormal —> Stress Echo, Stress SPECT, MRI, PET
—> if cannot exercise —> Pharmacological stress test
- ECG
—> ST elevation (transmural ischaemia)
—> ST depression + T inversion (subendocardial ischaemia with abnormal repolarisation)
—> easy to do, easy to interpret, cheap
—> but limited by abnormality in heart conduction / repolarisation, lower sensitivity / specificity - Stress Echo
—> Regional wall motion abnormality - Stress SPECT
- Cardiac MRI perfusion scan
—> can also look for scar formation, thinning of wall, ischaemia area (appear white on MRI)
—> harder to do, harder to interpret, high cost
—> but higher sensitivity / specificity - Pharmacological stress (for patients cannot exercise)
—> Vasodilator (**Dipyridamole / **Adenosine: coronary vasodilator) —> Steal phenomenon —> ↓ blood flow to ischaemic area —> exaggerate ischaemia —> manifestation on site of ischaemia
—> Inotrope (Dobutamine)
- Imaging
- ***CT coronary angiogram
Flowchart of Non-invasive investigations
No chest pain
—> Have CI for stress test / Symptoms warranting coronary imaging
—> ***Coronary imaging (CT / direct)
—> No CI for stress test
—> Symptoms not warrant coronary imaging
—> Able to exercise
—> Resting ECG interpretable / No previous revascularisation —> **Treadmill ECG study
—> Resting ECG not interpretable / previous revascularisation —> **Stress imaging
—> Not able to exercise —> ***Pharmacological stress imaging study
—> If inadequate information for Dx / prognosis / high risk (if worry to put patient under stress) —> ***Coronary imaging (CT / direct)
簡單而言: Treadmill ECG —> Stress imaging —> Pharmacological stress imaging study —> Coronary imaging (CT / direct)
Invasive investigations
Indication:
- unacceptable angina despite medical therapy
- non-invasive test results with high-risk features (e.g. large territory defect)
- angina / risk factors for CAD in setting of depressed LVEF
- for diagnostic purposes, in individual whom results of non-invasive testing are unclear
- Coronary angiogram
- catheter through artery —> inject contrast
- can be therapeutic
***Management of IHD
Treat to target: BP, Lipid, HbA1c
- Patient education
- Manage comorbid conditions
- DM, HT, HL
- use of drugs aggravating angina
- associated cardiac / non-cardiac diseases - Modify preventable risk factors
- smoking cessation + moderate alcohol consumption
- weight reduction
- regular aerobic exercise
- diet control (Mediterranean diet: low saturated / trans fat, high polyunsaturated fat, high fish oil, low glycaemic load, high fibre, high folate) -
**Pharmacological therapy
- Lipid lowering drugs (aim LDL-C **<1.4)
- Anti-platelet agents (esp. in secondary prevention)
- ACEI / ARB (CVD protection)
- β-blockers (Anti-ischaemic agents)
- CCB (Anti-ischaemic agents)
- Nitrates (Anti-ischaemic agents)
- Ivabradine, Ranolazine, Trimetazidine, Nicorandil (Novel agents) - Revascularisation procedures in selected patients
- PCI
- CABG (saphenous ring / internal mammary artery)
—> if fail medical treatment / uncontrolled
—> CABG preferable than PCI in:
—> **Unprotected left main
—> **Severe 3 vessel disease
—> ***2 vessel disease including a proximal LAD lesion
Lipid lowering drugs
- ***Statin (↓ LDL-C)
- ***Ezetimibe (NPC1L1 inhibitor)
- Bile-acid sequestrants (i.e. Resin, poorly tolerated ∵ GI SE)
- Mipomersen, Lomitapide (inhibit LDL / VLDL assembly + secretion in liver)
- PCSK9 inhibitor Ab (↓ degradation of LDL-R, effective in ↓ LDL-C, non-HDL-C, Lp(a))
