Podcast
Questions and Answers
What is the primary mechanism through which organic nitrates exert their vasorelaxant effects?
What is the primary mechanism through which organic nitrates exert their vasorelaxant effects?
Which of the following is a common adverse effect associated with the use of organic nitrates?
Which of the following is a common adverse effect associated with the use of organic nitrates?
What pharmacological action do organic nitrates primarily achieve to alleviate angina?
What pharmacological action do organic nitrates primarily achieve to alleviate angina?
Which of the following best describes the role of beta-adrenoceptor antagonists in the management of angina?
Which of the following best describes the role of beta-adrenoceptor antagonists in the management of angina?
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Which factor is primarily responsible for tolerance development in patients using organic nitrates for angina treatment?
Which factor is primarily responsible for tolerance development in patients using organic nitrates for angina treatment?
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In the context of stable angina, which clinical feature is characteristic of microvascular angina?
In the context of stable angina, which clinical feature is characteristic of microvascular angina?
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What is the primary action of sublingual organic nitrates in acute angina management?
What is the primary action of sublingual organic nitrates in acute angina management?
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Which of the following statements about the pathophysiology of stable coronary artery disease is true?
Which of the following statements about the pathophysiology of stable coronary artery disease is true?
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Which form of angina is characterized by symptoms occurring at rest or during nighttime due to coronary artery spasm?
Which form of angina is characterized by symptoms occurring at rest or during nighttime due to coronary artery spasm?
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What role does guanylate cyclase play in the mechanism of action of organic nitrates?
What role does guanylate cyclase play in the mechanism of action of organic nitrates?
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Which receptor subtype is primarily targeted by non-selective beta-blockers?
Which receptor subtype is primarily targeted by non-selective beta-blockers?
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Which of the following is a potential adverse effect of beta-blockers?
Which of the following is a potential adverse effect of beta-blockers?
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What is a mechanism by which calcium channel blockers exert their vasorelaxation effects?
What is a mechanism by which calcium channel blockers exert their vasorelaxation effects?
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Which of the following describes the use of nitrates in clinical practice for angina management?
Which of the following describes the use of nitrates in clinical practice for angina management?
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Which class of drugs is most likely to cause bradycardia as an adverse effect?
Which class of drugs is most likely to cause bradycardia as an adverse effect?
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What is the primary physiological effect of beta-blockers on the heart?
What is the primary physiological effect of beta-blockers on the heart?
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What substance is released from endothelial cells to induce vasodilation, which nitrates mimic or enhance?
What substance is released from endothelial cells to induce vasodilation, which nitrates mimic or enhance?
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In patients with asthma, which adverse effect of beta-blockers should be particularly monitored?
In patients with asthma, which adverse effect of beta-blockers should be particularly monitored?
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Which of the following statements best describes the role of calcium channel blockers in chronic stable angina?
Which of the following statements best describes the role of calcium channel blockers in chronic stable angina?
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Which of the following adverse effects is associated with potassium channel openers such as Nicorandil?
Which of the following adverse effects is associated with potassium channel openers such as Nicorandil?
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Stable Coronary Artery Disease is characterized by an imbalance primarily between myocardial O2 supply and demand.
Stable Coronary Artery Disease is characterized by an imbalance primarily between myocardial O2 supply and demand.
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Classic angina occurs without any obstruction in the coronary arteries.
Classic angina occurs without any obstruction in the coronary arteries.
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Microvascular Angina, or Syndrome X, has no angiographic evidence of obstructive coronary artery disease.
Microvascular Angina, or Syndrome X, has no angiographic evidence of obstructive coronary artery disease.
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Organic nitrates primarily work by increasing preload to alleviate angina symptoms.
Organic nitrates primarily work by increasing preload to alleviate angina symptoms.
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Prodrugs used in managing stable coronary artery disease must be converted in vivo to their active metabolites for effectiveness.
Prodrugs used in managing stable coronary artery disease must be converted in vivo to their active metabolites for effectiveness.
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What is the difference between classic angina and variant angina in terms of their clinical presentations?
What is the difference between classic angina and variant angina in terms of their clinical presentations?
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Describe the underlying pathophysiology that leads to microvascular angina or Syndrome X.
Describe the underlying pathophysiology that leads to microvascular angina or Syndrome X.
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Identify the major mechanisms by which organic nitrates provide relief from angina symptoms.
Identify the major mechanisms by which organic nitrates provide relief from angina symptoms.
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What are the main symptoms associated with stable coronary artery disease, especially in relation to pain characteristics?
What are the main symptoms associated with stable coronary artery disease, especially in relation to pain characteristics?
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Discuss how beta-adrenoceptor antagonists affect myocardial oxygen demand in patients with stable angina.
Discuss how beta-adrenoceptor antagonists affect myocardial oxygen demand in patients with stable angina.
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Study Notes
Stable Coronary Artery Disease
- Chronic or recurrent and acute ischaemic heart disease (IHD) syndrome
- Characterised by episodes of reversible or transient mismatch between myocardial oxygen demand and supply
- Commonly associated with transient chest discomfort
- May result in angina pectoris (strangling and choking pain in the chest)
Aetiology & Pathogenesis
- A mismatch or imbalance between myocardial oxygen demand and supply
- May be caused by:
- Atherosclerotic plaque-related partial obstruction of epicardial coronary arteries (classic angina)
- Transient, focal or diffuse, spasm of normal or mildly-diseased epicardial coronary arteries (variant angina)
- A primary dysfunction of small diameter (< 500 µm) intramural coronary arteries (microvascular angina)
Clinical Subtypes
- Two major clinical subtypes:
- Angina with obstructive CAD
- Angina without obstructive CAD (INOCA/NOCAD)
Angina with Obstructive CAD
- Classic or stable angina (angina of effort)
- Chest pain on exertion
- Fixed obstructive CAD (atherosclerotic plaque)
- ST-segment depression
Angina without Obstructive CAD (INOCA)
- Variant or Prinzmetal's angina (angiospastic/vasospastic)
- Microvascular angina (syndrome X)
Variant or Prinzmetal’s Angina (Vasospastic)
- Pain at rest or at night
- Focal or diffuse spontaneous coronary artery spasm
- ST-segment elevation (or ST-segment depression)
- Arrhythmias
Microvascular Angina (Syndrome X)
- Chest pain at rest or on exertion; pain persists after exertion
- Poor response to glyceryl trinitrate (GTN)
- No angiographic evidence of obstructive CAD
- Positive stress test - ST-segment depression during exercise
Underlying Coronary Pathology & Pathophysiology of Chronic Angina Syndromes
- Atherosclerosis (classic angina) - The main underlying pathology
- Progression from fatty streaks to fibrous plaques to complex plaques with a lipid core
- The lipid core may rupture, forming a thrombus and leading to infarction
- Coronary artery spasm (variant angina) - The main underlying pathology
- Transient, focal or diffuse, spasm of normal or mildly-diseased epicardial coronary arteries
- Caused by endothelial dysfunction contributing to coronary artery spasm
- Can be triggered by various factors, such as cold, stress, or smoking
- Microvascular dysfunction (microvascular angina) - The main underlying pathology
- Intramural coronary arteries smaller than 500µm
- Dysfunction possibly caused by endothelial dysfunction, abnormal vasomotor responses, and heightened response to vasoconstrictors
- Reduced coronary flow reserve
- Increased myocardial oxygen demand
Clinical Features
- Pain
- Location: Retrosternal, near the sternum
- Radiation: Throat, lower jaw, upper arms, back, epigastrium
- Character: Pressure, tightness, heaviness, discomfort, strangling, constricting, burning
- Duration: Brief, lasting a few minutes to hours
- Other symptoms:
- Dyspnoea
- Fatigue
- Nausea
- Diaphoresis
Principles of Clinical Management
- Medical treatment:
- Lifestyle modifications:
- Smoking cessation
- Diet modification
- Regular exercise
- Weight management
- Pharmacotherapy:
- Anti-anginal drugs:
- Organic nitrates & nitrites
- Beta-blockers
- Calcium channel blockers
- Potassium channel openers
- Sinus node (If current) inhibitors
- Late sodium current blockers
- Antiplatelet therapy:
- Aspirin
- Clopidogrel
- Statins
- ACE inhibitors
- Angiotensin II receptor blockers (ARBs)
- Anti-anginal drugs:
- Lifestyle modifications:
- Revascularization procedures
- Percutaneous coronary intervention (PCI):
- Balloon angioplasty (PTCA)
- Coronary stenting (BMS, DES)
- Coronary artery bypass graft (CABG)
- Percutaneous coronary intervention (PCI):
Drug Treatment
- Organic Nitrates & Nitrites:
- Cellular mechanism of vasorelaxation:
- In vivo conversion to NO
- Activation of guanylate cyclase => Increased cGMP
- Activation of protein kinase G (PKG) => Vasorelaxation
- Mechanisms of anti-anginal effect:
- Peripheral venodilatation => Reduced preload => Reduced myocardial oxygen demand (MVO2)
- Peripheral arterial & arteriolar dilatation => Reduced afterload => Reduced MVO2
- Coronary vasodilatation => Reversal of spasm & prevention of spasm
- Increased collateral blood flow
- Clinical use:
- Relief of acute angina attacks (GTN, amyl nitrite)
- Prophylaxis of chronic angina (GTN, ISDN, ISMN)
- Choice & mode of therapy depend on pharmacokinetic profile (sublingual, buccal, inhalation, transdermal, IV)
- Adverse effects:
- Flushing
- Throbbing headaches
- Postural hypotension & syncope
- Reflex tachycardia & increased myocardial contractility
- Tolerance (due to depletion of thiol (-SH) groups & physiological adaptation)
- Cellular mechanism of vasorelaxation:
Beta-Blockers
- History: First introduced in the mid-1960s for treatment of angina pectoris
- Chemistry: Structural analogues of isoprenaline (prototypes: propranolol, atenolol)
- Pharmacological action: Antagonise the effects of sympathetic nervous activation (e.g. noradrenaline & adrenaline) at beta-adrenoceptors
- 3 major subtypes of β-adrenoceptors:
- β1-ARs (heart & kidney)
- β2-ARs (heart, smooth muscle (e.g. vascular & bronchial))
- β3-ARs (adipocytes)
- Two broad classes of beta-blockers:
- Non-selective (e.g. propranolol)
- β1-receptor selective (cardioselective) (e.g. atenolol)
- 3 major subtypes of β-adrenoceptors:
- Mechanisms of anti-anginal effect:
- Haemodynamic effects => Reduced myocardial oxygen demand (MVO2):
- Reduced myocardial contractility
- Reduced heart rate
- Reduced systemic blood pressure
- Ancillary effects:
- Increased diastolic filling time => Increased myocardial perfusion
- Antiarrhythmic activity => Improved electrical stability
- Antiatherogenic & antithrombotic
- Haemodynamic effects => Reduced myocardial oxygen demand (MVO2):
- Clinical use: Prophylaxis of chronic stable angina (first-line)
- Adverse effects:
- Increased left ventricular (LV) size => Increased myocardial oxygen consumption
- Rebound phenomenon => Aggravation of angina
- Bronchoconstriction => Exacerbation of asthma
- Peripheral vasoconstriction => Cold extremities
- Myocardial depression => Risk of heart failure
- Masking of signs of impending hypoglycaemia
- Sexual dysfunction => Poor patient compliance
- CNS disturbances: Nightmares, depression, confusion
Calcium Channel Blockers
- History: Introduced in the 1970s for treatment of hypertension; later licensed for treatment of other cardiovascular diseases
- Pharmacological actions: Inhibit entry of calcium into cells via voltage-gated calcium channels (main effects on heart & vascular smooth muscle)
- Chemistry:
- Phenylalkylamines: Verapamil
- Dihydropyridines: Nifedipine
- Benzothiazepines: Diltiazem
- Cardiac effects (verapamil & diltiazem):
- Block of calcium influx into cardiac muscle cells => Decreased cardiac contractility
- Block of calcium influx into nodal & conducting cells => Reduced heart rate
- Vascular effects:
- Block of calcium influx into arterioles => Arteriolar dilatation
- Peripheral vasodilatation => Reduced systemic vascular resistance (SVR) => Reduced arterial blood pressure
- Coronary dilatation => Increased coronary blood flow, reversal of spasm, prevention of spasm
- Block of calcium influx into arterioles => Arteriolar dilatation
- Mechanisms of anti-anginal effect:
- Reduced myocardial oxygen demand:
- Reduced arterial blood pressure (afterload)
- Reduced myocardial contractility (verapamil & diltiazem)
- Reduced heart rate
- Increased myocardial blood flow:
- Coronary vasodilatation => Increased coronary blood flow, spasm reversal/prevention
- Reduced myocardial oxygen demand:
- Clinical use:
- Management of chronic stable angina (first-line)
- Management of variant angina
- Adverse effects:
- Mainly direct extensions of therapeutic effects
- Non-dihydropyridines (verapamil, diltiazem):
- Cardiodepression
- Bradycardia
- AV block
- Hypotension
- Headache
- Peripheral oedema
- Constipation
- Dihydropyridines (amlodipine, nifedipine, etc.):
- Hypotension
- Light-headedness
- Flushing
- Headache
- Peripheral oedema
Miscellaneous Agents
- Potassium channel openers:
- Nicorandil: Veno-dilatation => Reduced preload => Reduced MVO2; arterial dilatation => Reduced afterload => Reduced MVO2
- Sinus node (If current) inhibitors:
- Ivabradine: Inhibition of If => Reduced heart rate => Reduced MVO2
- Late sodium current blockers:
- Ranolazine: Inhibition of late INa => Anti-ischaemic effects
Revascularization Procedures
- Percutaneous coronary intervention (PCI):
- Balloon angioplasty (PTCA): Balloon catheter inserted to widen narrowed coronary arteries
- Coronary stenting (BMS, DES): Stent inserted to restore blood flow and prevent restenosis following PTCA
- Coronary artery by-pass graft (CABG): Section of blood vessel from another part of the body is grafted to bypass the blocked coronary artery
Stable Angina - Drug Treatment Algorithm (NICE 2011)
- Aims to balance symptomatic control with secondary prevention of cardiovascular effects
Management of Chronic Stable Angina (NICE 2011)
- The NICE guideline recommends the following management strategies:
- Risk factor modification and healthy lifestyle
- Antiplatelet therapy with low-dose aspirin
- Statin therapy to lower LDL-cholesterol
- Beta blockers as first-line treatment for symptom control and secondary prevention
- Calcium channel blockers as an alternative to beta-blockers for symptom control
- Long-acting nitrates for symptom relief, especially in stable angina
- Revascularisation (PCI or CABG) if medical management fails or for high-risk patients
Recommended Reading
- 2011 NICE Guideline for the Management of Stable Angina (CG 126) (updated: 25 August 2016)
- Management of Stable Angina: summary of NICE guidance
Chronic or Stable Coronary Artery Disease
- Stable coronary artery disease (SCAD) is a chronic or recurrent syndrome.
- SCAD is characterized by episodes of reversible or transient mismatch between myocardial oxygen demand and supply.
- This mismatch leads to myocardial ischemia or hypoxia without myocardial cell necrosis or death.
- SCAD is commonly associated with chest pain (angina pectoris).
Aetiology & Pathogenesis
- SCAD arises from an imbalance between myocardial oxygen demand and supply.
- It may be due to:
- Atherosclerotic plaque-related partial obstruction of epicardial coronary arteries (leading to classic angina).
- Transient, focal or diffuse, spasm of normal or mildly diseased epicardial coronary arteries (leading to variant angina).
- A primary dysfunction of small diameter intramural coronary arteries (leading to microvascular angina).
Clinical Subtypes
- Two major clinical subtypes:
- Angina with obstructive CAD.
- Angina without obstructive CAD (INOCA/NOCAD).
Angina with obstructive CAD
- Classic or Stable Angina:
- Chest pain on exertion.
- Fixed obstructive CAD (atherosclerotic plaque).
- ST-segment depression.
Angina without obstructive CAD (INOCA)
-
Variant or Prinzmetal’s Angina (Angiospastic/Vasospastic):
- Pain at rest or at night.
- Focal or diffuse spontaneous coronary artery spasm.
- ST-segment elevation (or ST-segment depression).
- Arrhythmias.
-
Microvascular Angina (Syndrome X):
- Chest pain at rest or on exertion, which persists after interruption of exertion and shows a slow/poor response to GTN.
- No angiographic evidence of obstructive CAD.
- Coronary microvascular dysfunction characterized by endothelial dysfunction, abnormal dilator responses, coronary microvascular spasm, heightened response to vasoconstrictors, reduced coronary flow reserve, etc.
- Positive stress test with ST-segment depression during exercise.
Clinical features
- Pain:
- Location: Retrosternal, near the sternum.
- Radiation: throat, lower jaw, upper arms, back, epigastrium.
- Character: pressure, tightness, heaviness, discomfort, strangling, constricting or burning.
- Duration: Brief, lasting a few minutes to hours.
- Precipitating Factors: Exertion, emotional stress, cold, heavy meals, smoking, alcohol.
- Relieving Factors: Rest, GTN, oxygen.
Drug Treatment of Stable Coronary Artery Disease (SCAD)
-
Organic Nitrates & Nitrites:
- Mechanism of action: In vivo conversion to NO, activating guanylate cyclase which increases cGMP, leading to activation of protein Kinase G (PKG) and vasorelaxation.
- Anti-anginal effects: Peripheral venodilatation (decreases preload), peripheral arterial & arteriolar dilatation (decreases afterload), coronary vasodilatation (reversal of spasm).
- Clinical use: Relief of acute angina attacks (GTN, amyl nitrite) and prophylaxis of chronic angina (GTN, ISDN, ISMN).
- Adverse effects: Flushing, throbbing headaches, postural hypotension and syncope, reflex tachycardia and increased myocardial contractility, tolerance.
-
β-Adrenoceptor Antagonists (β-Blockers):
- Mechanism of action: Block sympathetic nervous activation at β-adrenoceptors (β1-ARs - heart & kidney, β2-ARs - heart, smooth muscle, β3-ARs - adipocytes).
- Anti-anginal effects: Haemodynamic effects (reduced myocardial contractility, heart rate, and systemic blood pressure) and ancillary effects (increased diastolic filling time, antiarrhythmic activity, antiatherogenic & antithrombotic).
- Clinical use: Prophylaxis of chronic stable angina (first-line).
- Adverse effects: Increased LV size, rebound phenomenon, bronchoconstriction, peripheral vasoconstriction, myocardial depression, masking of signs of impending hypoglycaemia, sexual dysfunction, CNS disturbances.
-
Calcium Channel Blockers:
- Mechanism of action: Inhibit entry of Ca into cells via voltage-gated calcium channels, affecting heart and vascular smooth muscle.
- Cardiac effects (verapamil & diltiazem): Block of Ca influx into cardiac muscle cells (reduced cardiac contractility) and nodal & conducting cells (reduced heart rate).
- Vascular effects: Block of Ca influx into arterioles (arteriolar dilatation) leading to peripheral vasodilatation (decreased SVR and arterial BP) and coronary dilatation (increased coronary blood flow, spasm reversal/prevention).
- Anti-anginal effects: Reduced myocardial O2 demand (decreased arterial BP, myocardial contractility, heart rate) and increased myocardial blood flow (coronary vasodilatation).
- Clinical use: Management of chronic stable angina (first-line) and variant angina.
- Adverse effects: Generally extensions of therapeutic effects (cardiodepression (verapamil & diltiazem), hypotension, bradycardia, AV block, headache, peripheral oedema).
-
Miscellaneous Agents:
- Potassium channel openers: Nicorandil (veno-dilatation & arterial dilatation, leading to reduced preload and afterload).
- Sinus node (If current) inhibitors: Ivabradine (inhibition of If, leading to reduced heart rate).
- Late Sodium Current Blockers: Ranolazine (inhibition of late INa, leading to anti-ischemic effects).
Principles of Clinical Management of Stable Angina
-
Revascularization Procedures:
-
Percutaneous Coronary Intervention (PCI):
- Balloon Angioplasty (PTCA): Inflate a balloon inside the artery to compress the plaque and open the artery.
- Coronary Stenting: Placement of a stent (either bare metal (BMS) or drug-eluting (DES) stent) to keep the artery open.
- Coronary Artery Bypass Graft (CABG): Surgical procedure that bypasses the blocked coronary artery using a graft (usually saphenous vein or internal mammary artery) to improve blood flow.
-
Percutaneous Coronary Intervention (PCI):
Management Algorithm (NICE 2011)
-
Symptom control:
- Lifestyle modifications: Stop smoking, lose weight, exercise regularly, reduce stress.
- Medical therapy:
- Organic nitrates (GTN, ISDN, ISMN).
- β-blockers.
- Calcium channel blockers.
- Other drugs (nicorandil, ivabradine, ranolazine).
-
Secondary prevention of cardiovascular effects:
- Statins (e.g. atorvastatin)
- Antiplatelet agents (e.g. aspirin, clopidogrel).
- ACE inhibitors or ARBs (e.g. ramipril, valsartan).
-
Treatment Options:
- Medical Treatment
- Percutaneous Coronary Intervention (PCI)
- Coronary Artery Bypass Graft (CABG)
Recommended Reading
- 2011 NICE Guideline for the Management of Stable Angina (CG 126) (updated: 25 August 2016)
Chronic or Stable Coronary Artery Disease (SCAD)
- Stable Coronary Artery Disease (SCAD) is a chronic condition, characterized by episodes of reversible or transient mismatch between myocardial O2 demand and supply.
- Myocardial ischemia or hypoxia occurs without myocardial cell necrosis/death.
- Typically, chest discomfort or pain (angina pectoris) arises from the mismatch of myocardial O2 supply and demand.
Aetiology and Pathogenesis
- It arises from an imbalance between myocardial O2 demand & supply.
- There are several possible etiologies:
- Atherosclerotic plaque-related partial obstruction of epicardial coronary arteries: this is the most common cause, known as classic angina.
- Transient, focal or diffuse, spasm of normal or mildly-diseased epicardial coronary arteries: this leads to variant angina.
- A primary dysfunction of small diameter ( 500 µm) intramural coronary arteries: resulting in microvascular angina.
Clinical Subtypes
- Two major subtypes exist:
- Angina with obstructive CAD
- Angina without obstructive CAD (INOCA / NOCAD)
Angina with Obstructive CAD
- This is also known as Classic or Stable Angina (Angina of effort).
- Chest pain on exertion, related to fixed obstructive CAD (atherosclerotic plaque).
- ST-segment depression is usually observed.
Angina Without Obstructive CAD (INOCA)
- Consists of two subtypes:
- Variant or Prinzmetal’s Angina (Angiospastic/Vasospastic)
- Microvascular Angina (Syndrome X)
Variant or Prinzmetal's Angina
- Characterized by pain at rest or at night (not exertion).
- Focal or diffuse spontaneous coronary artery spasm.
- ST-segment elevation or depression can occur.
- Arrhythmias may also be present.
Microvascular Angina
- Chest pain occurs at rest or on exertion, and persists after exertion cessation.
- Slow or poor response to GTN (glyceryl trinitrate).
- No angiographic evidence of obstructive CAD.
- Characterized by coronary microvascular dysfunction, causing:
- Endothelial dysfunction
- Abnormal dilator responses
- Coronary microvascular spasm
- Heightened response to vasoconstrictors
- Reduced coronary flow reserve
- Positive stress test leading to ST-segment depression during exercise.
Clinical features
- Major signs and symptoms:
- Pain
- Location: retrosternal, near the sternum
- Radiation: throat, lower jaw, upper arms, back, epigastrium
- Character: pressure, tightness, heaviness, discomfort, strangling, constricting or burning
- Duration: brief, lasting a few minutes to arteries > arterioles
- Pain
Drug Treatments
-
Organic Nitrates and Nitrites
- Act as vasodilators, decreasing preload and afterload.
- They are metabolized to NO, activating guanylate cyclase and increasing cGMP, ultimately leading to smooth muscle relaxation.
- Clinical use:
- Relief of acute angina attacks: GTN, amyl nitrite
- Prophylaxis of chronic angina: GTN, ISDN, ISMN
- Adverse effects:
- Flushing & throbbing headaches
- Postural hypotension & syncope
- Reflex tachycardia and myocardial contractility
- Tolerance: depletion of thiol (-SH) groups & physiological adaptation
-
Beta-Blockers
- Block the effects of sympathetic nervous activation (noradrenaline and adrenaline) at β-adrenoceptors.
- Main types:
- Non-selective: e.g. propranolol
- β1-receptor selective: e.g. atenolol
- Mechanism of action:
- Reduce myocardial O2 demand:
- myocardial contractility
- heart rate
- systemic blood pressure
- Ancillary effects:
- diastolic filling time myocardial perfusion
- Antiarrhythmic activity electrical stability
- Antiatherogenic & antithrombotic
- Reduce myocardial O2 demand:
- Clinical use: Prophylaxis of chronic stable angina (first-line).
- Adverse effects:
- LV size myocardial O2 consumption
- Rebound phenomenon aggravation of angina
- Bronchoconstriction exacerbation of asthma
- Peripheral vasoconstriction cold extremities
- Myocardial depression risk of heart failure
- Masking of signs of impending hypoglycaemia
- Sexual dysfunction poor patient compliance
- CNS disturbances – nightmares, depression, confusion
-
Calcium Channel Blockers
- Inhibit entry of Ca into cells via voltage-gated calcium channels.
- They have significant effects on heart and vascular smooth muscle.
- Main types:
- Phenylalkylamines: verapamil
- Dihydropyridines: nifedipine
- Benzothiazepines: diltiazem
- Mechanism of action:
- Cardiac effects:
- Block of Ca influx into cardiac muscle cells cardiac contractility
- Block of Ca influx into nodal & conducting cells HR
- Vascular effects:
- Block of Ca influx into arterioles arteriolar dilatation
- Peripheral vasodilatation SVR arterial BP
- Coronary dilatation coronary blood flow; reversal of spasm; prevention of spasm
- Cardiac effects:
- Clinical use:
- Management of chronic stable angina (first-line).
- Management of variant angina.
- Adverse effects:
- Non-Dihydropyridines (Verapamil, Diltiazem)
- Cardiodepression
- Bradycardia
- AV block
- Hypotension
- Headache
- Peripheral oedema
- Constipation
- Dihydropyridines (Amlodipine, Nifedipine, etc)
- Hypotension
- Light-headedness
- Flushing
- Headache
- Peripheral oedema
- Non-Dihydropyridines (Verapamil, Diltiazem)
-
Miscellaneous Agents
- Potassium channel openers: Nicorandil - veno-dilatation preload MVO2; arterial dilatation afterload MVO2
- Sinus node (If current) inhibitors: Ivabradine - inhibition of If HR MVO2
- Late Sodium Current Blockers: Ranolazine - inhibition of late INa anti-ischaemic effects
Revascularization Procedures
- Percutaneous Coronary Intervention (PCI):
- Balloon angioplasty (PTCA)
- Coronary stenting: bare metal stents (BMS) and drug eluting stents (DES)
- Coronary artery by-pass graft (CABG)
Management of Chronic Stable Angina (NICE 2011)
- The recommended treatment plan for chronic stable angina includes:
- Symptom control: Manage the pain and discomfort associated with SCAD.
- Secondary prevention: Prevent future cardiovascular events.
- The treatment options are:
- Medical Treatment: Manage symptoms with medications.
- Percutaneous Coronary Intervention (PCI): Procedures for opening arteries.
- Coronary Artery Bypass Graft (CABG): Bypass obstructed arteries with grafts.
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Description
This quiz explores Stable Coronary Artery Disease, a condition marked by discrepancies between myocardial oxygen demand and supply, often resulting in chest discomfort. It covers the aetiology, pathogenesis, and clinical subtypes including obstructive and non-obstructive CAD. Test your knowledge on the specifics of angina and its various forms.
