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Cardiovascular drugs 1 Flashcards

1
Q

AF - pathophysiology

A

The pathogenesis of AF is now thought to involve an interaction between initiating triggers, often in the form of rapidly firing ectopic foci located inside one or more pulmonary veins, and an abnormal atrial tissue substrate capable of maintaining the arrhythmia. Structural heart disease underlies many cases of AF. Pulmonary vein triggers may play a dominant role in younger patients with relatively normal hearts and short paroxysms of AF, whereas an abnormal atrial tissue substrate may play a more important role in patients with structural heart disease and persistent or permanent AF.

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2
Q

What is fibrosis and loss of atrial muscle mass related to

A
  • Ageing
  • Chamber dilatation
  • Inflammation
  • Genetic
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3
Q

AF - risk factors

A
  • Hypertension
  • Valvular heart disease
  • Coronary artery disease
  • Cardiomyopathy
  • Congenital heart disease
  • Previous cardiac surgery
  • Pericarditis
  • Lung disease - PE, Pneumonia, COPD
  • Hyperthyroidism
  • Alcohol
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4
Q

AF - classification

A

Lone AF

Paroxysmal (<7 days)

Persistent (>7 days)

Permanent (>7 days ± Cardioversion)

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5
Q

AF - clinical features

A 
Asymptomatic
Palpitations
SOB
Chest pain 
Syncope
Pre-syncope
Heart failure
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6
Q

AF - Treatment

A
  • Rate control
  • Rhythm control
  • Anticoagulation
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7
Q

Should treatment be focused on rhythm or rate control

A

<48hrs duration - Rhythm

>48hrs duration - Rate control

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8
Q

When is rhythm control preferred

A
  • Symptom improvement
  • Younger patient
  • Heart failure related to AF
  • Adequacy of rate control
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9
Q

AF - Acute without heart failure rate control

A

1st line - Beta blocker or CCB(Diltiazem, verapamil)

2nd line - Add digoxin

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10
Q

AF - Acute with heart failure rate control

A

1st line - digoxin, amiodarone

2nd line - amiodarone

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11
Q

AF - Permanent or paroxysmal rate control

A

1st line - beta blocker or CCB

2nd line - Add digoxin

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12
Q

AF - Rhythm control - acute cardioversion, normal heart

A
  • Flecainide, sotalol
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13
Q

AF - Rhythm control - acute cardioversion, abnormal heart

A
  • Amiodarone
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14
Q

AF - Rhythm control - maintain sinus rhythm, normal heart

A
  • Flecainide, sotalol
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15
Q

AF - Rhythm control - Maintain sinus rhythm, abnormal heart

A
  • Amiodarone
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16
Q

PDE3 inhibitors

A

Activation of the sympathetic nervous system releases the neurotransmitter norepinephrine and increases circulating catecholamines (epinephrine and norepinephrine) which bind primarily to beta1-adrenoceptors in the heart that are coupled to Gs-proteins.

This activates adenylyl cyclase to form cAMP from ATP.

Increased cAMP, through its coupling with other intracellular messengers, increases contractility (inotropy), heart rate (chronotropy) and conduction velocity (dromotropy).

Cyclic-AMP is broken down by an enzyme called cAMP-dependent phosphodiesterase (PDE). The isoform of this enzyme that is targeted by currently used clinical drugs is the type 3 form (PDE3). Inhibition of this enzyme prevents cAMP breakdown and thereby increases its intracellular concentration

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17
Q

Non-cardioselective beta blockers

A
  • Propanolol
  • Carvedilol
  • Sotalol
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18
Q

Cardioselective beta blockers

A
  • Atenolol
  • Bisoprolol
  • Esmolol
  • Metoprolol
  • Nebivolol
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19
Q

Vasodilatory beta blockers

A
  • Labetalol

- Carvedilol

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20
Q

Rate limiting CCBs

A
  • Verapamil

- Diltiazem

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21
Q

Dihydropyridine CCBs

A
  • Amlodipine
  • Nifedipine
  • Felodipine
  • Lercanidipine
  • Nimodipine
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22
Q

Anticoagulation - CHA2DS2 VaSc

A 
C – Congestive heart failure=1
H – Hypertension=1 
A 2– Age >75years=2
D – Diabetes=1
S2 – Previous Stroke, TIA or thromboembolism=2
V   – Vascular disease=1
A –  Age 65-74 years=1
Sc – Sex category (female gender) =1

CHA2DS2VASc ≥2 = warfarin or direct oral anticoagulant

23
Q

Bleeding risk - HAS-BLED score

A

H – Hypertension = 1
A – Abnormal renal/liver function = 1 point each
S – Stroke in the past = 1
B – Bleeding history = 1
L – Labile INRs = 1
E – Elderly = 1
D – Drugs/Alcohol concomitantly = 1 point each

HAS-BLED ≥3 = significant risk of bleeding

24
Q

AF - Other treatments

A
  • Radiofrequency catheter or cryo-ablation

- Left atrial appendage occlusion(LAAO)

25
Q

Stroke - FAST

A

F- Face - Facial droop
A-Arms - Control of arms
S-Speech - Slurred
T - Time

26
Q

Stroke - lipid modification

A

For primary and secondary prevention

Exclude secondary causes of ↑ lipids - excess alcohol, uncontrolled diabetes, hypothyroidism, liver disease and nephrotic syndrome

Consider referral to a lipid specialist if:

Total serum cholesterol >7.5mmol/l + family history of premature coronary artery disease

Total serum cholesterol >9mmol/l

27
Q

Lipid modification - primary prevention

A

Offer atorvastatin for the primary prevention of CVD:

To people who have a 10% or greater 10‑year risk of developing CVD.

Adults with type 1 diabetes

People with chronic kidney disease

28
Q

Lipid modification - secondary prevention

A

Offer atorvastatin for the secondary prevention of CVD in any patient who has had a stroke or MI.

29
Q

Ezetimibe

A

Ezetimibe monotherapy is recommended as an option for treating primary (heterozygous‑familial or non‑familial) hypercholesterolaemia in adults in whom initial statin therapy is contraindicated or not tolerated

Ezetimibe, co‑administered with initial statin therapy might be appropriate

30
Q

Lipid lowering drugs

A
  • Nicotinic acid
  • Fibrates
  • Statins
  • Ezetimibe
  • Resins
31
Q

How do fibrates work

A

Fibrates lower blood triglyceride levels by reducing the liver’s production of VLDL (the triglyceride-carrying particle that circulates in the blood) and by speeding up the removal of triglycerides from the blood.

32
Q

How do resins work

A
  • Bile acid sequestrants are polymeric compounds that serve as ion-exchange resins
  • Bile acid sequestrants exchange anions such as chloride ions for bile acids. By doing so, they bind bile acids and sequester them from the enterohepatic circulation
  • The liver then produces more bile acids to replace those that have been lost
  • Because the body uses cholesterol to make bile acids, this reduces the level of LDL cholesterol circulating in the blood
33
Q

How does nicotinic acid reduce lipid levels

A

Nicotinic acid binds to its receptors Human Macrophage 74 A (HM74 A) / G Protein Coupled Receptor 109 A (GPR109 A) in adipocytes.19It is a G-protein coupled receptor
The ligand (nicotinic acid) recruits the inhibitory G protein coupled receptor. As a result there is decrease in cyclic Adenosine Monophosphate (cAMP) leading to decrease in activity of protein Kinase A.
This in turn results in a decreased activity of lipase; as a result, the breakdown of triacylglycerols (triglycerides) into fatty acids and glycerols is inhibited leading to a decrease in mobilization of fatty acids from adipocytes.
Consequently, there is a decrease of substrate (fatty acids) available to produce very low density lipoproteins (VLDL) in the liver.

34
Q

What are PCSK9 inhibitors

A

PCSK9 has medical importance because it acts in lipoprotein homeostasis. Agents which block PCSK9 can lower LDL particle concentrations. The first two PCSK9 inhibitors, alirocumab and evolocumab, were approved as once every two week injections, by the U.S. Food and Drug Administration in 2015 for lowering LDL-particle concentrations when statins and other drugs were not sufficiently effective or poorly tolerated

35
Q

HF pathophysiology

A

Poor ventricular function/myocardial damage (eg post myocardial infarction, dilated cardiomyopathy) –> heart failure –> decreased stroke volume and cardiac output –> neurohormonal response –> activation of sympathetic system + renin angiotensin aldosterone system –> vasoconstriction - increased sympathetic tone, angiotensin II, endothelins, impaired nitric oxide release, sodium and fluid retention - increased vasopressin and aldosterone –> further stress on ventricular wall and dilatation (remodelling) leading to worsening of ventricular function –> further heart failure

36
Q

HF - lifestyle measures for treatment

A
  • Exercise
  • Reduce alcohol consumption
  • Smoking cessation
37
Q

Drugs used for treatment of heart failure

A
  • Diuretics
  • ACEI
  • Beta-blockers
  • Aldosterone antagonists
  • ARBs
  • Hydralazine/nitrates
  • Digoxin
38
Q

Heart failure - diuretics

A

Loop diuretics - furosemide
Thiazides - bendroflumethiazide, metolazone(thiazide-like)
K+ sparing - Spironolactone(mineralocorticoid receptor antagonists), amiloride

39
Q

Loop diuretics

A
  • Na+/K+/Cl- symporter
40
Q

Thiazides

A
  • Na/Cl symporter
41
Q

K+ sparing

A
  • Epithelial Na channel
42
Q

HF - ACE inhibitors

A
  • Increase life expectancy vs placebo
  • Effect more marked in patients with more severe LV dysfunction
  • Benefit for all NYHA classes
  • Reduces risk of hospitalisation
43
Q

RAAS

A

Angiotensinogen –renin–> angiotensin I –ACE–> Angiotensin II –> Vasoconstriction + salt and water retention
(aldosterone secretion also leads to salt and water retention)

44
Q

Examples of ACE inhibitors

A

Ramipril
Lisinopril
Enalapril
Perindopril

45
Q

Examples of ARBs

A

Losartan
Candersartan
Valsartan

46
Q

Is it worth using beta blockers for management of heart failure

A

RCT/ meta analyses show that BB increase life expectancy vs placebo

All NYHA classes

Reduces hospitalisation

Evidence for bisoprolol, carvedilol and metoprolol

Low dose titrate up, monitor heart rate, BP, clinical progression

47
Q

HF - spironolactone

A

Patients with severe heart failure, NYHA III-IV

Increases life expectancy

Reduces hospital admission

Low dose (12.5-25mg)

48
Q

Chronic HF - Ivabradine

A

Ivabradine – Used with or in place of beta blocker if heart rate too high (>75 bpm)

49
Q

Chronic HF - hydralazine + nitrate

A

Used if ACEi/ARB not tolerated or contraindicated or in people of African origin

50
Q

Chronic HF - sacubitril (neprilysin inhibitor)/valsartan(ARB)

A 
- with New York Heart Association class II to IV symptoms and
a left ventricular ejection fraction of 35% or less and
who are already taking a stable dose of an ACE inhibitor or angiotensin II receptor antagonist.
51
Q

SGLT-2 inhibitors

A
  • Shown to be effective in reducing risk of heart failure
52
Q

Acute heart failure treatment

A

Basic measures:

  • Sit patient upright
  • High dose oxygen –> corrects hypoxia

Initial drug treatment:
Intravenous loop diuretics –> cause venodilatation and diuresis
Intravenous opitates/opioids(morphine/diamorphine) –> reduces anxiety and preload(venodilatation)
Intravenous, buccal, or sublingual nitrates –> reduce preload and afterload, ischaemia and pulmonary artery pressures

CONTINUE BETA BLOCKERS BUT DO NOT INITIATE

53
Q

HF - Other forms of therapy

A
  • Coronary revascularisation
  • Cardiac resynchronisation therapy
  • Cardiac transplantation

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