W7: Atherosclerosis II; SIHD; Angina; ACS; Stable CAD; Nutritional Aspects Flashcards
Describe the pathophysiology of stable angina.
• chest pain associated MI but no necrosis and symptoms relieve on rest/ GTN Supply demand mismatch due to ↓flow to myocardium via coronary art.
* obstructive disease, abn flow, infarction
=> pallor, tachy, tremor, systolic murmur, plateau pulse, ++JVP, oedema
Stable angina diagnostic tests
lipids LFTs Thyroidfunct.
cxr: oedema
ecg: ST depr., t-inversion
Stable Angina Severity CCS
I - only exertional
II - slight limitation, +stressors walking and stairs
III - marked limitation walking and stairs -stressors
Iv - any activity!
Explain the importance of diagnosis and treatment of stable angina (Pharma)
PROPHYLAXIS > STATINS; >3.5mmol/L cholesterol ↓LDL
> ACE I: stabilise endothelium and ↓plaque rupture
> ASPIRIN/CLOPIDOGREL: ↓PT aggregation
SYMPTOM CONTROL
> BB: atenolol, bisoprolol fumarate
> CCB: amlodipine
> central CCB: diltiazem/verapamil (rate-limiting)
> alt: Ik Ch. Blocker: Ivabradine ↓Sinus node rate (long-acting nitrate) + Nitrate, GTN: altered release + Nicorandil (long-acting nitrate)
Explain the importance of diagnosis and treatment of stable angina (Surgical)
- PCI: ↑Blood Flow
* PTransluminal Coronary Angioplasty * Stenting
- CABG: multi-vessel - symptom alleviation only!
Beta Blocker Pharmacology
B1 & B2 Receptor Antagonists (never cardioselective for B1)
*block symp. ↓HR, contr, and systolic wall tension
=> ↑diastole time = ↑perfusion of subendothelium.
C-I: asthma (B2), HF (dependent on symp.); Bradycardia
=> alt: IVABRADINE
SFX = fatigue, brady, MI risk (therefore progressive reduction)
CCB Pharmacology
⇥L-CaCh. influx = -ve ionotropic
VASODILATOR TYPE = AMLODIPINE
CENTRAL HR LIMITING = VERAPAMIL
CI: post-MI and unstable ang.
SFX: ankle oedema, headache, flushing, palpitations
Nitrovasodilators Pharma. => effects
GTN, ISOSORBIDE MONONITRATE, ISOSORBIDE DINITRATE (sustained releases)
*nitrate tolerance = n-free period
➩ ↑cGMP = relaxation and ↓preload and O2 consumption and requirements
2nd Line Rx for Stable CAD
NICORANDIL: ATPsens-K+ channel activator INHIBITING Ca influx, similar to AMLODIPINE CCB, VASC SMC RELAXATION
IVABRADINE: ↓SINUS NODE = ↓HR (alt. to BB or combined w/ BB in poorly controlled)
RANOLAZINE: INHIBITS INa channels (persistent/late Na) = ↓Ca levels and ↓Heart wall tension and O2 requirements
(Abx. drug-drug)
Cholesterol-Lowering Agents
HMG CoA Reductase Inhibitors; Post-MI
Anti-PT
P2Y12R on platelets
Aspirin inhibits PT and Txane
Describe the pathophysiology of myocardial infarction.
• ↑Unstable coronary lesion; • ↑fat plaque = ↑thrombus => gives rise to new symptoms related to CORONARY ARTERIES
Know the clinical presentation of myocardial infarction.
Chest pain discomfort; weight; tightening +sweat, nausea, breathless grey clammy, general unwell, ↑venous pressure = STEMI
Describe the characteristic ECG changes and other diagnostic aids for myocardial infarction
ECG:
* STE, Q (3d) = complete occl.
* STE acute MI, LAD block = anterolateral STEMI
* ST depr., T inv., (no q) = partial* blocked RCA = inferior STEMI
* nil STE but opp effect on opp side (V1 -> V2) = posterior MI TROPONIN MYOGLOBINCK-MB
=> qualifying (1) +ve biomarkers
(2) ischaemia; ecg; coronary problems; new cardiac dmg.
MI ACS Classification
Type 1 = Primary coronary occl.
Type 2 = Non thrombotic ischaemia. Mismatch 2º to ischaemia.
Type 3 = sudden cardiac death,
STE Type 4 = reperfusion -related: a) PCI b) stent thomb.
Type 5 = CABG associated MI, Q waves
Significance of Q waves
Previous MI (3 Days) Deep & wide = previous MI Deep and narrow = ventr. hypertrophy (normal = <0.2s)
Post MI Complications
- ARRYTHMIC
VF (common)
- MECHANICAL
tamponade, septal defect, papillary rupture
=> DEATH.
STEMI Tx
- THROMBOLYSIS
*PCI (2hrs) w/ DOAC(hep; enoxapain; fonda.)
* BALLOON + STENT (cathlab)
- FIBRINOLYSIS
*ALTEPLASE (2-12hr): fibrin-spec; plasminogen convered to plasmin => enzymatic brkdwn
* STREPTOKINASE: systemic and non-fibrin-spec
+ DAPT (Clopidogrel + Aspirin)
!risk of bleeds and Hx!
NSTEMI Tx
initial:
1. ASPIRIN: inhibit tx A2 prod; primary & secondary prevention (anti plt.)
+
FONDAPARINUX: inhibit Factor Xa (no need to monitor) s/cut injection (CI heparin) / HEPARIN: Xa and thombin inactivation; activated partial thromboplastin time (aPTT) monitoring!!
(antithrombin)
Use GRACE => low vs high
high: inclusion of angiography
- CLOPIDOGREL: P2YR antagonist inhibiting platelet aggr.
PRASUGREL
+ Aspirin
* CYP2C19 levels: genetic level efficacy. / TICAGRELOL, P2Y12 platelet inhibition / PRASUGREL
- ANGIOGRAPHY
- +BB if no C-I: indefinitine / VERAPAMIL | DILTIAZEM
(NICE 2024)
Long-Term Considerations
* ACE I for MI/ACS
* BB for AMI, NSTEMI+ACS, STEMI, post-ACS
*STATINS post discharge
Follow-Up & Non-Pharma in ACS
* ECG rpt.
* CARDIAC REHAB: lifestyle measures, exercise rehab.
