Atherosclerosis: Unmodifiable Risk Factors | family predisposition (premature atherosclerosis eg MI<55yrs)
age : >40yrs M >50yrs F
male gender
genetic abnormalities |
Atherosclerosis: Modifiable Risk Factors -1st line | Dyslipidemia
Hyperfibrinogenemia
Cigarette/ cigar smoking
Arterial Hypertension
Diabetes Mellitus
(NB: MI risk ↑es 4x, if >3 ↑es 10x ) |
Atherosclerosis: Modifiable Risk Factors - 2nd line | Obesity (BMI >30% above normal)
Physical inactivity
Mental stress + Type A personality
Hyperuricemia
- strengthen the impact of 1st line factors |
Atherosclerosis: Pathogenesis | 1- Endothelial injury due to risk factors or trauma
2- LDLs accumulate & aggregate, entering tunica intima
3- Macrophages oxidise LDLs via free radicals
4- Oxidised LDLs stimulate further leukocyte recruitment via chemoattractants releases by endothelial & SM cells
5- Monocytes engulf LDLs; accumulation of lipids and fatty streak development; cause cytotoxic damage to endothelial cells and cause dysfunction
6-Intimal smooth muscle proliferation &↑leukocyte recruitment result in atherosclerotic plaque formation
7- If plaque reaches coronary arteries, it can keep growing and cause stenosis OR rupture off; thrombosis/ embolism OR cause aneurysm by wall damage
8- ↓ O2 supply to myocardium, cellular acidosis and lactate release; in time it can cause ischemia and is called IHD |
Stable Angina Pectoris : definition | Pain >1month, not progressing & no exact time of disease beginning |
Stable Angina Pectoris : PAIN symptoms | PAIN
1) type: pressure/heaviness/squeezing/tightness/burning/numbness
2) when: physical or emotional exertion/cold/rich meals/tobacco/anger
3) where: sub/parasternal; mostly left or both sides/ levine's sign (between epigastrium and neck)
4) radiation: inner arm to forearm/wrist/left shoulder/epigastrium, sometimes neck/mandible/upper back
5) duration: 0.5-5 mins but sometimes 10-15 mins
6) relief: rest/sublingual nitroglycerine (1-3mins), elimination of factor |
Stable Angina Pectoris : other symptoms & signs | Other symptoms (Dyspnea, nausea, anxiety, cold sweats, general weakness, tremor, clouding of consciousness)
Signs (pallor, ↑ HR/BP, diffuse apex beat, gallop rhythm, paradoxical S2 due to prolonged LV ejection & mid-late systolic apical murmur due to ischemia of papillary muscles)
on palpation: ectopic systolic bulging / paradoxic movement |
Stable Angina Pectoris : Classification | Class I (only rapid/strenuous/ prolonged exertion); Rare
Class II (high but usual everyday physical load ); More frequent w/ nervous tension
Class III (low/moderate physical load); sometimes 1st hours of awakening
Class IV (slight tension, even at rest) |
Stable Angina Pectoris: Diagnostic Criteria | 1- Typical anginal pain
2- Ischemia on ECG at rest or exertion
3- Significant CA stenosis >75% |
Stable Angina Pectoris: Diagnosis | - Clinical signs
- Blood test (for risk factors/causes & DDx): CBC, lipids, electrolytes, Thyroid, Troponin, CRP, sugar, liver enzymes, Creatinine kinase & uric acid
- ECG (rest+24 hr - ST changes, T inversion,↓R, arrhythmia, BBB)
- Exercise Stress test: pathological if ST changes >1mm + anginal pain
- Xray (heart): degree of myocardial hypertrophy, the signs of left ventricular failure
- Echo (regional wall abnormality)
- SPECT w/Thallium, PET, multi-slice CT
- Angiography (MRI or Invasive) |
Stable Angina Pectoris: Treatment objectives | - To alleviate /prevent angina attack & improve QoL
- To perform timely diagnosis of acute MI
- To prevent sudden ischemic death |
Stable Angina Pectoris : Treatment - lifestyle changes | Change lifestyle to improve prognosis:
- quit smoking
- nutrition: reduce fat/salt/alcohol intake & more fruit/veg,
- if obese: reduce calories + exercise
- if HTN: reduce salt/alcohol
- exercise
Modify RFS: ( Lipid management: diet & anti-lipid drugs, BP: antihypertensives, DM, Weight, thromboses: reduce fats/smoking/aspirin) |
Stable Angina Pectoris : Drug therapy & Revascularisation | Drug therapy (nitrates + anti-ischemic improve quality of life, others for prognosis)
1- ↑O2 supply, = Nitrates (nitroglycerin, glycerol trinitrate, isosorbide mono/di nitrate), ACE inhibitors (captopril),Revascularization procedures (PCI, CABG)
2-↓ O2 demand = Nitrates, B-blockers (B1-metaprolol / B1&2-propanolol), Ca+ channel blockers (amlodapine), IF inhibitor (Ivabradine), Non-nitrate Anti-anginals (Ranolazine)
3- Myocyte metabolism adaptation= Anti-ischemic drugs (Trimetazidine, mildronate)
4- Prevention of adverse outcomes= Antiplatelet therapy to prevent TE (aspirin/clopidogril), Influenza vaccine, Statins (fluvastatin), RAAS blockade therapy
5- improve QoL + Prognosis( B-blockers, ACEI, Statins, Aspirin, CCBs) |
Unstable Angina: Definition | myocardial ischemia at rest or w/ minimal exertion in the absence of myocardial necrosis
ECG: ST segment depression + inverted T wave (acute ischemia) |
NSTEMI: Definition | myocardial necrosis in clinical setting consistent with acute myocardial ischemia |
Acute Coronary Syndromes : Types | - Unstable Angina
- Non-ST-Segment Elevation MI (NSTEMI)
- ST-Segment Elevation (STEMI) |
NSTE- ACS: Pathogenesis | 4 processes:
1- rupture of unstable atheromatous plaque
2- coronary arterial vasoconstriction
3- imbalance between the supply and demand of myocardium for oxygen
4- gradual intra-luminal narrowing of an epicardial coronary artery because of progressive atherosclerosis or post-stent restenosis
can occur simultaneously in any combination |
Unstable Angina: Clinical presentation | -Prolonged (>20mins) anginal pain at rest: retrosternal sensation of pressure/ heaviness radiating to left arm, neck or jaw
- sweating, pallor
- nausea, abdominal pain, vomiting
- dyspnea, syncope
- Atypical symptoms: epigastric pain, indigestion
- Physical exam: stable or in shock; excited/flashy/sweaty , BP↓ or↑, tachy/bradycardia
auscultation : gallop rhythm,, systolic murmur, pericardial friction sound (if pericarditis) |
MI: Clinical Presentation | - Pressure/ tightness in chest with radiation.
- shortness of breath
- diaphoresis (ex. sweating due to sympathetic innervation)
- nausea and vomiting (parasympathetic response)
- anxiety |
NSTE-ACS: Diagnostic Criteria | 1- Troponin elevation (not specific)
2- typical ischemic symptoms or ECG ischemic changes (ST depression of T wave inversion)
3- Imaging tests: echocardiography , coronary angiography |
NSTE- ACS: Diagnosis | 1- Clinical signs
2- ECG: ST changes - >1mm height), T inversion (if LBBB, ECG not useful) for MI: pathological Q waves
3- Biomarkers - < x5 ↑ troponin = Unstable Angina > x5 ↑ troponin = NSTEMI
4- Chest Xray - acute left ventricular insufficiency (due to stasis or edema) & heart dilation
5- Transthoracic echo - check LV structure (volume, size) and function (segment contractility, diastolic dysfunction), MI complications (rupture, aneurysm, thrombus, heart valves, pericardial effusion) |
NSTE-ACS: GRACE Risk Score (Mnemonic - CBCSTEAK) | - Creatinine
- Systolic BP
- Cardiac arrest at admission
- ST deviation
- Troponin, (elevated cardiac biomarkers)
- Elevated pulse rate
- Age
- Killip classification (I- no HF, II- rales/JVD, III- Pulmonary edema, IV- Cardiogenic shock/hypotension) |
NSTE-ACS: TIMI Risk Score | TIMI (each one is 1 point) - Mnemonic - AASSKPR
Age ≥65,
≥3 CAD risk factors (hypertension, hypercholesterolemia, diabetes, current smoker,family history of CAD)
Known CAD (stenosis >50%)
Aspirin use in past 7 days
Severe angina (>2 episodes in 24 hrs)
ST changes ≥ 0.5 mm
Positive cardiac marker |
NSTE-ACS: High Risk Patients | - Recurrent ischemia
- Dynamic ST changes
- Early post-infarction angina,
- Elevated troponins
- Hemodynamically unstable
- Major ventricular arrhythmias
- Diabetes,
- GRACE score >140 (Death/MI 30d. 12-30%) |
NSTE-ACS: Low Risk Patients | - No recurrent ischemia
- Isoelectric ST segment
- Only negative T wave or normal ECG
- Normal biomarker levels at baseline & after 6-12 hours
- GRACE score <109
(Death/ MI 30d. <2%) |
NSTE-ACS : Invasive strategy criteria | - Immediate (<2hrs) for very high risk criteria
- Early (<24hrs) for High risk criteria
- Invasive (<72hrs) for intermediate risk criteria
- Selective invasive for low risk criteria |
MI: Definition | evidence of myocardial injury (elevated cTn values) w/ necrosis in a clinical setting consistent with myocardial ischemia |
MI: Criteria | cTn >99th percentile & at least one of the following:
- symptoms of ischemia
- ECG changes indicative of ischemia: sig ST/T changes or LBBB
- Pathological Q wave
- Imaging: new loss of myocardium or new regional wall abnormality
-angiography/ autopsy: intracoronary thrombus |
MI: CLASSIFICATION | Type I : SPONTANEOUS MI- ischemia due to primary coronary event eg plaque rupture/erosion/fissure, coronary dissection, distal platelet embolism
Type II: ischemia due to ↑O2 demand eg HTN or ↓supply eg coronary artery spasm/embolism/arrhythmia/hypotension
Type III: related to sudden unexpected cardiac death ( w/ symptoms of myocardial ischemia + new ECG changes: ischemia or LBBB)
Type IVa: associated with PCI (w/ symptoms of MI+ cTn values >5x URL)
Type IVb: associated with documented stent thrombosis
Type V: associated with CABG (w/ symptoms of MI+ cTn >5x URL) |
MI : etipathogenesis | - disruption of atherosclerotic plaque
- leads to activation of thrombogenesis pathways: thrombus forms from platelet aggregates, fibrins & RBCs
- complete occlusion of epicardial vessel leads to large zone of ischemia
- if ischemia prolongs -> necrosis -> MI |
Other causes of elevated troponin: Cardiac disorders | - Heart failure
- Cardiomyopathy ( hypertrophic, viral )
- Hypertension
- Myocarditis, pericarditis
- Infiltrative disorders eg amyloidosis
- Injury
- Cancer |
Other causes of elevated troponin: Systemic disorders | - Pulmonary embolism
- Rhabdomyolysis
- Toxicity eg anthracycline
- Trauma
- Renal failure
- Sepsis
- Stroke
- Subarachnoid haemorrhage |
ACS w/ ST elevation: Treatment | - Stabilse patient : MONA
- if <120 mins: Primary PCI strategy + Re-perfusion
- if >120 mins: Fibrinolytic therapy for re-perfusions ( bolus of fibrinolytic eg Tenecteplase, alteplase, reteplase, streptokinase ) then either Routine or Rescue PI & Re-perfusion
- Long term : B-blockers/ ACEI (if patient w/ HF, LV dysfunction or DM) & Statins- should be continued indefinitely |
Peri-procedural anti-thrombotic medication in PCI | - Aspirin: LD 162-325 mg/day then 75-100mg/day
- P2Y12 inhibitor- Clopidogrel: LD 300-600mg/day then 75mg/day for at least 12m
- Anti-coagulants: LMWH 1mg/kg or Unfractionated heparin or Bivalrudin
- Glycoprotein IIb/IIIa inhibitors for high risk patients (recurrent ischemia, dynamic ECG changes or hemodynamically unstable) eg Abciximab, Tirofiban, Eftifibatide for 6-24hrs |
Fibrinolytic therapy : contraindications | - Aortic dissection
- Previous hemorrhagic stroke
- Previous ischemic stroke w/in 1 yr
- Active internal bleeding
- Intracranial tumour
- Pericarditis |
Myocardial Revascularisation | restoration of blood supply to ischemic myocardium to limit ongoing damage, reduce ventricular irritability & improve long-term and short-term outcomes in ACS patients
Modes:
- Fibrinolytic therapy,
- PCI w/ or w/out stent placement
- CABG |
Myocardial Revascularisation: Unstable Angina NSTEMI | - immediate perfusion not urgent
- Angiography w/in 24-48hrs of hospitalisation to identify coronary lesions requiring PCI or CABG
- Non-interventional approach & trail of medical management if angiography shows ( small area of myocardium at risk, lesion morphology not amenable to PCI, CA stenosis <50% or significant left main disease in CABG candidates) or patients are at high risk of procedure- related morbidity and mortality
- if persistent chest pain despite meds -> Immediate PCI or CABG |
MI: Early complications (<48hrs) | 1) Arrhythmias: ventricular fibrillation/flutter, ventricular extrasystoles, atrial fibrillation/flutter/premature beats , AV block( if inferior infarct), bradyarrhythmias
2) LV insufficiency/ Cardiogenic shock (SBP <90mmHg)
3) RV insufficiency
4) Acute pulmonary edema |
MI: Late complications (>48hrs) | 1) Cardiac aneurysm
2) Pericarditis
3) Remodelling (hypertrophy)
4) Rupture of the heart
5) Arrhythmias
6) Heart failure
- Stroke (emboli from LV)
- Venous thrombosis |