Acute Coronary Syndromes and Angina.. By Shapi.

INTERNAL MEDICINE
• INTERNAL MEDICINE
• ANGINA PECTORIS AND ACUTE CORONARY SYNDROMES:
Dr. Chongo Shapi (BSc.HB, MBChB)
- Medical Doctor.
2/26/2024 Dr. Chongo Shapi, BSc.HB, MBChB.. 1

ANGINA PECTORIS
• Angina is symptomatic reversible myocardial
ischaemia.
• Clinical Features include:
1. Constricting/heavy discomfort to the chest, jaw,
neck, shoulders, or arms.
2. Symptoms brought on by exertion.
3. Symptoms relieved within 5min by rest or GTN.
4. All 3 features = typical angina; 2 features =
atypical angina; 0–1 features = nonanginal
5. chest pain.

CONT’
• Other precipitants: Emotion, cold weather,
and heavy meals.
• Associated symptoms include: dyspnoea,
nausea, sweatiness, faintness.
• Features that make angina less likely: Pain that
is continuous, pleuritic or worse with
swallowing; Pain associated with palpitations,
dizziness or tingling.

CAUSES OF ANGINA PECTORIS
• Atheroma.
• Rarely: anaemia.
• coronary artery spasm.
• AS; tachyarrhythmias.
• HCM; arteritis/small vessel disease
(microvascular angina/cardiac syndrome X).

TYPES OF ANGINA
• Stable angina: Induced by effort, relieved by rest.
Has a good prognosis.
• Unstable angina: (Crescendo angina.) Angina of
increasing frequency or severity; Occurs on
minimal exertion or at rest. Associated with risk
of MI.
• Decubitus angina: Precipitated by lying flat.
• Variant (Prinzmetal) angina: (‘Vasospastic
angina’) Caused by coronary artery spasm (rare;
may coexist with fixed stenoses).

INVESTIGATIONS
• ECG: Is usually normal, but may show ST depression,
flat or inverted T waves or even signs of past MI.
• Blood tests: FBC, U&E, TFTs, lipids, HbA1c.
• Consider echo and chest X-ray.
• Further investigations are usually necessary to confirm
an IHD diagnosis.
• Angiography—Either using cardiac CT with contrast, or
transcatheter angiography (more invasive but can be
combined with stenting..
• Functional imaging: Myocardial perfusion scintigraphy,
stress echo (echo whilst undergoing exercise or
receiving dobutamine), cardiac MRI.

MANAGEMENT
• Address exacerbating factors: Anaemia,
tachycardia (eg fast AF), thyrotoxicosis.
• Secondary prevention of cardiovascular disease:
1. Stop smoking; exercise; dietary advice; optimize
hypertension and diabetes control.
2. 75mg aspirin daily if not contraindicated.
3. Address hyperlipidaemia
4. Consider ACE inhibitors, eg if diabetic.

CONT’
• PRN symptom relief: Glyceryl trinitrate (GTN)
spray or sublingual tabs.
• Advise the patient to repeat the dose if the
pain has not gone after 5min and to call an
ambulance if the pain is still present 5min
after the second dose.
• SE: headaches.

CONT’
• Anti-anginal medication: First line: B-blocker and/or
calcium channel blocker do not combine blockers with
non-dihydropyridine calcium antagonists). If these fail
to control symptoms or are not tolerated, trial other
agents.
1. B-blockers: eg atenolol 50mg BD or bisoprolol 5–
10mg OD.
2. Calcium antagonists: amlodipine—start at 5mg OD;
diltiazem—dose depends on formulation.
3. Long-acting nitrates: eg isosorbide mononitrate—
starting regimen depends on formulation.
Alternatives: GTN skin patches. SES: headaches, BP.

CONT’
4. Ivabradine: Reduces heart rate with minimal
impact on BP. Patient must be in sinus rhythm.
Start with 5mg BD (2.5mg in elderly).
5. Ranolazine: Inhibits late Na+ current. Start at
375mg BD. Caution if heart failure, elderly,
weight <60kg or prolonged QT interval.
6. Nicorandil: A K+ channel activator. Start with
5–10mg BD. CI: acute pulmonary oedema,
severe hypotension, hypovolaemia, LV failure.

CONT’
• Revascularization: Considered when optimal medical
therapy proves inadequate.
• Percutaneous coronary intervention (PCI): A balloon is
inflated inside the stenosed vessel, opening the lumen. A
stent is usually inserted to reduce the risk of re-stenosis.
• Dual antiplatelet therapy (DAPT; usually aspirin and
clopidogel) is recommended for at least 12 months after
stent insertion to reduce the risk of instent thrombosis.
• Specialist advice should be sought regarding antiplatelets if
the patient has a high bleeding risk or requires surgery.

CONT’
• CABG: Compared to PCI, patients undergoing
CABG are less likely to need repeat
revascularization and those with multivessel
disease can expect better outcomes.
• However, CABG is open heart surgery and so
recovery is slower and the patient is left with
two large wounds (sternal and vein
harvesting).

INTRODUCTION
• ACS includes unstable angina and myocardial
infarctions (MIs). These share a common
underlying pathology—plaque rupture,
thrombosis, and inflammation.
• However, ACS may rarely be due to emboli,
coronary spasm, or vasculitis in normal coronary
arteries.
• Myocardial infarction means there is myocardial
cell death, releasing troponin.
• Ischaemia means a lack of blood supply, ±cell
death.

CONT’
• MI’s have troponin rises, unstable angina does
not. An MI may be a STEMI—ACS with ST-
segment elevation (may only be present in V7–V9
if posterior STEMI) or new-onset LBBB; or an
NSTEMI—trop-positive ACS without ST-segment
elevation—the ECG may show ST depression, T-
wave inversion, non-specifi c changes, or be
normal.
• The degree of irreversible myocyte death varies,
and significant necrosis can occur without ST
elevation.

RISK FACTORS
• Non-modifiable: Age, gender, family history of
IHD (MI in 1st-degree relative <55yrs).
• Modifiable: Smoking, hypertension, DM,
hyperlipidaemia, obesity, sedentary lifestyle,
cocaine use.
• Controversial risk factors include: Stress, type
A personality, LVH, fibrinogen,
hyperinsulinaemia, homocysteine levels, ACE
genotype.

DIAGNOSIS
• An increase in cardiac biomarkers (eg
troponin) and either:
a) Symptoms of ischaemia, ECG changes of new
ischaemia, development of pathological Q
waves, new loss of myocardium, or
b) Regional wall motion abnormalities on
imaging.

CLINICAL FEATURES
• SYMPTOMS
1. Acute central chest pain, lasting >20min, often
associated with nausea,
2. Sweatiness, dyspnoea, palpitations. ACS without
chest pain is called ‘silent’; mostly seen in
elderly and diabetic patients. Silent MI’s may
present with: syncope, pulmonary, edema,
epigastric pain and vomiting, post-operative
hypotension or oliguria,
3. Acute confusional state, stroke, and diabetic
hyperglycaemic states.

CONT’
• SIGNS
1. Distress, anxiety, pallor, sweatiness, raised or
reduced pulse, raised or reduced BP, 4th heart
sound.
2. There may be signs of heart failure (Raised JVP,
3rd heart sound, basal crepitations) or a
pansystolic murmur (papillary muscle
dysfunction/rupture, VSD).
3. Low-grade fever may be present. Later, a
pericardial friction rub or peripheral oedema
may develop.

INVESTIGATIONS
1. ECG: ( STEMI: classically, hyperacute (tall) T waves, ST elevation, or
new LBBB occur within hours. T-wave inversion and pathological Q
waves follow over hours to days.
• NSTEMI/unstable angina: ST depression, T wave inversion, non-
specific changes, or normal. In 20% of MI, the ECG may be normal
initially. Paced ECGs and ECGs with chronic bundle branch block are
unhelpful for diagnosing.
• NSTEMI’s and may hinder STEMI diagnosis; in these cases, clinical
assessment and troponin levels are especially important.
2. CXR: Look for cardiomegaly, pulmonary oedema, or a widened
mediastinum. Don’t routinely delay treatment whilst waiting for a CXR.
3. Echo: Regional wall abnormalities.

CONT’
4. Blood: FBC, U&E, glucose, lipids, cardiac enzymes.
• Cardiac enzymes: Cardiac troponin levels (T and I) are
the most sensitive and specific markers of myocardial
necrosis. Different hospitals use different assays
• Check the required timing of troponin blood samples
where you work (eg two samples 3hrs apart).
• Other cardiac enzymes are sensitive but less specific;
their role in ACS diagnosis is decreasing as troponin
testing improves

MANAGEMENT
• ACS management depends on whether the ACS is ‘ST elevated’ or
not:
❑ ST elevated myocardial infarction (STEMI): this category includes
ACS with ST elevation on ECG but also ACS with new LBBB and
posterior Mis. Where ST elevation may only be seen with extra
leads (V7–V9), urgent revascularization is essential.
❑ ACS without ST elevation: Serial troponins are needed to
differentiate non-ST elevated
• MIs (NSTEMIs) (trop rise) from unstable angina (no trop rise).
• After the immediate actions described on treatment of ACS focuses
on managing symptoms, secondary prevention of further
cardiovascular disease, revascularization (if not already
undertaken), and addressing complications.

CONT’
• Symptom control: Manage chest pain with PRN GTN and opiates. If
this proves insufficient, consider a GTN infusion (monitor BP, omit if
recent sildenafil use). If pain is deteriorating, seek senior help.
Manage symptomatic heart failure.
• Patients should be strongly advised and helped to stop smoking
• Identify and treat diabetes mellitus, hypertension, and
hyperlipidaemia. Advise a diet high in oily fish, fruit, vegetables, &
fibre, and low in saturated fats.
• Encourage daily exercise. Refer to a cardiac rehab programme.
Mental health: flag to the patient’s GP if depression or anxiety are
present—these are independently associated with poor
cardiovascular outcomes.

CONT’
❑ Optimize cardioprotective medications
• Antiplatelets: aspirin (75mg OD) and a second antiplatelet agent (eg
clopidogrel) for at least 12 months to vascular events (eg MI,
stroke). Consider adding a PPI (eg lansoprazole) for gastric
protection. Anticoagulate, eg with fondaparinux, until discharge.
• B-blockade reduces myocardial oxygen demand. Start low and
increase slowly, monitoring pulse and BP. If contraindicated,
consider verapamil or diltiazem.
• ACE-i in patients with LV dysfunction, hypertension, or diabetes
unless not tolerated (consider ARB). Titrate up slowly, monitoring
renal function.
• High-dose statin, eg atorvastatin 80mg.
• Do an echo to assess LV function. Eplerenone improves outcomes in
MI patients with heart failure (ejection fraction <40%).

CONT’
❑Revascularization
• STEMI patients and very high-risk NSTEMI
patients (eg haemodynamically unstable) should
receive immediate angiography ± PCI.
• NSTEMI patients who are high risk (eg GRACE
score >140) should have angiography within 24h;
intermediate risk (eg GRACE 109–140) within 3d;
low-risk patients may be considered for non-
invasive testing.
• Patients with multivessel disease may be
considered for CABG instead of PCI

COMPLICATIONS
• Cardiac arrest
• Cardiogenic shock
• Left ventricular failure
• Bradyarrhythmias
• Tachyarrhythmias
• Right ventricular failure (RVF)/infarction
• Pericarditis: Central chest pain, relieved by sitting
forwards. ECG: saddle-shaped ST elevation.
Treatment: NSAIDS. Echo to check for effusion.

CONT’
• Systemic embolism: May arise from LV mural
thrombus. After large anterior MI, consider
anticoagulation with warfarin for 3 months.
• Cardiac tamponade: Presents with low cardiac output,
pulsus paradoxus, Kussmaul’s sign,3 muffled heart
sounds. Diagnosis: echo. Treatment: pericardial
aspiration
• Mitral regurgitation: May be mild (minor papillary
muscle dysfunction) or severe (chordal or papillary
muscle rupture secondary to ischaemia). Presentation:
pulmonary
• oedema. Treat LVF and consider valve replacement.

CONT’
• Ventricular septal defect: Presents with pansystolic murmur, raised
JVP, cardiac failure. Diagnosis: echo. Treatment: surgery. 50%
mortality in first week.
• Late malignant ventricular arrhythmias: Occur 1–3wks post-MI and
are the cardiologist’s nightmare. Avoid hypokalaemia, the most
easily avoidable cause. Consider 24h ECG monitoring prior to
discharge if large MI.
• Dressler’s syndrome: Recurrent pericarditis, pleural effusions, fever,
anaemia, and raised ESR 1–3wks post-MI. Treatment: consider
NSAIDS; steroids if severe.
• Left ventricular aneurysm: This occurs late (4–6wks post-MI), and
presents with LVF, angina, recurrent VT, or systemic embolism. ECG:
persistent ST-segment elevation. Treatment: anticoagulate,
consider excision.

THANK YOU!
• In an environment where their mouths speak
for them, I chose to allow my work ethic to
speak for me.

The End!

Acute Coronary Syndromes and Angina.. By Shapi.

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