Unstable Angina and NSTEMi

1. NSTE-ACS
NON-ST-ELEVATION
ACUTE CORONARY SYNDROMES
Dilina Aarewatte
Himesha Galgamuwa
Group 9A | TSMU

2. What are NSTE-ACS?
Non ST-elevation acute coronary
syndrome is characterised by
episodes of chest pain at rest or
with minimal exertion, which
increase in frequency or severity,
often with dynamic ECG changes.
NSTEMI
Unstable
Angina

4. Pathophysiology
● Most commonly caused by an imbalance
between oxygen supply and oxygen demand
resulting from a partially occluding thrombus
● This thrombus could be formed on a disrupted
atherothrombotic coronary plaque or on an
eroded coronary artery endothelium.
● The reduction of the blood flow caused by the
thrombus (and by embolization / debris) can
cause severe ischemia or myocardial necrosis.

5. ● Dynamic obstruction (e.g., coronary
spasm,as in Prinzmetal’s variant angina)
● Severe mechanical obstruction due to
progressive coronary atherosclerosis
● Increased myocardial oxygen demand
produced by conditions such as fever,
tachycardia, and thyrotoxicosis in the
presence of fixed epicardial coronary
obstruction.
Other causes:

6. Diagnosis
● Diagnosis is based largely on the clinical presentation
● Typically, chest discomfort is severe and has at least one
of three features:
○ it occurs at rest (or with minimal exertion), lasting
>10 minutes;
○ it is of relatively recent onset (i.e., within the prior
2 weeks); and/or
○ it occurs with a crescendo pattern (i.e., distinctly
more severe, prolonged, or frequent than previous
episodes).
● NSTEMI diagnosis is established with evidence of
abnormally elevated cardiac biomarker levels.

7. History and PE
● The chest discomfort, often severe, is typically located in the
substernal region or sometimes in the epigastrium, and
radiates to the left arm, left shoulder, and/or neck.
● Anginal “equivalents” such as dyspnea, epigastric discomfort,
nausea, or weakness may occur instead of chest pain and
appear to be more frequent in women, the elderly, and patients
with diabetes mellitus.
● The physical examination resembles that in patients with
stable angina and may be unremarkable.
● If the patient has a large area of myocardial ischemia or a large
NSTEMI, the physical findings can include
○ diaphoresis;
○ pale, cool skin;
○ sinus tachycardia;
○ a third and/or fourth heart sound;
○ basilar rales;
○ Hypotension (sometimes).

8. Electrocardiogram
● ST-segment depression occurs in 20 to
25% of patients; it may be transient in
patients without biomarker evidence of
myocardial necrosis, but may be
persistent for several days in NSTEMI.
● T-wave changes are common but are less
specific signs of ischemia, unless they are
new and deep T-wave inversions (≥0.3
mV).

10. Cardiac Biomarkers
● NSTEMI patients have elevated biomarkers of
necrosis, such as cardiac troponin I or T, which are
specific, sensitive, and the preferred markers of
myocardial necrosis.
● The MB isoform of creatine kinase (CK-MB) is a
less sensitive alternative. Elevated levels of these
markers distinguish patients with NSTEMI from
those with UA.
● There is a characteristic temporal rise and fall of
the plasma concentration of these markers and a
direct relationship between the degree of elevation
and mortality.

12. Risk Stratification
● The diagnosis of a non-ST elevation ACS
(NSTE-ACS) in the emergency department should
be followed by risk stratification and treatment.
● Clinical guidelines recommend an early invasive
strategy in higher risk NSTE-ACS.
● The Global Registry of Acute Coronary Events
(GRACE) risk score is a validated risk
stratification tool which has incremental
prognostic value for risk stratification compared
with clinical assessment or troponin testing alone.

13. Treatment and Complications
Medical Treatment
● Patients should be placed at bed rest with continuous ECG monitoring for ST-segment
deviation and cardiac arrhythmias.
● Ambulation is permitted if the patient shows no recurrence of ischemia (symptoms or ECG
changes) and does not develop an elevation of a biomarker of necrosis for 12–24 h.
● Medical therapy involves simultaneous Anti-ischemic and Antithrombotic treatments and
consideration of coronary revascularization

14. ANTI-ISCHEMIC TREATMENT
To provide relief and prevention of recurrence of chest pain, initial treatment should include bed rest,
nitrates, beta adrenergic blockers, and inhaled oxygen in the presence of hypoxemia
1. Nitrates
i. Sublingual or buccal spray - if the patient is experiencing ischemic pain
ii. Intravenous Nitroglycerin - If pain persists after three doses given 5 min apart
a. The rate of the infusion may be increased by 10 μg/min every 3–5 min
until symptoms are relieved, systolic arterial pressure falls to <100
mmHg, or the dose reaches 200 μg/min.
iii. Topical or Oral Nitrates - can be used when the pain has resolved, or they may
replace intravenous nitroglycerin when the patient has been pain free for 12–24h.
● Contraindications - The only absolute contraindications to the use of nitrates are hypotension
or the use of sildenafil or other phosphodiesterase-5 inhibitors within the previous 24–48 h

15. 2. Beta Blockers
● Started by the intravenous route in patients with severe ischemia, but this is contraindicated
in the presence of heart failure
● Oral beta blockade targeted to a heart rate of 50–60 beats/min is recommended.
3. Calcium Channel Blockers
● Heart rate–slowing calcium channel blockers, e.g. verapamil or diltiazem, are recommended
for patients who have persistent symptoms or ECG signs of ischemia after treatment with
full-dose nitrates and beta blockers and in patients with contraindications to either class of
these agents
❖ Additional medical therapy includes angiotensin-converting enzyme (ACE) inhibitors or, if these are not
tolerated, angiotensin receptor blockers.
❖ Early administration of intensive HMG-CoA reductase inhibitors (statins), such as atorvastatin 80
mg/d, prior to percutaneous coronary intervention (PCI), and continued thereafter, has been shown to
reduce complications of the procedure and recurrences of ACS.

16. ANTITHROMBOTIC THERAPY
1. Antiplatelet Drugs
Initial treatment should begin with the platelet cyclooxygenase inhibitor Aspirin.
● Contraindications are active bleeding or aspirin intolerance.
Dual Antiplatelet Therapy (Asprin + Platelet P2Y12 Receptor Blocker)
● In the absence of a high risk for bleeding, patients with NSTE-ACS should receive a platelet P2Y12
receptor blocker to inhibit platelet activation. The Clopidogrel is an inactive prodrug that is converted
into an active metabolite that causes irreversible blockade of the platelet P2Y12 receptor. When
added to aspirin it has been shown to confer a 20% reduction in cardiovascular death, MI, or stroke,
compared to aspirin alone, but to be associated with a moderate increase in major bleeding
Triple Antiplatelet Therapy (Asprin + Platelet P2Y12 Receptor Blocker + Reversible platelet P2Y12 inhibitor)

17. 2. Anticoagulants
(1) Unfractionated Heparin (UFH), long the mainstay of therapy
(2) Low-Molecular-Weight Heparin (LMWH), enoxaparin, which has been shown to be
superior to UFH in reducing recurrent cardiac events
(3) Bivalirudin, a direct thrombin inhibitor that is similar in efficacy to either UFH or LMWH
but causes less bleeding and is used just prior to and/or during PCI
(4) Indirect factor Xa inhibitor, fondaparinux, which is equivalent in efficacy to enoxaparin
but appears to have a lower risk of major bleeding

18. LONG-TERM MANAGEMENT
● Risk-factor modification
○ the caregiver should discuss with the patient the importance of smoking
cessation, achieving optimal weight, daily exercise, blood-pressure control,
following an appropriate diet, control of hyperglycemia (in diabetic patients), and
lipid management
● long-term therapy with five classes of drugs are directed
○ Beta blockers, statins and ACE inhibitors or
angiotensin receptor blockers are recommended for
long-term plaque stabilization.

19. PRINZMETAL’S VARIANT ANGINA
A syndrome of severe ischemic
pain that usually occurs at rest
and is associated with transient
ST-segment elevation. PVA is
caused by focal spasm of an
epicardial coronary artery, leading
to severe transient myocardial
ischemia and occasionally
infarction

20. ● Patients with PVA are generally younger and have fewer coronary risk factors (with the
exception of cigarette smoking) than do patients with NSTE-ACS.
● Cardiac examination is usually unremarkable in the absence of ischemia.
● The clinical diagnosis of PVA is made by;
■ The detection of transient ST-segment elevation with rest pain.
■ Multiple episodes of asymptomatic ST-segment elevation (silent ischemia).
■ Small elevations of troponin
● Coronary angiography demonstrates transient coronary spasm as the diagnostic
hallmark of PVA.
● Atherosclerotic plaques in at least one proximal coronary artery, and in these patients,
spasm usually occurs within 1 cm of the plaque.
❖ Hyperventilation or intracoronary acetylcholine has been used to provoke focal coronary
stenosis on angiography or to provoke rest angina with ST-segment elevation to establish
the diagnosis
Clinical and Angiographic Manifestations

21. TREATMENT
● Nitrates and calcium channel blockers are the main therapeutic agents.
● Aspirin may actually increase the severity of ischemic episodes, possibly as a result of the
sensitivity of coronary tone to modest changes in the synthesis of prostacyclin.
● The response to beta blockers is variable. Coronary revascularization may be helpful in patients
who also have discrete, flow-limiting, proximal fixed obstructive lesions.

22. ● Many patients with PVA pass through an acute, active phase, with frequent episodes of angina
and cardiac events during the first 6 months after presentation.
● Patients with no or mild fixed coronary obstruction tend to experience a more benign course
than do patients with associated severe obstructive lesions.
● Nonfatal MI occurs in up to 20% of patients by 5 years.
● Patients with PVA who develop serious arrhythmias during spontaneous episodes of pain are at
a higher risk for sudden cardiac death.
● In most patients who survive an infarction or the initial 3- to 6-month period of frequent
episodes, there is a tendency for symptoms and cardiac events to diminish over time.
PROGNOSIS

23. References
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syndromes: Risk scores, biomarkers and clinical judgment. International journal of cardiology. Heart & vasculature.
Retrieved July 8, 2022, from
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k%20patients%20for%20invasive%20management.
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Non-ST-Elevation Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association
Task Force on Practice Guidelines. Circulation. 2014 Dec 23;130(25):e344-426full-text or in J Am Coll Cardiol. 2014 Dec
23;64(24):e139

24. Thank You!