1. Acute coronary syndrome
Non-ST elevation myocardial infarction
(NSTEMI)/unstable angina (UA)

2. UA and NSTEMI are closely related conditions with similar clinical presentation, treatment, and pathogenesis but of varying severity. If there is biochemical evidence of myocardial damage, the condition is termed NSTEMI; in the absence of damage it is termed UA.
Unlike patients with a STEMI, in whom diagnosis is generally made on presentation in the emergency department, diagnosis of NSTEMI/UA may not be definitive on presentation and evolves over the subsequent hours to days. Therefore, management of patients with NSTEMI/UA is a progression through a number of risk stratification processes dependent on history, clinical features, and investigative results. These in turn determine the choice and timing of a number of medical and/or invasive treatment strategies.

3. Clinical presentation
There are three distinct presentations: • New-onset angina (in a patient without prior angina) • Rest angina (angina when patient is at rest; may occur in a patient with prior stable, exertional angina) • Increasing angina (in a patient with previously diagnosed angina for whom angina has become more frequent or longer in duration or requires a lower threshold to elicit)

4. NSTEMI/UA: diagnosis
Diagnosis in NSTEMI/UA is an evolving process and may not be clear on presentation. A combination of history, serial changes in ECG, and biochemical markers of myocardial injury (usually over a 24- to 48-hourperiod) determine the diagnosis.
Serial ECGs : Changes can be transient and/or fixed, especially if a diagnosis of NSTEMI is made.
• ST-segment depression of 0.05 mV is highly specific of myocardial ischemia (unless isolated in V1–V3, suggesting a posterior STEMI).
• T-wave inversion is sensitive but nonspecific for acute ischemia unless very deep ( 0.3 mV).
• Rarely, Q waves may evolve or there may be transient or new LBBB.

5. Serial biochemical markers of cardiac injury
These are used to differentiate between NSTEMI and UA, as well as to determine prognosis. Levels at 0, 6, and 12 hours after the last episode of pain. A positive biochemical marker (CK, CK-MB, or troponin) in the context of one or more of the ECG changes listed above is diagnostic of NSTEMI. If serial markers over a 24-hour period from the last episode of chest pain remain negative, UA is diagnosed.

6. Cardiac troponin T and I
Both of these are highly cardiac specific and sensitive, can detect “micro-
infarction” in the presence of normal CK-MB, are not affected by skeletal
muscle injury, and convey prognostic information (worse prognosis if posi-
tive). Troponins can be raised in nonatherosclerotic myocardial damage
(cardiomyopathy, myocarditis, pericarditis chronic renal failure) and should thus be interpreted in the context of the clinical picture.
Both TnT and TnI rise within 3 hours of infarction. TnT may persist up
to 10–14 days and TnI up to 7–10 days.
• CK levels do not always reach the diagnostic twice upper-limit of
normal and generally have little value in diagnosis of NSTEMI.
• CK-MB has low sensitivity and specificity. CK-MB isoforms improve
sensitivity (CK-MB2>1 U/L or CK-MB2/CK-MB1 ratio >1.5), but isoform assays are not widely available clinically.
• Myoglobine is non–cardiac specific, but levels can be detected as early
as 2 hours after onset of symptoms. A negative test is useful in ruling
out myocardial necrosis.

7. NSTEMI/UA: risk stratification
Early risk stratification
This should take place on presentation and forms part of the initial assessment used to make a diagnosis. It involves a combination of clinical features, ECG changes, and biochemical markers of cardiac injury. Patients are divided into high risk and intermediate/low risk.
• High-risk patients should be admitted to the CCU, follow an early invasive strategy, and be managed with a combination of :-
. ASA, clopidogrel, LMWH (or UFH), and/or gpIIb/IIIa antagonists
. Anti-ischemic therapy (first-line B-blocker, nitroglycerin)
. Early invasive strategy (inpatient catheterization and PCI within 48 hours of admission)
• Intermediate- to low-risk patients should be admitted to a monitored
bed on a step-down unit and undergo a second inpatient risk stratification once their symptoms have settled, to determine timing of invasive investigations. Initial management should include :-
• ASA, clopidogrel, LMWH (or UFH)
• Anti-ischemic therapy (first-line B-blocker, nitroglycerin)
• Undergo a late risk stratification in 48–72 hours from admission

8. Late risk stratification
This involves a number of noninvasive tests to determine the optimal tim-
ing for invasive investigations in intermediate/low-risk patients. It is gener-
ally performed if there have been no further episodes of pain or ischemia
at 24–48 hours after admission.
• Intermediate/low-risk patients who develop recurrent pain and/or
ischemic ECG changes, heart failure, or hemodynamic instability (in
the absence of a noncardiac cause) should be managed as a high-risk
• . High-risk patients from these assessments should also follow an early invasive strategy and intermediate/low-risk patients, a more conservative strategy.

9. NSTEMI/UA: medical management
1. Analgesia Morphine 2.5–5 mg IV. Acts as anxiolytic, reduces pain and systolic blood pressure through venodilatation and reduction in sympathetic arteriolar constriction. It can result in hypotension (responsive to volume therapy) and respiratory depression (reversal with naloxone 400 µg to 2 mg IV).

10. Antithrombotic therapy
2. Nitrates
• Nitroglycerin infusion (50 mg in 50 mL normal saline at 1–10 mL/hr) titrated to pain and keeping SBP >100 mmHg. T
3. B-Blockers
• These should be started on presentation. Initially use a short-acting agent (e.g., metoprolol 12.5–100 mg po bid), which if tolerated, may be converted to a longer acting agent (e.g., atenolol 25–1000 mg qd).
Rapid B-blockade may be achieved using short-acting IV agents such as metoprolol. Aim for HR of ~50–60 beats/min.
4. Calcium antagonists
• Diltiazem 60–360 mg po, verapamil 40–120 mg po tid. These aim to reduce HR and BP and are a useful adjunct to treatments 1–3 above.
Amlodipine/felodipine 5–10 mg po qd can be used with pulmonary edema and in poor LV function.
5. Statins (HMG-CoA reductase inhibitors)
High-dose statins (e.g., atorvastatin 80 mg qd) have been shown to reduce mortality and recurrent MI in the acute setting. The role of statins in primary and secondary prevention of cardiovascular events is well documented.
Antiplatelet therapy
All patients should be given aspirin and clopidogrel (unless contraindications)—gp IIb/IIIa antagonists to high-risk patients only.
Antithrombotic therapy
They should be used in conjunction with aspirin and clopidogrel in all patients on presentation and continued for 2–5 days after the last episode of pain and ischemic ECG changes.

11. Discharge and secondary prevention
• Length of hospital stay will be determined by symptoms and the rate of progression through the NSTEMI/UA pathway. Generally patients are hospitalized for 3–7 days.
• Secondary prevention remains of paramount importance and is similar in principle to that for STEMI patients.

12. Symptoms suggestive of ACS
Noncardiac diagnosis
Chronic stable angina
NSTEMI/UA
STEMI
Admit ,ASA, Clopidogrel, LMWH (UFH), NTG infusion, B-blocker, statin
Admit to CCU,Reperfusion ther.
Early risk stratifiction in E.R
Low risk
Intermid. risk
High risk
No,
Late risk stratification
Admit, monitor.
Sympt.cont.?
Yes, treat as
High risk
Admit to CCU
Early invasive strategy
Low risk
High risk
In patient angiog.
O.P angiography

13. Mention 3 characteristics of vulnerable atheromatus plaque.