Acute coronary syndrome

Dinesh k lamsal :MD

Background:

The initial diagnosis of acute coronarysyndrome (ACS) is

based entirely on history, risk factors, and, to a lesser
extent, ECG findings.
The symptoms are due to myocardial ischemia, the
underlying cause of which is an imbalance between supply
and demand of myocardial oxygen.
Internationally: In Britain, annual incidence of angina is
estimated at 1.1 cases per 1000 males and 0.5 cases per
1000 females aged 31-70 years. In Sweden, chest pain of
ischemic origin is thought to affect 5% of all males aged 50-
57 years. In industrialized countries, annual incidence of
unstable angina is approximately 6 cases per 10,000 people.
 Mortality/Morbidity:

• When the only treatment for angina was

nitroglycerin and limitation of activity.
• patients with newly diagnosed angina had a
40% incidence of MI and a 17% mortality rate
within 3 months.
• A recent study shows that the 30-day mortality
from ACS has decreased as treatment has
improved, a statistically significant 47% relative
decrease in 30-day mortality among newly
diagnosed ACS from 1987-2000.
• This decrease in mortality is attributed to aspirin,
glycoprotein (GP) IIb/IIIa blockers, and coronary
revascularization via medical intervention or
procedures
 Incidence :
• Sex: Incidence is higher in males among all patients
younger than 70 years. This is due to the cardioprotective
effect of estrogen in females. At 15 years postmenopause,
the incidence of angina occurs with equal frequency in
both sexes. Evidence exists that women more often have
coronary events without typical symptoms, which might
explain the frequent failure to initially diagnose ACS in
women.
• Age: ACS becomes progressively more common with
increasing age. In persons aged 40-70 years, ACS is
diagnosed more often in men than in women. In persons
older than 70 years, men and women are affected equally.

•
 Pathophysiology:
• Myocardial ischemia is most often due to atherosclerotic
plaques, which reduce the blood supply to a portion of
myocardium. Initially, the plaques allow sufficient blood flow
to match myocardial demand.
• When myocardial demand increases, the areas of narrowing
may become clinically significant and precipitate angina.
Angina that is reproduced by exercise, eating, and/or stress
and is subsequently relieved with rest, and without recent
change in frequency or severity of activity that produce
symptoms, is called chronic stable angina.
• Over time, the plaques may thicken and rupture, exposing a
thrombogenic surface upon which platelets aggregate and
thrombus forms. The patient may note a change in
symptoms of cardiac ischemia with a change in severity or
of duration of symptoms. This condition is referred to as
unstable angina.
 Contd… (1)
• The excessive mortality rate of coronary heart
disease is primarily due to rupture and thrombosis
of the atherosclerotic plaque.
• Inflammation plays a critical role in plaque
destabilization and is widespread in the coronary
and remote vascular beds. Systemic inflammatory,
thrombotic, and hemodynamic factors are relevant
to the outcome.
• Evidence indicates that platelets contribute to
promoting plaque inflammation as well as
thrombosis. A new theory of unbalanced cytokine-
mediated inflammation is emerging, providing an
opportunity for intervention.
 Contd …..(2)

• Patients with STEMI have a high likelihood of a

coronary thrombus occluding the infarct artery.
• Angiographic evidence of coronary thrombus
formation may be seen in more than 90% of
patients with STEMI but in only 1% of patients
with stable angina and about 35-75% of patients
with unstable angina or NSTEMI.
• However, not every STEMI evolves into a Q-
wave MI; likewise, a patient with NSTEMI may
develop Q waves
 Causes:
• Atherosclerotic plaque is the predominant cause.
Coronary artery vasospasm is less common.
• Alternative causes of angina include the following:
– Ventricular hypertrophy due to hypertension, valvular
disease, or cardiomyopathy
– Embolic occlusion of the coronary arteries
– Hypoxia, as in carbon monoxide poisoning or acute
pulmonary disorders
– Cocaine and amphetamines, which increase myocardial
oxygen demand and may cause coronary vasospasm
– Underlying coronary artery disease, which may be
unmasked by severe anemia
– Inflammation of epicardial arteries
– Coronary artery dissection
 Risk factors
Male gender
Diabetes mellitus (DM)
Smoking history
Hypertension
Increased age
Hypercholesterolemia
Hyperlipidemia
Prior cerebrovascular accident (CVA) - These patients constitute 7.5% of
patients with ACS and have high-risk features.
Inherited metabolic disorders
Methamphetamine use
Occupational stress
Connective tissue disease
 CLINICAL
• History: Typically, angina described as a sensation of chest
pressure or heaviness that is reproduced by activities or
conditions that increase myocardial oxygen demand.
• Some present with only neck, jaw, ear, arm, or epigastric
discomfort.
• Other symptoms, such as shortness of breath or severe
weakness, may represent anginal equivalents.
• A new case of angina is more difficult to diagnose because
symptoms are often vague and similar to those caused by
other conditions (eg, indigestion, anxiety).
• Patients may have no pain and may only complain of
episodic shortness of breath, weakness, lightheadedness,
diaphoresis, or nausea and vomiting.
• Patients may complain :Palpitations , Decreased exercise
tolerance
 Differential diagnosis: (on hx)
Stable angina
– Involves episodic pain lasting 5-15 minutes
– Provoked by exertion
– Relieved by rest or nitroglycerin
Unstable angina : Patients have increased risk for
adverse cardiac events, such as MI or death.
Three clinically distinct forms exist, as follows:
• New-onset exertional angina
• Angina of increasing frequency or duration or
refractory to nitroglycerin
• Angina at rest
 Contd ….
• Variant angina (Prinzmetal angina)
– Occurs primarily at rest
– Triggered by smoking
– Thought to be due to coronary vasospasm

Elderly persons and those with diabetes

• may have particularly subtle presentations and may complain of fatigue,
syncope, or weakness. Elderly persons may also present with only
altered mental status. Those with preexisting altered mental status or
dementia may have no recollection of recent symptoms and may have
no complaints whatsoever.
As many as half of cases of ACS
• are clinically silent in that they do not cause the classic symptoms
described above and consequently go unrecognized by the patient.
Maintain a high index of suspicion for ACS especially when evaluating
women, diabetics, older patients, patients with dementia, and those with
a history of heart failure.
 Diff . Dx. With others dis……
• Anxiety
• As
• Asthma
• Dcm
• Esophagitis
• Gastroenteritis
• Htn-ive ER
• Mi
• Percarditis
• Pneumothorax
• Pulmonary edema
 Physical:
• Physical examination results are frequently normal. If chest
pain is ongoing, the patient usually will lie quietly in bed and
may appear anxious, diaphoretic, and pale.
• Hypertension may precipitate angina or reflect elevated
catecholamines due to either anxiety or exogenous
sympathomimetic stimulation.
• Hypotension indicates ventricular dysfunction due to
myocardial ischemia, infarction, or acute valvular dysfunction.
• Congestive heart failure (CHF)
• Jugular venous distention
– Third heart sound (S3)
– A new murmur may reflect papillary muscle dysfunction
– Rales on pulmonary examination, suggesting left ventricular (LV)
dysfunction or mitral regurgitation
– Presence of a fourth heart sound (S4), a common finding in patients
with poor ventricular compliance due to preexisting ischemic heart
disease or hypertension
 Investigation
Lab Studies:
Troponin- for diagnosing myocardial necrosis. It is detectable in serum
3-6 hours after an MI, and its level remains elevated for 14 days.
CK-MB - levels begin to rise within 4 hours after MI, peak at 18-24 hours,
and subside over 3-4 days
lactase dehydrogenase – rises within 24 hours of MI , peak within 3-6
days, and returns to the baseline within 8-12 days
Cardiac markers -should be used liberally to evaluate patients with
prolonged episodes of ischemic pain, with new changes on ECG, or with
nondiagnostic or normal ECGs in whom the diagnosis of ACS or MI is
being considered.
C b c- is indicated to determine if anemia is a precipitant
b s l, renal function, and electrolytes levels, for patients with new-onset
angina.
Creatinine levels (For use ACE)
 Imaging Studies:
Chest x-ray: may demonstrate complications of ischemia, such as pulmonary edema ,
thoracic aneurysm or pneumonia.
Echocardiogram: identifying precipitants for ischemia, such as ventricular hypertrophy and
valvular disease.
Radionuclide myocardial perfusion imaging
Other Tests :ECG is the most important ED diagnostic test for angina
– Transient ST-segment elevations (fixed changes suggest acute MI):
In patients with elevated ST segments, consider LV aneurysm,
pericarditis, Prinzmetal angina, early repolarization, and Wolff-
Parkinson-White syndrome as possible diagnoses.
– Dynamic T-wave changes (inversions, normalizations, or hyperacute
changes): In patients with deep T-wave inversions, consider also
CNS events or drug therapy with tricyclic antidepressants or
phenothiazines.
– ST depressions that may be junctional, downsloping, or horizontal
– Diagnostic sensitivity may be increased by performing right-sided
leads (V4R), posterior leads (V8, V9), and serial recordings.
 TREATMENT
Prehospital Care:
• Obtain IV access.
• Administer supplemental oxygen.
• Aspirin should be given in the field, 162-325 mg chewed and
swallowed.
• Telemetry and prehospital ECG, if available, may be helpful
in selected circumstances. Certain EMS systems have
investigated protocols for prehospital administration of
thrombolytic therapy. This has not become a trend due to
unproven benefit and due to the increase in availability of
percutaneous coronary intervention (PCI) in many medical
centers as an alternative to thrombolysis for STEMI.
• Perform pulse oximetry.
• Administer sublingual or aerosolized nitroglycerin if chest
pain is ongoing and is felt to be cardiac in origin.
 Emergency Care :
• Goals of ED care are rapid identification of patients with STEMI,
exclusion of alternative causes of nonischemic chest pain, and
stratification of patients with acute coronary ischemia into low- and high-
risk groups.
• Obtain IV access, administer supplemental oxygen, and provide
telemetry monitoring if these procedures have not already been
accomplished in the prehospital phase. In addition, obtain a 12-lead
ECG as soon as possible after arrival.
• Complete a history and physical examination, with focus on risk factors
for coronary ischemia; onset, duration, and pattern of symptoms; and
early identification of complications of myocardial ischemia (eg, new
murmurs, CHF).
• Perform frequent reassessment of vital signs and symptoms in response
to administered therapies.
• Serial ECGs and continuous ST segment monitoring may be useful.
• Many EDs have an observation unit that may be an appropriate
disposition for patients who meet admission criteria.
• Medical therapy : Medication.
• Consultations: Cardiology
 MEDICATION
Drugs:
antiplatlets (aspirin-160-324 mg PO or chewed; suppository if
patient is unable to take PO medications )
Nitrates (Nitroglycerin-400 mcg SL or spray q5min, repeated up to 3
times, If symptoms persist, administer 5-10 mcg/min IV infusion )
Analgesics (Morphine sulfate - 2-4 mg IV q5-15min; titrate to
symptomatic relief or adverse effects (eg, lethargy, hypotension,
respiratory depression )
Anticoagulants (Heparin -- Augments activity of antithrombin III and
prevents conversion of fibrinogen to fibrin.)
dose : 80 U/kg IV bolus, followed by an infusion of 18 U/kg/h

Beta-adrenergic blockers (Metoprolol - 5 mg slow IV infusion q5min;

to a maximum dose of 15 mg or desired heart rate)
Low molecular weight heparins ( Enoxaparin-1 mg/kg administered
SC q12h in conjunction with oral aspirin (100-325 mg/d)
Adenosine diphosphate receptor antagonists (Clopidogrel-300 mg PO
loading dose, followed by 75 mg PO qd )
 Inpatients care
• Patients with unstable angina and/or ECG changes should be admitted to
a telemetry bed. A certain subset of patients with stable angina may be
treated as outpatients with antianginal agents, but close follow-up is
necessary.
• Patients with symptoms refractory to aggressive medical treatment, shock,
suspected or known aortic stenosis, or new or worsening mitral
regurgitation are at high risk. Management for these patients should
include the following:
– Admission to an intensive care unit setting
– Cardiology consultation
• Consideration for intra-aortic balloon pump (IABP) and early angiography
to delineate anatomy
• Continue antiplatelet and antianginal medications initiated in the ED.
Subsequent dosing is determined by symptomatic response and tolerance
of side effects.
• The routine use of lidocaine as prophylaxis for ventricular arrhythmias in
patients with ACS is not indicated. In MI, it has been shown to increase
mortality rates. Lidocaine may be used for patients with complex
ventricular ectopy or for patients with hemodynamically significant,
nonsustained, or sustained ventricular tachycardia.
 Complications:
• Acute myocardial infarction
• Cardiogenic shock
• Ischemic mitral regurgitation
• Arrhythmias
– Supraventricular arrhythmias (rare complication of
ischemia, may actually precipitate ischemic events)
– Ventricular arrhythmias; simple and complex premature
ventricular contractions (PVCs), and nonsustained
ventricular tachycardia (NSVT)
• Atrioventricular nodal blockade
– Usually transient in setting of reversible ischemia
– Treatment guided by location of block and hemodynamic
stability.
• Ventricular rupture occurs in the interventricular septum or
the LV free wall
 Prognosis:
• Patients with angina either go on to infarct or have their disease stabilized
by medical and/or interventional therapies. Patients with angina are a
heterogeneous group; therefore, prognosis varies with respect to stability of
disease, demographics, comorbidity, and current intervention.
• Patients with ACS with atrial fibrillation (AF) are associated with increased
morbidity and mortality (Mehta, 2003).
• Patients with ACS and DM, especially those with ST elevation, had
increased in-hospital mortality. Among patients with ACS and DM, those
receiving insulin had worse outcomes. Outcomes were similar for those on
hypoglycemic medication or on diet alone (Hasdai, 2003).
• In chronic stable angina, prognosis is generally excellent. Factors that have
been shown to impact prognosis include the following:
– Aspirin reduces progression to both nonfatal MI and cardiac death.
– Beta-blockers control anginal symptoms and reduce cardiac complications in
patients with hypertension.
– PTCA and revascularization improve the prognosis in high-risk patients.
– Poor prognostic factors include male sex, diabetes, and hypertension.
• In unstable angina, prognosis is determined by the ability to control
symptoms acutely, preventing progression to AMI. Factors associated with a
poorer prognosis include the following:
– Evidence of myocardial necrosis, as determined by elevated troponin T
– Delays in angiography in patients at high risk (Early angiography allows for triage
to medical therapy, PTCA, or revascularization.)