Post Graduate Diploma in EMERGENCY MEDICAL

SERVICES (PGDEMS)
HUB: Life Supporters Institute of Health Sciences
University: Tata Institute of Social Sciences

Project By
Dr.Chaitali choraghe

Under Guidance of
Dr.Paresh Navalkar

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CASE STUDY :- UNSTABLE ANGAINA

Tata Institute of social science

School Vocation Education

PGDEMS

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TABLE OF CONTENT

 Abstract
 Introduction
 Literature view
 Case presentation
 Management and outcome
 Discussion
 Current research/study
 Upcoming research/study
 Acknowledgement
 References

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 ABSTRACT
Unstable angina is one of the most common reasons for hospital
admission in the United States and causes substantial morbidity and
mortality.. Diagnosis of unstable angina is complicated by the dynamic
range of presentations, which can vary between atypical chest pain . In
this we see brief about unstable angina and its management.
Overcautious management can result in unnecessary hospital
admission, whereas inappropriate conservative strategies can cause
cardiac injury and death. To define treatment strategies for these
patients, the US Agency for Health Care Policy and Re search in March
1994 published guidelines on the diagnosis and management
of unstable angina. The emphasis is on diagnosis or exclusion of
coronary artery disease, establishment of the patient's risk for adverse
outcome, and triage to the most appropriate treatment regimen. The
guidelines emphasize the use of aspirin, heparin sodium, and beta-
blockers as the core therapy. Appropriate strategies are reviewed,
starting with intensive medical management and ending with patient care
after discharge.

Keywords:-

Acute coronary syndrome ,cardiac rehabilitation ,chronic stable angina

Aspirin, Heparin, Unstable Angina, Myocardial Infarction,Direct
Thrombin Inhibitor, low molecular weight

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 INTRUDUCTION
Unstable angina or sometimes referred causes unexpected
chest pain and usually occurs while resting. The most common
cause is reduced blood flow to the heart muscle because the
coronary arteries are narrowed by fatty build-ups
(atherosclerosis ) which can ruptured causing injury to the
coronary blood vessel resulting in blood clotting which blocks
the flows of blood to the heart muscles.
Unstable angina should be treated as an emergency. if you
have new ,worsening or persistent chest discomfort ,you need
to go to the ER. you could be having a heart attack which puts
you at increased risk for severe cardiac arrhythmias or cardiac
arrest ,which could lead to sudden death .

Causes:-
Blood clots that block an artery partially or totally are what
causes unstable angina .Blood clots may form, partially
dissolve and later form again and angina can occur each time a
clot blocks blood flow in an artery .

Symtoms :-
The pain or discomfort
 Often occurs while you may be resting, sleeping or
with little physical exertion.
 Squeezing ,Heaviness, Tightening
 Burning or aching across the chest, usually starting
behind the breastbone.
 This pain often spreads to the neck, jaw, arms
shoulders, throat, back or even the teeth.
Patient also complaint of symptoms including :-
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 Indigestion
 Heartburn
 Weakness
 Nausea
 Cramping shortness of breath
 Rest or medicine usually do not help relive it
 May get worse over time
 Can lead to a heart attack
 Pathogenic mechanisms in unstable
angina
 In the mid-1980s, several researchers10-12 suggested
that unstable angina was linked to non–Q and Q
wave MI, and that these conditions represented a
spectrum of disease in which plaque disruption or
fissuring led to thrombus formation and the acute
coronary syndrome. Intracoronary thrombus
formation was thought to explain the pathogenesis in
most patients with unstable angina. As opposed to MI
with ST-segment elevation in which the thrombus
was usually occlusive, the thrombus in unstable
angina was mural and did not result in total coronary
occlusion in 80% to 90% of patients (Figure
1).13 Non–Q wave infarction is positioned between
the other 2 conditions because there was more
frequent total occlusion of the culprit artery than in
unstable angina but less than in Q wave MI.14,15
 Nearly all pathologic evidence in acute syndromes
originates from autopsy studies.16Because short-term
mortality of unstable angina is low, autopsy data in
unstable angina represent a highly select population.
Aside from these, pathologic material in unstable
angina has been obtained mainly from atheromatous
plaque that is excised during directional atherectomy
of the culprit lesion.17,18 This analysis is subject to
sampling error because only a portion of the plaque
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 is removed. Accordingly, our understanding of its
pathogenesis derives mainly through other methods,
including angiography, angioscopy, and biochemical
studies.
 Thrombus Formation in Unstable Angina
 Results of angiographic studies10,19,20 suggest that
intracoronary thrombus formation or a complex lesion
(ulcerated or irregular plaque) is found in 50% to 80%
of culprit lesions, particularly if the presentation is
rest pain. Serial angiograms performed before and
after an episode of unstable angina, without an
intervening coronary intervention, have shown
progression of coronary artery disease in about 75%
of patients.21,22
 Recently, Dangas et al23 correlated coronary
morphologic features of the culprit lesion to the
Braunwald classification. There were significant
(P<.05) positive correlations between severity of the
unstable angina presentation and presence of an
intracoronary thrombus or complex lesion. Results of
angioscopic studies24 also indicate that intracoronary
thrombus or yellow plaque is found in most unstable
culprit arteries but infrequently in stable angina. The
thrombus in unstable angina has been characterized
as grayish-white and presumably platelet-rich,
whereas in MI it was red.25 Because the coronary
artery is usually totally occluded in MI, this red
thrombus is rich in fibrin and red blood cells,
superimposed on the platelet component and
potentiated by stasis of blood flow. Although
angiography is commonly used to detect thrombus, it
has low sensitivity relative to
26,27
angioscopy. However, angiography is relatively
specific (80%-90%) for the detection of thrombus or a
complex lesion.26,27 Small thrombi or mural thrombi
that do not cause luminal irregularity probably cannot
be detected angiographically. In conclusion,

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 thrombus formation on a presumed disrupted,
fissured, or eroded plaque is the most common
pathophysiological mechanism in unstable angina,
particularly when the presentation is that of acute rest
pain. However, it is unrealistic to assume that
thrombus formation can explain all unstable
presentations. For patients without rest pain, there
are less convincing data that thrombus is the
predominant cause. In our opinion, these patients
require further evaluation.
 Other Pathogenic Mechanisms in Unstable
Angina
 Other mechanisms might explain the clinical
syndromes of unstable angina. Inflammation has
been implicated. Inflammation plays a role in plaque
rupture, contributing to destabilization of the fibrous
cap of so-called vulnerable plaques by the secretion
of matrix metalloproteinases.28 Results of directional
atherectomy analysis of culprit lesions in unstable
angina show a higher percentage of the excised
plaque area infiltrated by inflammatory cells
compared with stable angina. One difficulty with
understanding the role of inflammation is the
interrelationship between thrombus formation and
inflammation. Tissue factor is found more commonly
in unstable vs stable plaques, and results of
histopathologic analysis29,30 of atherectomy
specimens show a strong association between
macrophage infiltration and tissue factor localization.
Local expression of tissue factor by macrophages
can lead to activation of the coagulation cascade.
Furthermore, activation of platelets might lead to
inflammatory reactions at the site of vascular
lesions.31 Another link between inflammation and
thrombosis might be lipoprotein(a). Recent
data32 suggest that lipoprotein(a), which is
considered atherosclerotic and thrombogenic, also

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 colocalizes in macrophage-rich areas in unstable
plaques. At the molecular level, the apolipoprotein A
portion of the lipoprotein(a) molecule has been
shown33 to be responsible for macrophage
chemoattraction.
 Another potential nonthrombotic mechanism for
unstable angina might be smooth muscle cell
proliferation. In lesions without angiographic
evidence of thrombus, some patients have an
abundant proliferation of smooth muscle cells on
directional atherectomy analysis of excised plaque
similar to that found in restenotic lesions.34 Again,
excluding a role for thrombus is difficult because one
third of lesions had thrombus demonstrated on tissue
analysis, although the angiogram suggested no
thrombus. Furthermore, thrombus might be a potent
stimulus for smooth muscle cell proliferation, along
with cytokines or growth factors released from
inflammatory cells or other stimuli, including
infectious agents like Chlamydia pneumoniae and
cytomegalovirus.35 Smooth muscle cell proliferation
without thrombus might play a role in unstable angina
in the restenotic lesion. Restenotic lesions do not
usually contain thrombus, yet their presentation might
be that of rest pain even with enzyme level elevation,
indicating non–Q wave MI (Figure 2).
 Finally, occasionally there are patients who present
with rest ischemia and ST-segment elevation in
whom vasospasm on an angiographically normal-
appearing vessel is present. However, most patients
with so-called Prinzmetal variant angina have fixed
and severe atherosclerotic lesions with
superimposed thrombus.
 Pathogenic vs Ischemic Mechanisms in Unstable
Angina
 In general, the pathogenesis of coronary disease
relates to the slow or rapid progression of

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 atherosclerosis. Ischemic mechanisms, on the other
hand, reflect an imbalance between myocardial blood
supply and oxygen demand. As physicians, we
evaluate patients with silent or clinical ischemia. In
unstable angina, transient decreases in blood supply
or even small increases in myocardial demand in the
presence of a new significant lesion might precipitate
ischemic manifestations of the disease, namely,
angina, by altering this balance. Transient decreases
in supply related to intracoronary thrombus formation
with spontaneous lysis or embolization, or transient
increases in vasomotor tone, might lead to rest pain.
Activated platelets release several vasoactive
substances that, in the presence of endothelial
dysfunction (impaired vasodilation), can result in
vasoconstriction at or distal to the lesion and a
transient decrease in blood flow. Although a
thrombus is usually present to explain or contribute to
decreases in blood supply, any process (thrombotic
or otherwise) that significantly perturbs this balance
can lead to unstable angina.

TREATMENT FOR UNSTABLE ANGINA:-

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First ,your healthcare provider will need to find the blocked
part or parties of the coronary arteries by performing a
cardiac catheterization. In this procedure a catheter is
guided through an artery in the arm or leg and into the
coronary arteries, then injected with a liquid dye through
the catheter. High speed x-ray movies record the course
of the dye as it flows through the arteries, and doctors can
identified blockage by tracing the flow. An evaluation of
how well your heart is working also can be done during
cardiac catheterisation Next, based on the extent of the
coronary artery blockage your doctors will discuss with
you the following treatment options

1)Percutaneous coronary
intervention(PCI):-
May be required to open a blockage coronary artery.
Briefly, this procedure involves undergoing cardiac
catheterisation following by using a catheter with a small
inflatable balloon at the tip .The balloon is inflated,
squeezing open the fatty plaque deposit located on the
inner lining of the coronary artery .
Then the balloon is deflated and the catheter is withdrawn.
This procedure is often followed by insertion of a stent to
then keep the coronary artery vessel propped open to
allow for improved blood flow to the heart muscles
2) coronary artery bypass graft surgery may be
indicated depending on the extent of coronary artery
blockage and medical history .in this procedure ,a blood
vessel is used to route blood around the blockade part
of the artery, forming a kind of detour.

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Before any of these procedure a doctor must find the
blockage part or parts of the coronary arteries. He or she
will guide a catheter through an artery in term or leg and
into the coronary arteries, then inject a liquid dye through
the catheter. High speed x-ray movies record the course
of the dye as it flows through the arteries and doctor can
identify blockages by tracing the flow .An evaluation of
how the heart works also can be done during cardiac
catheterisation.

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 Case presentation
This is a case of 50yrs old male patient presented with
complaint of left sided chest pain and palpitation.

Patient had left sided chest pain in the morning but after
taking rest he felt better, But on the same day in the
afternoon he had again the same episode of chest pain
which is not relieved by rest.

Patient told that he felt heaviness on the left sided of chest

radiating towards the left shoulder and had mild difficulty
in breathing , so releatives brought the patient in the
emergency room .

Patient was known case of hypertension since 3years ago

but 1 years ago he had not taken any medicine .

In the past history had same episode of the chest pain in

2008,but at the time doctors told that ECG was normal .

Personal habit the patient was chronic tobacco chewer

years and had taking alcohol occasionally

Patient did not have any major illness in the family history.

Patient was operated for Appendectomy before 2years

back When patient was brought to casuality,patient was
conscious and well oriented

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ON General examination

Temperture:-98.6F

Pulse -76b/min

BP-150/90mmHg,

RR-16b/min

,spo2-95%

,HGT-148mg/dl.

Systemic examination:-

CVS:-S1 &S2 heard

CNS:-conscious and well oriended

RS:- AEBE

GI:-soft

Management
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Patient came to the emergency department, patient
saturation was 95% so addministerd nasal cannula at 2lit
of O2 and spo2 maintained 98%.

The ECG was done and Blood investigation was sent to

lab (CBC, RFT , LFT ,Sr electrolyte , PT /INR, CPK-MB ,
Trop – I , HHH),send to lab

And in ECG shown T wave inversion in v1-v4

Due to ischemic changes, Tablet ecosprin 300mg ,Tablet

clopitab 300mg ,Tab Atorva 80mg was given on stat ,and
also inj pan 40mg , inj Emset 4mg /IV was given in
emergency department

Then patient was shifted to ICU and unstable angina

under evaluation ,In ICU department, seen cardiologist
,and patient advice for chest x-ray , 2D ECHO ,Lipid
profile ,and plan for CAG and then cardiologologist start
treatment

Inj monocef 1gm IV (1-0-1)

Inj PAN 40mg Iv (1-0-1)

Inj Emset 40mg (1-0-1)

Inj HEPARIN 4000IU 6hrly

Tab ecosprin 150mg-(0-1-0) ,

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Tab Atorva 80mg-(0-0-1)

Syp sucralfate 10ml(1-1-1)

As the x-ray,2DEcho and blood investigation report was

normal and also cardiac enzymes, Trop –T negative and
CPK-MB normal

As Trop-T negative and CPK-MB normal so patient

diagnosed as unstable angina.

Blood Investigation Report

Haematology PT Test 14.6

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 INR 1.19
Cardiac Enzymes Trop T Negative
CKMB 24
RFT BUN 11
Sr.Creat 0.8
LFT Total Bilirubin 1.2
SGOT 25
SGPT 25
Sr. Electrolytes NA+ 140
K+ 4.8
Cl 101
Lipid Profile LDL 158
HDL 60
Total Cholesterol 239

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LEGENDS

CARDIAC ENZYMES / CA RDIAC BIOMARKERS

Cardiac enzymes ― also known as cardiac biomarkers ― include

myoglobin, troponin and creatine kinase. Historically, lactate
dehydrogenase, or LDH, was also used but is non-specific. Cardiac
enzymes are released into the circulation when myocardial necrosis
occurs, as seen in myocardial infarction.

MYOGLOBIN

Myoglobin is released into circulation with any damage to muscle

tissue, including myocardial necrosis. Because skeletal muscle
contains myoglobin, this measurement is quite nonspecific for MIs.
The benefit in myoglobin is that a detectable increase is seen only
30 minutes after injury occurs, unlike in troponin and creatine
kinase, which can take between 3 and 4 hours.

TROPONIN

The enzymes troponin I and troponin T are normal proteins that are
important in the contractile apparatus of the cardiac myocyte. The
proteins are released into the circulation between 3 and 4 hours
after myocardial infarction and remain detectable for 10 days
following. This long half- life allows for the late diagnosis of MI but
makes it difficult to detect re-infarction, as can occur in acute stent
thrombosis after percutaneous coronary intervention, or PCI. There
are a number causes for troponin elevation not related to
myocardial infarction; however, troponin elevation is much more
sensitive than myoglobin and even creatine kinase.

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 CREATINE KINASE (CK)

Creatine kinase ― also known as creatine phosphokinase, or CPK

― is a muscle enzyme that exists as isoenzymes. The MB type is
specific to myocardial cells, whereas MM and BB are specific to
skeletal muscle and brain tissue, respectively. The CK level increases
approximately 3 to 4 hours after MI and remains elevated for 3 to 4
days. This makes it useful for detecting re- infarction in the window
of 4 to 10 days after the initial insult; troponin remains elevated for
10 days, making it less useful for this purpose.

Differential Diagnosis UNSTABLE ANGINA:-

Disease/Condition Differentiating Signs/Symptoms Differentiating Tests

Stable angina Pain occurs only in context of exertion ECG may be normal in the absence
or emotional stress, not worsening over of pain but may show ST
time, and relieved by nitrates or rest. depression during episodes of
angina or on stress testing.

Prinzmetal (variant Typically occurs without provocation ST elevation during acute

or vasospastic) and usually resolves spontaneously or episode. [3]
angina with rapid-acting nitrate. [3] Coronary angiography (invasive or
May be precipitated by emotional noninvasive) excludes severe
stress, hyperventilation, exercise, or a obstructive coronary artery disease
cold environment. [3] [47] but may show spasm. [3] (Fixed
Most episodes occur early in the lesions and spasm may coexist.)
morning. [3] Nonpharmacologic provocative
May be younger and/or smoker. [3] tests (e.g., cold pressor or
hyperventilation) or pharmacologic
Calcium-channel blockers suppress (e.g., acetylcholine) under
symptoms (beta-blockers do not supervision and in absence of
suppress symptoms). [47] contraindications to provocative
testing (left main disease, advanced

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Disease/Condition Differentiating Signs/Symptoms Differentiating Tests
3-vessel disease, presence of high-
grade obstructive lesions, significant
left-ventricular systolic dysfunction,
advanced heart failure) may be
diagnostic when invasive
assessment is not helpful. [3]

Non-ST-elevation Clinical presentation may be ECG may be normal or show ST

myocardial infarction indistinguishable. depression or T wave inversion.
Cardiac biomarkers (troponin,
creatine kinase [CK], CK-MB) are
elevated.

ST-elevation Clinical presentation may be ECG shows persistent ST elevation

myocardial infarction indistinguishable. in 2 or more leads. Cardiac
biomarkers (troponin, creatine
kinase [CK], CK-MB) are elevated.

Congestive heart Breathlessness, orthopnea, Echocardiogram shows reduced left

failure tachycardia, and peripheral edema are ventricular ejection fraction or signs
usually predominant. Chest pain may of diastolic dysfunction.
occur if coronary perfusion is poor.
CXR may show congestion,
cardiomegaly, or pleural effusion.
B-type natriuretic peptide: elevated.

Chest wall pain Onset often insidious, and may be
history of repetitive movement or minor
trauma. Pain may be reproduced on
palpation or movement. Not improved
with rest or nitrates but may be relieved
by local injection of lidocaine.
CXR or bone scan may show
skeletal pathology such as rib
fracture, osteoarthritis, or metastatic
tumor. Diagnosis of soft tissue
lesions is clinical.

Pericarditis Recent myocardial infarction, renal ECG: concave ST elevation in all

failure, chest irradiation, or associated leads except aVR; PR segment
connective tissue disease. depression.
Pain relieved by sitting up and leaning Echo: may show minimal pericardial
forward and is worse when lying effusion, but is frequently normal.
supine. If pleuropericarditis, the pain
may be worse or present only on
inspiration.
Pericardial rub may be heard.

Myocarditis May be preceded by viral infection. ECG may show evidence of

pericarditis or myopericarditis (ST

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Disease/Condition Differentiating Signs/Symptoms
Symptoms of myocarditis include chest
pain (which may be pleuritic as a result
of concomitant pericarditis),
palpitations, fatigue, or signs of heart
failure (e.g., peripheral edema,
increasing dyspnea, and weight gain).
Aortic dissection History of hypertension, or Marfan or CXR: may show wide mediastinum.
Ehlers-Danlos syndrome. Occasionally
precipitated by pregnancy.
Severe tearing chest pain radiating
between shoulder blades.
Unequal pulses, interarm differential
blood pressure, diastolic murmur of
Differentiating Tests
elevation or nonspecific ST-T
changes). Other findings include
arrhythmias or conduction
disturbances.
Echocardiogram is helpful in
excluding other causes of heart
failure (e.g., valvular heart disease).
Troponin levels are elevated in up
to one third of cases.
Serum viral antibody titers may
suggest recent viral infection, but
testing is rarely indicated in the
diagnosis of viral myocarditis or any
dilated cardiomyopathy, owing to its
low specificity and the delay of
rising viral titers, which would have
no impact on therapeutic decisions.
Antimyosin scanning helps in
diagnosis and when compared with
endomyocardial biopsy shows a
sensitivity of 83% and a specificity
of 53%.
MRI shows an area of delayed
hyper-enhancement that does not
match a coronary artery territory.
Endomyocardial biopsy is
necessary to establish a confirmed
diagnosis of myocarditis. Histologic
criteria for myocarditis are well
established. [48]However, routine
biopsy for establishing diagnosis of
myocarditis is rarely helpful
clinically, because histologic
diagnosis seldom has an impact on
therapeutic strategies, unless giant
cell myocarditis is suspected.
CT chest or transesophageal echo:
visualization of luminal flap will
confirm the dissection.
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Disease/Condition Differentiating Signs/Symptoms Differentiating Tests
aortic regurgitation.

Pulmonary Recent surgery, immobilization, ECG: sinus tachycardia, right

embolism prolonged air travel, or cancer.
Acute shortness of breath, pleuritic
chest pain, or syncope.
Hypoxia, cyanosis, elevated jugular
venous pressure with hypotension and
clear lung fields.
bundle branch block, S1Q3T3
pattern.
CXR: oligemic and hyperlucent lung
fields, wedge-shaped infarct if
pulmonary infarction.
V/Q scan: pulmonary embolism is
likely when an area of ventilation is
not perfused.
CT angiogram: reveals pulmonary
embolism/thrombus.

Pleuritis Recent viral infection or prodrome of CXR: may show resolving

infection. pneumonia.
Chest pain worse with inspiration.
Audible pleuritic rub.

Pneumothorax Underlying lung disease, trauma, or CXR: collapsed lung.

recent procedures (such as insertion of
central venous line).
Acute chest pain with shortness of
breath.
If large, will lead to tracheal deviation,
hyper-resonance, and decreased air
entry.

Perforated History of previous peptic ulcer Erect CXR and abdominal series:
abdominal viscus disease, diverticulitis, or recent bowel gas under the diaphragm.
biopsy.
CT abdomen: confirm the presence
Typically presents with abdominal pain. of free gas within the abdomen and
Chest pain is referred but may be peritoneal cavity.
mistaken for cardiac origin.
Abdominal examination shows
localized tenderness and, in cases of
peritonitis, generalized tenderness.

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 DISCUSSION

IN This case, patient came with chest pain and ECG

show lead V1 to V5 T inversion,so there will be ischemic
changes in anterio-lateralportion of heart.patient
provisionally diagnosed as unstable angina under
evaluation.as the cardiac enzymes (Trop-
T,CPKMB)negative ,so patient diagnosed as unstable
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angina /antiplatelates, anti –coagulant, statin and beta-
blockers are given ,,in this case ,we can also use
glycoprotein iib /iiia inhibitors to prevent further blocking
of coronary artery and to restore the perfusion of
myocardia .

Current research/study
OBJECTIVES: To describe common barriers that limit the effect of
guidelines on patient care, with emphasis on recommendations for triage
in the Agency for Health Care Policy and Research (AHCPR) Unstable
Angina Clinical Practice Guideline. DATA SOURCES: Previously
reported results from a prospective clinical study of 10,785 patients

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presenting to the emergency department (ED) with symptoms
suggestive of acute cardiac ischemia. STUDY DESIGN: Design is an
analysis of the AHCPR guideline with regard to recognized barriers in
guideline implementation. Presentation of hypothetical scenarios to ED
physicians was used to determine interrater reliability in applying the
guideline to assess risk and to make triage decisions. PRINCIPAL
FINDINGS: The AHCPR guideline's triage recommendations
demonstrate (1) poor interobserver reliability in interpretation by ED
physicians; (2) limited applicability of recommendations for outpatient
management (applies to 6 percent of patients presenting to the ED with
unstable angina); (3) incomplete specifications of exceptions that may
require deviation from guideline recommendations; (4) unexpected
effects on medical care by significantly increasing the demand for limited
intensive care beds; and (5) unknown effects on patient outcomes. In
addition, analysis of the guideline highlights the need to address
organizational barriers, such as administrative policies that conflict with
guideline recommendations and the need to adapt the guideline to
conform to local systems of care. CONCLUSIONS: Careful analysis of
guideline attributes, projected effect on medical care, and organizational
factors reveal several barriers to successful guideline implementation
that should be addressed in the design of future guideline-based
interventions.

Despite the growing number of patients discharged from hospital with a

diagnosis of unstable angina, the diagnostic procedures and treatment
of unstable angina are still greatly debated, as they have been for
patients with myocardial infarction. In recent years the definition and
classification of the clinical syndrome of unstable angina has been
subjected to numerous proposals by distinguished cardiologists.

An attempt to clarify and redefine practical guidelines for different

subgroups of patients has been developed and carried out by the US
Agency for Health Care Policy and Research (AHCPR).

The current medical approach to treatment of patients with unstable

angina is discussed in detail, analysing the role of antiplatelet
medications, β-blockers, nitrates, heparin and calcium antagonists. The
small subgroup of patients with refractory unstable angina should
undergo urgent coronary angiography and revascularisation. Previous
and current research on medical treatment with thrombolytic therapy,

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GPIIb/IIIa platelet receptor blockers and direct thrombin inhibitors is
outlined, keeping in mind one of the main aspects of pathophysiology of
the disease, that is ongoing thrombus formation.

In the future, a more aggressive strategy aimed at normalising the

atherogenic lipid profile in this very high risk group of patients should
be carried out, based on the positive results of lipid-lowering drug trials
both in primary and secondary prevention.

Upcoming research /study

Coronary angioplasty is known to mediate an inflammatory response.
Recently, we have characterized the transient systemic inflammatory
response after coronary stent implantation in patients with unstable
angina by measuring different soluble protein markers. In the present
study we have characterized the expression of various cellular activation
markers in neutrophils, monocytes and lymphocytes from the same
group of patients. Peripheral blood samples were taken before and 24 h,
48 h and 7 days after successful coronary stenting in 58 patients. Cell
surface markers (CD11b/CD18 and CD38) were analyzed by flow
cytometry to determine the activation of neutrophils, monocytes and T
lymphocytes. We found that coronary angioplasty with stent implantation
produces an increase in the cell surface expression of CD11b/CD18 in
neutrophils and CD38 in monocytes, following a similar time-course with
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a peak after 24 h, returning to basal levels after 48 h and a second peak
after 7 days. However, T lymphocytes were not found to be activated.
These results suggest that coronary stent implantation induces a
different pattern inducing soluble and cellular inflammation markers, and
therefore, they should be taken into account in patients undergoing stent
implantation to study clinical correlations.

The initiating event in unstable angina (USA) and non-Q-wave

myocardial infarction (NQMI) is the rupture of an atherosclerotic plaque
resulting in local thrombosis. The current standard treatment is the
administration of aspirin and heparin. The introduction of low-molecular-
weight heparin (LMWH) offers a potential alternative therapy. Clinical
mals have begun to examine the efficacy and safety of using LMWH in
the management of acute coronary syndromes. Two pivotal studies have
evaluated the effects of LMWH preparations on patients with USA or
NQMI: The ESSENCE and the TIMI 11B trials. These studies suggest
that LMWH plus aspirin is more effective and safer than unfractionated
heparin in preventing myocardial infarction, recurrent angina, or death.
Because of these differences, the American College of Cardiology and
the American Heart Association have updated their guidelines for the
treatment of USA and NQMI.

AKNOWLEDGEMENT
IN PREPARATION OF MY CASE STUDY, I HAD TO TAKE THE HELP
AND GUIDANCE OF SOME RESPECTED PERSON,WHO DESERVE
MY DEEPEST GRATITUDE. AS THE COMPLETION OF THIS CASE
STUDY GAVE ME MUCH PLEASURE, I would like to show my gratitude
Dr. paresh navlkar,LIHS for giving me good guideline for case study
throughout numerous consultations .I would also like to expand my
gratitude to all those who have directly and indirectly guided me in
writing this assignment .Many people ,especially my classmate and
family have made valuable comment suggestions on my paper which
gave me an inspiration to improve the quality bof the case study.

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REFERENCE

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