CARDIOLOGY

CASE STUDY
NAME ---Hemant Mahanand
ENROLLMENT No.--- 201941103034
2nd Year B.Sc Cardiology
 CASE 1

NON ST SEGMENT
ELEVATION
MYOCARDIAL INFARCTION
 PATIENT
DETAILS
• NAME - Rajesh Shah
• AGE - 66yrs
• GENDER - Male
• ADDRESS - Vadodara
• MARRITAL STATUS -Married
• RELIGION - Hindu
• OCCUPATION - Driver
• CONTACT DETAILS- +91952****23
• DATE OF ADMISSION -04-05-21
• DATE OF OPERATION - 12-05 -21
• DR's UNIT - Cardiology Unit
• WARD - OPD
• DIAGNOSIS -NSTEMI
• OPERATION - CABG
 Case Report
• A 66-year-old man with no previous cardiovascular
disease was admitted to the emergency
department for worsening chest pain and dyspnea.
• The patient referred the presence of intermittent
chest pain a month ago mainly at rest.
• No history of fever was present.
Medical History and
Cardiovascular risk factor
✴ Cardiovascular risk factors: type II diabetes.
mellitus, systemic hypertension, and mild
renal failure.
✴Family history: no family history of structural
heart disease
2013: hospital admission for interstitial
pneumonia complicated by respiratory failure
ALLERGIES
----none

MEDICATIONS
----Ramipril 5 mg,
atorvastatin 20 mg,
pantoprazole 20 mg
Insulin
VITAL SIGNS
– Temperature: 36.5 °C

– Heart rate: 95 bpm

– Arterial blood pressure: 150/80 mmHg

– Respiratory rate: 15 breaths/min

– Oxygen saturation: 99 %
PHYSICAL EXAMINATION
✴General : alert, awake, and oriented; restless

✴Neck : no jugular venous distention, no lymph

adenopathy, no carotid bruits

✴ Cardiovascular : regular and tachycardic rhythm,

apical soft proto-mesosystolic murmur (2/6 at the
Levine scale)

✴Lungs : no rales, rhonchi, or wheezes to aus-

cultation, normal percussion
✴ Abdomen : no hepatomegaly or splenomegaly, no
ascites, no masses, normal bowel sounds in all four
quadrants, soft, non-distended/non-tender, no
rebound or guarding, no costovertebral angle
tenderness

✴Extremities : no cyanosis or clubbing, no.

peripheral edema
ROUTINE LAB TEST
DIAGNOSIS
ECG - Right bundle branch block
Left anterior hemiblock
ST depression(>0.1mv) in (V3---V6)
ST elevation ---aVR
 Echocardiography:
• moderate concentric hypertrophy
(LV mass/BSA 135 g/m 2,relative
wall thickness 0.45)
• preserved LV global function
(estimated ejection fraction of 56
%) and hypokinesia of the middle
and apical anterior wall;
• normal dimension and function of
the right ventricle (TAPSE 20 mm,
FAC area 40 %);
• impaired relaxation of the left
ventricle (E/A < 0.75, E/E’ < 10);
• mild mitral and tricuspid
regurgitation;
• systolic pulmonary artery pressure
of 35 mmHg
CLINICAL COURSE AND
THERAPEUTIC MANAGEMENT
Clinical, instrumental, and laboratory data
allowed us to make diagnosis of SCA-NSTEMI:
ECG changes (ST depression >0.05 in more
than two contiguous leads), rise in cardiac bio-
marker levels, and normal left ventricle global
function with regional hypokinesia – no signs of
myopericarditis.
• According to guidelines, the patient was assessed with
established risk scores for prognosis and bleeding
(GRACE 120, intermediate risk; CRUSADE 30, low risk of
bleeding).
• Antiplatelet therapy with aspirin and ticagrelor (P2Y12
inhibitor) with a loading dose of 300 mg and 180 mg,
respectively, and anticoagulant therapy with
fondaparinux 2.5 mg/die were started. Intravenous
nitrate treatment and beta-blocker therapy (meto-prolol
2.5 mg ev.) were administered due to per-sistent angina
and tachycardia.
• ACE inhibitor(ramipril 5 mg) was continued, and high-
dose statin therapy (atorvastatin 80 mg) was initiated.
• The patient remained asymptomatic in the subsequent
hours despite an increase in cardiac biomarkers
(troponin I 15 ng/ml) at the laboratory analysis (6 h
after patient admission).
• Given a GRACE score of 120, an ECG suggesting a left
main or multivessel coronary artery disease (ST
depression in many leads with ST elevation in avR) and
the presence of high-risk criteria (signifi cant rise in
troponin) an early invasive strategy was performed.
• Thus, the patient underwent a coronary angiography
(<24 h) that showed triple- vessel disease with a
SYNTAX score >22
◾Considering the clinical status (asymptomatic
patient, progressive lowering in cardiac biomark-
ers: Tn I 10 ng/ml 12 h after patient admission)
and the unfavorable coronary anatomy (SYNTAX
score >22),
◾ the patient was sent for coronary
artery bypass grafting (CABG, class I A).
Ticagrelor was then discontinued,
◾And CABG was performed 5 days later without
procedural or bleeding complications.
◾The patient was then
transferred on day 12 to a postsurgery rehabilitation
center with a progressive improvement in functional
capacity and subsequently dismissed after 7 days.
◾ The therapy at discharge was dual-antiplatelet
therapy (aspirin 100 mg and ticagrelor 90 bid), ramipril
5 mg, atorvastatin 80 mg, metoprolol 50 mg bid,
pantoprazole 20 mg, and insulin therapy.
DISEASE CONDITION -
NSTEMI
• It is a type of heart attack that is
caused by mismatched oxygen
supply and demand to the heart
muscles.
• Leading to ischemic condition
which in turn leads to necrosis
of the heart muscle and
eventually heart attack.
• It does not show any st segment
elevation therefore it is difficult
to identify through ecg
 ETIOLOGY
Coronary artery disease (atherosclerosis). Plaques
made up mostly of cholesterol build up on your
artery walls and restrict blood flow.
Atherosclerosis is the most common cause of
myocardial ischemia
.
Blood clot. The plaques that develop in
atherosclerosis can rupture, causing a blood clot.
The clot might block an artery and lead to sudden,
severe myocardial ischemia, resulting in a heart
attack. Rarely, a blood clot might travel to the
coronary artery from elsewhere in the body.

Coronary artery spasm. This temporary tightening

of the muscles in the artery wall can briefly
decrease or even prevent blood flow to part of
the heart muscle. Coronary artery spasm is an
uncommon cause of myocardial ischemia.
PATHOPHYSIOLOGY
Atherosclerosis is a multifocal disease caused by
lipid accumulation that affects large-sized and medium-sized
arteries .
CAD is a dynamic process that leads to a progressive reduction in
the vessel size due to plaque formation.
NSTEMI is due to complete or partial occlusion of a coronary artery
or a mismatch between oxygen supply and demand.
ACS is generally precipitated by a plaque ruptureor erosion with
acute thrombosis or vasoconstriction leading to a sudden and
critical reduction in blood flow.
Inflammation plays a determinant role in plaque erosion and
subsequent thrombus formation.
CLINICAL PRESENTATION
• The more frequent symptom of ACS is retrosternal chest pain irradiating to the
left arm or to the neck sometimes described as retrosternal pressure or
heaviness.
• Dyspnea, diaphoresis, or nausea is often associated.
• Atypical presentation is common in older patients, women, and patients with
diabetes and may lead to a missed diagnosis .Exacerbation of symptoms
during physical exertion and reduction at rest is common.
• Relief of pain after administration of nitrates is also quite specifi c. UA is
characterized by the presence of new-onset angina, post-MI angina, or
crescendo angina.
• The presence of risk factors should be carefully evaluated as it signifi cantly
increases the probability of CAD diagnosis.
• The most common risk factors are male sex, family history of CAD, older age,
peripheral artery disease, diabetes mellitus, renal failure, previous
cardiovascular disease, and dyslipidemia.
MANAGEMENT
MEDICAL MANAGEMENT

• The therapeutic management of NSTEMI includes

the use of anti-ischemic and anti-thrombotic drugs
in combination to coronary revascularization.
 ANTI ISCHEMIC AGENT

• Oxygen insuffl ation: (4–8 L/min) if oxygen saturation is <90 %.

• Nitrate treatment (sublingual, oral, or intravenous) is indicated
to relieve angina and/or in patients with signs of heart failure (I;
C).
• Morphine 3–5 mg intravenously or subcutaneously, if severe
pain.
Oral beta blockers
Calcium channel blockers are recommended for symptom relief
in patients already receiving nitrates and beta-blockers
(dihydropyridine type) and in patients with contraindications to
beta-blockers (benzothiazepine or phenylethylamine type) (I; B).
 ORAL ANTIPLATETLET AGENT

◾ASA: loading dose of 150–300 mg, maintenance

dose of 75–100 mg daily (I; A).
◾ P2Y12 inhibitor should be added to aspirin and
maintained over 12 months (I; A).
◾Ticagrelor (180-mg loading dose, 90-mg twice daily
maintenance dose) is recommended for all patients
at moderate-to-high risk of ischemic events (I; B).
◾Prasugrel (60-mg loading dose, 10-mg daily
maintenance dose)
◾Clopidogrel (300-mg loading dose, 75-mg daily
dose)
 ANTICOAGULANTS

◾Fondaparinux (2.5 mg subcutaneously daily)

◾Enoxaparin (1 mg/kg twice daily)

GP IIb/IIIa Receptor Inhibitors

Among patients who are already treated with DAPT, the

addition of a GP IIb/IIIa receptor inhibitor (abciximab,
tirofi ban, eptifi batide) for high-risk PCI (elevated
troponin, visible thrombus) is recommended if the risk of
bleeding is low (I; B).
 SECONDARY PREVENTION

• Beta-blockers are recommended in all patients with

reduced LV systolic function (LVEF <40 %) (I; A).

• ACE inhibitors/ARB are indicated within 24 hr in all

patients with LVEF <40 % and in patients with heart
failure, diabetes, hypertension, or CKD, unless
contraindicated (I; A).
REVASCULARIZATION
THERAPY
PCI

• The main goal of PCI is to open up clogged

arteries, but there are different ways your
doctor can do that. PCI types include:
• Balloon angioplasty. A balloon is inserted and
inflated in your artery to press plaque out of
the way.
•
• Laser angioplasty. A laser is inserted on the
end of a catheter and vaporizes plaque.
•
• Rotational atherectomy. A special drill is
inserted into the artery to remove calcium
deposits.
Angioplasty with a stent.
A balloon is used to open
the artery and a
permanent metal coil is
placed to help keep the
artery open.
•
• Impella-supported PCI. A
tiny pump is inserted
into your heart through
your skin to help your
heart pump blood.
SURGICAL MANAGEMENT
CABG
• Coronary bypass surgery
redirects blood around a section
of a blocked or partially blocked
artery in your heart. The
procedure involves taking a
healthy blood vessel from your
leg, arm or chest and connecting
it below and above the blocked
arteries in your heart. With a
new pathway, blood flow to the
heart muscle improves.
 CASE 2

PERICARDITIS
 PATIENT DETAILS
• NAME - JAYESH PATEL
• AGE - 43 Yrs
• GENDER - Male
• ADDRESS - Vadodara
• MARITIAL STATUS -Married
• RELIGION - Hindu
• OCCUPATION - Business
• CONTACT DETAILS- +91952****23
• DATE OF ADMISSION -12-05-20
• DR's UNIT - Cardiology Unit
• WARD - OPD
• DIAGNOSIS -Pericarditis
CASE REPORT

A 43-year-old man was admitted to our cardiology

department, reporting a progressive chest pain
which referred to the neck and left shoulder within
the last 7 days.
Medical History and
Cardiovascular Risk Factors
• Previous medical history showed acute pericarditis
2 months ago and was treated with ibuprofen 600
mg PO bid for 10 days.
•
• Smoking (ten cigarettes a day) for 10 years.
◾ALLERGY
--- None

◾MEDICATION
---None
VITAL SIGNS
• Temperature: 36 °C

• • Heart rate: 82 bpm

•
• • Arterial blood pressure: 140/80 mmHg
•
• • Respiratory rate: 12 breaths/min
•
• • Oxygen saturation: 99 %
PHYSICAL EXAMINATION
◾General : alert, awake, and oriented. Well
developed and well nourished

◾ Neck : no jugular venous distention

◾ Cardiovascular : Regular rate and rhythm, S1 and S2 are

normal, mild systolic murmur at the apex, pericardial
friction rub, no gallops,
point of maximal intensity non-displaced and
non-sustained, no hepatojugular reflux
◾Lungs : clear to auscultation

◾Abdomen : no pulsatile masses, normal bowel

sounds in all four quadrants, no high-pitched
or tinkling sounds, resonant to percussion,
soft, non-distended/non-tender, no rebound or
guarding, no hepatosplenomegaly

◾ Extremities : no cyanosis or clubbing, no

peripheral edema
LAB TEST PERFORMED
DIAGNOSIS TEST
ECG
◾sinus rhythm
◾ Heart Rate --85 bpm
◾incomplete Right Bundle Branch
Block
◾ST Elevation --(all leads except aVR)
 ECHO
◾Cardiac
echocardiography showed
circumferential pericardial
effusion and normal
dimensions and function
of the cardiac chambers,
mild mitral regurgitation,
and mild inferior vena
cava (IVC) dilatation that
collapses with inspiration.

◾No signs of cardiac

tamponade.
 FINAL DIAGNOSIS

◾Recurrent idiopathic acute pericarditis.

◾ The patient was treated with colchicine in

combination with nonsteroidal anti-inflammatory
drugs (NSAID).
 DISEASE CONDITION -
PERICARDITIS
Pericarditis is an inflammation of
the pericardium.
Pericarditis is usually acute – it
develops suddenly and may last
up to several months. The
condition usually clears up after 3
months, but sometimes attacks
can come and go for years.
When you have pericarditis, the
membrane around your heart is
red and swollen, like the skin
around a cut that becomes
inflamed.
Sometimes there is extra fluid in
the space between the pericardial
layers, which is called pericardial
effusion.
 ETIOLOGY
Viral pericarditis is caused by a complication of a viral infection,
most often a gastrointestinal virus.
•
• Bacterial pericarditis is caused by a bacterial infection,
including tuberculosis.
•
• Fungal pericarditis is caused by a fungal infection.
•
• Parasitic pericarditis is caused by an infection from a parasite.
• Some autoimmune diseases, such as lupus, rheumatoid
arthritis and scleroderma can cause pericarditis. Other causes
of pericarditis include injury to the chest, such as after a car
accident
 PATHOPHYSIOLOGY
• Acute pericarditis develops quickly, causing
inflammation of the pericardial sac and often a
pericardial effusion. Inflammation can extend to the
epicardial myocardium (myopericarditis). Adverse
hemodynamic effects and rhythm disturbance are rare,
although cardiac tamponade is possible.
• Subacute pericarditis occurs within weeks to months of
an inciting event.
•
• Chronic pericarditis is defined as pericarditis persisting >
6 months.
•
Pericardial effusion is accumulation of fluid in the
pericardium. The fluid may be serous fluid
(sometimes with fibrin strands), serosanguineous
fluid, blood, pus, or chyle.

Cardiac tamponade occurs when a large pericardial

effusion impairs cardiac filling, leading to low cardiac
output and sometimes shock and death. If fluid
(usually blood) accumulates rapidly, even small
amounts (eg, 150 mL) may cause tamponade
 SIGNS AND SYMPTOMS

Palpitations may be the presenting complaint,

but chest pain is the cardinal symptom of pericarditis,
usually precordial or retrosternal with referral to the
trapezius ridge, neck, left shoulder, or arm.
The quality of the pain is usually pleuritic, but it range from
sharp, dull, aching, burning, or pressing, and the intensity
varies from barely perceptible to severe.
The pain is worse during inspiration, when lying flat, or
during swallowing and with body motion, and it may be
relieved by leaning forward while seated.
• Common associated signs and symptoms include
• low-grade intermittent fever, dyspnea/tachypnea
(a frequent complaint and may be severe with
myocarditis, pericarditis, and tamponade),
• cough, and dysphagia.
• In tuberculous pericarditis, fever, night sweats, and
weight loss were commonly noted (80%).
 MEDICAL MANAGEMENT
• Nonsteroidal anti-infl ammatory drugs (NSAIDs) are the
first-line therapy in acute pericarditis.
• High-dose aspirin, ibuprofen, or indomethacin may be
used for 1–3 weeks, but no single NSAID appears to be
more effective than the other [ 2 ].
• Colchicine has shown to be safe and effec-tive in
reducing recurrences [ 10 ].
• Pericarditis symptoms respond promptly to
corticosteroid therapy. Nonetheless, corticosteroids are
associated with increased recurrences and should only be
used when other therapies have shown to be ineffective.