Mdcu Comprehensive Cardio

MD Chula 2010

Comprehensive tutorial

y
Feb 2010

nl
O
se
U
Spectrum of Coronary Heart Disease
al
rn

• Chronic Ischemic Heart Disease
– Chronic stable angina
te

• Acute Coronary Syndromes
In

– Unstable angina / non ST elevation MI
– Acute ST elevation MI
• Sudden Cardiac Death
• Ischemic Cardiomyopathy
• Silent ischemia

MD Chula 2010

Coronary Heart Disease
Stable disease Acute Coronary Syndromes
(Stable plaque) (Active plaque)
• Chronic stable angina • UA / NSTEMI
• Ischemic • Acute ST elevation MI

y
cardiomyopathy • Ischemic sudden cardiac

nl
• Silent ischemia death

O
se
U

ACS and CSA
al
rn

CHEST PAIN
te

• Angina vs non-angina
• Typical vs atypical angina
In

• Exclude other life threatening non cardiac
chest pain
• STEMI vs NSTEMI/Unstable vs stable
angina
• Plaque rupture vs secondary UAE

MD Chula 2010

CHEST PAIN

•Location
• Exclude other life threatening non cardiac chest

y
pain ( next slide)
•Characteristic

nl
• STEMI vs NSTEMI/Unstable vs stable angina
•Radiation
•Exertion

O
•relief
se
U
ED Evaluation of
Patients With STEMI
al

Differential Diagnosis of STEMI:
rn

Other Nonischemic Cardiovascular
te

• Early repolarization
• Pericarditis •Brugada syndrome
• Wolff-Parkinson-
• Vasospastic angina •Myocarditis
White syndrome
•Hyperkalemia
In

• Hypertrophic • Deeply inverted T-
cardiomyopathy •Bundle-branch
waves suggestive of a
blocks
• Atypical angina central nervous system
lesion or apical
hypertrophic
cardiomyopathy
• LV hypertrophy with
strain

6

MD Chula 2010
ED Evaluation of
Patients With STEMI
Differential Diagnosis of STEMI: Other Noncardiac

Gastroesophageal reflux Cervical disc or neuropathic
(GERD) and spasm pain
Chest-wall pain Biliary or pancreatic pain
Pleurisy Somatization and
psychogenic pain disorder

y
Peptic ulcer disease
Panic attack

nl
O
se 7
U

CHEST PAIN
al
rn

te
In

• Exclude other life threatening non
cardiac chest pain ( next slide)

• STEMI vs NSTEMI/Unstable vs stable angina

MD Chula 2010
ED Evaluation of
Patients With STEMI
Differential Diagnosis of STEMI: Life-Threatening

Aortic dissection
Pulmonary embolus
Perforating ulcer

y
Tension pneumothorax
Boerhaave syndrome

nl
(esophageal rupture with mediastinitis)

O
se 9
U
ED Evaluation of
Patients With STEMI
al

rn

Aortic dissection Sudden onset
te

Pulmonary embolus Tearing pain
In

Perforating ulcer BP
Radiate to back
Boerhaave syndrome
Unequal pulse
Stroke

10

MD Chula 2010
ED Evaluation of
Patients With STEMI

Aortic dissection
Sudden onset
Pulmonary embolus
Dyspnea
Perforating ulcer
Tension pneumothorax hypoxemia

y
Boerhaave syndrome tachycardia

nl
Lung clear

O
Pleuritic pain
se 11
U
ED Evaluation of
Patients With STEMI
al

rn

Aortic dissection
te

Pulmonary embolus Epigastric pain
In

Perforating ulcer Guarding
Tension pneumothorax of liver dullness
Loss
Boerhaave syndrome

12

MD Chula 2010
ED Evaluation of
Patients With STEMI

Aortic dissection Sudden onset

Pulmonary embolus Tearing pain

Perforating ulcer BP

y
Radiate to
Boerhaave syndrome
back

nl
Unequal pulse

O
Stroke

se 13
U
ED Evaluation of
Patients With STEMI
al

rn

Sudden onset dyspnea
Aortic dissection Trachea shift
te

Pulmonary embolus Hyperresonance on
In

Perforating ulcer percussion
Tension pneumothorax Subcut.emphysema
Boerhaave syndrome

14

MD Chula 2010
ED Evaluation of
Patients With STEMI
Differential Diagnosis of STEMI:
Other Nonischemic Cardiovascular

• Early repolarization
• Pericarditis •Brugada syndrome
• Wolff-Parkinson-
• Vasospastic angina Position syndrome •Myocarditis
White related
• Hypertrophic •Hyperkalemia
• Deeply inverted T-
cardiomyopathy Sharp pain
waves suggestive of a
•Bundle-branch

y
blocks
• Atypical angina
Rubcentral nervous system

nl
lesion or apical
hypertrophic
cardiomyopathy

O
• LV hypertrophy with
strain
se 15
U

ACS and CSA
al
rn

CHEST PAIN
te

In

• Exclude other life threatening non cardiac chest pain
• STEMI vs NSTEMI/Unstable vs stable
angina

• UAE : Plaque rupture vs secondary UAE
• Risk stratification

MD Chula 2010



• Acute ST elevation MI
EKG

y
– non ST elevation MI

nl
– Unstable angina

O
• Silent ischemia
• Printzmetal angina se
U
al
rn

te

– Unstable angina
In

Cardiac
– non ST elevation MI marker
– Acute ST elevation MI

• Silent ischemia
• Printzmetal angina

MD Chula 2010

Spectrum of Acute Coronary Syndromes

Presentation Ischemic Discomfort
at Rest

Emergency No ST-Segment
ST- ST-Segment
Department Elevation Elevation

y
nl
+
+ +

O
In-
In-Hospital

Unstable Non STEMI STEMI
Angina se
(Non-Q-wave MI)
(⊕ : positive cardiac biomarker)
(Q-wave MI)
U
Further investigations for
al

“making diagnosis”
diagnosis”
rn

History
te

Intermediate
Low likelihood High likelihood
In

likelihood

- Excluded Need for
- Monitor, f/u risk stratification?

EST yes no

Stress imaging Rx
Coronary Angiography

MD Chula 2010

High risk
• Prolong pain >20 min
• S3 or rale
• Hypotension

y
• Pulmonary edema

nl
• New or worsening MR

O
• Dynamic ST change > 1 mm
• Troponin positive se
U
al

Intermidiate risk
rn

• Rest angina >20 min but relief by nitrate
te

• Nocturnal angina
In

• Age > 65 yrs

• Dynamic T wave change > 1 mm

MD Chula 2010

Low risk
• Resting angina < 20 min

• Normal or unchange EKG

y
nl
O
se
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Acute Coronary Syndromes
al

Management of Unstable Angina:
Risk evaluation
rn

Features Higher risk Lower risk
te

CAD-
CAD- likelihood - Known/suspect - Low
History - Prolonged, rest - Effort angina
In

chest pain - Angina > 2 wk
PE - Hemodynamic - Normal
instability
ECG - Dynamic ST - Normal / near-
near-
changes normal
- Deep inverted T
Troponin T or I - Positive - Negative

MD Chula 2010
Acute Coronary Syndromes

Management of Unstable Angina:
Risk evaluation
Unstable Angina

y
Higher risk Lower risk

nl
O
• Worse outcomes • Good prognosis
• CCU admission • Out-patient, ward
Out-
• Aggressive Rx se • Less aggressive Rx
U
al
rn
te

F Clinical predictors
In

F ECG

F Cardiac markers

MD Chula 2010

Cardiac markers in UA / NSTEMI

• Only useful in appropriate clinical settings
(ie. CP suspicious of ACS)
• Can be falsely elevated in many other

y
clinical conditions

nl
• Typical rise & fall is helpful to make

O
diagnosis of ACS
se
U

TIMI Risk Score
al
rn

1. Age > 65
2. Risk factor > 2 0 - 2 = Low risk
te

3. Known CAD (>50% stenosis)
(>50 %
In

4. Prior aspirin use (last 7 d) 3 - 4 = Int. risk
5. (2) Chest pain in the last 24 h
5 - 7 = High risk
6. ST changes on ECG
7. Elevated cardiac markers

MD Chula 2010

Current Management of ACS

Plaque rupture

Stable Unstable Non-Q Q-wave
angina angina wave MI MI

y
Non-ST elevation ACS ST elevation ACS

nl
O
ECG se
U
Fibrous Cap
al

Rupture
rn

Platelet Tissue Factor
Activation Release
te
In

Platelet TF binds & activate
Adhesion Factor VII

Platelet Extrinsic Coagulation
Aggregation Pathway Cascade

CLOT

MD Chula 2010

y
nl
O
se
U

Management of UA / NSTEMI
al
rn

• Prevent death / MI (Keep the artery from closing!)
te

– Prevent further propagation of thrombus
• Antiplatelet
In

• Anticoagulant
– Mechanical opening: revascularization (PCI, CABG)

• Relieve ischemia
– Anti-anginal agents
Anti-
– Revascularization (PCI, CABG)

MD Chula 2010

Recent Updates in NSTEMI: What’s New?

ESC Guidelines for the Management of NSTE-ACS June
2007

August
2007

y
nl
O
se 33
U
Updated Guidelines
al

Classes of Recommendations
rn

I IIa IIb III
Intervention is useful and effective
te

Evidence conflicts/opinions differ but
In

leans towards efficacy
Evidence conflicts/opinions differ but
leans against efficacy
Intervention is not useful/effective and
may be harmful

MD Chula 2010

Updated Guidelines
Weighing the Evidence

n 1994 version was starting point; literature searches
added more current reports

n Weight of evidence grades:
= Data from many large, randomized trials

y
= Data from fewer, smaller randomized trials,

nl
careful analyses of nonrandomized studies,

O
observational registries
= Expert consensus
se
U
al
rn
te

Medication
In

UAE / nonSTEMI

MD Chula 2010

Hospital Care
Anti-
Anti-Thrombotic Therapy
I IIa IIb III
Immediate Aspirin
Clopidogrel, if aspirin contraindicated
Aspirin + clopidogrel for up to 1 month,

y
if medical therapy or PCI is planned

nl
Heparin (IV unfractionated, scLMWH)
with antiplatelet agents listed above

O
Enoxaparin preferred over UFH unless
CABG is planned within 24 hours
se
U
Hospital Care
al

Clopidogrel Therapy
rn

I IIa IIb III
te

Aspirin + clopidogrel, for up to 1 month*
In

Aspirin + clopidogrel, for up to 9 months*
Withhold clopidogrel for 5-7 days for CABG

* For patients managed with an early conservative strategy, and
those who are planned to undergo early PCI

hGuidelines do not specify initial approach to using
clopidogrel when coronary anatomy is unknown

MD Chula 2010

Hospital Care
Platelet GP IIb/IIIa Inhibitors ( 1)
(1
I IIa IIb III
Any GP IIb/IIIa inhibitor + ASA/Heparin
for all patients, if cath /PCI planned
Eptifibatide or tirofiban + ASA/Heparin
for high-risk* patients in whom early
cath/PCI is not planned

y
nl
Any GP IIb/IIIa inhibitor for patients
already on ASA + Heparin + clopidogrel,

O
if cath /PCI is planned

se
* High-risk: Age > 75; prolonged, ongoing CP; hemodynamic instability;
rest CP w/ ST ∆; VT; positive cardiac markers
U
Hospital Care
al

Platelet GP IIb/IIIa Inhibitors ( 2)
(2
rn

I IIa IIb III
te

Eptifibatide or tirofiban + ASA/Heparin
for patients without continuing
In

ischemia in whom PCI is not planned
Abciximab for patients in whom PCI is
not planned

MD Chula 2010

Hospital Care
Anti-
Anti-Ischemic Therapy (1)
(1

I IIa IIb III
β-blocker (IV→oral) if not contraindicated
Non-dihydropyridine Ca2+ antagonist if β-
blocker contraindicated and no LV

y
dysfunction, for recurrent ischemia

nl
ACE inhibitor if ↑ BP persists with NTG+
β-blocker, for pts with CHF or diabetes

O
se
U
Hospital Care
al

Anti-
Anti-Ischemic Therapy (2)
(2
rn

I IIa IIb III
ACE inhibitor for all ACS pts
te

Extended-release Ca 2+ blocker instead
of β-blocker
In

Immediate-release Ca 2+ blocker with β-
blocker
Long-acting Ca2+ blocker for recurrent
ischemia, if no contraindications and
NTG + β-blocker used fully

MD Chula 2010

Early Invasive Strategy

Class I
l An early invasive strategy is indicated in patients who
have refractory angina or hemodynamic or electrical
instability (without contraindications). (LOE: B)

y
l An early invasive strategy is indicated in initially stabilized
patients (without contraindications) who have are high

nl
risk for clinical events. (LOE: A)

O
l In women with low-risk features, a conservative strategy
is recommended. (Level of Evidence: B)
se Anderson JL. J Am Coll Cardiol 2007;50:e1-157
U
Early Invasive vs Conservative
al

Strategy
rn

Class IIb
l In initially stabilized patients, an initially conservative
te

strategy may be considered for patients who have
elevated risk including those who are troponin positive.
In

(LOE: B)
l The decision to implement an initial conservative (vs.
invasive) strategy in these patients can consider MD
and patient preference. (LOE: C)
l An invasive strategy may be reasonable in patients with
chronic renal insufficiency. (Level of Evidence: C)

Anderson JL. J Am Coll Cardiol 2007;50:e1-157

MD Chula 2010

Early Invasive Strategy
Not Recommended

Class III

l An early invasive strategy is not recommended in patients with
extensive comorbidities, in whom the risks of revascularization are
likely to outweigh the benefits. (LOE: C)

y
l An early invasive strategy is not recommended in patients with

nl
acute chest pain and a low likelihood of ACS. (LOE: C)
l An early invasive strategy should not be performed in patients who

O
will not consent to revascularization. (LOE: C)

se Anderson JL. J Am Coll Cardiol 2007;50:e1-157
U
Hospital Care
al

Conservative vs. Invasive Strategies (1)
(1
I IIa IIb III
rn

Early invasive strategy in high-risk
patients with any of the following:
te

- Recurrent ischemia, despite meds
- Elevated Troponin I or T
In

- New ST-segment depression
ST-
- New CHF symptoms
- High-risk stress test findings
High-
- LV dysfunction (EF < 40%)
40%)
- Hemodynamic instability, sustained VT
- PCI within 6 months, prior CABG

MD Chula 2010

Hospital Care
Conservative vs. Invasive Strategies (2)
(2

I IIa IIb III
Either strategy in low- to moderate-risk
patients without contraindications to
revascularization

y
Early invasive strategy for patients with

nl
repeated ACS presentations, without
high-risk features or ongoing ischemia

O
se
U
al

Biological changes
Inflammation, abnormal flow dynamics,
rn

LDL oxidation, infection?, etc.
te

Antiplatelets PLAQUE DISRUPTION Anticoagulant
In

Platelet aggregation, thrombus formation

Mechanical obstruction
Ischemia
PCI Infarction CABG
Sudden death

MD Chula 2010

Diagnosis of UA/NSTEMI is Likely
Algorithm for an or Definite

Initial
ASA (Class I, LOE: A)
Invasive Clopidogrel if ASA intolerant (Class I, LOE: A)

Strategy Select Management Strategy
Proceed with an
Initial
Conservative
Strategy
Initial Invasive Strategy
Initiate Anticoagulant Rx (Class I, LOE: A)
Choices: enoxaparin or UFH (Class I, LOE: A)
Alternatives: bivalirudin or fondaparinux (Class I, LOE: B)

y
Prior to Angiography
Initiate at least one (Class I, LOE: A) or
both (Class IIa, LOE: B) of :

nl
Clopidogrel
IV GP IIb/IIIa inhibitor
Factors favoring both include:

O
Delay to Angiography
High Risk Features
Early recurrent ischemic discomfort

se
Proceed to Angiography
Anderson JL. J Am Coll Cardiol 2007;50:e1-157. Figure 7
U
Algorithm for Initial Conservative Strategy
al

Diagnosis of UA/NSTEMI is Likely
or Definite
rn

ASA (Class I, LOE: A)
te

Clopidogrel if ASA intolerant (Class I, LOE: A)

Select Management Strategy Proceed with
In

Invasive
Strategy
Conservative Strategy
Initiate Anticoagulation Rx (Class I, LOE: A):
choices: enoxaparin or UFH (Class I, LOE:
A) or fondaparinux (Class I, LOE: B), but
enoxaparin or fondaparinux are preferable
(Class IIA, LOE: B)

Initiate clopidogrel (Class I, LOE: A)
Consider adding GPIIbIIIa antagonist
IV eptifibatide or tirofiban (Class IIb, LOE: B)

(Continued)

MD Chula 2010
Algorithm for Initial Conservative Strategy
(Continued)

Any subsequent events necessitating
angiography?

Yes
No

Evaluate LVEF
(Class IIa, (Class I, LOE: B)

y
EF 0.40 or LOE: B)
EF greater
less
than 0.40
Stress Test

nl
(Class IIa, LOE: B)
Proceed to Dx Not Low Low Risk (Class I, LOE: A)

O
Angiography (Class I, LOE: A) Risk

Cont ASA indefinitely (Class I, LOE A)
Cont clopidogrel for at least one month (Class I, LOE A) and ideally up to
1 yr (Class I, LOE B)

se
DC IV GP IIb/IIIa if started previously (Class I, LOE A)
DC Anticoagulation Rx (Class I, LOE A)
U

Conclusions
al
rn

• Invasive strategy appears to be a better
strategy for intermediate- and high-risk
intermediate- high-
te

non-
non-ST elevation ACS patients
In

• This can only be accomplished by
– Aggressive antithrombotic agents (combined
antiplatelets, LMWH)
– Use of GPIIbIIIa inhibitors and stents in the
cath lab/PCI procedures

MD Chula 2010

Conclusions
• For low-risk (and some intermediate-
low- intermediate-
risk) patients, conservative
(selectively invasive) strategy is

y
appropriate

nl
• No one should go home without at

O
least non-invasive stress test
non-
se
U
al

Discharge/Post-
Discharge/Post-Discharge Medications
rn

I IIa IIb III
te

ASA, if not contraindicated
Clopidogrel, when ASA contraindicated
In

Aspirin + Clopidogrel, for up to 9 months
β-blocker, if not contraindicated
Lipid ↓ agents + diet, if LDL >130 mg/dL
ACE Inhibitor: CHF, EF < 40%, DM, or HTN

MD Chula 2010

Risk Factor Modification

I IIa IIb III
Smoking Cessation Counseling
Dietary Counseling and Modification

y
Cardiac Rehabilitation Referral

nl
HTN Control (BP < 130/85 mm Hg)

O
Tight Glycemic Control in Diabetics

se
U
Preparation for Discharge After UA/NSTEMI
al
rn

• Antiplatelet Rx
– ASA 75 - 162 mg/day
– Clopidogrel 75 mg/day
te

• Beta Blocker
• ACEI / ARB
– Especially if DM, HF, EF <40%, HTN
In

• Statin
– LDL <100 mg/dL (ideally <70 mg/dL)
• Secondary Prevention Measures
– Smoking Cessation
– BP <140/90 mm HG or <130/80 mm HG for DM or chronic kidney
disease
– HbA1C <7%
– BMI 18.5-24.9
– Physical Exercise 30-60 min at least 5 days/wk

MD Chula 2010

Acute STEMI

y
nl
O
se
U
al
rn
te
In

MD Chula 2010
ED Evaluation of
Patients With STEMI

Aortic dissection Tension pneumothorax
Pulmonary embolus Boerhaave syndrome
Perforating ulcer (esophageal rupture with
mediastinitis)

y
nl
O
se 59
U
ED Evaluation of
Patients With STEMI
al

Differential Diagnosis of STEMI: Other Cardiovascular and
rn

Nonischemic
te

Pericarditis LV hypertrophy with strain
Atypical angina Brugada syndrome
In

Early repolarization
Wolff-Parkinson-White Myocarditis
syndrome Hyperkalemia
Deeply inverted T-waves Bundle-branch blocks
suggestive of a central
nervous system lesion Vasospastic angina
or apical hypertrophic Hypertrophic
cardiomyopathy cardiomyopathy

60

MD Chula 2010
ED Evaluation of
Patients With STEMI
Differential Diagnosis of STEMI: Other Noncardiac

Gastroesophageal reflux Cervical disc or neuropathic
(GERD) and spasm pain
Chest-wall pain Biliary or pancreatic pain
Pleurisy Somatization and
psychogenic pain disorder

y
Peptic ulcer disease
Panic attack

nl
O
se 61
U
al

Ischemic myocardium potentially salvageable by reperfusion
rn

100
te

80 Ischemic myocardium
potentially salvageable
In

60 by intervention

40

20
Necrotic
myocardium

1 2 3 4 5 6 12 18 24 3 6 9 12 6
Reversible Irreversible
injury injury Hours Days Wks

MD Chula 2010
Options for Transport of Patients With STEMI and
Initial Reperfusion Treatment
• Patients receiving fibrinolysis should be risk-stratified to identify need
for further revascularization with percutaneous coronary intervention
(PCI) or coronary artery bypass graft surgery (CABG).
• All patients should receive late hospital care and secondary
prevention of STEMI.

Noninvasive Risk
Fibrinolysis
Stratification

y
Not Late
Rescue Ischemia Hospital Care
PCI Capable

nl
driven and Secondary
PCI Capable Prevention

O
PCI or CABG

Primary PCI
se 63
U

ACC/AHA Guideline for AMI
al
rn

Step 1 Access time and risk
te

• Time since onset of symptoms
In

• Risk of STEMI
• Risk of fibrinolysis
• Time required for transport to a skill PCI
lab.

MD Chula 2010

ACC/AHA Guideline for AMI

Fibrinolysis is generally prefered
• Early presentation
• Invasive strategy is not an option
• Delay to invasive strategy

y
• Prolong transport (door to balloon – door to

nl
neddele time > 60 minutes)

O
• Medical contact to balloon or door to balloon time
is > 90 minutes.

se
U
Reperfusion Options for STEMI Patients
Step 2: Select Reperfusion Treatment.
al

If presentation is < 3 hours and there is no delay to an invasive strategy,
rn

there is no preference for either strategy.
Invasive strategy generally preferred
§ Skilled PCI lab available with surgical backup
te

§ Door-to-balloon < 90 minutes
§ Door to balloon – door to neddele time < 1 hour
In

§ High Risk form STEMI
§ Cardiogenic shock, Killip class ≥ 3

§ Contraindications to fibrinolysis, including
increased risk of bleeding and ICH

§ Late presentation
§ > 3 hours from symptom onset

§ Diagnosis of STEMI is in doubt
66

MD Chula 2010
Contraindications and Cautions
for Fibrinolysis in STEMI

Absolute • Any prior intracranial hemorrhage
Contraindications • Known structural cerebral vascular lesion
(e.g., arteriovenous malformation)
• Known malignant intracranial neoplasm
(primary or metastatic)

y
• Ischemic stroke within 3 months EXCEPT

nl
acute ischemic stroke within 3 hours

O
NOTE: Age restriction for fibrinolysis has been removed
compared with prior guidelines.

se 67
U
al
rn

Absolute • Suspected aortic dissection
Contraindications
• Active bleeding or bleeding diathesis
te

(excluding menses)
• Significant closed-head or facial trauma
In

within 3 months

68

MD Chula 2010
Relative • History of chronic, severe, poorly controlled
Contraindications hypertension
• Severe uncontrolled hypertension on
presentation (SBP > 180 mm Hg or DBP >
110 mm Hg)
• History of prior ischemic stroke greater than

y
3 months, dementia, or known intracranial
pathology not covered in contraindications

nl
• Traumatic or prolonged (> 10 minutes) CPR
or major surgery (< 3 weeks)

O
se 69
U
al
rn

Relative • Recent (< 2 to 4 weeks) internal bleeding
Contraindications • Noncompressible vascular punctures
te

• For streptokinase/anistreplase: prior
exposure (> 5 days ago) or prior allergic
In

reaction to these agents
• Pregnancy
• Active peptic ulcer
• Current use of anticoagulants: the higher the
INR, the higher the risk of bleeding

70

MD Chula 2010

pitfall
Diagnosis
• Do not serial EKG
• Do not do EKGàDelay in Dx (atypical

y
presentation)

nl
• Miss Dx (aortic dissection )

O
se
U
al

pitfall
rn

Management
te

• Use too much time to Dx
In

• Delay treatment after Dx
• Do not beware of thrombolysis
contraindication
• Do not reassess sign of reperfusion

MD Chula 2010
Summary of Pharmacologic Rx: Ischemia

1st During Hosp DC +
24 h Hosp Long Term
Aspirin 162-325 mg 75-162 75-162
chewed mg/d p.o. mg/d p.o.
Fibrinolytic tPA,TNK,
rPA, SK

y
60U/kg (4000) aPTT

nl
UFH 12 U/kg/h (1000) 1.5 - 2 x C
aPTT 1.5 - 2 x C

O
Beta-blocker Oral daily Oral daily Oral daily

JACC 2004;44: 671
Circulation 2004;110: 588
se 73
U
Summary of Pharmacologic Rx: LVD, Sec. Prev.,
al

1st During Hosp Hosp DC +
24 h Long Term
rn

ACEI Anterior MI, Oral
Pulm Cong., EF < 40 Oral Daily
te

ARB ACEI intol., Daily Indefinitely
HF, EF < 40
In

Aldo No renal dysf, Same as
Blocker K+ < 5.0 mEq/L during
On ACEI, Hosp.
HF or DM
Statin Start w/o lipid Indefinitely,
profile LDL << 100

JACC 2004;44:671
2004;44:
Circ 2004;110:588
2004;110: 74

MD Chula 2010

This slide set was adapted from the 2007
Focused Update of the ACC/AHA Guidelines for
Management of Patients With ST-Elevation
Myocardial Infarction (Journal of the American
College of Cardiology published ahead of print
on December 10, 2007, available at
http://content.onlinejacc.org/cgi/content/full/j.jacc
.2007.10.001.

y
The full-text guidelines are also available on the

nl
Web sites:
ACC (www.acc.org) and,

O
AHA (www.americanheart.org)
se ACC/AHA 2007 STEMI Guidelines Focused Update
U
al
rn
te

Thienopyridines
In

ACC/AHA 2007 STEMI Guidelines Focused Update

MD Chula 2010

CLARITY-TIMI 28 Primary Endpoint:
Occluded Artery (or D/MI thru Angio/HD)

36% Odds Ratio 0.64
Occluded Artery or Death/MI (%)

25 21.7
Odds Reduction (95% CI 0.53-0.76)
20
P=0.00000036
15.0
15

y
10

nl
5

O
n=1752 n=1739 0.4 0.6 0.8 1.0 1.2 1.6
0
Clopidogrel Placebo
Clopidogrel Placebo better better
LD 300 mg
MD 75 mg
se
STEMI, Age 18-75
Sabatine N Eng J Med 2005;352:1179.
U
COMMIT: Effect of CLOPIDOGREL on
al

Death In Hospital
Placebo + ASA:
rn

1,846 deaths (8.1%)
Clopidogrel + ASA:
1,728 deaths (7.5%)
te

0.6% ARD
7% RRR
Dead

In (%)

P = 0.03

N = 45,852
No Age limit ; 26% > 70 y
Lytic Rx 50%
No LD given

Chen ZM, et al. Lancet. 2005;366:1607.

Days Since Randomization (up to 28 days) ACC/AHA 2007 STEMI Guidelines Focused Update

MD Chula 2010

24 h Hosp Long Term
Aspirin 162-325 mg
Clopidogrel
75-162 75-162
rPA, SK

y
60U/kg (4000) aPTT

nl
UFH 12 U/kg/h (1000) 1.5 - 2 x C
aPTT 1.5 - 2 x C

O

JACC 2004;44: 671
Circulation 2004;110: 588
se 79
U
al
rn
te

Anticoagulants
In


MD Chula 2010

Anticoagulants
I IIa IIb III Patients undergoing reperfusion with fibrinolytics
should receive anticoagulant therapy for a minimum of
48 hours (Level of Evidence: C) and preferably for the
duration of the index hospitalization, up to 8 days
I IIa IIb III (regimens other than unfractionated heparin [UFH] are
recommended if anticoagulant therapy is given for more
than 48 hours because of the risk of heparin-induced

y
thrombocytopenia with prolonged UFH treatment).

nl
(Level of Evidence: A)

O
Anticoagulant regimens with established efficacy
include:
♥ UFH (LOE: C)
♥ Enoxaparin (LOE:A)
♥ Fondaparinux (LOE:B)
se
U
Unfractionated Heparin
al

Advantages Disadvantages
rn

§ Immediate anticoagulation § Indirect thrombin inhibitor so
does not inhibit clot-bound
§ Multiple sites of action in
te

thrombin
coagulation cascade § Nonspecific binding to:
§ Long history of successful ― Serine proteases
In

clinical use ― Endothelial cells
(can lead to variability in level of
§ Readily monitored by aPTT and anticoagulation)
ACT
§ Reduced effect in ACS
― Inhibited by PF-4
§ Causes platelet aggregation

§ Nonlinear pharmacokinetics

§ Risk of HIT
Hirsh J, et al. Circulation. 2001;103:2994-3018. aPTT = activated partial thromboplastin time; ACT = activated coagulation time; PF-4 =
platelet factor 4; HIT = heparin-induced thrombocytopenia. ACC/AHA 2007 STEMI Guidelines Focused Update

MD Chula 2010

Low-Molecular-Weight Heparin
Advantages Disadvantages
§ Increased anti-Xa to anti-IIa activity → § Indirect thrombin inhibitor
inhibits thrombin generation more § Less reversible
effectively
§ Difficult to monitor
§ Induces ↑ release of TFPI vs UFH (no aPTT or ACT)
§ Not neutralized by platelet factor 4 § Renally cleared
§ Less binding to plasma proteins (eg, § Long half-life
acute -phase reactant proteins) → more
§ Risk of HIT
consistent anticoagulation

y
§ Lower rate of HIT vs UFH
§ Lower fibrinogen levels

nl
§ Easy to administer (SC administration)
§ Long history of clinical studies and
experience, FDA-approved indications

O
§ Monitoring typically unnecessary

SC = subcutaneous; aPTT = activated partial thromboplastin time;
ACT = activated coagulation time.
se
Hirsh J, et al. Circulation. 2001;103:2994-3018. TFPI = tissue factor pathway inhibitor; UFH = unfractionated heparin;

U
ExTRACT-TIMI 25: Primary End Point (ITT)
al

Death or Nonfatal MI
rn

15

UFH
12.0%
te

12
Primary End Point (%)

17% RRR
9.9%
In

9
Enoxaparin
Relative Risk
6
0.83 (95% CI, 0.77 to 0.90)
P<.001
3

Lost to follow-up = 3
0
0 5 10 15 20 25 30
Days after Randomization
Adapted with permission from Antman EM, et al. N Engl J Med. 2006;354:1477-1488. ACC/AHA 2007 STEMI Guidelines Focused Update

MD Chula 2010

Anticoagulants
For patients undergoing PCI after having
received an anticoagulant regimen, the following
dosing recommendations should be followed:

a. For prior treatment with UFH: administer
additional boluses of UFH as needed to support

y
I IIa IIb III
the procedure taking into account whether GP

nl
IIb/IIIa receptor antagonists have been
administered. (Level of Evidence: C) Bivalirudin

O
may also be used in patients treated previously
with UFH. (Level of Evidence: C)
se
Recommendation continues on the next slide.
U
Anticoagulants
al
rn

I IIa IIb III b. For prior treatment with enoxaparin: if the last SC
dose was administered within the prior 8 hours,
te

no additional enoxaparin should be given; if the
last SC dose was administered at least 8 to 12
hours earlier, an IV dose of 0.3 mg/kg of
In

enoxaparin should be given.

I IIa IIb III c. For prior treatment with fondaparinux: administer
additional intravenous treatment with an
anticoagulant possessing anti-IIa activity taking
into account whether GP IIb/IIIa receptor
antagonists have been administered.

MD Chula 2010

Anticoagulants
I IIa IIb III Because of the risk of catheter thrombosis,
fondaparinux should not be used as the sole
anticoagulant to support PCI. An additional
anticoagulant with anti-IIa activity should be
administered.

y
nl
O
U
al

rn

24 h Hosp Long Term
Aspirin 162-325 mg
Clopidogrel
75-162 75-162
te

In

rPA, SK
60U/kg (4000) aPTT
UFH
LMWH >
12 U/kg/h (1000)
UFH 2 x C
1.5 -
aPTT 1.5 - 2 x C

JACC 2004;44: 671
Circulation 2004;110: 588 88

MD Chula 2010

Beta-Blockers

y
nl
O
U
Beta-Blockers
al
rn

II IIa IIb III Oral beta-blocker therapy should be initiated in the first 24
hours for patients who do not have any of the following: 1)
signs of heart failure, 2) evidence of a low output state, 3)
te

increased risk* for cardiogenic shock, or 4) other relative
contraindications to beta blockade (PR interval > 0.24 sec,
2nd- or 3rd-degree heart block, active asthma, or reactive
In

airway disease).

I IIa IIb III It is reasonable to administer an IV beta blocker at the time of
presentation to STEMI patients who are hypertensive and who
do not have any of the following: 1) signs of heart failure, 2)
evidence of a low output state, 3) increased risk* for
cardiogenic shock, or 4) other relative contraindications to
beta blockade (PR interval > 0.24 sec, 2nd- or 3rd-degree heart
block, active asthma, or reactive airway disease).

MD Chula 2010

Beta-Blockers

I IIa IIb III IV beta blockers should not be administered to
STEMI patients who have any of the following: 1)
signs of heart failure, 2) evidence of a low output
state, 3) increased risk* for cardiogenic shock, or
4) other relative contraindications to beta
blockade (PR interval > 0.24 sec, 2nd- or 3rd-

y
degree heart block, active asthma, or reactive

nl
airway disease).

O
U
al
rn
te

Primary PCI
In


MD Chula 2010

Primary PCI
I IIa IIb III STEMI patients presenting to a hospital with PCI
capability should be treated with primary PCI within
90 min of first medical contact as a systems goal.

I IIa IIb III STEMI patients presenting to a hospital without PCI

y
capability, and who cannot be transferred to a PCI

nl
center and undergo PCI within 90 min of first
medical contact, should be treated with fibrinolytic

O
therapy within 30 min of hospital presentation as a
systems goal, unless fibrinolytic therapy is
contraindicated.
U
al
rn
te

Rescue and Late PCI
In


MD Chula 2010

Rescue PCI
A strategy of coronary angiography with intent to
perform PCI (or emergency CABG) is
recommended in patients who have received
fibrinolytic therapy and have:
I IIa IIb III

a. Cardiogenic shock in patients < 75 years who are

y
suitable candidates for revascularization

nl
I IIa IIb III
b. Severe congestive heart failure and/or pulmonary

O
edema (Killip class III)
I IIa IIb III
c. Hemodynamically compromising ventricular
arrhythmias.
U
al

Rescue PCI
rn

I IIa IIb III
perform rescue PCI is reasonable for patients in
te

whom fibrinolytic therapy has failed (ST-segment
elevation < 50% resolved after 90 min following
In

initiation of fibrinolytic therapy in the lead
showing the worst initial elevation) and a
moderate or large area of myocardium at risk
[anterior MI, inferior MI with right ventricular
involvement or precordial ST-segment
depression].


MD Chula 2010

Rescue PCI
I IIa IIb III
perform PCI in the absence of any of the above
Class I or IIa indications might be reasonable in
moderate- or high-risk patients, but its benefits
and risks are not well established. The benefits

y
of rescue PCI are greater the earlier it is initiated
after the onset of ischemic discomfort.

nl
O
U
al

Rescue PCI
rn

I IIa IIb III
perform PCI (or emergency CABG) is not
te

recommended in patients who have received
fibrinolytic therapy if further invasive
In

management is contraindicated or the patient or
designee do not wish further invasive care.


MD Chula 2010

Late PCI after Fibrinolysis or for Patients Not
Undergoing Primary Reperfusion

I IIa IIb III
PCI of a hemodynamically significant stenosis in a
patent infarct artery > 24 hours after STEMI may
be considered as part of a invasive strategy.

PCI of a totally occluded infarct artery > 24 hours

y
II IIa IIb III
after STEMI is not recommended in asymptomatic

nl
patients with 1- or 2-vessel disease if they are
hemodynamically and electrically stable and do

O
not have evidence of severe ischemia.

U
al
rn
te

Hospital Care
In


MD Chula 2010

Anticoagulants
I IIa IIb III It is reasonable for patients with STEMI who do not
undergo reperfusion therapy to be treated with
anticoagulant therapy (non-UFH regimen) for the
duration of the index hospitalization, up to 8 days.

y
I IIa IIb III
Convenient strategies that can be used include
those with LMWH (Level of Evidence: C) or

nl
fondaparinux (Level of Evidence: B) using the same

O
I IIa IIb III dosing regimens as for patients who receive
fibrinolytic therapy.
U
Emergency Management of Complicated STEMI
Clinical signs: Shock, hypoperfusion, congestive heart failure, acute pulmonary edema
al

Most likely major underlying disturbance?

Hypovolemia Low Output - Arrhythmia
Acute Pulmonary Edema
Cardiogenic Shock
rn

Administer Bradycardia Tachycardia
First line of action

Administer
• Furosemide IV 0.5 to 1.0 mg/kg
• Morphine IV 2 to 4 mg
• Fluids
• Oxygen/intubation as needed • Blood transfusions
• Nitroglycerin SL, then 10 to 20 mcg/min IV if SBP • Cause-specific Check Blood Pressure
te

greater than 100 mm Hg interventions See Section 7.7
• Dopamine 5 to 15 mcg/kg per minute IV if SBP 70 to Consider vasopressors in the ACC/AHA Guidelines for
100 mm Hg and signs/symptoms of shock present Patients With ST-Elevation
• Dobutamine 2 to 20 mcg/kg per minute IV if SBP 70 Myocardial Infarction
to 100 mm Hg and no signs/symptoms of shock
In

Check Blood Pressure Systolic BP Systolic BP Systolic BP Systolic BP
Second line of action

Greater than 100 mm Hg 70 to 100 mm Hg 70 to 100 mm Hg less than 70 mm Hg
NO signs/symptoms Signs/symptoms Signs/symptoms of shock
Systolic BP
of shock of shock
Greater than 100 mm Hg
and not less than 30 mm Hg
below baseline Nitroglycerin Dobutamine Dopamine Norepinephrine
10 to 20 mcg/min IV 2 to 20 5 to 15 0.5 to 30 mcg/min IV
mcg/kg per mcg/kg per
ACE Inhibitors minute IV minute IV
Short-acting agent such as
captopril (1 to 6.25 mg)
Third line of action

Further diagnostic/therapeutic considerations (should be considered in
nonhypovolemic shock)
Circulation 2000;102(suppl I):I-172-I-216.
Diagnostic Therapeutic
♥ Pulmonary artery catheter ♥ Intra-aortic balloon pump
♥ Echocardiography ♥ Reperfusion/revascularization
♥ Angiography for MI/ischemia
♥ Additional diagnostic studies

102

MD Chula 2010

Secondary Prevention and
Long-Term Management

y
nl
O
U
Secondary Prevention
al
rn

• Stop smoking – I (B)
• Clopidogrel 75 mg daily:
te

– PCI – I (B)
– no PCI – IIa (C)
In

• Statin goal:
– LDL-C < 100 mg/dL – I (A)
– consider LDL-C < 70 mg/dL – IIa (A)
• Daily physical activity 30 min 7 d/wk, minimum 5
d/wk – I (B)
• Annual influenza immunization – I (B)


MD Chula 2010
Secondary Prevention and Long Term Management

Goals Class I Recommendations

Antiplatelet
agents/
For all post-PCI STEMI stented patients without
anticoagulants: aspirin resistance, allergy, or increased risk of
Aspirin bleeding, aspirin 162 to 325 mg daily should be

y
given for at least 1 month after bare-metal stent
implantation, 3 months after sirolimus-eluting

nl
stent implantation, and 6 months after paclitaxel-
eluting stent implantation, after which long-term

O
aspirin use should be continued indefinitely at a
dose of 75 to 162 mg daily.
CHANGED
TEXT
U
al

rn

Antiplatelet
te

agents/ For all post-PCI patients who receive a drug-eluting
anticoagulants: stent (DES), clopidogrel 75 mg daily should be
In

given for at least 12 months if patients are not at
Clopidogrel high risk of bleeding.

For post-PCI patients receiving a bare metal stent
(BMS), clopidogrel should be given for a minimum
of 1 month and ideally up to 12 months (unless the
patient is at increased risk of bleeding; then it
should be given for a minimum of 2 weeks).

CHANGED
TEXT

MD Chula 2010

Goals Recommendations

Antiplatelet
For all STEMI patients not undergoing stenting
agents/
(medical therapy alone or PTCA without stenting),
anticoagulants: treatment with clopidogrel should continue for at
Clopidogrel least 14 d. (Class I; LOE: B)

y
Long-term maintenance therapy (e.g., 1 year) with

nl
clopidogrel (75 mg per day orally) is reasonable
in STEMI patients regardless of whether they

O
undergo reperfusion with fibrinolytic therapy or
do not receive reperfusion therapy. (Class IIa;
NEW LOE: C) se
RECS
U
al

rn

Antiplatelet Managing warfarin to INR = 2.0 to 3.0 for
te

paroxysmal or chronic atrial fibrillation or flutter is
agents/ recommended, and in post-STEMI patients when
anticoagulants: clinically indicated (e.g., atrial fibrillation, left
In

Warfarin ventricular thrombus). CHANGED
TEXT

Use of warfarin in conjunction with aspirin and/or
NEW clopidogrel is associated with increased risk of
REC bleeding and should be monitored closely.

In patients requiring warfarin, clopidogrel, and
aspirin therapy, an INR of 2 to 2.5 is recommended
NEW
REC with low dose aspirin (75 to 81 mg) and a 75 mg
dose of clopidogrel.

MD Chula 2010
Stepped Care Approach To Pharmacologic Therapy for Musculoskeletal
Symptoms with Known Cardiovascular Disease or Risk Factors for
Ischemic Heart Disease

• Acetaminophen, ASA, tramadol,
narcotic analgesics (short term)

• Nonacetylated salicylates

• Non COX-2 selective NSAIDs
Select patients at low risk

y
of thrombotic events

nl
• NSAIDs with some • Regular monitoring for sustained
Prescribe lowest dose
COX-2 activity hypertension or worsening of prior
required to control symptoms blood pressure control), edema,
worsening renal function, or

O
gastrointestinal bleeding.
Add ASA 81 mg and PPI to patients • COX-2 Selective
at increased risk of thrombotic • If these events occur, consider
events * NSAIDs reduction of the dose or
discontinuation of the offending drug,
a different drug, or alternative
* Addition of ASA may not be sufficient protection
against thrombotic events
Antman EM, et al. J Am Coll Cardiol 2008. Published ahead of print
se therapeutic modalities, as dictated by
clinical circumstances.
on December 10, 2007. Available at http://content.onlinejacc.org/cgi/content/full/j.jacc.2007.10.001 .
U
al

rn

Renin-
ACE inhibitors should be started and continued indefinitely in all
Angiotensin- patients recovering from STEMI with LVEF ≤ 40% and for those
te

Aldosterone with hypertension, diabetes, or chronic kidney disease, unless
System contraindicated. CHANGED
TEXT
Blockers: ACE
In

Inhibitors ACE inhibitors should be started and continued indefinitely in
patients recovering from STEMI who are not lower risk (lower
risk defined as those with normal LVEF in whom cardiovascular
NEW
REC risk factors are well controlled and revascularization has been
performed), unless contraindicated.

Among lower risk patients recovering from STEMI (i.e., those
NEW with normal LVEF in whom cardiovascular risk factors are well
REC controlled and revascularization has been performed) use of
ACE inhibitors is reasonable. (Class IIa; LOE: B)

MD Chula 2010


Renin-
Use of ARBs is recommended in patients who are
Angiotensin-
intolerant of ACE inhibitors and have HF or have had
Aldosterone
a STEMI with LVEF ≤ 40%. CHANGED
System TEXT

Blockers:
ARBs

y
It is beneficial to use ARB therapy in other patients

nl
NEW who are ACE-inhibitor intolerant and have
REC
hypertension.

O
NEW Considering use in combination with ACE inhibitors
REC in systolic dysfunction HF may be reasonable.
U
al

rn

Renin-
Angiotensin- Use of aldosterone blockade in post-STEMI
te

Aldosterone patients without significant renal dysfunction or
System hyperkalemia is recommended in patients who
In

Blockers:
are already receiving therapeutic doses of an ACE
Aldosterone
Blockade
inhibitor and beta blocker, have an LVEF of ≤ 40%
and have either diabetes or HF.
CHANGED
TEXT


MD Chula 2010


Beta- It is beneficial to start and continue beta-
Blockers blocker therapy indefinitely in all patients
who have had MI, acute coronary

y
syndrome, or left ventricular dysfunction
with or without HF symptoms, unless

nl
contraindicated.

O
CHANGED
TEXT

U
al
rn

te

Influenza Patients with cardiovascular disease
Vaccination should have an annual influenza
In

vaccination.

NEW
REC


MD Chula 2010

Post MI medical Rx

y
nl
O
se
U
al
rn
te

Chronic stable angina
In

MD Chula 2010

Risk stratification
yes High probability of
Clinical Assessment - co-morbid
co-
severe CAD
- Patient’s preference
Patient’
no
no
Suitable for EST

yes

Exercise ECG Test Intermediate-risk Stress Imaging Study

y
High-risk Low-risk
Low-risk Intermediate-risk High-risk

nl
O
Medical Treatment

Failure
se
Coronary Angiography
U
al
rn
te

Stress test
In

MD Chula 2010

Treatment
Ø Treatment that prevents death / MI (should
be highest priority)
l Antiplatelet agents

l Lipid lowering agents

l Beta-blocker in post MI patients
Beta-

y
l CABG in patients with left main or

nl
mulitvessels disease and LV dysfunction
l (ACE-inhibitors)
(ACE-

O
Ø Treatment that improves quality of life
l Antianginal therapy se
U

Treatment
al
rn

Ø Pharmacologic treatment that prevents
te

death / MI
l Antiplatelet agents
In

l Lipid lowering agents
Ø Antianginal therapy
Ø Treatment of risk factors
Ø Myocardial revascularization

MD Chula 2010

Revascularization
in patients with chronic stable angina
Ø Severe or limiting symptoms
l Despite maximal medical treatments
l Intolerable to medical treatment
Ø Large area of ischemia or high-risk noninvasive
high-

y
tests
Ø Malignant coronary anatomy:

nl
l Left main disease

O
l Triple vessels disease, esp. with abnormal LV
function
l Proximal LAD disease
Ø
se
Survivor of sudden cardiac death
U

CAUSES OF ANGINAL CHEST PAIN
al
rn

CORONARY ARTERIAL DISEASE
Fixed obstructive coronary disease
te

Coronary disease with dynamic flow limitation
Microvascular angina (Syndrome X)
In

VASCULAR DISORDERS
Variant angina
Coronary vasospasm (see Printzmetal angina)
Syndrome X (without obstructive vascular
disease)

MD Chula 2010

CAUSES OF ANGINAL CHEST PAIN
• CORONARY ARTERIAL DISEASE
• VASCULAR DISORDERS

OTHER CARDIAC DISORDERS
Aortic stenosis
Hypertrophic cardiomyopathy
Hypertensive heart disease and left
ventricular hypertrophy

y
Mitral valve prolapse

nl
Severe pulmonary hypertension and right
ventricular hypertrophy

O
SYSTEMIC DISORDERS PRECIPITATING ANGINA
Anaemia
Thyrotoxicosis
High-output states (e.g., arterio-venous shunts)
se
U
al
rn
te
In

MD Chula 2010

y
nl
O
se
U

CARDIOGENIC SHOCK: DIFFERENTIAL DX
al
rn

• Complications of acute MI
Extensive LV infarction and ischemia
te

Extensive RV infarction and ischemia
VSR
In

Acute, severe MR
Tamponade
With free wall rupture
Without free wall rupture
Arrhythmia (electrical complication)

MD Chula 2010


• Other conditions
• Acute MI with
Ischemic/infarcted bowel
Ruptured abdominal aortic aneurysm

y
Sepsis

nl
Hemorrhage
Anaphylaxis

O
Excessive β- or calcium channel blockade

se
U

al

rn

• Other conditions
Aortic dissection
te

Myocarditis
PE
Critical aortic or mitral stenosis
In

Hypertrophic cardiomyopathy with outflow
obstruction
Acute aortic or MR
Pericarditis with tamponade
LV apical ballooning/Takostubo cardiomyopathy
Metabolic/toxic
Calcium channel or β-blocker overdose
Acidosis, hyperkalemia, hypoxemia
Thyroid storm, myxedema coma

MD Chula 2010

y
nl
O
se
U
al

Aortic dissection
rn
te
In

MD Chula 2010

Types of Aortic Dissection

y
nl
O
se
U
al
rn
te
In

In
te
rn
al
U
MD Chula 2010

se
O
nl
y

MD Chula 2010

y
nl
O
se
U
al

Cardiac tamponade
rn
te
In

MD Chula 2010

• BECK TRIAD
• Pulsus paradoxus

y
nl
O
se
U
al
rn
te
In

Mdcu Comprehensive Cardio

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