Cardiovascular Diseases
Part 1
• Thanks to:
– SICP
– Andrea Davis RCIS, FSICP
– Wes Todd, Cardiac Self Assessment
– Morton Kern, MD
– Steve West , MD
– Ken Gorski RCIS
– Tom Maloney RCIS
– Merck
– Eli Lilly

Disclosure Information
Cardiovascular Diseases Part 1
Jeff Davis RCIS, FSICP
The following relationships exist related to this presentation:
None
Off label use of products will not be discussed in this presentation.

SICP’s RCIS Review
• Coronary Artery Disease
– Angina
• stable, unstable, prinzmetals/variant
• Myocardial Infarction
– NSTEMI, STEMI
• Heart Failure
– Left and right side heart failure
• Valve Disease
– AS, AI, MS, MR
• Cardiomyopathies
– Dilated, restrictive, hypertropic obstructive
• Pericardial
– Constrictive pericarditis, cardiac tampanode
• Shunts
– Atrial and ventricular septal defects, pfo’s
• Congenital Cardiac Anomalies

Risk Factors For CAD
• Family history
• Advancing age
• Male gender
• Total cholesterol >200, LDL>100
HDL< 35
• Hypertension
• Smoking
• Overweight/obesity
• Sedentary life-style
• Stress
• Diabetes Mellitus

Modify Risk Factors
• STOP SMOKING
• LOWER CHOLESTEROL –
– Drugs and Diet
• EXERCISE
• LOSE WEIGHT
• CONTROL HYPERTENSION
•
• CONTROL DIABETES...or…

Rupture!

• TWO PARALLEL
PROCESSES PLAY
IMPORTANT ROLE IN
ATHEROSCLEROSIS:
• First the fats:
LIPID ACCUMULATION &
OXIDATION
• Then the vessel deforms:
– ENDOTHELIAL
DYSFUNCTION causing
– Spastic vessels

Evolution of fibrous plaque
8. Muscle cells die
& harden plaque
-Calcium develops
Foam Cells
1 LDL Monocyte
Cell adhesion
factors macrophage
endothelium
1. LDL enters 3. Monocytes adhere & 4. cross 5. Macrophages Eat 6. muscle cells multiply &
2. & Oxidizes intima become macrophages Fat become Foam 7. enter intima
cells

Vulnerable Plaque
Rioufol et al. Circulation 2002;

7 y.o accident victim

ENDOTHELIAL SECRETION
• ENDOTHELIUM-DERIVED RELAXING
FACTORS
– NITRIC OXIDE
^ smooth-muscle-cell cyclic GMP
• ENDOTHELIUM-DERIVED CONTRACTING
FACTORS
– ENDOTHELIN-1
– potentiates renin & catecholamines

Classes of Angina
• Prinzmetals or Variant Angina
• Stable Angina
• Unstable Angina
• Acute Coronary Syndrome
– UA/NSTEMI
– STEMI

STABLE ANGINA
• Chest pain •Treatment
– Predictable •Diet and exercise
– Activity, emotional stress, •Modify risk factors
sex
– Relieved with rest, ntg •NTG
– Exacerbated by meals or •ASA
cold
– Pressure or tightness
•Beta blockers
– Duration 2-3 to 20-30 minutes •ACE inhibitors
– May radiate •Statins
• Levine sign •Calcium channel blockers
•PCI, stenting, CABG

ACS-The Plaque Ruptured

Results of ACS Pathophysiology
Plaque Disruption / Erosion
Thrombus Formation &
Embolization
Non-ST ST
Unstable
Elevation Elevation
Angina
MI MI

Fuster V, et al. N Eng J Med 1992;326:311-318. 2. Photos courtesy of Boehringer Ingleheim International GmbH, by Lennart
Nilsson

Coronary Artery Disease

Thrombus Formation and ACS
Plaque Disruption/Fissure/Erosion
Thrombus Formation
Old
Terminology: UA NQMI STE-MI
New Non-ST-Segment Elevation Acute ST-Segment
Terminology: Coronary Syndrome (NSTEMI-ACS) Elevation
Acute
Coronary
Syndrome
(STEMI-ACS)

Unstable Angina (UA)
• Partially occluding platelet-rich thrombus
• Inflammatory cells in arterial wall
• No permanent damage initially
• Increased risk for adverse cardiac events 30 days to 1
year (death, MI)
• ST depression is seen in only 20% who have angina
• ST depression >1mm correlates with an increased risk of
mortality
• Clinical forms
– New-onset exertional angina
– Angina of increasing frequency or duration; refractory to
nitroglycerin
– Angina at rest

Unstable Angina (UA)
– Aggressive medical treatment with ASA, GP IIa/IIIb
inhibitors, heparin, beta blockers, nitrates
– CABG or PCI may be necessary
– PCI may be preceded with antiplatelet (ASA,
clopidogrel, GP IIa/IIIb inhibitors) and antithrombin
(UFH or LMWH) therapies
– Hemodynamic support with IV fluids, PA pressure
monitoring and IABP may also be needed

11

Non ST Elevation Myocardial
Infarction (NSTEMI)
• Heart attack with damage
• Platelet aggregation occurs and thrombus is formed
• Cell markers are released which may lead to
spontaneous thrombolysis
• Brief, intermittent and incomplete coronary occlusion
• ST depression or T wave inversion may be present
• Increase in cardiac markers (troponins, CKmb) may be
present

ST Elevation Myocardial Infarction
(STEMI)
• Ischemic chest pain lasting over 30 minutes
• ST segment elevation >1mm in at least 2
contiguous leads
• Increase in Troponin and CKmb
• New-onset of LBBB may occur signifying extensive
muscle involvement
• Platelet aggregation and thrombus formation
continue causing blockage to persist
• Complete occlusion of blood flow causes muscle
infarct

Treatment of Acute Coronary
Syndrome
Initial Treatment of ACS
STEMI* UA/NSTEMI†
Antiplatelet, Antiplatelet,
anti-ischemic, or anti-ischemic, or
anticoagulant therapy anticoagulant therapy
Thrombolytics PCI or CABG PCI or CABG
Long-Term Medical Management
*Also known as Q-wave MI.
†
Also known as non–Q-wave MI.
Boden WE, et al. N Engl J Med. 2001;344:1939-1942.
Braunwald E, et al. J Am Coll Cardiol. 2000;36:970-1062.

These may continue to
Shift sides as DES becomes
The gold standard

ACS Medicine Cabinet
Anticoagulation
• Aspirin
• Heparin
• Low Molecular Weight Heparin
• GP IIb/IIIa Inhibitors
• Direct Thrombin Inhibitors
• Warfarin
• Statins (HMG Co-A Reductase Inhibitors)
• Early Medical vs Early Invasive therapy

ACS Medicine Cabinet
Anti-Ischemic Therapy
• Bed Rest
• Nitroglycerin
• Supplemental O2
• Narcotics (Morphine)
• Beta Blockade
• Calcium Channel Blockade ?
• Ace Inhibitor
• Diuretics
• Anti-arrthymics (PRN)
• Inotropic Agents (PRN)
• IABP (PRN)
• A compassionate listener

TREATMENT AMI
• FIBRINOLYTICS – decreasing
• DIRECT PCI STENTING- increasing
• PLATELET INHIBITION
CLOPIDOGREL (plavix) , ASA
• GP IIb-IIIa INHIBITORS
• CABG – really decreasing
• RISK FACTOR MODIFICATIONS
• STATINS- really increasing

Approved Fibrinolytic Agents
• Streptokinase
• Anistreplace
• Alteplase
• Reteplase
• TNKASE

Relative Contraindications to
Fibrinolytic Therapy
• Severe uncontrolled HTN on presentation (BP>180/110 mm Hg)
• HX of prior CVA or known intracerebral pathology
• Therapeutic use anticoagulants (INR>2-3)
• Recent Trauma (within 2-4 weeks)
• Noncompressible vascular puncture
• Recent (within 2-4 weeks) internal bleeding
• Streptokinase/anistreplase prior exposure or prior allergic Rxn
• Pregnancy
• Active PUD
• History of chronic hypertension

Absolute Contraindications to
Fibrinloytic Use
• Previous hemorrhagic Stroke
• Non-hemorrhagic Stroke or
cerebrovascular events within 1 year
• Known intracranial neoplasm
• Active internal bleeding (does not include
menses)
• Suspected Aortic Dissection

Complications of MI
• Dysrhythmias
– heart blocks
– Bundle branch block
– Ventricular Fibrillation
• CHF
• LV Aneurysm
• VSD
• MR

Ventricular Free Wall Mitral Regurgitation
Septal Rupture Rupture (Pap. M. dysfunction)
Incidence 1-2% 1-6% 1-2%
Timing 3-5 d p MI 3-6 d p MI 3-5 d p MI
Phy Exam murmur 90% JVD, EMD murmur 50%
Thrill Common No Rare
Echo Shunt Peric. Effusion Regurg. Jet
PA cath O2 step up Diast Press Equal. c-v wave in PCW
Images:Courtesy of W D Edwards (Mayo Foundation)
Data: Lavocitz. CV Rev Rpt 1984;5:948; Birnbaum. NEJM 2002;347:1426.

AHA COMPREHENSIVE
RISK FACTOR MANAGEMENT
♥ Blood pressure management
♥ Lipid management
♥ Physical activity
♥ Smoking cessation
♥ Weight management
♥ ACE inhibitors & Beta blockers
♥ Antiplatelet agents

A Guide to the Etiology,
Pathophysiology, Diagnosis,
and Treatment of Heart Failure
Created in association with
Dr. Philip B. Adamson, Director
Congestive Heart Failure Treatment Program
University of Oklahoma
Oklahoma City, Oklahoma

Heart Failure
A complex clinical syndrome in
which the heart is incapable of
maintaining a cardiac output
adequate to accommodate
metabolic requirements and
the venous return.

HF Incidence and Prevalence
• Prevalence
– Worldwide, 22 million1
– United States, 5 million2
• Incidence
– Worldwide, 2 million new cases annually1
– United States, 500,000 new cases
annually2
• HF afflicts 10 out of every 1,000 over age 65 in
the U.S.2
1 World Health Statistics, World Health Organization, 1995.
2 American Heart Association, 2002 Heart and Stroke Statistical Update.

New York Heart Association
Functional Classification
Class I: No symptoms with ordinary activity
Class II: Slight limitation of physical activity. Comfortable at rest,
but ordinary physical activity results in fatigue, palpitation,
dyspnea, or angina
Class III: Marked limitation of physical activity. Comfortable at rest,
but less than ordinary physical activity results in fatigue,
palpitation, dyspnea, or anginal pain
Class IV: Unable to carry out any physical activity without
discomfort. Symptoms of cardiac insufficiency may be present
even at rest

Etiology of Heart Failure
What causes heart failure?
– Ischemic Heart Disease
– Hypertension
– Idiopathic Cardiomyopathy
– Infections (e.g., viral myocarditis, Chagas’
disease)
– Toxins (e.g., alcohol or cytotoxic drugs)
– Valvular Disease
– Prolonged Arrhythmias

Left Ventricular Dysfunction
• Systolic: Impaired contractility/ejection
– Approximately two-thirds of heart failure patients
have systolic dysfunction1
• Diastolic: Impaired filling/relaxation
30%
(EF > 40 %)
(EF < 40%)
Diastolic Dysfunction
70%
Systolic Dysfunction
1 Lilly, L. Pathophysiology of Heart Disease. Second Edition p 200
Disease.

Determinants of Ventricular
Function
Contractility
Preload Afterload
Stroke
Volume
• Synergistic LV Contraction
• Wall Integrity
• Valvular Competence
Heart Rate
Cardiac Output

Left Ventricular Dysfunction
Volume Pressure Loss of Impaired
Overload Overload Myocardium Contractility
LV Dysfunction
EF < 40%
↑ End Systolic Volume
↓ Cardiac
Output
↑ End Diastolic Volume
Hypoperfusion Pulmonary Congestion

Sites of Failure
Right and Left Heart

Treatments of CHF circa Netter

Right Sided Heart Failure or
Peripheral Edema

Hemodynamic Basis for
Heart Failure Symptoms
LVEDP ↑
Left Atrial Pressure ↑
Pulmonary Capillary Pressure
Pulmonary Congestion

Left Ventricular Dysfunction
Systolic and Diastolic
• Symptoms • Physical Signs
– Dyspnea on – Basilar Rales
Exertion
– Pulmonary Edema
– Paroxysmal
Nocturnal Dyspnea – Pulsus Alternans
– Tachycardia – S3 Gallop
– Cough – Pleural Effusion
– Hemoptysis – Cheyne-Stokes
Respiration
– BNP may elevate

Right Ventricular Failure
Systolic and Diastolic
• Symptoms • Physical Signs
– Abdominal Pain – Peripheral Edema
– Anorexia – Jugular Venous
Distention
– Nausea
– Abdominal-Jugular
– Bloating Reflux
– Swelling – Hepatomegaly

Compensatory Mechanisms
• Frank-Starling Mechanism
• Neurohormonal Activation
• Ventricular Remodeling

General Measures
Lifestyle Modifications: Medical Considerations:
• Weight reduction • Treat HTN, hyperlipidemia,
diabetes, arrhythmias
• Discontinue smoking
• Coronary revascularization
• Avoid alcohol and other
cardiotoxic substances • Anticoagulation
• Exercise • Immunization
• Sodium restriction
• Daily weights
• Close outpatient monitoring

Pharmacologic/Medical Management
• Oxygen
• Digoxin
• Diuretics
• ACE Inhibitors
• Beta-Blockers
• Aldosterone Antagonists
• Angiotensin Receptor Blockers (ARBs)
• Dopamine/Dobutamine
• Intra Aortic Balloon Pump
• Underlying Cause

Cardiac Resynchronization Therapy
Patient Indications
CRT device:
– Moderate to severe HF (NYHA Class III/IV) patients
– Symptomatic despite optimal, medical therapy
– QRS ≥ 130 msec
– LVEF ≤ 35%
CRT plus ICD:
– Same as above with ICD indication

Summary
• Heart failure is a chronic, progressive disease that is
generally not curable, but treatable
• Most recent guidelines promote lifestyle modifications and
medical management with ACE inhibitors, beta blockers,
digoxin, and diuretics
• It is estimated 15% of all heart failure patients may be
candidates for cardiac resynchronization therapy
• Close follow-up of the heart failure patient is essential, with
necessary adjustments in medical management

Myocardial Infarction
• Left Heart MI
– Dec. SV, CO/CI, AO,
systemic perfusion
– Inc. LVEDP, LA/PCWP, PA,
pulmonary congestion
– Left side heart failure
• Right Heart MI
– Dec. PA, LVEDP, AO,
systemic perfusion
– Inc. RVEDP, RA/CVP,
systemic venous
congestion
– Right side heart failure

Thank You