Dr.Syed Imran
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Transcript of Dr.Syed Imran
Lahore: Jan 2011
Principles of Coronary Disease Evaluation & Management
Dr Syed Imran Ahmad MB, MRCP, FRCP (London)
Consultant Cardiologist (Clinical & Invasive) Head, Cardiology Section, Clifton Campus,
Faculty Member Ziauddin University, Karachi:&
Medilink Clinic, Clifton Karachi
Global Disease Mortality
0 5 10 15 20
Mortality (millions)Mortality (millions)
World Health Organization. World Health Organization. The World Health Report 2003: Shaping the Future.The World Health Report 2003: Shaping the Future. 2003. 2003.
Cardiovascular diseaseCardiovascular disease
Malignant neoplasmsMalignant neoplasms
InjuriesInjuries
Respiratory infectionsRespiratory infectionsCOPD and asthmaCOPD and asthma
HIV/AIDSHIV/AIDSPerinatal conditionsPerinatal conditionsDigestive diseasesDigestive diseases
Diarrhoeal diseasesDiarrhoeal diseasesTuberculosisTuberculosis
Childhood diseasesChildhood diseasesMalariaMalaria
DiabetesDiabetes
Atherosclerosis Is a Chronic Inflammatory Disease With LDL-C at the Core
•
Libby P. J Intern Med. 2000;247:349-358.
PHASE I: Initiation PHASE II: Progression PHASE III: Complication
CAD in relation to risk factorsProbability of CAD occurring within next 10 years
36
8
13
23
42
69
13
19
25
44
0 %
10 %
20 %
30 %
40 %
50 %
Women
Men
HBP (150-160) + + + + + +HDL (33-35) - + + + + +Chol (240-262) - - + + + +Cigarettes - - - + + +Diabetes - - - - + +LVH - - - - - +
Kannel WB, Europ.Heart J. 1992; 13:34-42
Integrated Cellular Mechanisms of Cardiovascular Disease
NO SynthesisNO Synthesis
VasoconstrictionVasoconstriction
ThrombosisThrombosis
SuperoxideSuperoxide
COX ActivityCOX Activity
Thromboxane AThromboxane A22
Prostaglandin HProstaglandin H22
ProstacyclinProstacyclin
InflammationInflammation
Leukocyte Leukocyte adhesionadhesion
EndothelialEndothelialpermeabilitypermeability
Angiotensin IIAngiotensin II
T-cell activationT-cell activation
EndothelinEndothelin
VasoconstrictionVasoconstriction
CalciumCalciummobilizationmobilization
Endothelial Dysfunction
DyslipidaemiaDyslipidaemiaHypertensionHypertension
Liao. Liao. Clin ChemClin Chem. 1998:44:1799-1808; adapted from Mason. . 1998:44:1799-1808; adapted from Mason. Cerebrovasc Dis.Cerebrovasc Dis. 2003;16(suppl 3):11-17. 2003;16(suppl 3):11-17.
DiabetesDiabetes SmokingSmoking
Coronary Arteries
Coronary Artery Disease
Angiogram of the left coronary artery and its branches
Initial Presentation of CAD May Be MI orInitial Presentation of CAD May Be MI orSudden Death: Sudden Death: Framingham Heart StudyFramingham Heart Study
MenMen
WomenWomen
0 20 40 60 80
MI or SuddenMI or SuddenDeath as InitialDeath as InitialPresentationPresentation46%
62%
% Patients% PatientsMurabitoMurabito et al. et al. Circulation.Circulation. 1993;88:2548-2555. 1993;88:2548-2555.
Patients Who Developed CAD (N=5144)Patients Who Developed CAD (N=5144)
Manifestations of CAD
• Chronic stable angina
• Unstable angina
• Vasospastic angina (Variant Angina)
• Silent ischaemia
• Myocardial infarction
• Congestive heart failure
• Sudden death (SCD)
Classification of stable angina
Severity I Conduct of daily work and activities without complaints (angina occurs only when load is extreme or over a
very extended period of time)
Severity II Slight restriction of daily work and activities (angina occurs when individual walks fast, climbs stairs or feels stressed)
Severity III Marked restriction of daily work and activities(angina occurs after walking a short distance, or climbing a flight of stairs)
Severity IV Daily work and activities not possible (angina constantly present)
Angina PectorisAngina Pectoris
– Angina is commonAngina is common
- - affects over 10% of men and women > 60affects over 10% of men and women > 60
– Angina is disablingAngina is disabling
- - quality of life can be poorquality of life can be poor
– Angina affects outcome variablyAngina affects outcome variably
- - 3% to 20% annual rate of cardiac events3% to 20% annual rate of cardiac events
Angina PectorisAngina Pectoris
– The The Holy TrinityHoly Trinity of treatment of treatment• Oral NitratesOral Nitrates• Beta BlockersBeta Blockers• Calcium AntagonistsCalcium Antagonists
• Statins and Anti plateletsStatins and Anti platelets
New mechanistic approaches to stable angina
Sinus node inhibition (ivabradine)
Late INa inhibition (ranolazine)
Rho kinase inhibition (fasudil) Metabolic modulation (trimetazidine)
Preconditioning (nicorandil)
OH3C O
H3C O
N
CH3
O CH3
O CH3
NO
N
CH3
H
CH3
CH3 O
O H
N
SO2 NHN
O
O NO2H
N
O
OHCH3
CH3
OCH3HN N N O
N
N
Acute Coronary Syndrome
Unstable anginaor NSTEMI
Temporary resolution of instability
Future high-risk lesion
AcuteSTEMI
Pathophysiology of ACS: Disrupted Plaque
Adapted from Yeghiazarians et al. Adapted from Yeghiazarians et al. N Engl J MedN Engl J Med. 2000;342:101-114.. 2000;342:101-114.
PlaquePlaquerupturerupture
Thin capThin cap
High High macrophagemacrophage
contentcontent
Large lipid coreLarge lipid core
Incomplete Incomplete coronarycoronaryocclusionocclusion
CompleteCompletecoronarycoronaryocclusionocclusion
Spontaneous lysis,Spontaneous lysis,repair, and wall repair, and wall
remodelingremodeling
Pathogenesis of ACS
White HD. Am J Cardiol. 1997; 80(4A):2B-10B.
Cumulative 6-month mortality from CAD
0 1 2 3 4 5 6
5
10
0
15
20
25
Months after hospital admission
Dea
ths
/ 100
pts
/ m
onth
Acute MIUnstable anginaStable angina
Duke Cardiovascular Database
N = 21,761; 1985-1992Diagnosis on adm to hosp
EARLY RISK STRATIFICATION
• In all patients with CP the likelihood of Acute coronary Ischaemia should be determined (High, Intermediate and Low)
• The process of early RS focuses on:Anginal SymptomsClinical ExaminationECG findings Biomarkers of
Cardiac Injury
Why Early Risk Stratification?• Assessment of prognosis, based upon the likelihood of
death/MI should set the pace of Initial Evaluation & Management of ACS.
• The process of RS is needed for
– Selection of the site of care (CCU, Monitored unit, OPD)
– Selection of Therapy specially newer agents like GP
IIb/IIIa inhibitors
– Determination for the need of an early invasive course.
Tools for Risk Assessment(12-lead ECG)
• It remains the sheet-anchor of the decision making for evaluation and management in CP
• A tracing during CP is of particular importance.• High Risk: • ST-segment deviation > 0.05 mV• New or presumed new LBBB
• Sustained VT• Intermediate Risk:• T wave inversion or presence of Q waves• Low Risk:• No ECG changes during CP
Anginal Symptoms
• High Risk:• Accelerating Tempo of CP in preceding 48 hrs or
prolonged CP for >20 min• Intermediate Risk:• Recent prolonged angina at rest for >20 min now
resolved; Rest angina of <20 min.• Low Risk:• New onset Angina with no other High/Intermediate
risk features on symptoms or ECG.
BIOMARKERS• Biomarkers of Cardiac Injury should be
measured in all patients with suspected ACS
• Cardiac Specific Troponin (cTnT or cTnI) is the preferred marker, if available.
• CK-MB is also acceptable
• Total CK (without MB), AST, LDH are considered useless now in this setting.
Principles of Hospital Care in ACS
• Bed Rest
• Continuous ECG monitoring in a CCU for Ischaemia/Arrhythmia
• Nitrates S/L followed by an IV infusion
• Pulse Oximetry with Oxygen if needed
• Morphine Sulphate IV if pain persists and specially with LVF
• Beta Blockade with first dose IV, if CP persists
Principles of Hospital Care in ACS
• ACE-I, early on ( a lot of evidence with drugs like Ramipril: also evidence with ARB e.g. Valsartan)
• Antiplatelets (Aspirin and Clopidogrel)
• Anticoagulants (UFH/LMWH or Fondaparinux)
• Statins
• Early Invasive vs. planned ischaemia driven
Lipid Management in Clinical Practice
• For patients with CHD or diabetes, a new, lower optimal goal for LDL-C is <70 mg/dl —NCEP Coordinating Committee Circulation 2004;110:227–239
What is an appropriate therapeutic target for LDL-C?
Changes to NCEP ATP III LDL-C Goals
Modification
Modification
2+ risk factors (10-year risk 20%)
CHD or CHD risk equivalents(10-year risk >20%)
Risk Category
Optional goal of <100 mg/dl (2.5 mmol/L)
for 10%–20% risk group
Optional goal of <70 mg/dl (1.8 mmol/L)
<130 mg/dl (3.4 mmol/L)ATP III
<100 mg/dl (2.5 mmol/L)ATP III
LDL-C GoalPublication
NCEP=National Cholesterol Education Program; ATP III=Adult Treatment Panel III
Adapted from Grundy SM et al Circulation 2004;110:227–239; Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults JAMA 2001;285:2486–2497.
Rationale for Lower LDL-C Goals
• Both HPS and PROVE IT suggest that additional benefit may be obtained by reducing LDL-C levels to substantially less than 100 mg/dl (2.5 mmol/L)
• Recent trials indicate that there is no threshold below which lower LDL-C concentrations provide no further benefit
Adapted from Grundy SM et al Circulation 2004;110:227–239; HPS Study Group Lancet 2002;360:7–22; Cannon CP et al N Engl J Med 2004;350:1494–1502; O’Keefe JH et al J Am Coll Cardiol 2004;43:2142–2146; Stamler J et al JAMA 2000;284:311–318; Chen Z et al BMJ 1991;303:276–282.
Investigations in CAD
• Non-invasive Testing:
– Echocardiography (Resting and Stress)– ETT– Myocardial Perfusion Studies (Thallium)– CT Angiogram– Cardiac MRI– PET
Investigations in CAD
• Invasive Testing:
– Selective Coronary Angiography & Ventriculography
– Invasive Electrophysiological (EP) Studies
Further Management
• Medical Treatment
• Interventional Treatment– Percutaneous Coronary Intervention (PCI)
– Surgical Intervention (CABG)
Prognosis in CAD
• More closely related to – Left Ventricular Function; &
– Extent of Coronary Disease
than
– The severity of Symptoms
Thank You
Dr Syed Imran Ahmad MB,FRCP(London)