2. Introduction
• Stable Ischemic Heart Disease is most commonly (?) caused by
atheromatous plaque that gradually narrows one or more of the
epicardial coronary arteries.
• IHD - Leading cause of death worldwide.*
• Burden of CAD shifting to lower socioeconomic groups.
• Increase in CV risk factors.
• WHO – estimated rise in CAD deaths in 2020 – 11.1 million (7.6
million in 2005).*
AHA: International Cardiovascular Disease Statistics.Dallas,AHA 2009
5. Removing stenoses does not
consistently treat IHD
• COURAGE trial (N=2,287) evaluation of PCI on top of medical
therapy (optimal ?), 30% of patients were still symptomatic with
angina 1 year after PCI.
• Incidence of angina was not significantly different.
• No difference in composite end point.
Boden et al, Optimal medical therapy with or without PCI for stable coronary disease.
N Eng J Med 2007;356:1053-16.
11. • Is there any benefit of achieving lower BP (target <120 mm
hg) compared to usually recommended (target <140 mm Hg)?
• Does normalisation of BP in CVD patients has any benefit
of CV outcomes?
12. ACCORD BP study
• High risk Type 2 Diabetics
• Intensive therapy (SBP<120mm Hg) vs Standard therapy( SBP
<140mm Hg).
• 4733 pts
• The primary composite outcome was nonfatal MI, nonfatal stroke, or
death from CV causes.
• The mean follow-up was 4.7 years.
Effects of Intensive Blood-Pressure Control in Type 2 Diabetes Mellitus
The ACCORD Study Group
N Engl J Med 2010; 362:1575-1585.
13. In patients with type 2 diabetes at high risk for cardiovascular
events, targeting a SBP of <120 mm Hg, as compared with <
140 mm Hg, did not reduce the rate of a composite outcome of
fatal and nonfatal major cardiovascular events.
14. • Are ACEI beneficial in patients with normal LV function but
at risk of CV events?
• Role of ACEI beyond improving LV dysfunction?
(pleiotropic effects)
15. HOPE trial
The Heart Outcomes Prevention Evaluation
Study
• Vascular disease or diabetes plus one other CV risk factor, not
known to have low LVEF or HF(<40%).
• 9297 pts.
• >55 years of age.
• Ramipril (10 mg/day) vs placebo
Effects of an Angiotensin-Converting–Enzyme Inhibitor, Ramipril, on Cardiovascular Events in High-Risk Patients.
The Heart Outcomes Prevention Evaluation Study Investigators
N Engl J Med 2000; 342:145-153
16. End points/Results
• Primary - composite of MI, stroke or death from CV causes.
P<0.001
Conclusion : Ramipril significantly reduces the rates of
death,myocardial infarction,and stroke in a broad range of
high –risk patients who are not known to have a low ejection
fraction or heart failure.
17. HOPE - Summary of Results
• Patients randomized to ramipril had risk
reductions of:
– MI, stroke, CV death -22%
– CV death -25%
– MI -20%
– Stroke -31%
– Revascularization procedures* -16%
– New onset of diabetes -32%
*Revascularization procedures included PTCA, CABG or peripheral angioplasty
N Engl J Med, January 20, 2000
18. • Does addition of ACEI over conventional therapy in
patients with stable CAD have a favorable outcome?
• Does the effects of ACEI apply to low risk CAD patients?
19. EUROPA trial
EUropean trial on Reduction Of cardiac events with
Perindopril in stable coronary Artery disease
• Low risk patients with stable CAD
• 12,218 pts
• Perinodpril (8mg/day)
• Follow up (mean 3.4 yrs)
Primary – Composite of CV mortality, nonfatal MI, and cardiac
arrest.
Secondary – Composite of total death, nonfatal MI, and cardiac
arrest; heart failure; revascularization (PCI/CABG); and stroke.
Lancet 2003 Sep 6;362(9386):782-8
20. EUROPA Trial
CV death/non-fatal MI/
cardiac arrest
p=0.0003
8.0%
9.9%
0%
5%
10%
15%
Perindopril Placebo
3.5%
4.1%
0%
1%
2%
3%
4%
5%
Perindopril Placebo
European Society of Cardiology 2003
CV Mortality
p=0.107
Among patients with stable CAD, treatment with the ACE-I
perindopril was associated with a reduction in the primary
endpoint of cardiovascular mortality, non-fatal MI, and cardiac
arrest compared with placebo.
21. PEACE trial
Prevention of Events with Angiotensin Converting
Enzyme Inhibition
• 8290 pts,Double blind, placebo controlled
• Trandolapril (4mg/d) vs placebo .
• Primary end point – death from CV causes,MI or coronary
revascularization.
• Mean age of patients – 648 yrs,
• LVEF 58 9 %
N Engl J Med 2004; 351:2058-2068
22. Results
• 72% underwent revascularization previously.
• 70% received lipid lowering drugs.
• Primary end point was seen in 21.9% (trandolapril) vs 22.5% (placebo)
(p= 0.43) .
23. PREVENT study
Prospective Randomized Evaluation of the Vascular Effects
of Norvasc Trial
• Amlodipine (Norvasc) vs placebo (5 mg -10 mg) {RCT}
• Angiographically documented CAD – slowing of progression of
lesions with baseline of 30% stenosis.
• Reduction in atherosclerosis in carotids by IMT.
• Rates of clinical events
• 825 pts,36 months
Circulation.2000; 102: 1503-1510
24. Conclusions— Amlodipine has no demonstrable effect on angiographic
progression of coronary atherosclerosis or the risk of major
cardiovascular events but is associated with fewer hospitalizations for
unstable angina and revascularization.
25. CCBs
Trial Regimen Protocol Results
CAPARES trial Amlodipine 10
mg/day
2 weeks before
angioplasty
Less incidence of
angina (p = 0.04)
EST,48hr ambulatory
ECG at 2 weeks and
20 weeks post PTCA
Exercise induced
ischemia reduced by
40%(p=0.009)
Ischemia of Holter
ECG reduced by
28%(p=0.009)
ACTION study Long acting nifedipine No effect on major or
CV events
(n=7665 pts) 52% hypertensives Reduced need for
PTCA /CABG
Can J Cardiol. 2000 Jul;16 Suppl D:8D-11D
Expert Rev Cardiovasc Ther . 2008 Sep;6(8):1055-62
26. CARISA trial
Combination Assessment of Ranolazine In
Stable Angina trial
• Effect of ranolazine over the OPTIMAL MEDICAL therapy.
• Symptomatic stable CAD pts.
• OMT –Atenolol ,amlodipine or diltiazem
• 750mg or 1000 mg Ranolazine vs placebo
Twice-daily doses of ranolazine increased exercise capacity and provided
additional antianginal relief to symptomatic patients with severe chronic
angina taking standard doses of atenolol, amlodipine, or diltiazem,
without evident adverse, long-term survival consequences over 1 to 2
years of therapy.
JAMA 2004 Jan 21;291(3):309-16.
27. What is the mechanism of action of trimetazidine?
28. Trimetazidine
• Metabolic agent
• Inhibits the enzyme 3-ketoacyl coenzyme A thiolase,the terminal
enzyme in b oxidation pathway.
• Enhances glucose metabolism.
• Energy production with less oxygen consumption.
• Improves endothelial function by increasing NO production.
Drugs. 1999 Jul;58(1):143-57
29. TRIMPOL II
• Efficacy and tolerability of trimetazidine in combination with
metoprolol.
• Randomized,double blind,parallel group,placebo controlled
study.
• 426pts
• Placebo or trimetazidine 20 mg tid over metoprolol 50 mg bd.
• TMT at baseline,4 weeks,8 weeks,12 weeks.
After 12 weeks, there were significantly greater improvements in the
Metoprolol+trimetazidine group in
Time to 1 mm ST segment depression,
Total workload,
Time to onset of angina,
maximum ST segment depression,
mean weekly number of angina attacks,
mean weekly nitrate consumption, and
grade of anginal pain.
There was no evidence of any development of tolerance to trimetazidine.
The tolerability of trimetazidine was excellent.
European Heart Journal (2001) 22, 2267–2274
30. STUDY DRUGS No. ASSEESSMENT RESULTS
TACT CT+TMZ (60 mg) vs
CT +placebo
117 pts Exercise capacity TED – increased
by 89 seconds,
TI increased by
99 sec
TA +100 sec
A/W decreased
by 51%.
VASCO
angina
study
70 mg/d TMZ,140mg/d
TMZ in CSA
645 pts Exercise capacity TED increased
by 6%,TI
increased by
9.6%
Chazov et al ,Am J Ther 2005;12(1):35-42.
Vitale C et al, Int J Cardiol.2103;168(2)1078-81.
TED –TOTAL EXERCISE DURATION
TI – TIME TO 1mm ST DEPRESSION
TA -TIME TO ANGINA
A/W – ANGINA PER WEEK
32. • Chronic stable angina with LV systolic failure on OMT
• 10,917 pts
• 5mg bid – 7.5 mg bid
• Ivabradine did not improve the CV death rate or hospital admissions
rates for acute MI or acute heart failure.
Sub group analysis –
• Among patients with RHR > 70 /min – reduction in hospital
admissions for non fatal MI, unstable angina and coronary
revascularization. Cardiology, 2008;110(4):271-82
33. • Elevated HR an established marker of CV risk.
• Chronic CAD without HF and HR >70/min.
• CCS II angina
• Ivabradine 10 mg bid vs placebo
• THR 55-60/min
N Engl J Med 2014; 371:1091-109
34. • No difference in primary end point or CV deaths.
• Increase in the incidence of the primary end point among patients with
activity-limiting angina ( p=0.02 ).
• The incidence of bradycardia was higher with ivabradine than with
placebo (18.0% vs. 2.3%, p<0.001).
CONCLUSIONS :
Among patients who had stable coronary artery disease
without clinical heart failure, the addition of Ivabradine to
standard background therapy to reduce the heart rate did not
improve outcomes.
35. TRIAL drug Follow up Results
SAPAT trial
(2035 pts)
1 st trial in CSA
Aspirin (75 mg /d) 50 months Primary outcome – 34%
reduction (p =0.003)
Secondary events
reduction by 22-33%
Non significant adverse
events
CAPRIE trial Clopidogrel (75
mg/d)vs Aspirin
(325 mg/d)
36 months 8.7% relative decrease in
the risk of vascular
death,ischemic stroke,or
MI among patients with
established
atherosclerotic vascular
disease.(p=0.043)
Lancet1992 Dec 12;340(8833):1421-5.
Lancet 1996 Nov 16;348(9038):1329-39.
ANTI PLATELETS
36. CAPRIE: Superior Efficacy of Clopidogrel
versus ASA
*MI, ischemic stroke or vascular death
†Intent-to-treat analysis (n=19,185)
CAPRIE Steering Committee. Lancet 1996; 348: 1329–1339.
0
4
8
12
16
0 3 6 9 12 15 18 21 24 27 30 33 36
Months of follow-up
Cumulativeeventrate*(%)
ASA
Clopidogrel
8.7%† RRR
(p=0.043)
20
Patients with recent ischemic stroke, recent MI or symptomatic PAD
37. CAPRIE: Clopidogrel Reduced the Rate of
Rehospitalization
Bhatt DL et al. Am Heart J 2000; 140: 6773.
*Rehospitalization for ischemia (angina pectoris, TIA, limb ischemia) or bleeding (gastrointestinal,
intracranial or other)
†On-treatment analysis (n=19,099)
Patients with recent ischemic stroke, recent MI or symptomatic PAD
5 10 15 20 25 30 35
9.1%† RRR
(p=0.018)
Months of follow-up
Cumulativeeventrate*(%)
0
5
10
15
20
ASA
Clopidogrel
38. CHARISMA trial
• Dual antiplatelet therapy.
• 15603 pts,28 months
• Clinically evident CVD or having risk factors
• Clopidogrel 75mg/d + aspirin 75-162 mg/d vs palcebo + aspirin
75 mg/d
Am Heart J 2004 Aug;148(2):263-8
39. Overall Population: Primary Efficacy Outcome (MI,
Stroke, or CV Death)†
† First Occurrence of MI (fatal or non-fatal), stroke (fatal or non-fatal), or cardiovascular death
*All patients received ASA 75-162 mg/day
§The number of patients followed beyond 30 months decreases rapidly to
zero and there are only 21 primary efficacy events that occurred beyond
this time (13 clopidogrel and 8 placebo)
Bhatt DL, Fox KA, Hacke W, et al. NEJM 2006.
Cumulativeeventrate(%)
0
2
4
6
8
Months since randomization
0 6 12 18 24 30
Placebo + ASA*
7.3%
Clopidogrel + ASA*
6.8%
RRR: 7.1% [95% CI: -4.5%, 17.5%]
p=0.22
40. • In this trial, there was a suggestion of benefit with clopidogrel
treatment in patients with symptomatic atherothrombosis and a
suggestion of harm in patients with multiple risk factors.
• Overall, clopidogrel plus aspirin was not significantly more
effective than aspirin alone in reducing the rate of myocardial
infarction, stroke, or death from cardiovascular causes
41. Women and CAD
HERS
The Heart and
Estrogen/Progesti
n Replacement
Study
Estrogen + progestin in
post menopausal women
CAD pts No morbidity or
mortality benefit
Increased risk of
DVT,PE
Postive – reduction
in
LDL(10%),increase
d HDL by (11%)
HERS II Follow up of patients
enrolled in HERS
6.8yrs
2321 post
menopaus
al women
Increased risk of
VTE
JAMA. 1998;280(7):605-613
JAMA 2002 Jul 3;288(1):58-66.
42. WHI
Compared with the placebo, estrogen plus progestin resulted
in:
• Increased risk of MI,stroke
• Increased risk of DVT,PE
• Increased risk of breast cancer
• Reduced risk of colorectal cancer
• Fewer fractures
• No protection against mild cognitive impairment and increased risk
of dementia (study included only women 65 yrs)
https://www.nhlbi.nih.gov/whi/index.html
43. Compared with the placebo, estrogen alone resulted in:
• No difference in risk for MI
• Increased risk of stroke
• Increased risk of DVT,PE
• Uncertain effect for breast cancer
• No difference in risk for colorectal cancer
• Reduced risk of fracture
44. 4S trial
Scandinavian Simvastatin Survival Study
• Benefits of Cholesterol lowering in 4,444 pts with CAD.
• TC : 212-309 mg/dl
• Prior MI and angina pectoris.
• Simvastatin 20mg/day – 40 mg/day
• Goal of cholesterol - 116-200 mg/dl
• Primary – Total mortality
• Secondary – Major adversed coronary events
• Tertiary – Effect on PTCA/CABG procedures,event free survival.
Lancet,Vol 344, 8934, p1383–1389, 1994
48. • What is the trial which showed high dose statin is beneficial
in management of CSA patients and is safe with less
complications related to drug?
49. AVERT trial
Atorvastatin Versus Revascularization Treatment
• Aggressive lipid therapy (atorvastatin 80 mg/d) or PTCA followed by
usual care(lipid lowering drugs also included).
• 18 month study
• 341 pts.
• LDL>115mg/dl, TG>500mg/dl, CCS II, Bruce protocol > 4 min,
stenosis >50% in coronaries.
• Primary – cardiac death,cardiac arrest,need of PTCA/CABG
• Secondary – time to ischemia event,worsening angina,changes in
lipoproteins.
Mean percentage diameter of coronary stenosis – 80%.
Interesting points:
1.Reduction of ischemic events in atorvastatin group by 36%.
(p=0.048)
2.Long time for occurrence of ischemia > 6 months (p=0.03)
3.Routine use of atorvastatin(80mg/day) – safe – only four
developed complications.
Can J Cardiol. 2000 Jan;16 Suppl A:11A-3A
50. TNT
Treating to New Targets study
• 10,003 pts
• Atorvastatin 10 mg vs atorvastatin80 mg.
• Target of LDL -100 mg/dl for 10 mg and
75 mg /dl for 80 mg
Am J Cardiol. 2004 Jan 15;93(2):154-8.
51. No difference in all cause mortality between
high dose and low dose atorvastatin
57. ABCDE of SIHD patient
management
• A –Aspirin, Antianginals
• B – Betablockers, Blood pressure control
• C – Cholesterol management,C igarette cessation
• D – Dietary improvements, Diabetes control.
• E – Education and Exercise.
ESC/EHA Guidelines for stable CAD,2012
61. COURAGE trial
Clinical Outcomes Utilizing Revascularization and
Aggressive DruG Evaluation
• PCI + OMT vs OMT
• Severe angiographic disease of one or more vessels(>70%
stenosis),and either classic symptoms or documented ischemia
on provocative testing.
• 2287 pts randomized.
• Follow up 2.5-7 yrs (median 4.6 yrs).
Circulation. 2008; 117: 1283-1291.
62. What is the motto?
Test
a strategy of routine anatomically driven PCI plus OMT
versus
a strategy of selective,ischemia driven PCI, if needed for
failure of initial OMT.
63. Results
• Death or MI occurred with similar frequency in both arms
(p=0.62).
• No difference in hospitalization for ACS (p = 0.56) or MI
(p=0.33).
• Less angina at 1 and 3 yrs but not at 5 yrs in PCI pts.
• Increased PCI in patients on OMT.
Conclusion:
As an initial management strategy in patients with SIHD,
PCI did not reduce death,MI or other major CV events when added to
OMT.
64.
65.
66. Important features of COURAGE
cohort
• Highly symptomatic at baseline.
• Clinical comorbidities.
• High prevalence of objective evidence of myocardial ischemia.
• Extensive angiographic CAD.
67. Patient cohort
• 42-43% no angina or class I angina
• 30% SVD
• 35% LAD
• EF -61%
• DES was not routinely available.
68. What went wrong?
• 1.low cardiac mortality in stable angina patients.
• 2.improved endothelial function over long term on OMT.
• 3.collateralization - alleviation of symptoms in patients on OMT.
• 4.Adherence of patients on OMT (80%).
• 5.Benefits of PCI were diluted - disease progression in other vessels
or the failure to provide complete revascularization initially.
• 6.ACS can occur at site other than severe stenosis.
69. Subgroup analysis
No difference between PCI plus OMT vs OMT in
• CCS class II or III angina
• Diabetes
• Low LV EF
• Multivessel CAD
71. FAME 2 Trial
• FFR < 0.8 in one or more visually stenotic coronary arteries(>50%
stenosis)
• FFR+ PCI + OMT vs OMT
• 1632 pts (2 yrs)
• Premature termination (Highly significant reduction in composite end
point at 7m).
• 68% RR reduction in PCI vs OMT (12.7% vs 4.3%) (p<0.001)
• Lower rate of urgent revascularization in PCI group.(1.6% vs11.1 %)
( p < 0.001)
N Engl J Med 2012; 367:991-100
72.
73. How was the positive result?
• No uptitration of Medical therapy in patients who were
symptomatic.
• Patients who were symptomatic were randomized to PCI without
objective evidence of ischemia or biomarker positivity.
• 52% patients underwent early revascularization.
• PATIENTS WERE NOT ON OPTIMAL MEDICAL
THERAPY
74.
75. FFR strategy
• FFR helps in stenting of lesions which are physiologically
siginificant (FFR <0.80) rather than
anatomically(>50%stenosis),thereby decreasing the new
disease which is as a result of PCI+ stenting.
76. • What is the latest advanced technology with relation to
FFR?
• What is the Trial evidence?
77. Instantaneous wave free ratio(iFR)
• Vasodilator free pressure-only measure of the hemodynamic
severity of a coronary stenosis.
• Alternative to FFR
• CLARIFY study.
• VERIFY study.
• RESOLVE study.
• Further studies needed to take on iFR as effective replacement for
FFR.
80. CABG vs Medical Therapy
CABG improves the survival rate among patients with
• High risk stable angina.
• 3V CAD
• Impaired LV function.
• Substantial LMCA stenosis.
• CASS (Coronary Artery Surgery Study)
• ECSS (European Coronary Surgery Study)
• VATS(Veterans Administration Cooperative Study)
81.
82.
83. Why CABG was superior?
• Studies were done in era of low awareness of benefit of OMT.
• No trials have been done so far in comparison of CABG with OMT
84.
85. PCI vs CABG
S.No Trial Profile No .of patients
Follow up
Result
1 EAST Mmultivessel CAD 400pts ,8 yrs No benefit of PCI
Left main disease Non significant improved
survival in CABG
2. BARI Multivessel CAD 7 yrs No difference
Diabetics Better survival rate with
CABG (76.4% vs55.7%)
3. ARTS Multivessel CAD 1,200 pts,1 -5 yrs No difference
Diabetics Increased mortality in PCI
4. ARTS 2 DES was used Similar rate of
revascularization
Multivessel CAD
J Am Coll Cardiol. 2001;38(1):143-149
86. S.No Trial Profile Follow up Result
5 BARI2D trial Type2DM+CAD
PCI or CABG vs OMT
No difference between two
groups.
Revascularization wise
greater freedom of events in
CABG group (p=0.01)
NEJM 2009;360:2503-12
87.
88. SYNTAX trial
SYN ergy between PCI with TAXus and cardiac surgery
• 3VD or LMCA
• Multivessel PTCA vs CABG
CABG PCI P value
Primary End point
Death,stroke,MI,repeat revascularization
12.3% 17.6% 0.002
Secondary end point death,stroke,MI 7.7% 7.6% 0.98
Repeat revascularization 5.9% 13.5% < 0.001
Rate of stroke 2.2% 0.6% 0.003
Circulation: Cardiovascular Interventions.2009; 2: 463-467
N Engl J Med 2009; 360:961-972
89. Class I indication for evaluation of LMCA or Multivessel
disease(ACC/AHA 2013 PCI guidelines).
• Grading of coronary anatomy on basis of
– lesion location
– Complexity
– Functional impact
• Assess patients at individual level.
• Helps in CABG vs PCI
Low score 0-22
No difference
Intermediate 23-32
No difference
High score >32
CABG was better
90.
91. STICH trial
• 1212 ICMP with reduced EF.
• 462 deaths over 56 months of follow up.
• CABG did reduce CV deaths (p=0.09).
• Sudden deaths were reduced in CABG (p=0.041).
• Fatal pump failure events (p=0.05).
• Protective effect of CABG occurred after 24 months.
• Post procedure deaths increased in CABG patients.
• Fatal MI were lower.
Conclusion:
Addition of CABG to medical therapy is beneficial
in patients with stable angina and reduced EF(ICMP)
Beneficial effects were seen after 2 years.
Panza et al,JACC 2013
92.
93.
94. • What is meant by Unprotected Left Main Disease?
• What is Left Main Equivalent?
• In what proportion of patients undergoing angiography,is
Unprotected Left main disease seen?
95. • 4% cases
Asymptomatic , non flow limiting , angiographically insignificant
disease(< than50%)
Ostial,Ostio proximal
Shaft : Mid, distal or diffuse Left main
Bifurcation lesion
Non functional CABG grafts ( eg: LIMA occlusion makes LAD
unprotected).
Left main equivalent: significant (70 percent or more) stenosis of
proximal left anterior descending (LAD) artery and proximal left
circumflex artery
96. Left main disease arm (SYNTAX trial)
CABG PCI P value
Primary outcome Same
Stroke 2.7% 0.3% 0.009
Repeat
revascularization
6.5% 11.8% 0.02
N Engl J Med 2009; 360:961-972
97. FREEDOM trial
• Diabetics with MVD
• PCI+DES vs CABG
• 1900 pts
• 29% were women
• 83% had TVD.
• Primary outcome occurred more frequently in PCI group (p=0.005).
• MI decreased in CABG group(p<0.001)
• Stroke was most common in CABG group.(p=0.03)(5.7 vs 2.4)
N Engl J Med 2012; 367:2375-238
99. TRIAL DESIGN NO. RESULT
PRECOMBAT N = 1454
Premier of
RandomizEd
COMparison of
Bypass Surgery
versus Angioplasty
Using Sirolimus-
Eluting Stent in
Patients with Left
Main Coronary
Artery Disease
Prospective
Open label
Randomized trial
First trial in UPLMD
Sirolimus stent vs
CABG
IVUS has been used. PCI with sirolimus
eluting stent appears a
potential alternative to
CABG with a
noninferior incidence
of 2-year MACCE for
patients with ULMCA
stenosis.
LE MANS 105 pts
Study of unprotected
LEft MAiN Stenting
versus bypass
surgery
Randomized
Open label
Direct stenting in PCI
Bifurcation
technique ,Initial
stent to LAD then
Cullotte or Prov T if
necessary.No crush
stenting
IVUS advised
PCI noninferior to
CABG
N Engl J Med 2011;364:1718-27
LEMANS trials, J Am Coll Cardiol 2008
103. TRIAL DESIGN NO. RESULTS
SWISS II
Swiss
Interventional
Study on Silent
Ischemia Type
II
PCI effect in patients
with silent ischemia
post MI
201 Pts
PCI vs OMT
Aspirin 100
mg/d
Statin 80 mg/d
PCI better
Less MACE (p=0.001)
Lower rates of ischemia (p=0.03)
LVEF preserved at 1 yr
DANAMI PCI or CABG vs
OMT
503 Pts
Follow up 1.2-
4.5 yrs
PCI vs CABG better
Non significant improvement in
mortality.
Less MI (p=0.03)
Less angina
(p<0.001)
OAT 2166 pts The 4-year cumulative primary event
rate was 17.2% in PCI and 15.6% in
OMT (P=0.20).
Rates of MI (fatal and nonfatal) were
7.0% and 5.3% ; (P=0.13). Rates of
nonfatal reinfarction were 6.9% and
5.0%, P=0.08); There was no
interaction between treatment effect
and any subgroup variable
JAMA, 2007 May 9;297(18):1985-91
Circulation.1997; 96: 748-755
N Engl J Med 2006; 355:2395-240
105. EECP
• The Multicenter Study of Enhanced External Counterpulsation
(MUST-EECP):
• 139 pts
• EECP vs OMT
• Exercise duration increased in both groups, (p < 0.3).
• Time to >1-mm ST-segment depression increased significantly from
baseline in active CP compared with inactive CP (p < 0.01).
• More active-CP patients saw a decrease and fewer experienced an
increase in angina episodes as compared with inactive-CP patients (p
< 0.05).
• Nitroglycerin usage decreased in active CP but did not change in the
inactive-CP group. The between-group difference was not significant
(p = 0.7).
EECP reduces angina and extends time to exercise-induced
ischemia in patients with symptomatic CAD.
Treatment was relatively well tolerated and free of limiting
side effects in most patients.
J Am Coll Cardiol. 1999;33(7):1833-1840
107. EXCEL trial
• Abott cardiovascular systems
• XIENCE PRIME or XIENCE V vs CABG in left main disease.
Inclusion criteria :
• Unprotected left main coronary artery (ULMCA) disease with
angiographic diameter stenosis (DS) ≥70% requiring
revascularization, or
• Main Equivalent Disease
• Silent ischemia, stable angina, unstable angina or recent MI.
http://www.invasivecardiology.com/issue/4148
108. Angiographic exclusion criteria:
• Left main diameter stenosis <50%
• SYNTAX score ≥33
• Left main reference vessel diameter <2.25 mm or >4.25 mm.
• Results yet to be published.. Dec 2016
111. Conclusions
• OMT is essential in all patients with stable angina.
• In patients with Diabetes,TVD – CABG >PCI.
• PCI+DES > PCI +BMS with relation to restenosis.
• In left main, PCI+DES = CABG > OMT.
• Asymptomatic Post MI pts. OMT = PCI or CABG.
112. • CABG – mortality benefit, morbidity benefit, less target
vessel revascularization,increased risk of stroke.
• PCI - improved quality of life, less angina, but increased
revascularization,restenosis,mortality.
• SYNTAX SCORE > 33 – CABG.
113. The appearance of a disease is swift as an
arrow; its disappearance slow, like a thread.
When a disease relapses there is no cure.
---Chinese proverb